الفهرس 
PATHOPHYSIOLOGY OF PERIOPERATIVE MYOCARDIAL INFARCTIONOnly 14 pages are availabe for public view
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Abstract
Three-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, commonly known as statins, have been proven to be highly effective drugs for reducing cholesterol.
Besides the lowering of LDL-C, statins seem to have other, so-called pleiotropic effects, which may, among other effects, stabilize atherosclerotic plaques during surgical procedures.
Although the pathophysiology of perioperative myocardial infarction (MI) is not entirely understood, two different main theories are employed. The first is oxygen supply–demand mismatch, caused by an increase in oxygen demand in the setting of fixed coronary artery stenosis. The second, similar to MIs occurring in the nonoperative setting and which is thought to play a major role in the occurrence of perioperative MIs, is coronary plaque rupture, which leads to thrombus formation and subsequent vessel occlusion. Major contributors to coronary plaque rupture include surgical stress, tachycardia and hypertension.
Coronary plaques at high risk of rupture are known as vulnerable plaques. The prevalence of vulnerable plaques is high, even in patients without any signs or symptoms. It is impossible to predict the time it will take the vulnerable plaque to become unstable, due to the many factors influencing this process.
Surgery imposes an extra myocardial workload, resulting in mechanical stress, stress-induced inflammation and possible vascular spasms. This can cause vulnerable plaques to become unstable, leading to plaque rupture with resulting thrombus formation, vascular occlusion, myocardial ischemia and eventually MI.
Rupture of a vulnerable plaque is the result of a combination of many factors that can be grouped into two main mechanisms. The first is the combination of intrinsic characteristics of individual plaques including plaque morphology that promote plaque instability. The second is the combination of extrinsic forces ”e.g. inflammation and hypercoagulability” that influence stress on the plaque, triggering plaque disruption. The pleiotropic properties of statins lead to plaque stabilization and prevent myocardial ischemia.
Perioperative statins administration is associated with a reduced incidence of adverse cardiovascular events, including unstable angina pectoris, myocardial infarction (MI), cardiac death, atrial fibrillation, and stroke. Moreover, the beneficial effects of statin therapy are not limited to patients with hypercholesterolemia.
A major deterrent for perioperative statin therapy has been the fear of statin-induced myopathy and rhabdomyolysis. Perioperatively, there are many factors increasing the risk of statin induced myopathy, such as impaired renal function after major surgery, and multiple drug use during anesthesia. Moreover, the use of analgesic agents and postoperative pain may mask signs of myopathy. Failure to detect statin-induced myopathy may then lead to continuous statin use and the subsequent development of rhabdomyolysis and acute renal failure.
Considering the low incidence of statin-induced myopathy and rhabdomyolysis, the potential benefits of perioperative statin use seem to outweigh the potential hazards.