Download CORONARY ARTERY DISEASE: A REVIEW OF RISK FACTORS

CORONARY ARTERY DISEASE: A REVIEW OF RISK FACTORS
Viquar Fatima Qureshi1*, Fathima Aamer1, Mohammad Rehan Qureshi1
Roohi Fathima2 and Mohammad Farhan Qureshi2
Deccan College Of Medical Sciences, Hyderabad, Andhra Pradesh, India and
Foothills Medical Center, University of Calgary, Calgary, Alberta, Canada.
‫لا‬.‫( والعوامل المدييلة يلي‬CAD) ‫أجريت محاولة لمراجعة العالقة بين أمراض الشرايين التاجية‬
‫مللن اباللاار الرةيألللية بمللراض الشللرايين التاجيللة الفيل الللوليبط ةللط اب شللية الما للة ويشللم‬
‫ م قيلاي المواوملة ل أللولين‬،‫ م ملرض الألل رلم الأللم ةم الفيل ةلط يملوز الل‬،‫ارتباع ضلط الل‬
‫للرا الورايللة م يوام ل تر يايللة وبي يللةم‬،‫ مللن العوام ل اب‬،‫ومواألتيين ةللط اللل‬.‫والزي ل اي ةللط الللو‬
‫موز والألللعرا الحراريللةم‬،‫يع ا جتمللايطم الزيللاي ةللط ت للاوت اللل‬،‫الجل م الع للر والعللرعم اللل‬
‫ م‬،‫ابا م الفي ةط يملوز الل‬.‫ا لت‬
‫ا فباض ال شاط ال ايعطم والتطيرا الم احاة (قياي ي‬
‫ م ملط أيملا ي تأللامع ةلط‬،‫ اب ألل‬،‫ل‬.‫المواومة ل ألولينم الفيل اللوليبط ةلط اب شلية الما لة م ج‬
‫اص لاعض العوامل ملل‬، ‫قياي احتمالية أمراض الشرايين التاجية ةط اار الألن أُي ط امتما‬
‫يللة وأ للواع الشللواةق‬،‫ال احيللة ال بألللية ا جتماييللةم طريوللة الحيا مالعوامل الوراييللة والاي يللة والم ا‬
‫مويةم ت يب الشلرايينم‬،‫ م مجموية أمراض ابويية ال‬،‫الحر م الج م ا و اع ال مث م ةور ال‬
‫اق الت بألط وابيراض الجا اية ل يوية واإلشعاع‬.‫الأل رلم أمراض ال يى والج‬
Abstract
An attempt is made to review the relationship between coronary artery disease
(CAD) and its risk factors. The major risk factor for CAD is endothelial dysfunction,
including hypertension, diabetes, obesity, dyslipidemia, increased insulin resistance,
and hyperhomocysteinemia. The other factors such as genetic, constitutional,
environmental, gender, ethnicity, social support, increased fat and calorie intake,
decreased physical activity and associated changes (increased inflammatory markers,
dyslipidemia, insulin resistance, endothelial dysfunction and oxidative stress) are also
associated with increased risk for CAD in elderly. Special emphasis is given to the
factors such as, psychosocial, life style, environmental, genetic, immunological, free
radical species, gender, menopause, anemia, comorbidity, hypertension,
atherosclerosis, diabetes, renal disease, pulmonary disease, side effects of therapeutic
drugs and radiation.
___________________________________
1* Author for correspondence
1
2
Deccan College of Medical Sciences, Hyderabad, Andhra Pradesh, India
Foothills Medical Center, University of Calgary, Calgary, Alberta, Canada.
Introduction
Complications of cardiovascular disease, including, myocardial infarction,
peripheral vascular disease, angina, stroke and heart failure caused by CAD are the
leading cause of death in adults in the United States, accounting for about one-third of
all deaths in subjects over 35 years of age [1]. Coronary events are caused by the
rupture of an atherosclerotic plaque with subsequent thrombosis formation. Despite
great strides the knowledge of coronary artery risk factors remain poorly defined. The
purpose of this article is to update the literature on different risk factors for CAD and
offer suggestions to reduce the risk of CAD.
