The article uses correlation quantitative research as the method for research. The method uses two variables to test or determine their relationship to the topic of the research. The use of this method exposes the outcome of the research to risks associated with biasness, manipulation, and control. The use of this article by nurses in their practices would have the risks associated with having negative outcomes of the practices and the majority of their patients developing more complicated issues.
The method used is subject to manipulation and biases during the research and cannot achieve the required outcomes. This is due to the use of the variable that may have a little relationship and thus the research may have to false the research outcomes (Anthony & Jack, 2009). This causes the outcomes or the reached findings to be unreliable for use. For instance, in the article, the strong correlations were noted among depression, sleep, and fatigue (Crane, 2005). However, the research indicated that only 32.7% of the women exposed to sleep and depression suffer from myocardial infarction.
The findings indicate that majority of the women meet the minimal kilocalories required per week to prevent myocardial infarction (Crane, 2005). These findings though they have their recommendations, may not be fully reliable as they may have some contradicting issues between the variables.
To avoid these risks; the research method needs to be elaborative and has different approaches. The use of experimental research would have reliable findings, as the methods used to sample out the data are generally better than for correlation (Anthony & Jack, 2009). The method has low risks of biasness, control, and manipulation as it involves randomization of samples that make every sample in the population to have a given probability.
References
Anthony, S. & Jack, S. (2009). Qualitative case study methodology in nursing research: An integrative review. Journal on Advanced Nursing, 65(6):1171-81.
Crane, P. (2005). Fatigue and physical activity in older women after myocardial infarction. Heart & Lung, 34(1), 30-37.
Myocardial Infarction is a disease of the heart that is caused by occlusions in the coronary arteries. The circulation of blood through the ventricles is reduced and the capacity of the heart to absorb oxygen is diminished. Artherosclerosis is mainly implicated with myocardial infarction.
MI is primarily evaluated using the ECG readings in which the ST-segment is usually elevated. By, analyzing the morphology of the ECG inconjuction with other tests, the condition can be correctly evaluated. The coronary occlusions can be dissolved using thrombolytic therapy.
In this case study, the close collaboration between nursing and other interventions illustrates the clinical procedure for handling patients with myocardial infarction in a hospital setting. It also gives insight into the complications of MI that may occur in a patient together with the necessary interventions from the nursing staff. The study questions are answered sequentially as follows;
Mr. Jones gradually developed symptoms of myocardial infarction. He started by experiencing excruciating chest pain that radiated to his jaw and left arm, shortness of breath (dyspnea) and diaphoresis (sweating), which culminated in sudden unconsciousness (syncope). These are the typical signs and symptoms of myocardial infarction.
They do not present immediately but gradually. The classic symptom of myocardial infaction is usually chest pains, which radiate to other parts of the body such as the left and right arms, lower jaw, neck, back, and the epigastrium, which resemble the heartburn.
Often, MIs are caused by accumulation of atherosclerotic plaque, which stimulates the forming of intracoronary thrombus. Intracoronary thrombus results in the occlusion of the coronary artery. This gives rise to insufficient circulation of blood through the ventricles hence myocardial infarction. The level of occlusion determines the severity of MI (Cotran, Kumar & Robbins, 1994).
Many other conditions that are uncommon can cause the coronary artery to block and thereby cause a myocardial infarction. They include rare inflammation of coronary arteries, a blood clot in another place of the body other than the ventricle e.g., in the heart chamber, a wound near the heart through a stab, the spasmal effects of taking cocaine on the coronary artery, and complications arising from heart surgery and/ or another rare heart conditions.
An ECG is performed to compare cardiac activities in the ventricular areas. The ST segment elevation is used to indicate on the ECG. Mr. Jones ECG signal indicated that there was an ST-segment elevation in leads II, III, and aVf on the ECG, which is indicative of MI. however, the ECG alone cannot be used to reliably diagnose myocardial infarction. It should be noted that the ECG also evaluates other heart conditions.
Consequently, the morphology and the principal components of the signal may give contradictory diagnosis. For instance, myocardial infarction is evaluated by observing the characteristics of the ST segmement. An elevation of the segment is indicative of possible myocardial infarction. However, the ST segment elevation is also indicative of the inherited type of cardiac arrhythmia called Brugada Syndrome. Consequently, other tests are necessary including laboratory tests, urine and blood sample analysis etc..
Cardiac enzymes are used as biomarkers that are evaluated to determine the heart function. There are particularly useful in evaluation of myocardial infaction although they are essential in assessment of other conditions that may lead to increment in cardiac biomarker level (Rao, Miller, Rosenbaum, & Lakier, 1999).
Cardiac enzymes such as creatine kinase-MB are ordered when the severity of myocardial infarction needs to be determined. The level of cardiac proteins in the blood corresponds to the severity of the myocardial infarction in the patient. Therefore, by determining these enzymes it makes the work of risk stratification of patients with myocardial infarction easier.
Once admitted to the CCU, It is the prerogative of the nurses to measure the blood pressure, changes in the heart and respiratory rates related to the physical examination of the patient. The most common examination performed on patients with suspected myocardial infarction is an ECG, which often indicates the presence of abnormalities in the left ventricle. In addition, laboratory tests of blood proteins related to the heart is performed to indicate if degeneration of myocardial cells is present.
MI results in diminished supply of oxygen to the heart due to the degeneration of cardiac cells. Consequently, the capacity of the heart to extract oxygen from blood may be compromised. The significance of using oxygen to make sure that the red blood cells are saturated maximally to compensate for the hearts diminished ability to extract the oxygen.
Mr. Jones oxygen demands clearly outstripped supply oxygen dosage ameliorated the situation before comprehensive diagnosis and treatment ensued (Cotran, Kumar & Robbins, 1994). Administration of oxygen supplements treatment of patients with MI. Mr. Jones had shortness of breath and an episode of syncope. As treatment ensued, his oxygen supply had to be stabilized through administration of supplemental oxygen.
Myocardial infarction may give rise to other cardiac conditions that may need proper medical attention. Such conditions include the Wenckebach (Type 1) and Type 2 disarrhythmias. Wenckebach or Type I block is an intermittent cardiac conduction failure. In Wenckeback, conduction reduces as conduction velocity progressively reduces until failure of cardiac electrical conduction occurs. The ECG pattern of the condition shows the PR interval getting progressively longer until the non-conducted wave occurs.
Thrombolytic therapy initiates cardiac hemorrhage in patients with myocardial infaction. It is initiated to dissolve the coronary clots thereby easing the flow of blood and supply of oxygen to the heart. However, this therapy is not suitable in certain conditions such as recent surgery, stroke in the recent past, high blood pressure e.t.c.
The thrombolytic drugs are known to cause hemorrhage elsewhere in the body that can be life threatening in scenarios where a patient underwent surgery recently or is hypertension is present. In the case of Mr. Jones, he became unconscious as soon as he arrived at the reception. In addition, he had very high pressure at 130/92, which made it inappropriate to initiate thrombolytic therapy (Marcus, et al, 2007).
Myocardial infarction is associated with complications such as angina, free wall rupture, reinfarction, extension of infarct, heart failure, aneurysms, cardiogenic shock, valve dysfunction, arrhythmias, central nervous system (CNS) or peripheral embolisation, pericarditis, and psychosocial complications. Mr. Jones developed arrhythmias which were corrected by administration of drugs.
The ECG is the common procedure for diagnosis of myocardial infarctions. However, other diagnostic tests can be carried out on Mr. Jones. They include blood and urine tests, swabs, diagnostic and lab tests, and pathology testing. Pathology testing is important as myocardial infarction could have been caused by a certain underlying pathogen. These tests are performed in order to confirm presence of myocardial infarction because an ECG cannot provide a comprehensive assessment of the condition.
References
Cotran R., Kumar V. & Robbins S. (1994). Robbins Pathologic Basis of Disease. 5th Ed. Philadelphia, PL: WB Saunders Press.
Marcus, et al. (2007). The utility of gestures in patients with chest discomfort American Journal of Medicine, 120(1), 839.
Rao P., Miller S., Rosenbaum R., & Lakier J. (1999). Cardiac troponin I and cardiac enzymes after electrophysiologic studies, ablations, and defibrillator implantations. American Journal of Cardiology, 84(4), 470.
Myocardial infarction is a very serious medical issue and it needs to be treated as soon as possible. Every nurse should have the knowledge about this condition and should know how to treat a patient who is suffering from this condition. According to the Australian Bureau of statistics Ischaemic heart disease was top leading cause of death in Australia in 2017 and heart failure was number thirteen cause of death for men and number eleven for women in Australia (Australian bureau of statistics, 2018). This essay will discuss and analyse the pathophysiology of Myocardial infarction. Fist it will go through pathophysiology of ST-Elevation Myocardial Infarction, then symptoms of this condition and pathophysiology of the symptoms to analyse reasons that patient have those symptoms.
In myocardial infarction one or more than one parts of myocardium can be permanently damaged as a result of low oxygen supply because coronary arteries are blocked and they cannot transfer enough blood to cardiac muscles and myocardium cells start to die which is known as necrosis (Farrell, 2017). One of the biggest contributors to myocardial infarction is atherosclerosis and there are lots of evidence to suggest that high concentration of low density lipoproteins (LDL) in blood can start and help atherosclerosis to progress (Lu & Daugherty, 2015). First the process starts with a damage in endothelial layer, then it transfers LDL from blood into tunica intima and LDL become oxidised LDL, after that endothelial cells discharge a protein named monocyte chemoattractant protein which is responsible for bringing monocytes to the site of injury and after monocytes enter the intima they turn to macrophages. Macrophages try to fight ox-LDL and after ingesting them they eventually become foam cells. These new foam cells discharge more chemokines and monocyte chemoattractant protein forces SMCs to come into intima, then platelet-derived growth factor is secreted by Foam cells, SMCs and macrophages. Then foam cells and macrophages release Interleukin IL-12 which causes T cells to be activated and it is a contributor to plaque growth, then interferon IFN-γ is discharged by T cells and then they bring more macrophages into intima and the process repeats itself which starts to build up plaque and eventually cause atherosclerosis (Hao & Friedman , 2014). Thrombus generation at the site of plaque rupture is effected by local flow disturbances, plaque vulnerability and systematic thrombotic propensity involving platelets hyperactivity, inflammation and blood vulnerability. Platelets adhesion is initiated by binding of glycoprotein Ib-V-IX receptor to Von Willebrand factor (vWF) glycoprotein receptor binds to collagen. After adhesion platelets form monolayer at the site of rupture, they release two agonists thromboxane A ( TxA2 ) and adenosine diphosphate (ADP). These two receptors play a role in in platelets activation and activation of GPIIb/IIIa receptors. Thrombus is formed when activated GPIIb/IIIa receptors bind between platelets through fibrinogen. Thrombin promotes more platelets activation and the formation of procoagulant platelet surface and larger amounts of thrombin created. At the end thrombin converts fibrinogen to fibrin and as a result a fibrin network and platelet fibrin clot is formed (Waksman et al, .2014). Then fatty tissues and thrombus make coronary arteries narrow and interrupts blood flow to cardiac cells, if doctors do not address this issue as soon as possible myocardial cell start to die as a result of low oxygen and the body does not have the balance for oxygen supply and demand anymore (Montecucco et al., 2016).
Myocardial infarction has many symptoms including angina, diaphoresis and, nausea, shortness of breath, elevated cardiac troponin and creatine (Jevon, 2012). All these symptoms have pathophysiology explanations and they will be analysed one by one.
Angina is usually a severe pain in the chest which can radiate to neck, jaw and left arm. It can come from Ischaemic or coronary diseases and it could be a sign of myocardial infarction (Wolters Kluwer Health, 2014). Angina is a visceral pain and visceral pain is caused by autonomic nervous system. During a cardiac pain afferent sympathetic nerve activity is affected by adenosine which is responsible for signalling pain from heart to brain. Afferent sympathetic neurones pass from myocardium to superior cardiac plexus, then they go through sympathetic ganglion chain to the dorsal horn of the spinal cord. After that they connect to neurons in Lamina I and V. it is possible that this is the point at which signals occurs between somatic and visceral afferent pathways and because cardiac sympathetic plexi, spinal cord and ganglion chain have many connections angina pain can be felt in many parts of upper body (Leach & Fisher , 2013).
