Smoking and Risk of Cardiac Disease - Research Paper Example

 Cardiac disease is a major contributor for mortality and morbidity all over the world including the United States. One of the devastating consequences of heart disease is massive heart attack which has almost 100 percent mortality. There are several risk factors for cardiac disease, some of which are preventable. The most significant preventable factor is smoking. Several studies have associated smoking with risk of cardiac disease. Infact, both passive and active smoking are associated with cardiac disease and hence in several countries in the world, smoking in public places has been banned. The specific cardiac disease that is caused by smoking is ischemic heart disease. While there are several views as to how smoking causes cardiac disease, most experts agree that there are several mechanisms through which smoking leads to the development of cardiac disease. Smoking is associated with many health-related problems and hence is a major health-related issue. It is a leading cause of illness and death all over the world. A smoker is at risk of developing cancers of the throat, mouth, lungs, bladder and esophagus and also heart attack. Research has shown that smoking increases the risk of lung, throat and mouth cancers by 14 times, cancer of the esophagus by 4 times, chances of death through heart attack by two times and chances of bladder cancer by 2 times (Bernstein, EmedicineHealth). Other health-related problems occurring due to cigarette smoking are emphysema, chronic bronchitis, peptic ulcer disease, pneumonia, cancer of the lip, cancers of the larynx and pharynx, malignancies of the abdomino-pelvic organs like pancreas, bladder and kidneys and also cancer of the cervix. Cigarette smoking can also increase the risk of burns (Bernstein, EmedicineHealth). In this essay, the role of smoking in the development of cardiac disease will be discussed. This will be preceded by an overview of ischemic heart disease. The thesis statement in this essay is “What is the relationship between smoking and cardiac disease?” Ischemic heart disease or IHD or coronary heart disease is a condition in which there is oxygen deprivation to the muscles of the heart as a result of decreased blood flow and perfusion and is accompanied by inadequate removal of the products of metabolism (Zevitz, Emedicine). This is the most common form of heart disease and a leading cause of premature death in the developed countries (Zevitz, Emedicine). The hallmark feature of this condition is imbalance between the supply and demand of oxygen of the myocardium which can occur either due to increased myocardial oxygen demand or decreased myocardial oxygen supply or both. It can manifest as one of these: anginal discomfort, ST-segment deviation on ECG, decreased uptake of technetium 99 or thallium 201 in images of myocardial perfusion and ventricular function impairment (Zevitz, Emedicine). Ischemia to the myocardium results from disease in the coronary arteries. The disease is most often due to formation of atheroma and its consequences like thrombosis. Coronary arteries can be affected in other conditions also like aortitis, polyarteritis, certain connective tissue disorders and in some congenital anomalies like fistula, malformation of major coronary artery and anomalous origin of coronary artery (Mcpherson, Medscape). Atheroma, also known as atherosclerosis is nothing but patchy focal disease of the intima of the artery. Of all the arteries in the body, coronary arteries are at increased risk of developing atheroma (Ross, p.443). The beginning of these plaques occurs in the second or third decade and gradually progresses. Initially, the circulating monocytes migrate into the intima of the arteries and take up oxidised low density lipoprotein from the plasma. These cells then become lipid-laden foam cells (Mcpherson, Medscape). Once these foam cells die, the contents of the cells are released which are mainly lipids. These form fatty streaks. Smooth muscles cells of the artery migrate in and around the fatty streaks and proliferate to form a plaque. The plaque encroaches into the lumen and also erodes the media layer of the artery. Gradually a thick collagen -rich fibrous tissue encapsules the plaque which is then called mature fibrolipid plaque. Mature plaques can rupture or fissure creating a pathway for blood to enter. The blood then disrupts the arterial wall. Disruption of arterial wall compromises the vessel lumen and precipitates thrombosis and vasospasm, all of which cause decrease in the blood flow through that vessel (Schachinger, p.1899). Sometimes, the rupture itself can cause occlusion of the vessel or can cause rapid growth of the plaque which occludes the vessel resulting in acute coronary syndrome (Stone, p.226). According to a report by the U.S. Department of Health and Human Services, "More than 61 million Americans suffer from some form of cardiovascular