Coronary artery disease extent

There can be a number of underlying causes of CHE. The most prevalent is the lack of oxygenated blood reaching the heart muscle itself because of coronary artery disease with myocardial infarction (111). Hypertension and valvular disease can contribute to CHE as well, but to a lesser extent in terms of principal causes for the disease. 

Ischemic heart disease (IHD) is also called coronary heart disease (CHD) or coronary artery disease. The term ischemic refers to a decreased supply of oxygenated blood, in this case to the heart muscle. Ischemic heart disease is caused by the narrowing of one or more of the major coronary arteries that supply blood to the heart, most commonly by atherosclerotic plaques. Atherosclerotic plaques may impede coronary blood flow to the extent that cardiac tissue distal to the site of the coronary artery narrowing is deprived of sufficient oxygen in the face of increased oxygen demand. Ischemic heart disease results from... 

The statins have been demonstrated to markedly lower plasma LDL levels (and triglyceride levels to a lesser extent). In fact, statins were approved by the US FDA on the basis of a surrogate endpoint reduction in plasma cholesterol levels. Since we know that increased plasma cholesterol levels are correlated with increased risk of coronary artery disease, it seems logical that reducing plasma cholesterol levels would lead to reduced risk. That turns out to be true in this case. However, see the case of hormone replacement therapy (HRT) for women for a more complex example, discussed below. 

By 1996 over 500,000 coronary interventions were performed annually, which has more than doubled to today s current standard. These pioneers have paved the way for interventional procedures that now serve as the standard of care for symptomatic coronary artery disease. While coronary intervention remains in its adolescent stage, the quality of care has increased substantially and the bar is ever increasing as to the extent coronary interventions play in our society s healthcare. 

Pharmacokinetics According to the product label, the pharmacokinetics of eptihbatide are linear and dose proportional. Plasma elimination half-life is approximately 2.5 hours. The extent of eptihbatide binding to human plasma protein is about 25% its mean volume of distribution is 185mPkg. Clearance in patients with coronary artery disease is 55-58 ml/kg per hour. Clinical studies have included 2418 patients with serum creatinine between 1.0 and 2.0mg/dl without dose adjustment. No data are available in patients with more severe degrees of renal impairment, but plasma eptihbatide levels are expected to be higher in such patients. Patients in clinical studies were older than the subjects in clinical pharmacology studies, and they had lower total body eptihbatide clearance and higher eptihbatide plasma levels. Men and women showed no important differences in the pharmacokinetics of eptihbatide. 

In the past half a century, scientists and public health officials have gradually come to realize that the two leading causes of mortality in Western nations, heart disease and cancer, are associated to a certain though unknown extent with life style, including dietary factors. This association is somewhat better established for coronary artery disease than it is for cancer. Based on current knowledge, many organizations have offered dietary advice to the public (1-9). However, the scientific community has reached no clear consensus about the nature of the association between diet and chronic diseases and the extent to which dietary modification can decrease the risk, especially cancer risk (5 6 10 U). 

In a study from the Mayo Clinic (M4), a group of male patients undergoing diagnostic coronary angiography for chest pain or suspected coronary artery disease had plasma cholesterol and triglyceride, HDL cholesterol, and apoA-I concentrations measured. Whereas HDL cholesterol discriminated to some extent between those with and those without important coronary artery disease (and total cholesterol and triglyceride did not discriminate at all), apoA-I levels provided an almost perfect prediction of obstructive coronary artery disease. Some caveats on the interpretation of apoA-I levels in this and other studies have been noted by Blackburn (B34). 

Further support for using blood pressure as a surrogate endpoint is provided by the concordance of evidence from a number of clinical trials in which blood pressure lowering with low-dose diuretics and P-blockers was shown to reduce the incidence of stroke/ coronary artery disease/ and congestive heart failure in hypertensive patients (19). Of particular interest is a meta-analysis that was conducted to compare the extent of blood pressure reduction achieved in different clinical trials with the maximum benefit that was anticipated on epidemiolgic grounds (Table 17.3) (20). The decrease in stroke incidence anticipated for a 5- to 6-mm Hg average reduction in diastolic blood pressure was fully realized with only 2 to 3 years of antihypertensive therapy. 

