Several trials have shown that lipidlowering intervention also lowers coronary events and mortality:
The Familial Atherosclerosis Treatment Study (FATS) showed that in men with coronary artery disease and high apolipoprotein B levels, intensive lipid-lowering therapy slowed coronary lesion progression, accelerated regression, and decreased the incidence of cardiovascular events.
The Scandinavian Simvastatin Survival Study (4S) showed a lower mortality rate from acute myocardial infarction in patients treated with simvastatin vs placebo. Recent follow-up of the same population shows that simvastatin therapy is safe in coronary artery disease for up to 8 years and yields continued survival benefit.
In the West Of Scotland COronary Prevention Study (WOSCOPS), pravastatin significantly decreased the incidence of myocardial infarction and cardiovascular death without increasing noncardiovascular mortality in men with moderate hypercholesterolemia and no history of myocardial infarction.
The Cholesterol And Recurrent Events (CARE) study showed that the benefit of cholesterol-lowering therapy extends to the majority of coronary patients whose cholesterol levels are average.
These studies also showed that lipid-lowering therapy lowers coronary morbidity and mortality more rapidly than does the physical regression of atherosclerosis. Several animal and human studies have confirmed that hypercholesterolemia increases the susceptibility of myocardium to ischemic insult by various nonath-erosclerotic mechanisms. Wang et al provided important data on the cardiovascular effects of dyslipidemia, showing that dyslipidemia per se, especially an elevated LDL cholesterol, impairs outcome in myocardial infarction, measured by the postinfarct radionuclide left ventricular ejection fraction, and that this effect is independent of its atherogenic properties. They made the interesting observation that the severity of coronary atherosclerosis, measured by the Gensini score and number of diseased vessels, is not an independent predictor of the postinfarct left ventricular ejection fraction. In other words, the detrimental effect of dyslipidemia is independent of atherogenicity, and related more to endothelial dysfunction, the cardiomyocyte, coagulation, and other cellular functions.
As described in these animal models, hypercholesterolemia does not affect cardiovascular function only through atherosclerotic mechanisms. Underdevelopment of the collateral circulation and augmentation of the no-reflow phenomenon result from the interaction of microvascular endothelial dysfunction. Platelet hyperaggregability plays a major role in increasing myocardial damage.
Dyslipidemia has also been shown to impair anticoagulation mechanisms by increasing the levels of plasminogen activator inhibitor, decreasing those of tissue plasminogen activator, and enhancing platelet aggre-gability. Dyslipidemic thrombophilicity may in part explain the observation by Wang et al that patients with higher serum cholesterol levels have a significantly lower infarct artery patency rate. This is independently associated with a lower postinfarction ejection fraction, despite a similar rate of thrombolytic therapy use.
Serum lipid levels can also influence sarcolemmal membrane composition, of which cholesterol is a common and relatively prominent component. A high membrane cholesterol content affects the enzymes required for energy production and the movement of Ca2+ through specific channels in cardiomyocyte membranes, thus influencing cardiac contractility.
These findings imply that dyslipidemia impairs baseline left ventricular systolic function and the extent of compensatory hyperkinesia, resulting in a lower postinfarct ejection fraction.
pathophysiology; dyslipidemia; hypercholesterolemia; left ventricular systolic function; myocardial infarction; mortality
How does dyslipidemia affect left ventricular systolic function after a first acute myocardial infarction? Photo Gallery
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