Protecting the Heart: A Practical Review of the Statin Studies

H. T. Ong, MBBS (Mal), MRCP (UK), M Med (Sing), FRCP (Glasg, Edin), FCCP (USA), FAMM (Mal)

In This Article

Getting Aggressive: MIRACL and ADVERT

Besides lowering cholesterol levels, statins are known to modify endothelial function, stabilize plaques, and reduce inflammation and thrombus formation. The MIRACL study[23] looked at the effect of atorvastatin used early in the acute coronary syndromes. A total of 3086 patients with unstable angina or non-Q wave myocardial infarction were randomly assigned to placebo or atorvastatin 80 mg daily between 24 and 96 hours of admission. After a follow-up of 16 weeks, atorvastatin therapy produced a significant reduction of primary end point, which was defined as death, nonfatal myocardial infarction, cardiac arrest, or recurrent symptomatic ischemia (RR 0.84; 95% CI 0.70-1.00). Unfortunately, there was no significant change in death, nonfatal myocardial infarction, or cardiac arrest, and the benefit is seen in the reduction of recurrent ischemia. Thus, while this study established the safety and efficacy of statins in the acute coronary setting, it also suggests that more benefit will come from other therapeutic intervention when dealing with unstable angina and myocardial infarction.[24,25] The patient with an acute coronary syndrome is facing life-threatening consequences of the sudden occlusion of coronary blood flow. For treatment to make the most impact, it must result in quick and significantly increased coronary flow; this is something hypolipidemic therapy does not do.

The value of aggressive cholesterol reduction was investigated in comparison with coronary angioplasty in the AVERT study.[26] Patients with stable angina advised for percutaneous intervention were studied. Out of 341 patients recruited, 177 had an angioplasty as advised initially; the other 164 did not have an angioplasty but were instead initiated on 80 mg per day of atorvastatin. After a follow up of 18 months, patients assigned to the aggressive lipid-lowering therapy had a significantly longer time to the first ischemic event, as well as a lower incidence of ischemic events, although the latter just failed to reach statistical significance (P = .048, not significant after adjustment for interim analysis). The safety of aggressive lipid reduction therapy was confirmed, and there is a suggestion that it may be as efficacious as percutaneous intervention in managing patients with stable angina pectoris. In fact, trials of angioplasty vs medical therapy in stable angina pectoris have shown that angioplasty does not reduce the incidence of myocardial infarction and has no effect on coronary mortality.[27,28] In fact, most myocardial infarctions are due to the sudden disruption of the mildly stenotic lesions, and not the progression of previously severely narrowed plaques.[29] Since angioplasty treats only those severely stenotic lesions and does nothing to the mildly stenotic plaques, it cannot have a big impact in reducing myocardial infarction. Moreover, there is increasing evidence that acute coronary syndromes develop in the setting of a systemic inflammatory state.[30,31] Since the statins also have an anti-inflammatory and plaque stabilization effect, it stands to reason that they would be better able to prevent plaque rupture than angioplasty, which only targets a local stenotic plaque.[32,33,34] Further work is needed in this area, but it does seem that drug therapy has much to offer in preventing the adverse effects of atherosclerosis.


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