The second symptom of MI is diaphoresis which means excessive sweating. There are two possible reasons for excessive sweating in MI. The first reason is sympathetic nervous system starts to stimulate and produces sweating to protect the body from pain, but this explanation does not explain the absence of sweating in other painful diseases such as trauma, burn. The second explanation is activation of the sympathetic nervous system because of hypotension which has caused by acute MI (Gokhroo et al., 2015).
Another symptom is nausea and there are two explanations for nausea in patients with myocardial infarction. The first possible reason could be injured and necrotic cardiomyocytes discharge metabolites such as pyruvic acid and lactic acid, then these metabolites stimulate autonomic nerve peripheral receptors and it causes nausea. The second explanation is reduced function of heart as a result of myocardial necrosis and occlusion of coronary arteries which can trigger Bezold-Jarisch reflex and can cause nausea (Guo et al., 2015).
One of the most important symptom is shortness of breath and it happens because when cardiac cells die and coronary arteries are occluded the body needs more oxygen and heart cannot give enough oxygen to the body , the heart receives the a signal to increase rate of breathing because oxygen demand is more than oxygen supply (Berliner et al, 2016).
Another symptom of myocardial infarction is increases level of troponin which is responsible for cardiac cells contraction. When the cardiac cells start to die, they release troponin into blood stream and it causes the troponin to elevate (Popp, 2013). Creatine also is another enzyme that exists in heart muscles and skeletal muscles and body releases creatine after infarction to blood stream (Mythili & Malathi, 2015).
So, myocardial infarction pathophysiology and symptoms of this condition have been explained. The mortality rate of MI keeps declining because of advancement in medical therapy.
References
Australian bureau of statistics. (2018), Causes of Death, Australia, 2017 https://www.abs.gov.au/ausstats/abs@.nsf/Lookup/by%20Subject/3303.0~2017~Main%20Features~Australia’s%20leading%20causes%20of%20death,%202017~2
Farrell, M. (2017). Smeltzer and Bare’s textbook of medical – surgical nursing. Wolters Kluwer.
Lu , H. , & Daugherty , A. (2015) . Atherosclerosis, 35 (3) , 485-491. https://www.ahajournals.org/doi/pdf/10.1161%2FATVBAHA.115.305380
Hao, W., & Friedman, A. (2014). The LDL-HDL Profile Determines the Risk of Atherosclerosis: A Mathematical Model, 9(3): e90497. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0090497
Montecucco, F. Carbone, F.Schindler, T, (2016). Pathophysiology of ST-segment elevation myocardial infarction: novel mechanisms and treatments. Volume 37, Issue 16, 21 April 2016, Pages 1268–1283, https://doi.org/10.1093/eurheartj/ehv592
Waksman, R. Gurbel, P. Gagila, M. (2014). Antiplatelet therapy in cardiovascular disease. Wiley Blackwell
Jevon, P. (2012). Angina and heart attack. Oxford university press. https://ebookcentral.proquest.com/lib/rmit/reader.action?docID=975545
Leach, A. Fisher, M. (2013). Myocardial ischaemia and cardiac pain – a mysterious relationship. 7(1) , 23–30. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4590151/
Gokhroo, R., Ranwa, B., Kishor, K., Priti, K., Ananthraj, A. Gupta, S., Bisht, D. (2015).
Sweating: A Specific Predictor of ST-Segment Elevation Myocardial Infarction Among the Symptoms of Acute Coronary Syndrome: Sweating In Myocardial Infarction (SWIMI) Study Group. 39, 2, 90–95. https://onlinelibrary.wiley.com/doi/pdf/10.1002/clc.22498
Guo, Z., Yang, X., Chen, M., Liu, J., Li, X., Zhang, Y. (2015). Impact of Cardiogenic Vomiting in Patients with STEMI: A Study from China. 21. 3792–3797. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4674008/
Berliner, D., Schneider, N., Welte, T., Bauersachs, J. (2016). 113(49): 834–845. https://dx.doi.org/10.3238%2Farztebl.2016.0834
Popp, R. (2013). Troponin: Messenger or Actor? Journal of the American College of Cardiology, 61, 611-614. https://doi.org/10.1016/j.jacc.2012.11.024
Mythili, S., Malathi, N. (2015). Diagnostic markers of acute myocardial infarction. 3(6): 743–748. https://doi.org/10.3892/br.2015.500
Zipes, D., Libby, P., Bonow, R., Mann, D., Tomasseli, G., (2019).Braunwald’s Heart Disease. A textbook of cardiovascular medicine (11th ed.). Elsevier
First of all, there are many things or as we called it as factors that may lead to increase the possibility of having this specific disease in real for the person, by ding it or using it.
First, alcohol using or consuming: it is actually one of the main causes that increasing the possibility of having this specific disease in real for the person comparing to the others factors so, people who are drinking alcohol the chances of having this specific disease in real for the person will be increased for them comparing to who do not drink alcohol. The main reason for that done is by increasing the level of low-density lipoproteins in the blood circulatory that is then will affect the morbidity and mortality of the patient which also increase the occurring of thrombosis, increasing the amounts of triglycerides, blood pressure, heart rate and all these increasing amounts will cause atrial fibrillation and anoxia which there will lowering the ability of the muscles of the heart to do its work so producing then this specific disease in real for the person.
Second, smoking is another factor that is actually increase the happening of producing this specific disease in real for the person percentage. The main reason for that is the smoking factor does is by increasing the amounts of LDL cholesterol which is actually bad for the body the main reason for that is having high amounts of lipids instead of proteins which is actually needed by the body and also having high amounts of triglycerides which then as result will decrease the amounts of HDL cholesterol which is normally has the high amounts of proteins that is useful for the body.
Third, hypertension which is actually the increasing will be for the two parts of hypertension measurements which are systolic and diastolic which then increase the blood pressure of patient in a high way which then as a result will increase the possibility of having this specific disease in real for the person though especially in patient who are suffering from hypertension when they are in their older ages. The main reason for that is having hypertension is actually increase the possibility of having or suffering from atherosclerosis which the as a result will cause producing this specific disease in real for the person.
Fourth, obesity or BMI or what we called it as body mass index is actually cause the producing of this specific disease in real for the person where the lipids around the whole body and there is specifically two types of it which are obesity in the upper part of the body and the another type is lower part when it is accumulated the blood vessels actually the demand blood and oxygen needed by the heart does not reach the heart which then as a result having the weakness of the heart muscles which then the person will suffer from this specific disease in real for the person.
Fifth, diabetes mellites which has the abbreviation and what we called it as DM and it is mainly has many types, but there are specifically two types that cause and help suffering from this specific disease in real for the person. The main reason of this disease is actually the pancreatic part of the body is unable to produce the main thing to maintain the level of sugar in the body which is insulin as a result specifically type two diabetes which we called it as non-insulin dependent diabetes mellitus people who actually have this type of DM they will suffer from MI or what we called it as myocardial infarction which may be in its acute form.
Finally, the history of the family and it is actually may increase the chance of having this specific disease in real for the person and the main reason for that is actually the genetic information that transformed to the person from his or her parents.
The pathophysiology of the discussed disease already which that is actually explaining how the patient getting in this disease, there are many ways and now we will starting with patients have atherosclerosis in their blood circulatory system which then will cause a gradual obstruction to the wall of the blood vessels of the coronary artery of the heart and as a result the patients will have the ischemia where this part of the heart does not have enough amount of blood and energy which is actually required for that pat to does its work so now there is no lots of hemoglobin and heme in the blood which is actually the main one to carry the oxygen to the tissues and cells of the organ. Also, if the patient is suffering from arterial spasm or what we called it as closure of the vessel so the blood cannot pass through which is actually a sudden reversible obstruction which then causes ischemia which means low amounts of blood reach a specific part of the organ which then will cause low passage of the oxygen which is normally needed by the organ to wok which then will cause angina and increasing the possibility of having thrombolysis which is mainly the one that is increased having the disease which is called unstable angina and this disease is acute and need to be treated in the hospital. Finally, the presence of three types of accumulated the lipids at once which then actually increases the risk of having this specific disease in real for the person to happen which are atherosclerosis, plaque split and thrombus which are sudden and usually irreversible which makes them more risky and occlusion is already occurred to the blood vessels which then causes ischemia and hypoxia to the organ and the presence of permanent thrombus because their actions are irreversible which as a result enhancing necrosis to happen which means the death of that organ because of low amount of oxygen is present and finally enhancing the presence of this specific in real for the person.
The diagnosis can be done by doing one of these three to determine the suffering of this specific disease in real for the person and let us start with the usual clinical features that are done the physician so, if the doctor observed that the patient has these symptoms such as chest pain, shock, low grade fever which is less than normal, having indigestion where the patient actually suffering from difficulties in digesting the foods. The second diagnosis can be done for the patient is by checking the serum cardiac markers which are actually enzymes by determining their levels in the serum of the body such as creatinine phosphokinase where we also called it as (CK) as an abbreviation also lactic dehydrogenase where we called it as (LDH) and finally we use the cardiac specific troponins where we can called it also as (cTn). The final way that we use to diagnosis patient with this specific disease is by checking the ECG changes by checking the wave of the ECG such as ST segment if there is an elevated in its level, the person will may have this specific disease in real for the person, also checking T wave inversion and finally the appearance of huge and deep Q waves.
The treatments that mainly used for this specific disease when in it is observed on the patient are many such as thrombolytic drugs, antihypertensive drugs sch as beta blockers, ACE inhibitors and vasodilators. Also, lipids lowering drugs, antiplatelet and anticoagulant drugs.
First of all we have to know about heart, heart is a fist-sized muscular organ that is located in the center of the chest behind sternum slightly titled to the left, it is basically double pump, it provides the force needed to circulate the blood through the two major circulatory systems and it is composed of four chambers (two thin walled blood receiving, the atria and two thick walled blood pumping, the ventricles). Myocardial infarction (acute myocardial infarction or MI) is a serious medical emergency in which blood flow to the heart is abruptly and completely blocked in coronary artery, ordinarily by atherosclerosis (plaque) which it is accumulation of fats, cholesterol, white blood cell ,calcium and other substances then it will become blood clot. When an individual having an acute myocardial infarction (MI) has abrupt chest pain that is felt behind the sternum and sometimes travels to the left side of the neck or left arm, more over the person may have sweating, vomiting, shortness of breath, nausea, anxiety, heartbeats, vomiting, fatigue and weakness. These symptoms are partially different in women because women experience fewer symptoms than men, however in some cases the person does not have chest pain, shortness of breath, sweating or other symptoms, these cases are called (silent) myocardial infarctions case. Most important risk factors to this disease are obesity, high blood pressure, elder age, lack of physical activity, previous cardiovascular disease, both type of diabetes, tobacco smoking, excessive of drinking alcohol, high levels of certain types of lipid in blood such as (triglycerides, low-density lipoprotein (LDL) cholesterol and other types of cholesterol), low levels of high density lipoprotein (HDL) cholesterol in blood, the use of amphetamines and cocaine and stressful, one of the most important risk factor is diabetes which it is an abnormality, body could not produce or could not response to the insulin hormone, it leads to hyperglycemia. The main way to determine if a person has had myocardial infraction (the investigations to diagnosis MI) are using echocardiogram (which it is ultrasound to provide moving picture on heart and vessels) and ECG (it is a simple test that is used to detect electrical signals produced by heart, also we can determine it by testing blood for substances that damaged heart muscle released it, common blood tests to diagnosis (MI) are both type of troponin (troponin I and troponin T) and creatine kinase (CK-MB). Let’s move on to the treatments of myocardial infarction, treatments for myocardial infarction are percutaneous coronary intervention also known as angioplasty which it is opening blocked blood vessels especially coronary artery to restore normal blood flow to heart by using balloon through a catheter (long thin tube) through a small puncture of arm or leg artery to blocked artery of the heart, also we can do thrombolysis also known as fibrinolytic therapy which it is the process of dissolution of blood clot by medications such as the (anistreplase, reteplase and streptokinase…..), immediate treatments for suspected myocardial infarction includes aspirin which it prevents further blood from clotting, sometime nitroglycerin and other pain medication is used to treat chest pain and also sometime doctors use oxygen supplement, in a case if the person has diabetes we can treat him or her by coronary bypass surgery Also known as coronary artery Bypass graft (CABG) surgery, it is a surgical process that surgeon uses another blood vessels from other area of your body to bypass damaged blood arteries in order to restore normal blood flow to your heart.