Risk Factors for Coronary Artery Disease
1.
Psychosocial Factors:
Interest in the link between psychosocial factors and CAD has recently
increased. Literature reports identified a number of psychosocial factors including
chronic stress, socioeconomic status, depression, personality traits, social support and
immigrant status which have link with CAD.
1.1.
Chronic Life Stress
The chronic life stress includes work stress, job strain, and effort-reward
imbalance, marital and domestic stress. Work stress tends to be greater in individuals
of lower socioeconomic status, and is also associated with lower social support,
conventional cardiovascular risk factors, less education and certain psychological
traits [2]. Low job control is more common in lower socioeconomic status groups, and
about half of the inverse social gradient in CAD incidence is attributable to low
control at work [3]. Studies in Finland, Germany and the UK have shown that Job
strain and effort-reward imbalance has been linked to more rapid progression of
carotid atherosclerosis and risk of CAD [4] Marital stress predicts depressive
symptoms in women and women with established CAD who report high marital stress
have a poorer prognosis [5].
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1.2.
Socioeconomic Status
Established evidence shows that low socioeconomic status is associated with
adverse health outcomes. Low socioeconomic status is also an established risk factor
for the development of CAD [6,7]. Horne et al., [8] found lower socioeconomic
status, including residential economic status and economic status, predicted increased
risk of death/myocardial infarction in a large population of patients with significant,
angiographically-defined CAD at baseline. These studies supported the idea that
socioeconomic status-related morbidity and mortality involve complex combinations
of factors (e.g., economic, educational, psychological, social and also residential
status). Further studies of residence status-related risk are warranted, as are studies of
socioeconomic status in secondary-prevention cohorts and with preventive
interventions.
1.3.
Depression
Depression and coronary heart disease may be related in several ways: (1)
there is epidemiological evidence that high levels of depressive symptoms in male and
female patients are associated with an increased risk of myocardial infarction and a
higher mortality following an acute cardiac event. Furthermore, patients developing
depression after myocardial infarction have more complications, including cardiac
arrhythmias. (2) In patients with a chronic coronary heart disease depression also
results in a worse cardiac functional status with more frequent and severe chest pain,
more physical limitation, less treatment satisfaction and a lower perceived quality of
life. Non-compliance with drug therapy is also more prevalent in depressed cardiac
patients. (3) The possible pathophysiological mechanisms leading to more frequent
complications of coronary heart disease in patients with depression are not fully
explained, but could partly be due to higher sympatho-adrenergic stimulation and
3
increased platelet aggregation [9].
In a study on the role of psychosocial factors of time urgency/impatience,
achievement striving/competitiveness, hostility, depression, and anxiety on long-term
risk of hypertension, Yan et al., [10] found time urgency/impatience and hostility are
associated with a dose-response increase in the long-term risk of hypertension in
young adults.
1.4.
Personality Traits
Literature reports have focused that hostility and anger are the potential risk
factors for cardiovascular disease including CAD. However, the confounding effects
of gender, ethnicity, social support, increased fat and calorie intake, decreased
physical activity, and alcohol and tobacco weaken the correlation [11].
1.5.
Social Support
In England, 16% of men and 11% of women report a severe lack of social
support. Low social support causes greater psychological distress [12]. The adverse
effects of stressful life events can be ameliorated by social support; socially isolated
people may experience augmented stress [13].
1.6.
Obesity
Obesity is widely recognized as a risk factor for CAD. Literature reports
suggest that it can become a risk factor only when accompanied by hypertension,
hyperlipidemia, impaired glucose tolerance, etc. In a survey conducted on a relatively
homogeneous group of 527 Konkani subjects, Mooteri et al., [14] demonstrated a high
prevalence of CAD despite a lack of significant obesity.
