Heart Diseases and Their Pathophysiology

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Table of Contents

Introduction
Heart work
Angina pectoris
Acute ischemic heart disease
Asymptomatic hyperglycemia
Conclusion
References

Introduction

Cardiovascular disease is the leading cause of death. One of every two women will die of a heart attack, stroke, or other cardiovascular illness. In 2002, 444,000 men and 479,000 women died of cardiovascular disease (Mahrman, 2006). Moreover, strokes caused 56,645 deaths in men and 87,124 deaths in women. In comparison, 246,000 women died of cancer of all forms; specifically, 43,100 women died of breast cancer, and 55,900 women died of lung cancer.

Thus, more than twice as many women died of cardiovascular disease than cancer (Mahrman, 2006). That ratio increases to 10:1 when deaths caused by cardiovascular disease are compared with deaths from accidents, chronic obstructive pulmonary disease, and pneumonia or influenza. Once coronary artery disease develops, women do not have a survival advantage over men. In fact, in every age group, women with coronary disease have a higher risk of death from a coronary event than men.

Most of the risk factors for coronary artery disease are similar for men and women. These risk factors include diabetes, hyperlipidemia, hypertension, smoking, family history, obesity, and aging. The main types of heart diseases are coronary heart disease, cardiomyopathy, cardiovascular disease, ischaemic heart disease, heart failure, hypertensive heart disease, inflammatory heart disease, and valvular heart disease.

Heart work

The heart is a unique muscle capable of generating its stimulation. The automaticity of specialized cardiac muscle fibers results in rhythmic impulses that are then transmitted to the remainder of the cardiac muscle (Mahrman, 2006). The finely orchestrated timing of the conducted impulse produces sequential systole in the atrium and ventricle, thus allowing efficient cardiac output. The primary pacemaker of the heart is the sinus node, a group of specialized cells located in the sulcus terminalis of the high right atrium, between the superior vena cava and the base of the right atrial appendage.

The impulse emitted from the sinus node excites adjacent atrial tissue in a progressive wavefront that produces atrial contraction. The electrical bridge between the atria and ventricles is the atrioventricular (AV) junction, a complex group of structures beginning with the AV node, which transmits the impulse slowly and provides time for active ventricular filling during atrial systole. The impulse then travels throughout the ventricles in a rapid, uniform wavefront by way of the penetrating bundle of His, the bundle branches, and the Purkinje fiber system, the net result of which is synchronized ventricular systole.

High shear stress may be involved in activating blood elements, which then have increased contact with possibly altered areas of the endothelium in the areas of low shear stress and blood flow. These factors initially give rise to typically eccentric plaques in predisposed regions (Mahrman, 2006). The zones with the greatest predilection for severe coronary atherosclerosis are the proximal left anterior descending coronary artery, the proximal right coronary artery, and the area of the distal right coronary artery just proximal to the origin of the posterior descending branch. As coronary atherosclerosis progresses, extensive remodeling of the vessel wall occurs.

In vascular segments with advanced atherosclerosis, all three layers of the arterial wall are involved and show intimal thickening, medial degeneration, adventitial fibrosis, and lymphocyte infiltration. At this stage, plaques may be concentric or eccentric. Medial degeneration allows for vascular dilatation, which tends to preserve the luminal diameter until the growth of atherosclerotic plaque is very advanced. An approximate 50% narrowing of luminal diameter is required to produce a lesion that impairs the increased blood flow required to meet high myocardial oxygen needs. An even greater reduction in luminal diameter is needed to impair baseline myocardial blood flow (Mahrman, 2006).

Less bulky coronary plaques associated with subcritical coronary stenosis are also subject to acute changes that can lead to sudden coronary thrombotic occlusion. The extent of anatomic coronary disease in symptomatic patients varies greatly (Klabunde, 2004). Notwithstanding, critical coronary stenoses often develop in the presence of multifocal and diffuse disease, which can lead to underestimation of the extent and severity of coronary atherosclerosis on coronary arteriograms also is common.

In most patients, an acute myocardial infarction cannot be seen anatomically. “Platelet aggregates in the coronary circulation have been documented in a significant subset of patients, particularly in those with a history of unstable angina pectoris” (Mahrman, 2006, p. 54). Thus, clinicopathologic studies are consistent with three major mechanisms of sudden cardiac death: ischemia-induced ventricular arrhythmia without acute myocardial infarction, acute myocardial infarction with ventricular arrhythmia, and primary ventricular arrhythmia associated with old myocardial damage and altered electrical conduction (Klabunde, 2004).

Angina pectoris

Angina pectoris is the clinical term used to describe chest pain resulting from a relative oxygen deficiency in heart muscle (Klabunde, 2004). The coronary heart disease syndromes are stable angina pectoris, unstable angina pectoris, variant angina (Prinzmetal’s angina), acute myocardial infarction, non-Q-wave infarction (usually nontransmural), and Q-wave infarction (usually transmural). Most individuals with angina have underlying atherosclerotic heart disease.