Outline:
tiredness after surviving myocardial infarction
ischemic heart disease
patients with diabetes and cardiovascular disease
Why some patients sometime complaining of tired after surviving myocardial infraction?
Some patients feels tired after surviving myocardial infarction because when Myocardium is damaged and prevented from having oxygenated blood flow during a myocardial infarction, scar tissue is formed on the damaged myocardium, it leads to reduce efficiency of pumping blood in the affected area (cardiac output reduced), it means blood flow in the body reduced too and it causes reducing supply of oxygen as well as nutrient in all of the body also wash out of metabolic waste reduced so it is why tiredness and fatigue produced and the level of this tiredness is depending on the location and size of the scar tissue. Like Dr. Pia alsen, Author of the study, observed:
“Many people experienced the tiredness as different and new, not related to physical effort, daily activity or a lack of rest; it occurred unpredictably and may not attributed to definite cause”
Sometime some medication that you are taking for the disease of the heart can also cause Tiredness , such as the statin drugs (which they are most common for cholesterol-lowering drugs, statin also known as lipid-lowering medicine and it reduces the illness and mortality in the person who are at high risk of cardiovascular disease , example of statin Crestor and Lipitor….) and beta blockers could make you feel tired (beta blockers are a group of drug also known as beta-adrenergic blocking agents, and it is used to reduction of high blood pressure, manage abnormal heart rhythms and to protect the heart from a second heart attack after a first heart attack, example of beta blockers atenolol and betaxolol…..etc.), it is important to know that tiredness can also be found in depression, iron deficiency, thyroid and other medical conditions. It is possible to have both heart disease and second condition that is also contributing to your tiredness. So every survivors of myocardial infarction need doctor’s advice for lifestyle because they will be tired even by taking shower.
What is ischemic heart disease and what is pathophysiology of ischemic heart disease?
Ischemia is define as inadequate blood supply (circulation) to a local place due to blockage of blood vessels supplying to that place, Ischemic heart disease which also known as coronary heart disease (CHD), it causes the loss of oxygen and nutrients to myocardial tissue (imbalance between supply of oxygen and demand of oxygen to the myocardium) because of poor coronary blood flow(because of narrowed coronary artery) and the metabolic waste product accumulates is myocardium, this disease is nearly epidemic in the western world. About 250,000 people a year die in the United States because of ischemic heart disease without being hospitalized. It is more prevalent in white and elderly age. But how it happens? Atherosclerosis is the most common cause of ischemic heart disease (CHD). Atherosclerosis is known as fibrous fatty plaque which it is accumulations of fatty (especially LDL cholesterol), fibrous cap (collagen and smooth muscle), foam cells (macrophages, smooth muscle) which they are necrosis because of keep engulfing LDL cholesterol , possibly including calcium deposits and endothelium covers all of it, gradually narrow the coronary artery lumens, which reduces the volume of blood that can flow through them. This can lead to myocardial infarction (a temporary deficiency of blood flow to the heart) and eventually necrosis (heart tissue death). Atherosclerosis has two types (stable plaque and unstable plaque) the difference is in the proportion of the structure, stable plaque has [ fibrous cap which it is thick, less foam cells (macrophages and large smooth muscles containing LDL cholesterol) and less extracellular fat] it has less chance to rupture so it is why it is called stable plaque, in opposite unstable plaque has [ fibrous cap which it is thin, less foam cells (macrophages and large smooth muscles containing LDL cholesterol) and more extracellular fat] because of thin fibrous cap this type is unstable and has more chance to rupture and create blood clot. When endothelium with basement membrane have been damaged because of hypertension (high blood pressure), stress and any toxic material such as nicotine from smoking…. plaque material are really thrombogenic so because of the primary homeostasis , a lots of platelets attaches to the collagen and accumulates with red blood cells then coagulation cascade has been activated and secondary homeostasis will initiate, it stimulates more platelet to accumulates and fibrin clot formed, so blood clot formed and coronary artery blocked. Most people with 70% luminal obstruction do not experience the limitation of the blood flow and symptoms of ischemic heart disease while they are at rest, It occurs when the oxygen demand increases (usually during emotional stress and exercise), but people with 90% luminal obstruction can experience the limitation of blood flow and the symptoms of it at any situation even during rest. We should be aware of that most cases of ischemic heart disease involves left ventricle, a few cases of ischemic heart disease involves right ventricle, this difference refers to the properties of left ventricle and right ventricle, left ventricle has 1.5 thickness, high tension and its pressure is about 0-120 millimeter mercury so it needs more oxygen but right ventricle has 0.3 to 0.5 thickness, low tension and its pressure is about 0-25 millimeter mercury so it needs less oxygen. Ischemic heart disease has four types (myocardial infarction, stable angina, cardiac sudden death, unstable angina). Genes implicated with ischemic heart disease, Overwhelming evidence confirms a genetic link to ischemic heart disease (CHD). Researchers have identified more than 250 genes that may play a role in ischemic heart disease, ischemic heart disease commonly results from combined effects of multiple genes. These effects make the genetics of Ischemic heart disease very complicated because many genes can influence a person’s risk. Some of the most important genes linked to ischemic heart disease include [low density lipoprotein (A protein that removes LDL from blood stream, a mutation in this Gene is responsible for familial hypercholesterolemia ), apolipoprotein E, apolipoprotein B and apolipoprotein A…..etc.]. Treatment of ischemic heart disease is near to the treatment of myocardial infarction, but it Focus more on 3 goals (reducing myocardial oxygen demand, increasing the oxygen supply, alleviating pain), also controlling modifiable risk factors is really important. Interventions may be non-invasive or invasive.
How patients with diabetic mellitus present?
Diabetes is an important risk factor and major cause of cardiovascular disease and development of coronary artery disease, unfortunately patients with diabetes suffer more from an excess coronary artery disease and patients with diabetes mellitus present in as many as 30% of patients hospitalized with acute myocardial infarction. Mortality rate in the patients with diabetic in acute myocardial infarction was reported to be very high and at least double the mortality rate in the patients without diabetes, despite improvement of the treatment of acute myocardial infarction, the mortality rate of the patients with diabetes is still double compare with patients without diabetes. After adaptation of the size of infarction (injury), patients with diabetes have more chance to have a congestive heart failure than patients without diabetes. Diabetes leads to hyperglycemia which it associates with obesity, hypertension, and dyslipidemia and diabetes is an important factor to increase atherosclerosis plaque formation and thrombosis, the pathophysiology of vascular damage in diabetes is complex and involves abnormalities in endothelial cells, vascular smooth muscle cells, and platelet function, As a result of all these pathological changes, the development of atherosclerotic, patients with diabetes appear to have a greater number of ruptured plaques, plaques in people with diabetes is a complex progressive process, characterized by early vascular inflammation and endothelial dysfunction, leading to monocyte recruitment and subsequent formation of fatty streaks. Over the years, this leads to atherosclerotic plaques that in a pro inflammatory and pro-thrombotic context become unstable and prone to rupture. The choice of the most appropriate (glucose-lowering medications) will help the physicians to reduce the excess of cardiovascular risk in diabetic patients.
Patients with diabetes have higher levels of triglycerides and very low density lipoprotein cholesterol (VLDL) and lower levels of high density lipoprotein cholesterol (LDL) than do patients without diabetes, patients with diabetes have high levels of plasma protein and increase it red cell aggregation and possibly decrease red cell deformability, induced platelet aggregation have been shown to be higher in patients with diabetes than in patients without diabetes, plasma fibrinogen levels are elevated in diabetic patients and have been shown to correlate with myocardial infarction and sudden death in diabetic men because of the rapid formation of blood clot, factor VIII and factor VIII ristocetin cofactor are elevated in diabetic patients, fibrinopeptide A in thrombin may also be elevated in diabetic patients, also because of the deficient production of prostacyclin, endothelial dysfunction or damage is more in patients with diabetes and preventing a normal repair of ongoing endothelial damage, that is why mortality rate by myocardial infarction is double in patients with diabetes compare patients without diabetes. Screening for Coronary Artery Disease in Diabetic Patients, Coronary artery disease (CAD) is often asymptomatic in diabetic patients, and up to sixty percent of myocardial infarctions may be clinically silent and detected only by systematic electrocardiogram screening, these patients often experience atypical symptoms of ischemia such as fatigue or shortness of breath during physical activity in the absence of typical chest pain.
Conclusion
Myocardial infarction or heart attack is an irreversible damage of myocardial tissue caused by lack of oxygenated blood due to atherosclerosis and blood clot in coronary artery, then myocardial tissue may become necrosis. Because of the physiological changes of the heart after myocardial infarction, the person that survived from myocardial infarction has unidentified and unexperienced tiredness (fatigue), and they have never been tired like that, the level of tiredness is depending on the location and size of damaged myocardial tissue. Ischemic heart disease that is known as coronary artery disease is a situation that blood flow has been reduced to the myocardial tissue and it leads to imbalance between oxygen supply and oxygen demand, it has many reason but most important and most common cause is atherosclerosis which it is accumulation of fat, macrophages, smooth muscle and calcium…..etc. So because of the atherosclerosis the coronary artery narrowed and blood flow has been reduced to that specific area of myocardial tissue. Patients with diabetes are at high risk to die by myocardial infarction (MI) due to physiological changes that occurs inside diabetic patients, they have a lots of unstable atherosclerosis plaque and so they will rupture at any time, it is why patients with diabetes need more screening.
In this essay, I will be discussing the different cellular/tissue engineering methods that could be implemented as a treatment strategy for the patient’s many conditions, while explaining why using these treatment strategies will be beneficial to the patient.
One of the patient’s conditions is hypertension (high blood pressure) caused when the pumping of blood around the body and the resistance measure of blood flow in blood vessels is affected with a blood pressure reading measured above 140/90 mmHg (High blood pressure (hypertension), 2019). The impact of having persistent blood pressure causes continuous stress on blood vessels impacting other organs such as the brain and kidneys and their function, increasing the risk of other health conditions such as heart attacks (myocardial infarctions) (High blood pressure (hypertension), 2019). The treatment of hypertension involves the use of various medications such as ACE inhibitors that help to reduce blood pressure through the relaxation of the blood vessels (High blood pressure (hypertension) – Treatment, 2019). Calcium channel blockers help to reduce blood pressure through the widening of blood vessels (High blood pressure (hypertension) – Treatment, 2019). Even with several different treatments available to treat hypertension, there are many side effects through prolonged use like headaches and dizziness and tiredness (High blood pressure (hypertension) – Treatment, 2019).
Another of the patient’s condition was having two myocardial infarctions (heart attack) caused by a blockage preventing the supply of blood to the heart, causing severe damage to surrounding heart muscles (Heart attack, 2019). One potential complication of having a myocardial infarction is it can affect other areas of the body, with a reduced supply of blood, preventing the maintenance of other cellular functions (known as a cardiogenic shock) (Heart attack, 2019). Many other potential complications that can arise from having a myocardial infarction is both serious and potentially life-threatening; these complications include arrhythmia are abnormal heartbeats, in which the beating of the heart rapidly increases before stopping leading to cardiac arrest, another is the rupturing of the heart, in which all the muscles, wall and valves of the heart are torn apart (Heart attack, 2019). All these complications can rapidly occur and can often lead to the death of the patient (Heart attack, 2019).
After a myocardial infarction, the types of treatment used is dependent on the severity; medication used is to dissolve any blood clots present, with surgery used to restore blood flow to the heart (treatments for heart attack, 2019). One procedure used is a coronary artery bypass graft, which involves using a blood vessel from another area of the patient’s body such as an arm or leg and is then attached to the coronary artery, to direct blood flow around the arteries, improving blood flow and the amount of oxygen supplied to the heart (treatments for heart attack, 2019).