1.7.
Smoking
Cigarette smoking is a known risk factor for CAD and sudden cardiac death
(SCD). Literature reports suggest association of smoking with the elevation of IL-2
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and sP-selectin serum levels in patients with stable CAD [15]. Current cigarette
smoking is a powerful independent predictor of SCD risk in patients with CAD.
Patients who quit smoking experienced a significant reduction in SCD risk [16].
However, the effect of continued cigarette smoking and smoking cessation on SCD
risk in patients with established CAD is subject to controversy. Wang et al., [17]
reported a high prevalence of overweight and/or smoking patients with coronary heart
disease in rural China. Smoking is also found to be the most significant independent
risk factor for lower extremity arterial disease, associated with claudication and
amputation [18]. Nevertheless, a survey conducted in a relatively homogeneous group
of 527 Konkani subjects revealed a high prevalence of CAD despite a lack of smoking
[14]. Kaamotho et al., [19] also found low prevalence of cigarette smoking in a study
on risk factors for CAD.
2.
Environmental Factors
Air pollution--the 20th century's other "big smoke"--deserves consideration as
a 2nd cause. Auto exhaust blankets the world's cities. It consists of smoke and other
effluents of petroleum vaporization and combustion that emanate from the crankcases
and exhaust pipes of trucks and automobiles. Auto exhaust gases fit the timeline, and
their increasing amounts parallel the worldwide rise in coronary heart disease.
Increasing doses of these chemicals imitate cigarette smoke and stimulate
inflammation in the lungs. They appear to be absorbed into the blood, where they
cause inflammation in blood vessels, increased blood pressure, and clogged coronary
arteries [20].
3.
Genetic Factors
CAD is a complex, multifactorial disorder in which interactions among
various genetic and environmental influences play an important role. Genetic
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epidemiological studies have suggested that several gene polymorphisms, including
those in the genes for angiotensin-converting enzyme and paraoxonase increase the
risk for CAD in individuals with type 2 diabetes [21]. Polymorphisms in the genes for
insulin-like growth factor-I and lipoprotein lipase have been shown to increase the
risk of both CAD and type 2 diabetes [17, 22].
There are certain genetic defects that affect activities of some enzymes
(cystathionin β-synthase, methyltransferase and 5, 10-methylenetetrahydrofolate
reductase) which may lead to homocystinuria. Heterozygosity for deficiency of
cystathionin β-synthase is known to be linked with arthrosclerosis and thrombotic
disease including CAD [23].
Adiponectin gene locus, chromosome 3q27, is the candidate site for CAD.
Adiponectin I164T mutation is associated with the metabolic syndrome and coronary
artery disease. The I164T mutation in the adiponectin gene is reported to be a
common genetic background associated with the metabolic syndrome and CAD in the
Japanese population [24]
The Von Willebrand factor (VWF) may be causally associated with coronary
heart disease or merely be a marker of endothelial damage. The G allele of the -1793
C/G promoter polymorphism in the VWF gene has been associated with higher
plasma levels of VWF. Van der Meer et al., [25] found a clear association of G allele
of the -1793 C/G polymorphism in the VWF gene with an increased risk of Coronary
heart disease.
4.
Immunological Factors
A lot of literature data indicate a relationship between local and systemic
inflammatory/immune activation and the pathogenesis of atherosclerosis. In
atherosclerotic conditions the activation may be modified by a couple of factors that
6
exert damaging effects on the vascular wall [15].
Inflammation and the recruitment of monocytes into the artery wall are
thought to be important aspects in the initiation and progression of atherosclerosis.