In summary, oxysterols are known to exist in atherosclerotic lesions and have been demonstrated in cell-culture experiments to have profound cellular effects that could influence the development, progression, and reversal of atherosclerosis. The key question in this field of research, however, is whether the concentrations of oxysterols in vivo are high enough to influence atherogenesis. Thus far, only the oxysterol-activated nuclear transcription pathway has been directly supported by in vivo data, and even in this case the precise roles and identification of the activating oxysterols in vivo have not yet been elucidated. Moreover, to the extent that oxysterols are generated in vivo and not just obtained from the diet, their role in human atherosclerosis has been questioned by clinical trials showing little or no protective effect of antioxidants on atherosclerotic coronary artery disease (K.J. Williams and E.A. Fisher, 2005). 

Our patient population was predominantly male, consistent with the demography of the UAE and the protection conferred in premenopausal women from accelerated coronary artery disease as well as the age distribution of the population. Thus, the number of women studied was very low. Several studies have shown that when thrombolysis is initiated less than 3 hours after the onset of chest pain, mortality is remarkably low (11,12). Most of our patients were treated early. The mean time from onset of chest pain to treatment was 3.25 hours. This would, to some extent, account for the low mortality. 

Norhammer A, Malmberg K, Diderholm E, Lagerqvist B, Lindahl B, Ryden L, Wallentin L. Diabetes mellitus The major risk factor in unstable coronary artery disease even after consideration of the extent of coronary artery disease and benefits of revascularization. 1 Am Coll Cardiol 2004 43 585-591. 

A study in 13 patients with coronary artery disease found that irbesartan 150 mg daily reduced the extent and severity of perfusion defects after dipyridamole-induced stress. ... 

We have also studied the distribution of coronary artery atheroma in a series of 300 patients to determine which factors were responsible and have shown that the usual risk factors, proximality of the lesion and presence of bifurcations are the most important causative factors (Halon et al., 1983). Since coronary artery disease is more common, we have studied regional ventricular function by frame-by-frame analysis of cineangiograms and are able to show the pattern of contraction on a 3-dimensional reference axis which takes into account the position on the ventricular circumference, time of the cardiac cycle and extent of contraction. This can be converted into a simple contour map which shows the 3-dimensional picture in a 2-dimensional plane (Sapoznikov et al., 1983). 

Dugi KA, Schmidt N, Brandauer K, et al. Activity and concentration of lipoprotein lipase in post-heparin plasma and the extent of coronary artery disease. Atherosclerosis 2002 163 127-134. 

In addition to coronary sclerosis, evidence is accumulating that high Lp(a) levels may be important in the development of cerebrovascular and peripheral arterial disease, as well (J6, T8, U2). Lp(a) levels not only correlated well with clinical endpoints such as transient ischemic attack and cerebral infarction, but also were associated with the extent and severity of carotid atherosclerosis, as assessed by bidirectional Doppler ultrasound (K23, M33, Z2). 

Diitiazem [dil TYE a zem] has cardiovascular effects that are similar to those of verapamil. It reduces the heart rate, although to a lesser extent than verapamil, and also decreases blood pressure. In addition, diitiazem can relieve coronary artery spasm and is therefore particularly useful in patients with variant angina. The incidence of adverse side effects is low. Figure 18.4 shows treatment of angina in patients with concomitant diseases. 

Diseases of the heart and circulatory system, cardiovascular diseases, have long been the leading cause of mortality in Europe and North America, and total cholesterol and low-density lipoprotein (LDL) cholesterol are the two most important risk factors for coronary heart disease. Decreased arterial compliance of the arteries is thought to contribute to systolic hypertension and coronary artery insufficiency. A number of nutraceuticals have been used for long-term prevention or symptom reduction in cardiovascular diseases, notably soy products, tea flavonoids, octacosanol, n-3-polyunsaturated fatty acids (PUFAs), and, to a lesser extent, melatonin, Pycnogenol, resveratrol, coenzyme QIO, lycopene, and DHEA. 

There appears to be little relationship between the historical features of angina and the severity or extent of coronary artery vessel involvement. Therefore, one may speculate that severe symptoms might be associated with multivessel disease, but no predictive markers exist on a routine basis. 

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