The final condition of the patient is non-insulin dependent diabetes (type II diabetes) in which glucose levels in the blood continuously builds up; insulin is a hormone produced by the pancreas and is released after eating, helping with transporting glucose from the blood into cells around the body to be used for energy (What You Need to Know About Type 2 Diabetes, 2019). In type II diabetes, the body begins to display resistance to insulin isn’t efficiently used, causing stress on the pancreas as a higher level of insulin is required to help with the uptake of glucose; eventually leads to further damage to the cells of the pancreas, as an insufficient level of glucose can affect many cells and the maintenance of cellular functions (What You Need to Know About Type 2 Diabetes, 2019).
Some symptoms of type II diabetes commonly identified are constantly feeling hunger and a dry mouth, excessive thirst, a lack of energy and fatigue (What You Need to Know About Type 2 Diabetes, 2019).
Type II diabetes can be controlled through dietary changes by including foods with high fibre content and regular exercise to help maintain blood glucose levels (What You Need to Know About Type 2 Diabetes, 2019). If these changes aren’t sufficient, there are many medications used, to maintain blood glucose levels, metformin helps to lower the level of glucose helps to improve how the body can respond to insulin; another example is dipeptidyl peptidase-4 inhibitors are a type of medication used to help decrease blood glucose levels to ensure it is maintained at the optimal level (What You Need to Know About Type 2 Diabetes, 2019).
Regenerative medicine is scientific research, focusing on the construction of cellular sources or treatments for implementation in the repair or replacement of damaged tissues and organs caused by many diseases (Regenerative medicine – Tissue Regenix, 2020). Regenerative medicine focuses on addressing obstacles, such as an increasingly ageing population, by helping to reduce healthcare costs; and by providing better management of symptoms commonly present in many chronic diseases, or through the development of cures to replace current treatments used for many chronic diseases (What we do · UK Regenerative Medicine Platform, 2018).
For the patient’s many conditions, the use of regenerative therapies could prove to be beneficial, as it could help to relieve the patient of his symptoms and may help to restore normal function through the replacement of damaged tissues and organs; as the patient has suffered from myocardial infarctions and both hypertension and type II diabetes.
Regenerative therapies focusing on the treatment of hypertension is required to ensure an optimal blood pressure reading between 90/60 mmHg or 120/80 mmHg is measured, supporting both the pumping and resistance of blood flow around the body.
An example of current research involves the use of cell-derived exosomes focused on therapies for use in treating cardiovascular diseases such as hypertension (Chimenti and Frati, 2018). The patient suffers from hypertension is at risk of having a stroke or kidney disease. The current treatment used for the patient involves a combination of medication used to control blood pressure. In some patients, they are still unable to maintain optimal blood pressure levels (Chimenti and Frati, 2018).
This research has shown that the interaction between both immunity and inflammation plays a significant role in the development of hypertension (Chimenti and Frati, 2018). Angiotensin II is a factor found to be involved in regulating blood pressure and has also been identified in the initiation of inflammation in both blood vessels and the kidney, showing angiotensin II is the central mechanism involved in hypertension development (Chimenti and Frati, 2018).
Cardiosphere-derived cells are a type of cardiac progenitor cells (CPC) have been studied for many diseases including myocardial infarction and Duchenne muscular dystrophy, it has shown that using these cardiosphere-derived cells through the secretion of exosomes helps to enhance tissue repair by exhibiting antiapoptotic and antifibrotic factors through modulation of the inflammatory response, tested using a mouse model and inducing hypertension in these mice. As shown in figure 1, it demonstrates the effects of using these cardiosphere-derived cells on fibrosis reduction (Chimenti and Frati, 2018).
]Figure 1. A diagrammatic representation of the functioning of cardiac progenitor cell exosomes containing Y RNAs is present in many cell types; the function of extracellular Y-RNA fragments is still unknown (Chimenti and Frati, 2018). The presence of the Y4 RNA RV-FYF1 from the 56-nucleotide fragment, found within cardiac progenitor cell exosomes is significantly involved in the protection of cardiac cells along with controlling the expression and release of IL-10, having an effect on resident macrophages, leads to a reduction in the accumulation of fibrosis within organs such as the heart (Cambier et al., 2018).
The results showed that using these CDC exosomes have shown numerous effects when tested using a cardiac hypertrophy model induced by angiotensin II, as both inflammation and hypertension are interlinked, as enhanced secretion of IL-10 exerts many anti-inflammatory effects, helping to mitigate cardiac hypertrophy along with improved kidney function without altering blood pressure level (Cambier et al., 2018).
By using these exosomes, it showed a reduction in the expression of proinflammatory cytokines such as IL-1b and IL-6 from the heart; as inflammation is commonly identified in cardiac hypertrophy and myocardial infarction, using these CDC exosomes can help to initiate both cell proliferation and structural remodeling of cardiac cells without triggering hypertension by blocking the function of Angiotensin II (Cambier et al., 2018). The use of these exosomes helps to improve tissue repair and would be beneficial to the patient, as it could help to prevent both fibrosis in organs such as the heart without inducing hypertension and could help to relieve the patient of fatigue and shortness of breath.
Although the findings demonstrate that using these CDC exosomes would be beneficial in the treatment of many cardiovascular diseases such as hypertension, the transition from using an animal to human models would be difficult, as the effects shown in the animals may not be the same for when tested in humans. The use of exosomes exhibits many beneficial effects, but integration in human trials would be difficult, as you are unable to track the exosomes in the body. This shows the impact of regenerative therapy in the treatment of cardiovascular diseases isn’t apparent and doesn’t show if this therapy has long-term benefits for the patient.
Regenerative therapies focusing on the treatment of myocardial infarction is to ensure the functioning of the heart is similar to normal function; by preventing fibrosis and arrhythmia with focus on repairing damaged muscles and valves and the walls of the heart. By using regenerative therapies, it could be beneficial to the patient, as it could help to restore normal function through the replacement of damaged vessels, induced by myocardial infarction and hypertension using tissue-engineered vascular grafts.
For cardiovascular disease, one treatment is blood vessel bypass surgery using autologous blood vessels; an advantage of this treatment is long-term patency is achieved; some issues identified are further trauma caused by surgery to the patient and obtainment of these autologous vessels for treatment is often insufficient (Li, Li, Xu and Zhang, 2019). By replacing this with artificial blood vessels, it would help to prevent the use of multiple surgeries for the patient, limiting further trauma and helping to potentially restore normal function of tissues and blood flow following myocardial infarction (Li, Li, Xu and Zhang, 2019).
Figure 2. A diagrammatic representation of the three fabrication methods used to manufacture tissue-engineered grafts, which includes sheet tissue engineering using a 2D cell sheet around a cylindrical base forming a tube that is shaped and developed into a tissue-engineered graft; the second method involves the joining of microtissues into a cylindrical mould, which is shaped and developed into the tissue-engineered graft (Li, Li, Xu and Zhang, 2019). The third method is bioprinting involves incorporating cells and materials together, forming the tissue-engineered graft (Li, Li, Xu and Zhang, 2019). (Image from (Pashneh-Tala, MacNeil and Claeyssens, 2016)
In tissue engineering, the production of a decellularized matrix involves using detergents and solvents in the decellularization of tissues helps to remove cellular material, that would initiate an immune response when administered to the patient, as shown in figure 3.
Figure 3. A diagrammatic representation of the decellularized matrix used to manufacture tissue-engineered grafts, one type are autografts commonly used, in which both the tissue and extracellular matrix are decellularized (Pashneh-Tala, MacNeil and Claeyssens, 2016). Following this is the extraction of the patient’s cells, which is seeded with stem cells onto the scaffold forming the tissue-engineered graft (Pashneh-Tala, MacNeil and Claeyssens, 2016). (Image from Pashneh-Tala, MacNeil and Claeyssens, 2016).
A current treatment used for myocardial infarction is a surgical procedure called coronary artery bypass graft, which involves using a blood vessel from another area of the patient’s body such as an arm or leg and is then attached to the coronary artery, to direct blood flow around the arteries, improving blood flow and the amount of oxygen supplied to the heart (treatments for heart attack, 2019).
Although using coronary artery bypass has been shown to improve blood flow after myocardial infarction; for the patient using a regenerative therapy that incorporates the use of tissue-engineered grafts could potentially be more beneficial, as the patient has previously had two myocardial infarctions, there would be extensive damage caused to both the tissues and vessels of the heart affecting the function of other organs within the body due to limited blood supply; and could result in the further development of conditions or diseases impacting the patient’s everyday life, that could potentially result in the death of the patient.
By implementing tissue-engineered grafts in the treatment strategy for the patient, it would help to limit the need for multiple surgeries; while helping to restore normal function of blood vessels and the heart improving blood flow around the body, helping to prevent issues with the functioning of other organs. The tissue-engineered grafts may also help to treat the patient’s hypertension, as the grafts maintain blood pressure, it improves blood flow around the body and could potentially help to alleviate the patient of his symptoms such as shortness of breath and fatigue.
For many regenerative therapies, such as tissue-engineered grafts, there are still issues that need to be addressed, which includes an incompatibility between the graft and the patient’s blood vessels could lead to rupturing of the grafted vessel, leading to the insufficient function of the graft making it unsuitable for long-term treatment (Li, Li, Xu and Zhang, 2019). If the issues are addressed, it could be an effective long-term treatment for the patient, as shown above.
Regenerative therapies focusing on the treatment of non-insulin dependent diabetes is to ensure both glucose and insulin levels are maintained at an optimum level to help maintain normal cellular function in the body.
An example of research involves the use of human mesenchymal stem cells for the production of insulin-producing cells for the treatment of non-insulin dependent diabetes.
Mesenchymal stem cells can self-renew and differentiate into various cell types like bone and muscle cells; these stem cells have shown to be effective in the treatment of many diseases like non-insulin dependent insulin, which for the patient is ineffectively treated using available treatments (Kim and Park, 2017).
Figure 3. A diagrammatic representation of manufacturing processes such as using stem cells, reprogramming damaged islet cells or generating new islet cells in the pancreas (Zhou and Melton, 2018).
The use of mesenchymal stem cells for the treatment of non-insulin dependent diabetes has many advantages, that could be beneficial in long-term treatment for the patient; as mesenchymal stem cells can be isolated easily and expanded (Kim and Park, 2017). The mesenchymal stem cells can be obtained from a donor if there are limited islet cells extracted from the patient. Although using stem cells could have many potential advantages, there are still some disadvantages from using this type of therapy, which includes limited replication of these cells, would require the patient to have multiple doses of stems cells for treatment to ensure the benefits of this regenerative therapy are maintained (Kim and Park, 2017).
Overall, there are many potential benefits of using regenerative therapy, that could be used in the patient’s treatment strategy, as shown in the given examples, these therapies could help the patient to manage symptoms such as shortness of breath and fatigue, as a result of non-insulin dependent diabetes. The use of regenerative therapy could also help to potentially cure or reverse some of the damage caused to tissues or organs, as a result of diseases/ conditions such as myocardial infarction.
References:
Cambier, L., Giani, J., Liu, W., Ijichi, T., Echavez, A., Valle, J. and Marbán, E., 2018. Angiotensin II–Induced End-Organ Damage in Mice Is Attenuated by Human Exosomes and by an Exosomal Y RNA Fragment. Hypertension, [online] 72(2), pp.370-380. Available at: [Accessed 27 March 2020].
Chimenti, I. and Frati, G., 2018. Cell-Derived Exosomes for Cardiovascular Therapies. Hypertension, [online] 72(2), pp.279-280. Available at: [Accessed 22 March 2020].
Healthline. 2019. What You Need To Know About Type 2 Diabetes. [online] Available at: [Accessed 21 March 2020].
Kim, H. and Park, J., 2017. Usage of Human Mesenchymal Stem Cells in Cell-based Therapy: Advantages and Disadvantages. Development & Reproduction, [online] 21(1), pp.1-10. Available at: [Accessed 29 March 2020].
Li, Z., Li, X., Xu, T. and Zhang, L., 2019. Acellular Small-Diameter Tissue-Engineered Vascular Grafts. Applied Sciences, [online] 9(14), p.2864. Available at: [Accessed 28 March 2020].
nhs.uk. 2019. Heart Attack. [online] Available at: [Accessed 20 March 2020].
nhs.uk. 2019. High Blood Pressure (Hypertension) – Treatment. [online] Available at: [Accessed 20 March 2020].
nhs.uk. 2019. High Blood Pressure (Hypertension). [online] Available at: [Accessed 26 March 2020].
nhs.uk. 2019. Treatments For Heart Attack. [online] Available at: [Accessed 20 March 2020].