disease, including high blood pressure, coronary heart disease, stroke, congestive heart failure, and other conditions. More than 2,600 Americans die every day because of cardiovascular diseases, about 1 death every 33 seconds." More than 1.1 billion people who fall in the above 15 years age-group smoke cigarettes and there are about 4 million deaths every year globally due to tobacco consumption. It has been estimated, in the next decade, the death toll will rise to 100 millions a year (Pohrehn and Squier, 2000). This number will actually exceed the total deaths caused by AIDS, automobile accidents, tuberculosis, maternal mortality, homicide and suicide, all these combined. Such are the implications of tobacco consumption globally. The main problem arises because of exports of tobacco from developed countries to developing and under-developing countries. Thus tobacco consumption is a global health problem. There are many risk factors for the development of ischemic heart disease. Advanced age is one of the most important risk factors. As age advances, the number and size of the plaque increases and thus increases the risk of coronary artery event. Men are at increased risk of development of IHD than women (Zevitz, Emedicine). However, the risk is same after menopausal age in women. Family history of coronary artery disease increases the risk of ischemic heart ailment. This is either due to genetic factors or due to similar diet, eating habits, lifestyle and smoking. Research has shown that 40% of risk of developing IHD can be attributable to genetic factors and 60% to environmental factors. Also, it is important to note that other risk factors like hyperlipidemia, hypercholesterolemia and hyperfibrinogenemia are also influenced by genetic factors. There is some research which has shown common deletion polymorphism of angiotensin converting or ACE enzyme gene. This gene mutation has been linked to increased levels of ACE in the blood which also increases the risk of coronary artery disease ((Mcpherson, Medscape). The most avoidable cause of IHD is smoking. Research has proved a strong, consistent and dose related association between smoking and IHD. The risk is highest in young people. The risk decreases significantly after quitting smoking for 6 months. Consumption of tobacco, especially in the form of smoking is a leading cause of death and causative factor for many other conditions. Other forms of tobacco also lead to various health ailments. Research has shown that both active and passive smoking can produce health related hazards. Highest rates of passive smoking exposure is seen in cafes, restaurants and bars, followed by work place and then homes of relatives, friends and acquaintances. The quality and lifespan of smokers depends on the severity and number of smoking related illness and other associated comorbid conditions. Consumption of alcohol and other illicit drugs, sedentary lifestyle and stresses life can increase the mortality and mobility related to smoking (Bernstein, EmedicineHealth). Hypertension, both systolic and diastolic, increase the risk of IHD. Hypercholesterolemia contributes to premature coronary artery disease. The risk is directly related to plasma levels of LDL cholesterol and inversely related to HDL cholesterol. Hypertriglyceridemia also increases the risk of IHD. Certain hemostatic factors like hyperfibrinogenemia and increased factor VII levels increase the risk of coronary thrombosis and myocardial infarction. Regular exercise in the form of brisk walking or cycling or swimming for atleast 20 minutes for 2-3 times in a week increases HDL cholesterol, lowers blood pressure, decreases blood clotting and promotes collateral vessel formation and thus reduces the risk of IHD ((Mcpherson, Medscape). Hence lack of physical activity is considered as one of the risk factors for IHD. Diabetes mellitus allows diffusion of existing coronary atheroma and thus increases the risk of IHD. Diabetes is frequently associated with obesity and physical activity, both of which are again risk factors for IHD. Obesity, by itself, is an independent risk factor for IHD. Heavy consumption of alcohol is associated with hypertension and increases the risk of cardiac events. Deficiency of polysaturated fatty acids or PUFA in the diet is associated with increased incidence of IHD. Low levels of antioxidants like vitamin C and vitamin E are independent risk factors for coronary artery disease (Zevitz, Emedicine). IHD can manifest as any one of the following: Angina, myocardial infarction, heart failure, arrhythmias and sudden death. Myocardial infarction or MI occurs when the imbalance between supply and demand of oxygen to the heart muscle or myocardium becomes critical enough to cause myocardial necrosis (Alpert et al, 2000). This mostly occurs as a result of rupture of plaque in a coronary vessel leading to sudden reduction of blood supply to the concerned portion of myocardium. Smoking is strongly associated