There is an increase of IL-6 or sVCAM-1 in atherosclerosis progression and its
clinical consequences including CAD [26]. Smoking is known to affect a number of
inflammatory markers in CAD patients [15]. Smoking-induced endothelial
dysfunction may lead to elevation of IL-2 and sP-selectin serum levels and
consequent inflammatory activation within a vascular wall mediated by cytokines and
adhesion molecules. The elevation of IL-2 and sP-selectin serum levels caused by
smoking cigarette is found to be associated with stable CAD. CAD patients who have
never smoked are characterized by delayed onset of angina and increased sTNFR 2
concentrations [15]. Cesari et al., [27] suggested an important role for IL-6 and TNFalpha in clinical as well as sub-clinical CAD. They found CRP C-reactive protein had
a weaker association with CAD than the cytokines in older men and women.
5.
Role of Free Radical Species
Low density lipoprotein (LDL) is oxidatively modified by endothelial cells
and macrophages in the arterial wall. Oxidatively modified LDL (Ox-LDL) is known
to be involved in the initiation and development of atherosclerotic lesions [28]. The
uptake of Ox-LDL by macrophage and smooth muscle cells leads to the formation of
foam cells, which accumulate lipid droplets [29]. The Ox-LDL exhibits several cell
biologic activities, i.e., it enhances the interaction between leukocytes and endothelial
cells, inhibits endothelial cell migration, induces endothelin secretion from endothelial
cells and macrophages, and induces apoptosis in vascular smooth muscle cells. In a
recent study, Zhang et al., [30] found increasing circulating levels of Ox-LDL to be a
significant risk factor for CAD.
7
An imbalance between oxidative damage and antioxidative protection in
association with the pathophysiology of atherosclerosis has been suggested to cause
CAD. In patients with CAD, erythrocyte glutathione and Glutathione peroxidase were
significantly lower than those found in controls. Patients with CAD are reported to
have higher malondialdehyde and lower total plasma protein thiol levels than the
controls, which represent the oxidative damage products of lipid and proteins [31].
6.
Gender
Studies on hypertensive pregnancies and conventional risk factors in women
<66 years, revealed diabetes, hypertension, hypercholesterolemia, advanced age,
smoking, and pre-eclampsia to be independent risk factors for subsequent CAD in
women [32]. While, Kamotho et al., [19] suggested diabetes mellitus, hypertension,
dyslipidaemia, age in male gender, as the significant risk factors for CAD.
Cardiovascular disease continues to be the leading cause of death in women over age
50 in the United States. Significant differences exist between men and women in the
prevalence, incidence, and treatment outcomes of cardiovascular disease, particularly
CAD. The presenting features of CAD may vary between men and women, and the
diagnostic evaluations of such symptoms may differ based solely on gender [33].
However, In a cross-sectional autopsy study of the arterial surface involvement with
atherosclerosis among the Greenlanders, no significant differences between females
and males were found in either the risk factors or prevalence and extent of
atherosclerosis in the aorta and in the coronary arteries [34].
7.
Menopause
Menopause is a physiologic phase of a woman's life, due to the changes of
their hormonal status. Fastidious symptoms may be associated with changes in the
metabolism together with new cardiovascular risk factors, particularly aggressive for
8
the female cardiovascular system, unprepared because of the protection due to the
fertile period. Changes of the lipid profile, obesity, hypertension, glucose intolerance
and diabetes mellitus may intervene as severe risk factors. Cardiovascular disease
represents therefore the most frequent cause of mortality and morbidity also in the
female gender more than cancer either in the United States as in Europe [35]. The
risks related to post-menopause are mainly due to the abrupt interruption of estrogen,
which has indirect protective effects on lipid, glycidic metabolism and direct effects
on vessel function [33, 35].
8.
Anemia
In animals, experimentally induced CAD significantly inhibits the
hemodynamic response to surgical blood loss; anecdotal evidence in humans
corroborates these findings. Erythropoietic response to surgical blood loss may also
be blunted in patients with CAD. Regardless of whether anemia is the result of a
preexisting condition or surgical blood loss, its presence worsens outcomes in patients
with CAD who undergo cardiac surgery. The combination of coronary artery disease
and anemia has resulted in acute myocardial infarction as well. Finally, anemia after
noncardiac surgery is associated with an increased risk of myocardial ischemia,
potentially creating a cycle in which blood loss and myocardial ischemia exacerbate
each other (36).