Pashneh-Tala, S., MacNeil, S. and Claeyssens, F., 2016. The Tissue-Engineered Vascular Graft—Past, Present, and Future. Tissue Engineering Part B: Reviews, [online] 22(1), pp.68-100. Available at: [Accessed 29 March 2020].
Tissueregenix.com. 2020. Regenerative Medicine – Tissue Regenix. [online] Available at: [Accessed 21 March 2020].
UK Regenerative Medicine Platform. 2018. What We Do · UK Regenerative Medicine Platform. [online] Available at: [Accessed 22 March 2020].
Zhou, Q. and Melton, D., 2018. Pancreas regeneration. Nature, [online] 557(7705), pp.351-358. Available at: [Accessed 29 March 2020].
Ischemic heart disease (IHD) is the leading cause of death around the world. IHD develops, when coronary arteries become narrowed and it is mainly due to atherosclerosis. Many people don’t know they have IHD, until they develop angina or a heart attack.
Aim: To know the etiology, risk factors, symptoms, morphology of myocardial infarction and complications.
Etiology: IHD is due to accumulation of lipoproteins, which lead to formation of the atheromatous plaque that will narrow the coronary artries and decrease the blood supply to the heart leading to ischemia. The resulting ischemia may be complicated by myocardial infarction.
Risk factors: They are divided into controllable (High blood pressure, high cholesterol, smoking, diabetes, stress, Being overweight or obese) and non-controllable risk factors (as family history, age and gender).
Morphology of myocardial infarction: The myocardium shows coagulative necrosis and centeral yellow area surrounded by hyperemic border. The scar completes after 2 months. Microscopically, there is hypereasinophilic myocyte with loss of the nuclei with phagocyte infiltration, which appears basophilic. The coronary artery shows thrombosis and the plaque may ulcerate.
Complications: They may include: acute pulmonary edema, heart rupture (left ventricular wall rupture, ventricular septal rupture and papillary muscle rupture), left ventricular aneurysm, ventricular pseudoaneurysm, carcinogenic shock, pericarditis and pulmonary hemorrhage, arrhythmia and sudden death from lethal arrhythmia.
Introduction:-
The IHD is has one of the highest mortality rates around the world. It develops mainly, when arteries of the heart become too narrow. Many risk factors can increase the chance of developing IHD. It has very serious complications discussed in this review.
Aim: To know the etiology, risk factors, clinical symptoms, morphology of myocardial infarction and complications.
Etiology:-
IHD is a cardiovascular disorder occurring due to atherosclerosis or atherosclerotic occlusions of the coronary arteries in most cases (Mendis et al., 2011).
When the endothelial function of the arterial wall disrupts, atherosclerosis begins due to the accumulation of lipoprotein droplets in the intima of the coronary vessels (Badimon et al., 2012).
Plaque can start to collect along the blood vessel walls, when we are young, building up gradually as we get older. That buildup inflames the vessel walls and raises the risk of blood clot and heart attack. The plaque makes the inner walls of the blood vessels sticky. Some Things like inflammatory cells, lipoproteins, and calcium attach to this plaque while travelling through the bloodstream.
As a result of accumulation of more of these materials along with cholesterol, the artery walls become narrower & obstruction of blood flow may occur, which leads to a mismatch between myocardial oxygen demand and supply (Cassar et al., 2009).
Risk Factors:-
There is no single cause for coronary heart disease, but ‘the risk factors’ can increase your chance of developing it.
A. Controllable risk factors: (controlled through lifestyle changes and medication)
Smoking: It promotes coronary occlusion, as it produces endothelial denudation and platelet adhesion to subintimal layers, thereby increasing the build of fatty materials and platelet‐derived growth factor‐mediated proliferation of smooth muscle cells, which narrows the artery. Smokers have been reported to have 70% more IHD mortality than non-smokers (US Department of Health and Human Services, 1990).
Diabetes: particularly, diabetes mellitus or type 2 diabetes (Haffner, 1999).
Cholesterol: Low levels of high-density lipoprotein cholesterol, high levels of very low‐density lipoprotein (VLDL) cholesterol & high levels of total VLDL triglycerides have been reported as risk factors for IHD in patients with type2 diabetes (Laakso et al., 1993).
Blood Pressure: Atherosclerosis could be aggravated by arterial hypertension. Hypertension has also been frequently associated with metabolic disorders like insulin resistance or hyperinsulinemia and dyslipidemia, which are known to be risk factors of IHD (DeFronzo & Ferrannini, 1991).
Obesity: Excess body fat in the abdominal visceral could lead to atherosclerotic disease (Matsuzawa et al., 1995).
Hyperuricemia: Some studies have indicated an association between hyperuricemia and the risk of IHD (Zalawadiya et al., 2015).
Stress: Various physiological changes produced by stress (such as elevated blood pressure, reduced insulin sensitivity, elevated hemostasis, and endothelial dysfunction) may be relevant to cardiovascular diseases (Steptoe & Kivimäki, 2012).
B. Uncontrollable risk factors:-
Family history: It is an important determinant of IHD risk, but one that is hard to quantify (Pandey et al., 2013).
Age: The risk of IHD increases with age (Teramoto et al., 2013).
Gender: Men are more liable to develop IHD at an earlier age than women. However the risks increase in postmenopausal women (Stangl et al., 2002).
Ethnicity: Asian indians have a higher risk of heart disease as compared to other ethnic origins (Enas et al., 2001).
Clinical presentation:-
Angina pectoris: It is a chest pain on exertion, in cold weather or in emotional situations. Patients may experience nausea, vomiting, sweating and enhanced anxiety (Kosuge et al., 2006).
Myocardial infarction, heart failure & sudden cardiac death (Kannel, 2002).
Morphology of myocardial infarction in pre & post interventional era: The pathological diagnosis of myocardial infarction depends on the coagulative necrosis of the myocardium, repairing feature and detection of thrombosis in the coronary arteries (Robbins & Cortan, 2005).
Myocardium: The non reperfused myocardial infarction shows coagulative necrosis (Robbins & Cortan, 2005). 12-14 hours the myocardium is dark motling. 1-3 days there is centeral yellow area surrounded by hyperemic border. 7-10 days the border gets red-gray. 7-8 weeks the scar starts from the periphery to the center. After 2 months the scar completes. The microscopic appearance before 12 hours, there is hypereasinophilic change in the myocyte, but it’s poorly informative (Madrigal et al., 1979). After 12 hours start of coagulative necrosis with loss of the nuclei. The neutrophilic infiltration begins from 1-3 days (figure 3). Day 3-7 phagocytosis of the border and fragmentation of the myocyte. After 1 week beginning of the granulation tissue. Dense collagen deposits (3-8 weeks). Complete scar develops in the second month (Robbins & Cortan, 2005). After 2 months the collagen becomes dense and compact and the myocardium is acellular.
Coronary artery:-
A plaque with thrombosis is found at autopsy in about 90% of patients died from myocardial infarction and not treated by thrombolysis or percutaneous coronary angioplasty. The plaque ruptured in about 75% of cases and erosion in minority of cases (Arbustini et al., 1999). The lesion is large atherosclerotic plaque with cap ulceration and superimposed thrombosis. The thrombosis is red with small platelets (in the head), fibrin and red cells (in the body & tail) (Arbustini et al., 1991).
Post thrombolytic & post percutaneous coronary angioplasty era:
Reperfusion in myocardial infarction restores the coronary flow using thrombolytic and percutaneous coronary angioplasty (Antman et al., 2004). The great effectiveness occurs with percutaneous coronary angioplasty, when done within the first 12 hours from the beginning of the ischemia (Abustini et al., 1999).
Morphology of myocardium:-
The gross appearance of the reperfused myocardial infarction is hemorrhagic. The microscopic examination shows coagulative necrosis with red cells infarction (figure 4).
The small vessels show thromboembolism. The vessels may be damaged and worsen the hemorrhagic invasion. This may lead to swelling of the cells and may prevent the reperfusion (non-reflow) phenomenon (Rezkalla & kloner, 2002). If the reperfusion occurs before the necrosis, the area at the risk will be rescued. The scar of the reperfused myocardial infarction has more angiogenesis than non-reperfused one. The result of the reperfusion is limitation of the infarction and improvement of the function (Antman, 2004).
Coronary artery:-
The reperfused myocardial infarction culprit is expected to be patent. It may show hemorrhagic invasion, thrombosis and ulceration (Prati et al., 2003). New filters are used to collect thrombosis and plaque to limit the small vessels impairment (Stone et al., 2005).
Myocardial infarction complications:-
• Acute pulmonary edema:
Pulmonary edema is associated with a 20-40% 30-day mortality rate, It occurs as an acute event with the beginning of ST-elevation myocardial infarction (STEMI) or reinfarction or as the climax of slowly progressive congestive heart failure during the first days after myocardial infarction (MI) (Pena-Gil et al., 2005).
• Heart rupture:
a) Left ventricular free-wall rupture occurs in 1-6% of all patients admitted with STEMI. Risk factors include: first MI, anterior infarction, old age, female sex, hypertension, no collater,als, and intake of corticosteroids or non-steroidal anti-inflammatory drugs. The main determinants in preventing rupture are early reperfusion and collateral circulation (Nakumura et al., 1992) (Pallak et al., 1994).
b) Ventricular septal rupture rarely occurs. The frequency of acute rupture of inter-ventricular septum declines during reperfusion period. Rupture site can rapidly expand and cause sudden hemodynamic collapse (Crenshaw et al., 2000).
c) Papillary muscle rupture rarely occurs. The diagnosis is made on the basis of clinical and imaging findings.
Left ventricular aneurysm:
It occurs in the left anterior wall, combined with left anterior descending occlusion and wide infarcted area (Tikiz et al, 2001).
Ventricular pseudoaneurysm:
It is a rare complication. It occurs as a result of rupture of ventricular free wall and is covered by overlying adherent pericardium. The pathologic features depend on interval of time between beginning of MI & death and also the extent of hemorrhage. The myocardial wall shows fissuring. Coagulative necrosis is one of the myocardial changes (Neven et al, 2005).
Arrhythmias:
They are common in patients with STEMI and occur early after development of symptoms. The mechanisms for ventricular tachyarrhythmia include loss of transmembrane resting patients, development of foci of enhanced automaticity (Carmeliet, 1999).
Lethal arrhythmias / sudden death:
They are one of the most common causes of death in non-hospitalized patients with acute MI (Perron & Sweeney, 2005).
Cardiogenic shock:
It is frequently caused by extensive left ventricular dysfunction, other common causes include mechanical complications (acute mitral regurgitation & ventricular septal rupture) (Hochman, 2003).
Mitral regurgitation (MR):
It occurs as a consequence of papillary muscle, lateral wall infarction. It has poor diagnosis if accompanied with cardiogenic shock. The area of infarction seems to be less extensive in case of papillary muscle and wall infarction than papillary displacement (Hochman, 2003).
Pericarditis:
It occurs in transmural STEMI including the whole thickness of the myocardial wall to the epicardium. Patients with pericarditis have larger infarcts, lower ejection fraction and higher risk of congestive heart failure (Shahar et al., 1994).
Acute pulmonary hemorrhage:
It is a rare complication that occurs in patients who undergo primary percutaneous transluminal coronary angioplasty (PTCA) and are treated with glycoprotein IIb/IIIa inhibitors. The pathological diagnosis is important to confirm the alveolar invasion by red blood cells. Bleeding complications are common in women than in men (Razakjr et al., 2005) (Ali et al., 2003).
Conclusion:
IHD is the leading cause of death worldwide and have many risk factors (as high cholesterol, smoking, diabetes, obesity, hypertension & aging). It has very serious complications (as pulmonary edema, aneurysm, rupture arrhythmia & carcinogenic shock).
