Abstract
Randomized trials have established that statin treatment reduces coronary events in primary prevention and in patients with stable coronary artery disease. In unstable coronary artery disease, however, the pathophysiological background is distinct, and the potential benefits of statin therapy have not been evaluated until recently. Data from animal models and clinical studies indicate that statin treatment can influence a spectrum of molecular and cellular mechanisms that are intimately related to the pathogenesis of acute coronary syndromes; these include the reduction of circulating levels of atherogenic lipoproteins (very low density lipoprotein, very low density lipoprotein remnants, intermediate density lipoprotein, and low density lipoprotein) and thus of arterial lipid deposition and the attenuation of inflammation, modulation of thrombogenesis and thrombolysis, improvement of endothelial dysfunction, and reduction of ischemia/reperfusion injury. Indeed, findings from prospective and observational studies have demonstrated that statin treatment significantly improves clinical outcome after acute coronary syndromes. Therefore, early initiation of statin therapy after an acute coronary event not only enhances adherence to treatment but also preempts the occurrence of new events. In this review, we discuss recent important developments in our knowledge of the clinical evidence of the beneficial effects of early statin therapy in acute coronary syndromes and the biological mechanisms that underlie them.
Absolutely!!! It's the best time to begin treatment. The only exception would be for those people whose ACS is due solely to cigarette smoking and even then the anti-clotting effects of statins should be helpful. So absolutely!!!
It has repeatedly been shown that statins decrease morbidity and mortality in patients with atherosclerosis, thus supporting their use for the primary and secondary prevention of ischemic heart disease. Different pathological pathways that are triggered in the setting of acute coronary syndrome (ACS), such as endothelial dysfunction, activation of inflammatory and coagulation cascades, and thrombus formation, are known to be inhibited by statins, thereby justifying the use of these agents in patients with ACS. Several recent prospective controlled clinical trials have demonstrated the safety and, in some cases, the efficacy of statins when administered early after ACS. An increasing number of publications have reported, however, that statins may confer a beneficial effect not only in early secondary prevention, but also in the direct treatment of ACS (ie, when statins are administered as first-line treatment in clinically unstable patients). This therapeutic option is supported by the following: numerous experimental studies demonstrating a protective effect of statins under conditions of acute ischemia; analysis of different registries and trials, which has demonstrated a more favourable prognosis for statin-treated patients at the time of acute myocardial ischemia; and small clinical trials reporting a lower periprocedural infarction rate during coronary intervention or lower levels of several prognostic biomarkers, in addition to a lower incidence of cardiovascular events associated with statin therapy.
Early initiation of statin therapy after an acute coronary event not only enhances adherence to treatment but also preempts the occurrence of new events.