Atherosclerosis Smoking

Effect of vitamin C and E supplementation on susceptibility of plasma lipoproteins to peroxidation induced by acute smoking, Atherosclerosis 85 47-54. 

Klein LW. Cigarette smoking, atherosclerosis and the coronary hemodynamic response. A unifying hypothesis. J Am Col Cardiol 1984 4 972-974. 

Classic risk factors of atherosclerosis must first and foremost be fought with lifestyle interventions such as diet, physical activity, and smoking cessation. Indeed, and although it effectively relieves angina, simply... 

Cardiovascular disease (CVD) is one of the leading causes of death worldwide. There are a number of established risk factors including serum cholesterol levels, smoking and family history, which are responsible for between 50 and 75% of the CVD cases, with the remainder due to factors that cause atherosclerosis. Estrogen treatment such as hormone replacement therapy is known to protect against CVD by decreasing the levels of low-density... 

Factors that predispose an individual to IHD are listed in Table 4—2. Hypertension, diabetes, dyslipidemia, and cigarette smoking are associated with endothelial dysfunction and potentiate atherosclerosis of the coronary arteries. The risk for IHD increases two-fold for every 20 mm Hg increment in systolic blood pressure and up to eight-fold in the presence of diabetes.5,6 Physical inactivity and obesity independently increase the risk for IHD, in addition to predisposing individuals to other cardiovascular risk factors (e.g., hypertension, dyslipidemia, and diabetes). 

The development of CHD is a lifelong process. Except in rare cases of severely elevated serum cholesterol levels, years of poor dietary habits, sedentary lifestyle, and life-habit risk factors (e.g., smoking and obesity) contribute to the development of atherosclerosis.3 Unfortunately, many individuals at risk for CHD do not receive lipid-lowering therapy or are not optimally treated. This chapter will help identify individuals at risk, assess treatment goals based on the level of CHD risk, and implement optimal treatment strategies and monitoring plans. 

The disturbance of balance between superoxide and nitric oxide occurs in a variety of common disease states. For example, altered endothelium-dependent vascular relaxation due to a decrease in NO formation has been shown in animal models of hypertension, diabetes, cigarette smoking, and heart failure [21]. Miller et al. [22] suggested that a chronic animal model atherosclerosis closely resembles the severity of atherosclerosis in patients. On the whole, the results obtained in humans, for example, in hypertensive patients [23] correspond well to animal experiments. It is important that endothelium-dependent vascular relaxation in patients may be improved by ascorbic acid probably through the reaction with superoxide. 

Figure 22.6 How various factors increase the risk of atherosclerosis, thrombosis and myocardial infarction. The diagram provides suggestions as to how various factors increase the risk of development of the trio of cardiovascular problems. The factors include an excessive intake of total fat, which increases activity of clotting factors, especially factor VIII an excessive intake of saturated or trans fatty acids that change the structure of the plasma membrane of cells, such as endothelial cells, which increases the risk of platelet aggregation or susceptibility of the membrane to injury excessive intake of salt - which increases blood pressure, as does smoking and low physical activity a high intake of fat or cholesterol or a low intake of antioxidants, vitamin 6 2 and folic acid, which can lead either to direct chemical damage (e.g. oxidation) to the structure of LDL or an increase in the serum level of LDL, which also increases the risk of chemical damage to LDL. A low intake of folate and vitamin B12 also decreases metabolism of homocysteine, so that the plasma concentration increases, which can damage the endothelial membrane due to formation of thiolactone.

Zwijsen, R. M., L. H. de Haan, J. S. Costing, H. L. Pekelharing, and J. H. Koeman. Inhibition of intercellular communication in smooth muscle cells of humans and rats by low density lipoprotein, cigarette smoke condensate and TPA. Atherosclerosis 1990 85(1) 71-80. 

NO also reduces endothelial adhesion of monocytes and leukocytes, key features of the early development of atheromatous plaques. This effect is due to the inhibitory effect of NO on the expression of adhesion molecules on the endothelial surface. In addition, NO may act as an antioxidant, blocking the oxidation of low-density lipoproteins and thus preventing or reducing the formation of foam cells in the vascular wall. Plaque formation is also affected by NO-dependent reduction in endothelial cell permeability to lipoproteins. The importance of eNOS in cardiovascular disease is supported by experiments showing increased atherosclerosis in animals deficient in eNOS by pharmacologic inhibition. Atherosclerosis risk factors, such as smoking, hyperlipidemia, diabetes, and hypertension, are associated with decreased endothelial NO production, and thus enhance atherogenesis. 

However, if a man smokes, eats to the point of obesity, and has elevated blood glucose and elevated blood pressure, his peripheral nervous system wires do not respond adequately to the let s have intercourse signal from the brain—in other words, neurological innervation of the penis is rendered faulty, usually by diabetes (Fig. 14—12). Furthermore, there may not be much pressure in the plumbing — there may be atherosclerosis of the arterial supply of the penis from hypertension and hypercholesterolemia—when cGMP says relax the smooth muscle and let the... 

Cardiovascular diseases are the leading cause of death in the Western world. Basically, atherosclerosis manifests itself in three major organs and thereby leads to severe secondary diseases. Coronary disease results from atherosclerosis of the coronary arteries and culminates in myocardial infarction when vessels are occluded by a thrombus. In the brain, atherosclerosis gives rise to arterial thrombi or ruptures that result in a stroke. Atherosclerosis in the kidney leads to renal failure. Since these diseases significantly lower life expectancy, early recognition and elimination of risk factors (hypertension, diabetes mellitus, hyperlipidemia, and smoking) that promote atherosclerosis are essential. 

The findings suggest several mechanisms that might contribute to the adverse effect of smoking on atherosclerosis. 

Homer D, Ingall TJ, Baker HL et al. (1991). Serum lipids and lipoproteins are less powerful predictors of extracranial carotid artery atherosclerosis than are cigarette smoking and hypertension. Mayo Clinic Proceedings 66 259-267 Hooper L, Capps N, Clements G et al. (2004). Foods or supplements rich in omega-3 fatty acids for preventing cardiovascular disease in patients with ischemic heart disease. 

Howard G, Wagenknecht LE, Burke GL et al. (1998). Cigarette smoking and progression of atherosclerosis the Atherosclerosis Risk in... 

As we age, the body produces less and less NO, especially when LDL cholesterol levels are high, when we smoke cigarettes, when we gain weight, when we live sedentary lifestyles, and when we develop type 2 diabetes and sugar levels rise in the blood. Reduced production of NO leads to arterial constriction that limits blood flow, elevates blood pressure, increases blood clot production, and results in more rapid cell death and cardiovascular disease. For reasons yet to be determined, blacks produce less NO than whites do, which may explain why the incidence of hypertension is higher in that community. And while there is an association, we don t know whether a decreased production of NO contributes to the development of type 2 diabetes or whether that form of diabetes results in less NO. Decreased NO production has also been correlated with the early development of atherosclerosis. In 2005, Russian scientists at the Scientific Sessions of the American Heart Association reported their findings that a decline in NO production parallels increases in blood pressure from mild to severe. 

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