Cardiovascular diseases (CVD) are the number one cause of death globally. An estimated 17.9 million people died from cardiovascular diseases in 2016, representing 31% of all global deaths. Pakistan is there in the list of developing countries of the world and the contribution cardiovascular disease (CVD) of developing countries to the global weight of CVD is more than 80 %. Myocardial infarction (MI) is the most prominent cause behind all these mortalities (World Health Organization, 2018). Myocardial infarction is caused by complete blockage of the coronary artery due to a thrombus attach to a rapture plaque. They may have some modifiable and non-modifiable risk factors. Patient may present in emergency department with severe chest pain, dysrhythmias, shortness of breath, and sweating. Due to occlusion of blood supply, cardiac muscle damaging started. Most of the death are due to ventricular fibrillation after ischemia. Myocardial infarction is an emergency situation which requiring immediate diagnosis and treatment. It should be recognized immediately to avoid the consequences. In developing countries, due to different issues including poverty, socioeconomic status, and lack of facilities it’s difficult to identify the proper diagnose. Knowledge regarding myocardial infarction, their signs and symptoms, risk factors provides beneficiary sources in proper identification and treatment. All health care professionals have a good knowledge regarding the patients of cardiovascular diseases. First goal for being a health care professionals in management of myocardial infarction is to diagnoses the condition in very rapid manner. The research topic “What is nurses’ knowledge and practices about streptokinase administration and monitoring among myocardial infarction emergency room (ER)?” was selected.
Aims of the study:
The aims of the study are to assess:
What is the knowledge and practices of nurses about streptokinase injection administration and monitoring among myocardial infarction in the emergency room (ER)?
What is different protocol used for administration of streptokinase in emergency room (ER)?
Background /significance of the research topic:
The reasons behind for selection of this topic are: As working as a charge nurse in ER patient census for usage of streptokinase was huge, due to which medication errors occurred. I have observed different incidences while administrating streptokinase (SK) to myocardial infarction patients i.e. nurses did not follow the protocol streptokinase. It was seen that Foleys Cather inserted after administration of streptokinase and patient started severe bleeding. Another incident was observed that patient was shifted to cardiac care unit (CCU) without proper instruction after SK administration and patient came out of bed and went to washroom due to which he got Cerebrovascular Accident (CVA). Once misinterpretation of electrocardiogram (ECG) also created a big problem. These incidents were different causes, but 80% of these were due to gap in knowledge and practices of nurses. Furthermore, due to overcrowding nurses were not able to give proper attention to the patient. These all incidences have directly effected on patients, which lead to mortality or increased the stay of patients. Most of the time it was seen that patient came with a single problem i.e. myocardial infarction but a single mistake created a lots of problem for him. Therefore I am keen to interest to study the knowledge and practices of nurses regarding streptokinase form myocardial infarction patient in ER.
Tools for measurement of knowledge level of nurses for SK:
Searching from different publications, which given different tools in form of questionnaire, I also want to develop self-development tools will be uses for data collection from participants. The tools will be consist on questionnaires regarding knowledge, attitude and practices of nurses for administration and monitoring of streptokinase drug in emergency rooms. The study design will be quantitative study.
The purpose of the literature review are: identify the gap and inconsistences in the body of knowledge, select proper theoretical frame work and guided propped study. Its helps to refines not only research questions but also selecting suitable design. Furthermore the intervention are developed and refined based of literature review (Polit & Beck, 2013).
Search strategy:
For searching different publications, different search engines i.e. PubMed, Google Scholar, Wiley online library, Journal of Cardiovascular Nursing were searched. Different keywords were used: streptokinase, Nurses knowledge, monitoring and administration, myocardial infarction. The Boolean operator “AND” and “OR” were mostly used for getting significant hits and relevant publications. The Boolean operator “AND” gave condensed and relevant publications regarding the topic and. All publication condensed by Boolean operator “OR” tried to discuss comparison instead of relationship between keywords. An inclusion criteria was kept for the systemic literature search from different databases .articles publication from 2010 to 2019, publication written in English language and participant should be nurses. Although, some publication were out of range according to date of publication criteria but there were a lot of significant literature review regarding the topic and helpful in study. Most of the publication retrieved from different databases were descriptive studies designs and none of publication was available in Pakistani context (See appendix B).
After conducting the literature review from different search engine, 12 relevant publications were selected for review.
Literature Review and synthesis:
In 17th century the idea about angina and chest pain, their risk factors, pathophysiology were known, but there were no proper treatments for it. Till 1950, the treatments for myocardial infarction (MI) were palliative rather than curative. After that the drugs that show effect for treatments off MI were anticoagulants. Furthermore, after 1947 different clinical trials were started on the streptokinase (anticoagulant). Until 1979, the direct administration of streptokinase into the coronary arteries was not tried and it was performed by a small group of patients. The risk intracoronary streptokinase (SK) administration can be classified as cardiac and extra cardiac (Sikri, & Bardia, 2007).An common practice, in all over the world when patients present with chest pain enter to emergency room, nursing staff should have a suspicious of cardiac pain. After taking history and 12 leads Electrocardiogram (ECG) the initial therapy for restoration of perfusion to prevent further damage to the second layer of heart myocardium is given. The initial therapy such as Morphine, Oxygen, Nitroglycerin and Aspirin (MONA) are used for stabilizing the patient’s conditions. While streptokinase therapy is used to dissolve a clot and reopen the arteries or veins, but it cannot be used in all conditions. The administration of streptokinase depend upon the specific criteria and protocol. Nurses who working in emergency rooms, are expected to be knowledgeable about the characteristics of the therapy and able to make decision for administration of streptokinase (Mustafa & Elfaki, 2017). The American Heart Association (AHA) and the World Health Organization (WHO) recognized the key role that nurses and other team members play in supporting the goal to reduce cardiovascular diseases and disability by 25 % in 2025. Nurse’s knowledge is a significant role in proper management and prevention of early morbidity and mortality due to myocardial Infarction. For determination of nurses knowledge about drugs used during emergency management of acute myocardial infarction, Mustafa and Elfaki (2017) conducted a study and reported that most level of knowledge among trained nurses about streptokinase and regard their complication were poor and there were inverse correlation. As streptokinase used for the reopening of arteries and veins, sometime it can lead to undesirable effects. So nurses must be a good observer to master these problems. Nurses should aware about the window periods of streptokinase. Streptokinase prepared, administered, and monitored by nursing staff, that they had an experienced working in emergency department. One of the adverse effect of streptokinase is dysrhythmias, can lead to ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT), which required prompt defibrillation. A study conducted by Mustafa and Elfaki in 2016, regarding the attitude of nurses to defibrillate a rhythmic patient and was found low, shows that 82% of nurses did not fibrillate the patient until the doctor attended. Nurses think that defibrillation is the doctor responsibility. Furthermore, delay in defibrillation could lead to brain death, so patient needs quick interventions and should not be wait for doctor. Being a nurse, it’s our responsibility to know that brain death can occur less than four minutes if blood supply is interrupted (Mustafa & Elfaki, 2016). One of the aspect related to the competency and knowledge of nurses is to, quickly identify the adverse reaction. As streptokinase should be administer through intravenous infusion of 1.5 million units is given over 30 to 60 minutes. Their rapid infusion can lead to hypotension (Aylward, 1996). Sometime, streptokinase causes transient blood pressure loss in many patients and in some of them would also create allergic reactions including rash, fever, and bronchospasm. Another rare complication is cerebral hemorrhage (Zad, 2014). Before deciding for antiplatelet therapy, the identification of different risk factory is necessary. Although the therapy can decrease the risk of ischemic but it can increase the risk of moderate or severe bleeding. Therefore, it is important to carefully select the candidate for extended dual antiplatelet therapy. Selection should be performed on the basis of certain guidelines, while the risk between the ischemic events and risk of bleeding should be balanced. Bobadilla (2018) identified different bleeding risks calculators such as TIMI and CRUSADE, they are designed for the acute setting. Other calculators, HAS-BLED and HEMORR2HAGES are also used. According to Umanath (2012), “A thrombolytic therapy will be considered successful if there was no documented infiltration of the AV access or extravasation of thrombolytic agent”. According to American college of Cardiology (ACC) and American Heart Association (AHA) guidelines emphasize implementing reperfusion as soon as possible after the patient enter the medical system as the most important feature of managing ST Elevation Myocardial Infarction (STEMI). Furthermore, it seems that the chances of mortality is decreasing when fibroblastic therapy is started in initial three hours after symptoms onset. Streptokinase therapy is the sample option to manage STEMI du to its general accessibility, lack of requirement of specialized skills, and ability to rapidly reinstate perfusion when administered in a timely manner (Spinler, 2006). Spinler (2006) identified different causes which can delay to reperfusion and effective treatment are: hesitation of patient to contact health personal, delays due to patients transport issues are common, delays in effective STEMI management may occur in emergency rooms due to overcrowding , lack of proper communication among departmental staff or lack of proper protocol of STEMI patients.
Conclusion:
Although in all developing countries as well as in some develop countries the administration of streptokinase for myocardial infarction is still in high level, but different studies discussed in literature review, identified gap in knowledge, attitude and practices of nurses regarding administration of streptokinase in myocardial infarction. It seems that nurses have experiences of Critical Care Unit (CCU), Emergency Room (ER) ranging from different years but they don’t have knowledge regarding streptokinase and their administration. They just follow the colleagues without any logical reasoning. Nurses working in Emergency Rooms (ER), will be certified for advanced cardiac life support (ACLs) and Basic life support (BLS). Nurses should be aware about the window period, main adverse effects, pre and post teaching of the streptokinase.
In last it is concluded, that the competency in term of knowledge, attitude and practices of nurses directly affect patient with myocardial infarction and receiving streptokinase.
There is a lot of research literature on the topic of behavioral sciences and medicine that suggests psychological and social factors may play a direct role in organic coronary artery disease (CAD) pathology. However, there are many people in the scientific community who regard this evidence with skepticism. This paper critically examines research on risk factors for acute myocardial infarction. Two key variables identified as possible psychosocial risk factors for CAD are addressed: depression and lack of social support. The evidence shows that there is a considerable psychological and social impact on patients with coronary heart disease CAD, which can lead to acute myocardial infarction. Denollet and Brutsaert (1998) have found that lack of social support and depression can result in cardiac events independently of established medical risk factors (Carney, 1998). In particular, there is substantial evidence that depression is a risk factor for cardiac morbidity and mortality, both for patients without clinical evidence of coronary heart disease at index examination and for patients with established coronary disease (Orth-Gomer and Kristina, 2007). The relationship is most clear in the case of patients with a recent acute myocardial infarction (Freedland, 2004).
Pathophysiology of Heart Disease
Coronary heart disease refers to a set of conditions resulting from coronary atherosclerosis, the accumulation of plaque in coronary arteries. The atherosclerotic process is quite complex and happens over a span of many years. It involves a series of biochemical processes in interaction with various risk factors (Ross, 1999). The first symptoms of coronary heart disease may include anginal chest pain resulting from decreased cardiac blood flow (ischemia), myocardial infarction (heart attack), or sudden death as a result of serious disturbances of cardiac rhythm (arrhythmias). Due to the complex nature of the coronary disease, various psychosocial and behavioral variables can be linked to different aspects of the disease process.
The acute emergency is known as myocardial infarction, or heart attack is usually caused by a blockage in one of the coronary arteries that supply blood to the heart muscle. The blockage typically occurs when a blood clot lodges in an area already narrowed by arteriosclerosis. Symptoms of myocardial infarction include a crushing pain in the chest radiated to the arm, the jaw, and the neck, although in some cases, there are no symptoms at all. Acute myocardial infarction (MI) is defined as the death of myocardial cells (Rubin, 1995). The seriousness of the infarction depends upon the amount of heart muscle affected, how long the area is deprived of blood, and whether it affects the natural pacemaker of the heart, setting off arrhythmias. Death of heart muscle tissue and heart failure may result; damage to other vital organs, including the brain, may occur if the heart is unable to pump necessary oxygen and blood to them.
Investigative Topic
The paper investigates the two key factors that lead to acute myocardial infarction in a person who is just recovering from a cardiac problem. The two factors are depression and social support.