However, angina may also develop in some people with ventricular hypertrophy, “left ventricular outflow obstruction, severe aortic valvular regurgitation or stenosis, cardiomyopathy, or a dilated ventricle or ventricles in whom coronary artery stenosis is not present” (Klabunde, 2004, p. 53). Transient myocardial ischemia followed by reperfusion may lead to protracted recovery of segmental ventricular function, known as myocardial stunning. This is probably caused by cellular calcium overload and generation of free radicals Stunned myocardial segments may contribute to the development of CHF when the area of ischemia or infarction is large. Ischemia can lead to chronic depression of segmental ventricular function, known as myocardial hibernation (Klabunde, 2004).

Acute ischemic heart disease

Acute ischemic heart disease is often initiated by secondary changes that occur in atherosclerotic plaques. Coronary lesions at risk for acute changes are atheromatous plaques with thin fibrous capsules and large cores of lipid-rich debris. Hemodynamic trauma, local attachment, and activation of platelets and blood cells, and the cytotoxic effects of plaque contents all contribute to endothelial injury and plaque disruption (Lilly, 2006).

The process of injury and disruption can advance to include an influx of blood components, an increase in intraplaque pressure, and an outward rupture of the fibrous capsule. Intraluminal and intramural thrombus and intraplaque hemorrhage often develop. Intraplaque hemorrhage also can occur without plaque surface changes (Esselstyn, 2007). Such hemorrhages, which arise from leakage from intraplaque vessels, are rarely clinically significant. Vasospasm induced by vasoactive products released from activated platelets can contribute to coronary occlusion. In some cases, the coronary arteries are free of atherosclerosis, and the clinical syndrome results from one of a diverse (Lilly, 2006).

The clinical syndromes of acute ischemic heart disease are angina pectoris, sudden cardiac death, and acute myocardial infarction. Ordinary angina pectoris is usually associated with significant atherosclerotic narrowing of one or more of the major coronary arteries. The clinical syndromes of acute ischemic heart disease are angina pectoris, sudden cardiac death, and acute myocardial infarction. Ordinary angina pectoris is usually associated with significant atherosclerotic narrowing of one or more of the major coronary arteries. Sudden cardiac death is associated with significant atherosclerotic narrowing of at least one coronary artery in 90% of cases. Multifocal myocardial scarring or healed infarction (Esselstyn, 2007).

Heart diseases typically become evident in men in the prime of life, usually in their mid-50s, whereas in women, it generally develops 10 to 20 years later than this. Thus, many studies of this problem have included mostly men, and our knowledge about the coronary disease in women has largely been extrapolated from studies primarily focused on men (Klabunde, 2004). Although the risk factors for atherosclerosis are similar in men and women, there are enough differences that it is important to address coronary disease in women as a specific issue.

The most obvious difference between men and women is the presentation of coronary disease in women in the older, postmenopausal years (Esselstyn, 2007). Other important gender differences include the less specific clinical manifestations of coronary disease in women, the greater difficulty of diagnosis, and the more severe consequences of myocardial infarction when it occurs in women.

Asymptomatic hyperglycemia

Asymptomatic hyperglycemia also increases risk in women. Diabetes may negate the protective effect of estrogen in younger women. Intensive treatment of hyperglycemia has been shown to delay the onset and to slow the progression of retinopathy, nephropathy, and neuropathy (Klabunde, 2004). Cholesterol profiles of women and men differ with age. This change in lipid levels may help explain the increased incidence of coronary artery disease in older women (Klabunde, 2004).

Epidemiologic studies have confirmed that high cholesterol is a risk factor for coronary disease in women, Hypertension is more common in older women than in older men. Although hypertension is a risk factor for women, studies of hypertension have included mostly men. Conflicting results have been reported from the few trials that have involved women. Smoking is an important modifiable risk factor for men and women.

Although smoking increases the risk of a first myocardial infarction, the increased risk is eliminated within 2 to 3 years after quitting smoking. However, more men than women have recently quit smoking. In women, the risks of smoking and the use of oral contraception are additive. (Mahrman, 2006).

Family history and obesity, particularly obesity in a truncal distribution, are significant risk factors for both women and men. A family history of coronary disease and truncal weight distribution, although not modifiable factors, should alert the physician to the possibility of coronary disease in women who have these risk factors. The clinical presentation of coronary disease is often more subtle in women than in men. For example, angina pectoris is a less specific sign of coronary disease in women than in men. Although angina is the most common presentation of coronary disease in women, only one-half of women who reported having angina had significant coronary artery disease (Mahrman, 2006).

Conclusion

The onset and severity of heart disease differ between women and men. However, risk factors for heart disease have been studied more extensively in men. Only since the 1980s have they been studied in large, carefully designed clinical trials in women. Many factors (including oral contraceptive use, menopause, hormone replacement therapy, and cultural and social roles) contribute to the sex difference and may act synergistically with known heart disease risk factors (smoking, elevated cholesterol levels, and obesity) to increase risk. Several large studies have shown a substantial increase in the incidence and mortality of heart disease in diabetics. Hypertension is important to risk factors for cardiovascular morbidity and mortality.

References

Esselstyn, C. B. (2007). Prevent and Reverse Heart Disease. Avery.

Lilly, L. S. (2006). Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty. Lippincott Williams & Wilkins; 4th edition.

Klabunde, R. E. (2004). Cardiovascular Physiology Concepts. Lippincott Williams & Wilkins; Pap/Cdr edition.

Mahrman, D. E. (2006). Cardiovascular Physiology. McGraw-Hill Medical; 6 edition.

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