Coronary artery disease development

A 69-year-old woman with stable angina and mild single-vessel coronary artery disease developed acute myocardial ischemia within a week of starting venlafaxine (75 mg/day). 

Mammals lack the ability to synthesize astaxanthin or convert dietary astaxanthin into vitamin A. Unlike p-carotene, astaxanthin has no pro-vitamin activity in these animals. Astaxanthin has been shown in both in vitro and in a study with human subjects to be effective for the prevention of the oxidation of low-density protein, suggesting that it can be used to prevent arteriosclerosis, coronary artery disease, and ischemic brain development. A number of astaxanthin health products are under study. 

The risk of gout increases as the serum uric acid concentration increases, and approximately 30% of patients with levels greater than 10 mg/dL (greater than 595 pmol/L) develop symptoms of gout within 5 years. However, most patients with hyperuricemia are asymptomatic. Other risk factors for gout include obesity, ethanol use, and dyslipidemia. Gout is seen frequently in patients with type 2 diabetes mellitus and coronary artery disease, but a causal relationship has not been established. 

Contrary to LDL, high-density lipoproteins (HDL) prevent atherosclerosis, and therefore, their plasma levels inversely correlate with the risk of developing coronary artery disease. HDL antiatherogenic activity is apparently due to the removal of cholesterol from peripheral tissues and its transport to the liver for excretion. In addition, HDL acts as antioxidants, inhibiting copper- or endothelial cell-induced LDL oxidation [180], It was found that HDL lipids are oxidized easier than LDL lipids by peroxyl radicals [181]. HDL also protects LDL by the reduction of cholesteryl ester hydroperoxides to corresponding hydroperoxides. During this process, HDL specific methionine residues in apolipoproteins AI and All are oxidized [182]. 

The formation of atherosclerotic plaques is the underlying cause of coronary artery disease (CAD) and ACS in most patients. Endothelial dysfunction leads to the formation of fatty streaks in the coronary arteries and eventually to atherosclerotic plaques. Factors responsible for development of atherosclerosis include hypertension, age, male gender, tobacco use, diabetes mellitus, obesity, and dyslipidemia. 

It is well-established that an elevated level of cholesterol, particnlarly that carried largely in the form of LDLs, is an independent risk factor for the development of atherosclerosis and its sequelae, including coronary artery disease (leading to heart attacks), strokes, and peripheral arterial disease. 

There is a mutant gene that produces an inactive receptor and patients with this mntant snffer from high levels of LDL-cholesterol in their blood. They have a markedly increased risk of developing atherosclerosis and coronary artery disease. 

As discussed above, obesity is associated with dyslipidemia, a condition where high levels of low-density lipoprotein cholesterol (LDL-C) is common. Elevated LDL-C is strongly associated with an elevated risk of coronary artery disease and for this reason a number of lipid-lowering therapies that target LDL-C have been developed. These include bile-acid sequestrants (BAS), statins (HMG-CoA reductase inhibitors), cholesterol absorption inhibitors, and fibrates. ... 

Reduction in risk of Ml, stroke, and death from cardiovascular causes - In patients 55 years of age or older at high risk of developing a major cardiovascular event because of a history of coronary artery disease, stroke, peripheral vascular disease, or diabetes that is accompanied by at least 1 other cardiovascular risk factor (eg, hypertension, elevated total cholesterol levels, low FIDL levels, cigarette smoking, documented microalbuminuria). 

It is indicated in premature infants exposed to high concentration of oxygen, correction of established vitamin E deficiency, in patients at risk of developing vitamin E deficiency, nocturnal muscle cramps, intermittent claudication, fibrocystic breast disease, coronary artery disease and as an antioxidant. 

The primary indication for antidepressant agents is the treatment of MDD. Major depression, with a lifetime prevalence of around 17% in the USA and a point prevalence of 5%, is associated with substantial morbidity and mortality. MDD represents one of the most common causes of disability in the developed world. In addition, major depression is commonly associated with a variety of medical conditions—from chronic pain to coronary artery disease. When depression coexists with other medical conditions, the patient s disease burden increases, and the quality of life—and often the prognosis for effective treatment—decreases significantly. 

The effects of coenzyme Q10 on coronary artery disease and chronic stable angina are modest but appear promising. A theoretical basis for such benefit could be metabolic protection of the ischemic myocardium. Double-blind, placebo-controlled trials have demonstrated that coenzyme Q10 supplementation improved a number of clinical measures in patients with a history of acute myocardial infarction (AMI). Improvements have been observed in lipoprotein a, high-density lipoprotein cholesterol, exercise tolerance, and time to development of ischemic changes on the electrocardiogram during stress tests. In addition, very small reductions in cardiac deaths and rate of reinfarction in patients with previous AMI have been reported (absolute risk reduction 1.5%). 

If a normal person is given an inhibitor for HMG-CoA reductase, cholesterol synthesis is inhibited in the liver. Lower levels of cholesterol then signal the synthesis of increased levels of LDL receptors. This increases the uptake of LDL into the liver and reduces serum LDL. In a patient with FH, this has little effect because there are no LDL receptors. The only effect is that the liver does not make as much cholesterol and does not contribute as much to serum LPT, levels. The new liver will make normal amounts of LDL receptors and have normal uptake of LDL from the blood. This result will dramatically lower serum LDL levels and prevent the new heart from developing coronary artery disease. If the liver transplant had not been done, the heart transplant would have been to no avail. 

Chronic diseases caused by physical inactivity and inappropriate diet consumption are epidemic in modem Western society. Chronic diseases develop over a lifetime, with clinical sequelae occurring many years after the underlying pathogenesis of the disease has occurred. As we move ahead in the 21st century, cardiovascular diseases (i.e., coronary artery disease, hypertension, stroke, and heart failure), type 2 diabetes, metabolic syndrome, and cancer are the leading killers in Western society and are increasing dramatically in developing nations. 

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