Clinical Depression
Clinical depression is a syndrome that includes depressed mood and other symptoms such as changes in weight, insomnia, fatigue, and markedly diminished interest or pleasure (Am. Psychiatr. Assoc. 1994). The lifetime prevalence rate is reported to be 13% for major depression and 5% for dysthymia in the general population (Kessler et al. 1994). Depression rates are higher in cardiac patients, especially post-myocardial infarction patients, with studies reporting prevalence rates of 16-23% (Schleifer et al. 1989). As many as 30% of cardiac patients may have depressive symptoms (Frasure-Smith et al. 1995). Depression rates do not appear to increase markedly with the severity of cardiovascular disease or increased disability (Carney et al. 1987, Frasure-Smith et al., 1995).
Carney et al. (1988) found that patients with cardiovascular disease who met the criteria for major depression were 2.5 times more likely to develop a serious cardiac complication over the next 12 months than non-depressed patients. More than a dozen subsequent studies have controlled for other risk factors and yielded similar results. For example, Frasure-Smith and colleagues followed 222 patients after their first MI. These patients received structured psychiatric examinations within 15 days of their first MI and were followed for 18 months. After controlling for other independent risk factors, depression was associated with a 3.5-fold risk of mortality. This risk is comparable to other major risk factors for mortality, such as congestive heart failure and left ventricular function (Frasure-Smith et al. 1993, 1995).
Depression as Risk-Factor for AMI
Studies show that the risk of cardiovascular disease associated with depression increases in a linear manner and that depressive symptom are sufficient to increase risk in the absence of major depressive disorder. Moreover, some aspects of depression or some characteristics may increase the risk of morbidity or mortality. For example, vital exhaustion refers to fatigue, irritability, and demoralized feelings and has been associated with the development of coronary artery disease and other cardiac events in healthy and already suffering patients (Kop et al. 1994). In one study, the presence of exhaustion predicted adverse clinical outcomes in CAD patients undergoing coronary angioplasty, a non-surgical cardiac procedure (Kop et al. 1994). These results could not be attributed to the pre-existing disease. Similarly, the absence of hope has also been identified as a possible risk factor. Thus, many studies have linked psychological factors with the development and worsening of coronary artery disease.
Depression and cardiovascular illness – Discussion of Findings
Depression is expected to have an enormous impact on the worldwide burden of disease in the coming years. The diseases with the strongest impact are predicted to be ischemic heart diseases and major depression because of their high prevalence (about 5% of the population is depressed) and their strong effects on QoL (Quality of Life). According to a recent study by Jonge et al. (2006), it has been found that depression after myocardial infarction is a risk factor that reduces the quality of life and increases cardiac complaints at 12 months after the first Myocardial infarction. The study included a cohort of 468 adults with MI from four hospitals in the north of the Netherlands between September 1997 and September 2000. A case-control study including 11,119 patients with a first MI and 13,648 age- and sex-matched control subjects from 262 centers in Asia, Europe, the Middle East, Africa, Australia, and North and South America was conducted to investigate the relation of psychosocial factors to the risk of myocardial infarction (MI). It was found that depression was more common among the cases (24.0 vs. 17.6%). Those reporting depression were 1.55 times more likely to have an MI than those who did not have depression. These findings were consistent across regions, in different ethnic groups, and in both sexes. This study was conducted by Rosengren et al. (2004) for the Interheart and concluded that psychosocial stressors are associated with an increased risk of acute MI.
According to a Harvard Health Publication (2007), people with post-heart attack depression are two to three times more likely to have another heart attack or to die prematurely compared with survivors who don’t have depression. The report also says that depression that occurs for the first time during recovery from a heart attack appears to be more dangerous than depression that started before the attack.
The study titled “Minor Depression as a Cardiac Risk Factor After Coronary Artery Bypass Surgery” by Rafanelli et al. (2006) reports that psychosocial factors have a huge impact on coronary artery bypass grafting patients. It has been found from this study that observer-rated minor depression is a potential risk factor for cardiac events 6–8 years after coronary artery bypass grafting surgery. The available data suggest that depression, in general, assessed by self-rated methods, could be a risk factor for cardiac events in this population. The study is limited by its small sample size that included only six subjects with minor depression (Rafanelli et al., 2006). Blumenthal and colleagues (2003) showed that not only patients with moderate-to-severe depression before coronary artery bypass grafting but also patients with mild or moderate-to-severe depression that persisted for 6 months after coronary artery bypass grafting had higher death rates than those without depression. It is likely that depression is thought of as an understandable and inevitable reaction to the severe circumstances accompanying coronary artery bypass surgery, and, as a result, it is not always treated. Therefore it is possible that minor depression could be underestimated and under-treated even more frequently than major depression. Because of this neglect to treat minor depression, it can become a significant factor that increases psychological and physical vulnerability. Though there is no scientific link between depression, cardiac morbidity, and mortality, there are various explanations by which depression may be linked to cardiac morbidity and mortality. These explanations are based on social, behavioral, and biological mechanisms (Blumenthal, 2003). The authors of the study, Rafanelli et al. (2006), point out that there is some difficulty in assessing depression after surgery because of the overlap between symptoms of depression and those of cardiac disease.
What kind of depression increases the risk of cardiac events, and what type of events are involved? – This is the question addressed in this study by Horsten et al., which suggests an increase in the combined risk of “revascularization, cardiac mortality, and myocardial infarction in women who report two or more out of nine depression symptoms”(Frasure-Smith and Lespeurance, 2000). Most previous research highlighting depression-related risks for mortality and myocardial infarction in coronary artery disease patients has found the risk to be concentrated in the approximately 25 to 30% of patients with the highest level of depression. In this study, however, the risk was seen to be present even if there was a mild case of depression with just about two symptoms.
Why does depression occur in patients with cardiac problems?
The November 2001 report published by the British Heart Foundation says that heart disease is caused by depression. To quote: “the individual meaning and threat of having heart disease and of its treatment are precipitants of depression.” The main reasons for depression are constitutional vulnerability (family history of emotional problems, previous episodes), adverse social circumstances, and pre-existing chronic depression. The report further holds that depression may be a primary risk factor for the onset and also for mortality in established diseases. Minor depressive symptoms are frequent in the early days and weeks after an acute event, and 15-20% of those with infarction or angina suffer major depressive disorder (BHF, 2001). Moreover, heart failure causes fatigue and malaise, which are similar to the symptoms of depression. Low mood occurs in 15-20% of patients, and moreover, this also interferes with acceptance of medical advice and treatment. Generally, it has been found that depressive symptoms are common in the immediate weeks following surgery. Some drugs used for treating hypertension can also cause a lowering of mood (BHF, 2001).
Several behavioral and physiological mechanisms have been proposed for the association between depression and cardiovascular illness. Depressed individuals certainly are more likely to engage in risk-related behaviors such as smoking or lack of physical activity, which can lead to heart diseases (Carney et al., 1995). However, after control of traditional risk factors and risk-related behaviors, depression was found to be still associated with poor cardiac outcomes, suggesting that other factors are involved (Glassman & Shapiro 1998). Depression is also associated with high levels of certain chemicals in blood and urine, and there is evidence that hyper-excretion of such chemicals decreases after treatment with tricyclic antidepressants. Thus treatment of clinical depression using antidepressants can increase the risk of heart disease. Depressed individuals tend to have reduced heart rate variability (beat-to-beat fluctuations in heart rate) (Stein et al., 2000). Low heart rate variability is associated with poor cardiovascular outcomes. It has been proposed that weakening of the heart through low heart rate leaves the heart vulnerable to unopposed stimulation by the sympathetic nervous system and more susceptible to malignant cardiac arrhythmias and sudden death. Because increased mortality in depressed patients is largely attributable to an increased risk of sudden death, it has been proposed that problems in the heart increase the risk of depressed individuals and make them more susceptible to lethal arrhythmias (Frasure-Smith et al. 1993, 1995; Gorman & Sloan 2000). There is also evidence that the association between depression and cardiovascular disease is mediated, at least in part, by changes in blood platelet function (Musselman et al. 1996).
It is also possible that depression contributes “both to myocardial ischemia and to other factors that promote lethal ventricular arrhythmias in ischemic myocardium”(Skala et al., 2006). Thus, the evidence linking depression to increased risk of morbidity and mortality in coronary artery disease (CAD) is quite significant. Moreover, it has been found that these data also relate depression with symptoms in patients who are already suffering from established CAD.
Limitations of these findings
It is not clear whether symptoms of depression alone, in the absence of clinical depression, are sufficient to increase the risk for cardiovascular disease. Individuals with depressive symptoms are more likely to develop the coronary disease over time, but there is no evidence so far to suggest whether or not their symptoms developed into major depression over the time course of the follow-up period.
Depression may also be inherently associated with other behavioral or biological risk factors for coronary disease. For example, depression is associated with feelings of fatigue and lack of interest in activities, which may result in a sedentary lifestyle. The mechanisms by which depression is linked with increased coronary risk in cardiac patients are not entirely clear and may involve biological markers such as reduced heart rate variability and parasympathetic function, impaired platelet reactivity, or behavioral factors such as associations with other psychosocial risk factors or reduced compliance with medical regimens. Further studies of these mechanisms might suggest additional useful targets for possible interventions.
Social Support
Social support refers to having a variety of social contacts available as resources for one’s personal benefit (Cohen et al., 2000). Structural support refers to the existence of social bonds and interconnections between social bonds. Social support is generally measured in terms of marital status, the number of people in one’s household, and a number of social contacts. These measures are often considered in combination with social integration. Functional support refers to the usefulness of one’s social contacts in providing specific functions, such as emotional support, tangible or instrumental aid, feelings of belonging, and informational support (Cohen et al., 2000).
The most effective social support interventions occur naturally. The quality of the support provided is said to be good when it facilitates treatment compliance (Coppotelli and Orleans, 1985) (Antman et al., 2004). Over protectiveness and withholding information or worries from the patients by family members or vice versa can worsen conditions and lead to bad outcomes (Suls et al., 1997; Clarke et al., 1996). Some methods of providing social support include telephone follow-up, cardiac rehabilitation, or other group events can be effective methods of support for socially isolated individuals (Houston-Miller et al., 1995) (Antman et al., 2004).
Horsten et al. (2000) have reported that symptoms of depression and lack of social integration 3–6 months after discharge for an acute coronary syndrome can have independent negative impacts on 5-year prognosis in women 65 years of age and younger. In their 1998 quantitative angiography study, involving a sub-sample of the current study patients, the authors found that major coronary stenoses were significantly more common in women with low social integration. Thus, it makes sense that the combined end-point of revascularization, myocardial infarction, and cardiac deaths would also be linked to low social integration in the full sample.
The first indication that social support could be linked to mortality after myocardial infarction (MI) was elucidated 25 years ago in the Beta-Blocker Heart Attack Trial. This trial involved interviews with 2320 male survivors of acute MI. Results showed that social isolation and high levels of stress were associated with a 4-fold increase in mortality at 3 years when compared with men with low-stress levels and low social isolation scores (Mookadam, 2004).
The importance of social support in this context of myocardial infarction
The impact of social support on premature mortality after acute myocardial infarction deserves detailed study for several reasons: First, as a predictor of 1-year mortality, low social support is equivalent to many of the classic risk factors, such as elevated cholesterol level, tobacco use, and hypertension. Second, treatment of acute myocardial infarction is costly. Because low social support is associated with increased 1-year mortality, neglecting the role of social support may diminish the possible gains obtained during treatment. Therefore, lack of social support should be considered a risk factor for subsequent morbidity and mortality after a myocardial infarction (Mookadam, 2004). In fact, social isolation is associated with increased mortality and morbidity, with an odds ratio of 2.0 to 3.0 (Mookadam, 2004).
Explaining the link between Social Support and Myocardial Infarction
The mechanism/mediator role of social isolation is not very clear. Experts feel that there is a complex interaction of determinants that influence biological, social, psychosocial, and behavioral factors. Social isolation can cause anxiety that can lead to stress. This stress activates the neurohormonal and physiologic pathways. On the other hand, social support can exert social control over the patient by health-promoting behaviors of others.
Social support networks may provide support resources such as medical referral networks, group therapy, or informational opportunities relating to employment. Many biological processes, such as endocrine responses, immune responses, etc., are influenced by lack of social support, and such imbalances are known to be injurious to arterial walls and the myocardium itself (Mookadam, 2004).