9.
Comorbidity
As the population ages, physicians are increasingly required to make decisions
concerning patients with multiple co-existing illnesses (comorbidity). Many trials of
CAD therapy have excluded patients with significant comorbidity, such that there are
limited data to guide the management of those patients. Comorbid disease is strongly
associated with long-term survival in patients with CAD [37].
9
9.1.
Hypertension
Hypertension may be associated with increased body mass index, with insulin-
resistance, sodium retention, increased blood viscosity and estrogen deficiency with
increased smooth muscle cell proliferation which determines an increase in systemic
vascular resistance. It is a common cardiovascular disease and considered as the most
significant risk factor in the development of stroke, congestive heart failure, renal
insufficiency, arterial lesions in general, coronary heart disease and myocardial
infarction. Hypertension is common among obese people and is related to smoking
habits and drinking alcohol [19,38]. Haukkamaa et al., [32] found hypertensive
pregnancies to be independent risk factor for CAD among young women.
Although numerous cross-sectional studies have reported associations of
hypertension, hypercholesterolemia, diabetes, smoking, and/or obesity with the
presence of CAD, correlations of these risk factors for myocardial infarction with the
degree or progression of CAD have been less consistent. Nevertheless, these risk
factors are generally assumed to be major determinants not only of myocardial
infarction, but of the degree of CAD as well. On multiple regression analysis, none of
these risk factors was associated with degree of CAD. Three other variables (age,
high-density lipoprotein-cholesterol and free testosterone, often show an independent
association with degree of CAD. These variables may be stronger predictors of degree
of CAD than are blood pressure, cholesterol, diabetes, smoking, and body mass index
[39].
Baweja et al., [40] found CAD to be significantly associated with stroke,
systemic hypertension, diabetes mellitus, end-stage renal disease, and family history
of stroke and myocardial infarction. The increased incidence of adverse
cardiovascular events in patients with aortic sclerosis is associated with CAD and
10
inflammation, not a result of the effects of valvular heart disease per se [41].
9.2.
Atherosclerosis
Atherosclerosis, characterized by cholesterol-laden plaques, is nearly universal
in western society, with extensive involvement of coronary, carotid and major arteries
of the leg [42]. Whether imaged directly by carotid ultrasound or detected by reduced
ankle blood pressures, symptoms of intermittent claudication in the leg, or clinically
apparent coronary heart disease, atherosclerosis of the major arteries is consistently
associated in general populations with elevations in plasma cholesterol levels,
Smoking and diabetes are also major contributors to atherosclerosis [18].
9.3.
Diabetes
Among risk factors for CAD, diabetes mellitus is a major contributor, not only
in the development of CAD but also to outcome various manifestations of the disease.
In fact, increasing levels of blood glucose, even below the level of established
diabetes, serve as predictors of increased risk [43]. Despite improvement in the
management of patients with unstable coronary syndromes, unstable CAD is still
linked to a substantially increased mortality and morbidity among diabetic patients
[44]. All the complications except for CAD were more frequent in men with type 1
diabetes mellitus. Risk factors that correlated with all chronic diabetic complications
were diabetes duration and arterial hypertension. Age, lipid abnormalities, smoking
and alcohol consumption, family history were associated with varying degrees of type
1 diabetes mellitus complications. In patients with microangiopathy, neuropathy and
CAD the following components of metabolic syndrome were found: obesity,
hypertension, dyslipidemia implying the contribution of insulin resistance to the
pathogenesis of these complications [45].
Insulin resistance plays a significant role as a major risk factor of CAD [46].
