Risk Factors for Acute Myocardial Infarction

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Introduction

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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