Social Support and Myocardial Infarction – Discussion of findings
In a study by Bucher (1994), it was found that patients who had a first myocardial infarction and had social support are less likely to die than those with no social support. In this study, five out of nine of the cohorts showed that no social support increased the risk of death. Relative risks for the five cohorts ranged between 1.47 to 5.62. The studies also showed that the increased risk of death with no social support was increased more for men than women. Two intervention studies demonstrate reduced mortality with community interventions (RR~0.5 for sudden death rates). This proves decisively that lack of social support in the case of patients who had myocardial infarction can lead to death.
On the positive side, it has been found more recently that social relationships and social support may influence recovery from a myocardial infarction (MI). In a panel study by Kathleen Ell and Julian Haywood (1984), the role of social support in MI recovery was explored. It was tested if it can contribute towards multiple recovery outcomes. The study utilized analysis of data collected through structured interviews during acute hospitalization (N = 114) and again 6 months later (N = 75) and one year later (N = 60). It was found that there are statistically significant associations between measures of support and psychological, functional, and physical outcomes (Ell and Haywood, 1984).
Social support and Cardiac events
The literature suggests two major models explain the impact of social support: the main effect and the stress-buffering models. In the main effect model, social support has an impact on disease outcomes regardless of other physical or psychosocial risks.
According to the main effect model, it has been hypothesized that social integration has an impact on cardiac outcomes because integrated patients may be more likely to receive medical treatment or be more motivated to alter risk factors. The stress-buffering model suggests that social support is beneficial only in the presence of ‘high stress’ or high psychological risk. Supposing that depression is a ‘high stress’ situation, the stress-buffering model suggests that perceived social support should act to buffer the impact of depression on cardiac events. In a sample of 887 men and women following myocardial infarction, it has been found that very high levels of support buffered the impact of depression on mortality. Depressed individuals with high support did not experience a depression-related increase in risk. Further, high levels of support predicted improvements in depression symptoms over the first post-myocardial infarction year in depressed patients.
Many other earlier studies have confirmed the association between low social support and the risk of cardiovascular disease. In a 6-year follow-up of residents of South Sweden, Orth-Gomer and colleagues (Orth-Gomer & Johnson 1987) determined that the third of their sample having the lowest number of social contacts were at 50% greater risk of coronary heart disease mortality than those with higher numbers of social ties. In a prospective study in the United States, Vogt and colleagues (1992) followed members of a health maintenance organization for 15 years. Hospital records were then examined to identify the incidence of MI. After controlling for standard risk factors, such as hypertension and obesity, they determined that those individuals reporting a wide range of different types of social contacts were less likely to have a heart attack than those who were less socially integrated.
Social support also plays an important role in mortality from preexisting cardiovascular disease. In 1984, Ruberman and colleagues first reported that more socially isolated men were at greater risk of death following an MI. A 4-year follow-up study found that patients who lived alone after a heart attack were at greater risk for recurrent fatal and nonfatal coronary events (Case et al. 1992). Similarly, individuals who were not married and had no relatives have been observed to be more likely to die in the 5 years following an MI. At least 6 other studies have yielded similar results. Berkman and colleagues suggest that lack of emotional support may be the reason why social isolation often results in greater post-MI mortality (Berkman et al. 1992). In their longitudinal study, emotional support was measured prospectively, and patients were followed for 6 months. Even after controlling for age, the severity of MI, and co-morbidity, individuals reporting no sources of emotional support had a threefold higher risk of mortality than those reporting one or more sources.
Limitations of Findings
Data from these studies convincingly suggest that social support plays an important role in the development and progression of coronary disease. The specific aspects of social support that are important and the mechanisms by which social support may affect disease are less clear. Many studies are difficult to compare because each uses a different instrument to measure social support. Further, many studies fail to report the psychometric properties of the instrument chosen to measure social support. Research in this area would be better understood if there were more standardized measurement tools that are also psychometrically accurate. Another important consideration in social support research is the nature of the study samples used. Many studies of social support are conducted on women, based on the popular assumption that females would be more responsive to social support than males. However, the epidemiological data suggest that, in fact, men may be more responsive to social support than women (Orth-Gomer & Johnsson 1987). The specific needs of the individual may also mediate the beneficial effects of social support. Epidemiological data suggest that a minimum number of social contacts are necessary for cardiovascular health for women in urban areas (Orth-Gomer & Johnsson 1987). However, women in rural settings have smaller social networks and do not experience negative cardiovascular effects. Orth-Gomer & Johnsson (1987) have speculated that women who live in urban areas lead more unstable lives owing to greater changes and contradictory demands from multiple social roles, and therefore require larger social networks.
Another factor to be considered is that not all social contacts provide support. Social relationships may involve demands for attention or assistance, conflict, and criticism. Further, the number of supportive relationships an individual has appears to be only weakly correlated with the number of non-supportive relationships they have. It has long been suggested that social integration may actually be harmful if it is accompanied by interpersonal conflict or problems. There is now increasing evidence that positive, supportive relationships are associated with lower levels of cardiovascular and neurohormonal reactivity, whereas non-supportive relationships are associated with heightened physiological stress responses. Therefore, the nature of social relationships may be as important as the number and should be measured as well. Although low levels of support are associated with increased risk for cardiac events, it is not clear what types of support are most associated with clinical outcomes in healthy persons and coronary heart disease patients. There also is little evidence that improving low social support reduces coronary heart disease events (Frasure-Smith and Lesperance, 2000).
In the case of coronary artery disease, the strongest evidence for risk factors such as depression and social support exists in the health psychology and behavioral medicine field. But medical practitioners do not accept these findings for the following reasons: the fact that the literature contains many studies with various design limitations, such as small or selected samples among studies reporting positive (or negative) results, or lack of appropriate control groups; inconsistent results among studies; and doubts about the actual clinical relevance of behavioral variables and interventions. There are also inconsistencies in defining and measuring various psychosocial measures and gaps in knowledge regarding the applicability of various psychological risk factors in different demographic and health groups. Finally, it is not clear that depression or lack of social support can affect all patients and all cardiac endpoints in the same way or to the same degree. These factors may have different effects on both cardiac physiology and cardiac endpoints for different people.
Counter Arguments
There is some confusion regarding the contribution of depression towards myocardial infarction. Are depressed MI patients really depressed, or do they only seem so because some depressive symptoms mimic cardiac symptoms? Do depressed MI patients have a poorer prognosis primarily because they have more severe disease or because of depression? It is assumed that cardiac symptoms are an unbiased marker of the severity of underlying disease, regardless of depression status. But it is possible that depressed patients report more cardiac symptoms, regardless of disease severity. The second implicit assumption is that more severe disease causes depression, rather than the other way around. This is perhaps the more conservative assumption, but the actual interrelationship is likely to be complex, and we should not prematurely ascribe the adverse effect of depression to disease severity before we have a better understanding of this interrelationship. There is also some confusion regarding the nature and meaning of social support. Another confusing question is: Is every aspect of our social relationships supposed to be supportive and to provide a clear and unambiguous health benefit to a person?
Conclusion
Extensive evidence from multiple sources proves that psychological and psychosocial variables can have a significant impact on organic manifestations of coronary artery disease. In this paper, only a few studies have been considered in the realm of psychological or social risk factors. However, it can be seen that there is substantial evidence for the effects of psychosocial variables such as depression and social support on cardiac events. There can be both major and contributing factors that play a huge role in causing a chronic cardiac event in patients recovering from myocardial infarction. The major risk factors that can not be changed are heredity (inherited traits), male sex, and increasing age. The contributing factors are those that result from modifiable lifestyle habits such as tobacco smoke, high cholesterol, high blood pressure, and physical inactivity. The latest research shows that psychosocial factors such as depression and social isolation can cause myocardial infarction in patients recovering from a chronic cardiac event. Depression and social isolation can work indirectly by leading to contributing factors of myocardial infarction or directly through various mechanisms. Studies show that they are both linked to chronic cardiac events.
Thus, it can be concluded that depression and lack of social support can increase the risk of myocardial infarction in a patient with cardiac problems.
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This element refers to AMI patients who have a history of smoking. In regard to the measure, individuals receive smoking cessation counseling during their hospital stay (“Adult smoking cessation advice/counseling,” 2010). A patient is considered eligible for this standard if he or she has smoked cigarettes at some point during the twelve months before hospitalization. The measure is highly important for AMI since quitting smoking can decrease morbidity and mortality in people. Individuals who attend at least brief smoking cessation sessions from their healthcare providers are more inclined to stop smoking. Unfortunately, it is noted that smoking cessation counseling is not provided to all patients with AMI (“Adult smoking cessation advice/counseling,” 2010).
Median Time to Fibrinolysis
This measure involves the average time from arrival to the delivery of “fibrinolytic agent in patients with ST-segment elevation or left bundle branch block (LBBB) on the electrocardiogram (ECG) performed closest to hospital arrival time” (“Median time to fibrinolysis,” 2010). Median time to fibrinolysis is necessary for AMI since it serves as a strong predictor of patient outcomes. When fibrinolysis is delayed by an hour, the likelihood of death is 2 to 1000. According to national guidelines, the most relevant time to fibrinolysis is 30 minutes upon hospitalization (“Median time to fibrinolysis,” 2010). Despite recommendations, many elderly AMI patients do not receive fibrinolytic therapy on time.
Median Time to Primary Percutaneous Coronary Intervention (PCI)
This measure is defined as the average time from arrival to PCI in individuals hospitalized with ST-segment elevation or LBBB on the ECG. The significance of this standard is justified by the decrease in morbidity and mortality in patients who are given primary angioplasty right after hospitalization (“Median time to primary PCI,” 2010). The effectiveness of PCI is increased if it is applied early. According to national guidelines, the prompt initiation of PCI is recommended for patients indicating ST-elevation MI.
The Pathophysiology of Acute Myocardial Infarction and Nursing Interventions
Acute myocardial infarction is reflected in patients through ST-segment elevation. AMI is the outcome of erosion or rupture of an atherosclerotic plaque “with thrombotic occlusion of an epicardial coronary artery and transmural ischaemia” (Heusch & Gersh, 2017, p. 774). The size of the resulting infarction can vary depending on the following factors:
the size of the ischemic area that is at risk;
the period and frequency of coronary occlusion;
the range of coronary microvascular dysfunction and the degree of residual collateral blood flow (Heusch & Gersh, 2017).
The progressive development of MI depends on the innate collateral circulation as well as resistance to myocardial ischemia. 30-50% of the risk area is possible to be affected and, as a result, saved by reperfusion after 4-6 hours from the onset of angina symptoms in the patient (Heusch & Gersh, 2017). Even upon 12 hours of coronary occlusion, there is still a possibility of interventional reperfusion which can eliminate the size of the infarct.
One of the most effective measures for AMI patients is PCI. Research indicates that patients receiving this intervention are more likely to develop hypertension, diabetes, or dyslipidemia but less likely to develop the peripheral vascular disease, chronic lung disease, or heart failure within two weeks (Wayangankar et al., 2016). Another productive approach is a secondary prevention intervention (Harbman, 2014). This nurse practitioner measure is reported to enhance the attainment of such objectives as blood pressure, smoking cessation, attendance at cardiac rehabilitation, physical activity, and other improvements (Harbman, 2014).
Harbman, P. (2014). The development and testing of a nurse practitioner secondary prevention intervention for patients after acute myocardial infarction: A prospective cohort study. International Journal of Nursing Studies, 51(12), 1542-1556.
Heusch, G., & Gersh, B. J. (2017). The pathophysiology of acute myocardial infarction and strategies of protection beyond reperfusion: A continual challenge. European Heart Journal, 38(11), 774-784.
Median time to fibrinolysis. (2010). Web.
Median time to primary PCI. (2010). Web.
Wayangankar, S. A., Bangalore, S., McCoy, L. A., Jneid, H., Latif, F., Karrowni, W., … Klein, A. (2016). Temporal trends and outcomes of patients undergoing percutaneous coronary interventions for cardiogenic shock in the setting of acute myocardial infarction: A report from the CathPCI Registry. JACC: Cardiovascular Interventions, 9(4), 341-351.