11
There are many metabolic consequences of insulin resistance and multiple conditions
associated with insulin resistant states. The most obvious pathology associated with
insulin resistance is type 2 diabetes mellitus, but other manifestations include
hypertension, central obesity, a hypercoagulable state, and dyslipidemia. The
atherogenic dyslipidemia associated with insulin resistant states is characterized by
hypertriglyceridemia; an increase in very-low-density lipoprotein secretion from the
liver; an increase in atherogenic small, dense low-density lipoprotein; and a decrease
in high-density lipoprotein cholesterol. Each of these lipid abnormalities is an
independent risk factor for CAD, and in concert, the cardiovascular risk is magnified.
Therefore, insulin resistant states should be identified as early as possible in patients,
and these lipid abnormalities should be assessed and treated [47]. Factors beyond the
extent of flow-limiting coronary lesions are of considerable importance for outcome
in diabetic subjects with unstable coronary syndromes [48].
9.4.
Renal Disease
In a study on identification of the association of atherosclerotic CAD and
pulse pressure with renal disease progression in patients with mild chronic renal
disease, Kim et al., [49] found atherosclerotic CAD and pulse pressure to be
associated with renal disease progression. End stage renal disease is found to be
significantly associated with cardiovascular diseases including CAD [40].
9.5.
Pulmonary Disease
Pulmonary fibrosis and atherosclerosis have many similarities at the
histopathologic level. Moreover, fibrotic lung diseases exhibit systemic effects and
have the potential to affect the vasculature beyond the lung. Recent studies [50]
revealed a significant association between fibrotic lung disorders with CAD. Gowda
et al., [51] found acute pulmonary edema (after cardioversion of arrhythmiaas) to be
12
associated with cardiac diseases including CAD.
9.6.
Side Effects of Therapeutic Drugs
Widespread human exposure to a variety of drugs, chemicals, and biologic
products and recent awareness of their toxic manifestations has led to the recognition
of many diseases including cardiovascular, renal, neurologic abnormalities, metabolic
acidosis, disseminated intravascular coagulation, or pulmonary diseases [52].
There is a growing concern about an increased risk for cardiovascular disease
in HIV infected patients receiving antiretroviral therapy. This risk could be related to
metabolic abnormalities associated with long-term use of antiretroviral drugs. In fact,
well recognized cardiovascular risk factors such as hypertension, dyslipidaemia,
diabetes mellitus and central fat deposition are increasingly seen in HIV patients on
antiretroviral therapy. These factors can also be associated with non reversible risk
factors, such as male sex, age greater than 40 years and family history of premature
CAD. In addition, cigarette smoking and sedentary life style may predispose these
patients to significant cardiovascular disease [53].
The association of highly active antiretroviral therapy regimens that include
protease inhibitors with metabolic and somatic disorders has raised concerns about the
possibility of an increased risk of CAD in patients with HIV infection. In a recent
study, Barbaro et al., [54] found protease inhibitors to accelerate the onset of CADrelated events in young, male, heavy smokers who develop metabolic disorders and
lipodystrophy during therapy.
Some anti-depressant medications, on the other hand, may also cause cardiac
symptoms and increase the risk in patients with coronary heart disease. The use of
tricyclic antidepressants has been shown to result in a higher relative risk of
myocardial infarction even after adjustment for other cardiovascular risk factors.
13
Tricyclic anti-depressants may have direct cardiac effects, such as QT-prolongation
with ventricular arrhythmias, orthostatic hypotension and, less frequently, myocardial
dysfunction [9].
9.7.
Radiation
People with Hodgkin's disease and breast cancer often receive therapeutic
irradiation to the chest (mediastinum) as an element of treatment. While the therapy
often cures the malignancy, it has been implicated in causing late-onset heart disease.
In a related study, Friedlander et al., [55] found therapeutic irradiation of the chest
resulted in the inadvertent inclusion of the heart within the irradiation field.
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