with myocardial infarction. According to Gerace (WebMD), in the US, 20 percent of all deaths related to heart disease are directly related to cigarette smoking, because smoking is a major contributing factor for coronary artery disease. The risk of heart disease is directly related to the number of cigarettes smoked per day. Those who smoke one pack of cigarettes per day are twice likely to suffer from coronary artery disease. The risk of smoking persists as long as the smokers continue to smoke. Women who smoke and also take birth control pills are are increased risk of not only heart attack, but also stroke and peripheral vascular disease. It is not only active smoking that causes heart disease, but also passive smoking (Gerace, WebMD). Smoking increases the risk of heart disease by decreasing oxygenation to the heart, increasing heart rate and increasing blood pressure (Czernin, 395). Heart derives its energy from oxidation of substrates. The oxygen consumption of the heart depends on many factors like heart rate, systolic wall tension, contractility, activation and depolarisation, shortening against a load, maintenance of cell viability in basal state, maintenance of active state, fatty acid uptake and direct metabolic effect of catecholamines. As the heart rate increases, the oxygen consumption of the heart increases (Zevitz, Emedicine). Smoking also increases blood clotting and causes damage to the cells lining coronary arteries and other blood vessels (Gerace, WebMD). Smoking also causes decrease in HDL cholesterol and decreased exercise tolerance. According to Heitzer and Meinertz (p.30), "Smoking causes acute hemodynamic alterations such as increase in heart rate, systematic and coronary vascular resistance, myocardial contractility, and myocardial oxygen demand. These short-term effects could lower the ischemic threshold in smokers with coronary artery disease and contribute to the increased risk for acute cardiovascular events." The initiating event for atherosclerosis is thought to be endothelial damage and several long term studies have demonstrated direct toxic effects with regard to structural changes in the human endothelial cells (Vallance, p.342). Endothelium has a functional role in the regulation of vascular tone, leukocyte adhesion, platelet endothelial interactions, smooth muscle cell proliferation and leukocyte adhesion. It also interferes with the synthesis and release of various vasoactive substances like the nitric oxide. The main cause for endothelial dysfunction subsequent to smoking is increase in oxygen free radicals which inactivate the important vasodilator nitric oxide leading to vasoconstriction. Smoking also increases oxidative modification of LDL (Heitzer and Meinertz, p.30). Another important effect of smoking is the systemic inflammatory response leading to raised C-reactive protein and leucocyte counts. Thrombosis is due to the prothrombotic effects of smoking caused due to alterations in the function of platelets, fibrinolysis and imbalance between prothrombotic and antithrombotic factors. Among the modifiable risk factors for cardiovascular disease, smoking is the most significant one. Though it initially starts are as a "behavioural choice" or "habit", it soon becomes an acquisition and transforms the nicotine-receptor density and neurophysiological function. During smoking throusands of chemicals are inhaled which initiate and accentuate atherosclerosis by influencing various aspects of the cardiovascular system like vascular dysfunction, vasomotor activity, lipid oxidation, development of atheroma and finally thrombosis (Pipe, 145). In any patient with cardiovascular disease, the priority management is smoking cessation. The benefits of quitting smoking accrue rapidly and decreases the risk of disease progression, hospital readmission and overall mortality (Pipe, 145). According to Morita (1914), cessation of smoking improves the peripheral vasomotor response. There is some evidence that even passive smokers have lower vasomotor response and this imporves after decreased exposure to smoking. In a study by these authors, they reported that "coronary vasomotor abnormality assessed by MBF response to the CPT was improved at 1 mo after smoking cessation and that the findings indicate that coronary endothelial dysfunction may be reversible within 1 mo after smoking cessation in healthy young smokers” (Morita, 1914). Thus, smoking is a strong risk factor for development of ischemic heat disease due to several mechanisms, the most significant of which is endothelial damage and atheroma formation. Both passive and active smokers are at risk. The risk is directly proportional to the number of cigarettes consumed and it decreases after cessation of smoking. Thus, every attempt must be made by health care professionals and others to decrease smoking, especially in those who are already have an established heart disease. 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