In comparing the Monitored Atherosclerosis Regression Study (MARS) [1] with another recently published coronary prevention trial that also tested reductase inhibitors against placebo, it appears that a decreased coronary event rate may be related to the particular reductase inhibitor.

The MARS trial was a randomized, double-blind, placebo-controlled, multicenter angiographic trial testing the effects of lovastatin on the progression of coronary artery disease in patients with angiographically proven coronary disease. Most patients had multiple risk factors for the disease. Treatment with diet and lovastatin (80 mg/d) for 2.2 years had a favorable effect on lipoprotein levels and angiographically proven coronary disease progression compared with diet and placebo. However, no statistical differences were noted between the placebo and lovastatin groups in regard to coronary events (myocardial infarction, percutaneous transluminal coronary angioplasty, coronary artery surgery, coronary death, and unstable angina). Another randomized, double-blind, placebo-controlled multicenter trial tested pravastatin in persons with cholesterol levels of 5.2 to 7.8 mmol/L (200 to 300 mg/dL) and additional coronary risk factors [2]. Most had known coronary disease manifested by angina or previous myocardial infarction.

Pravastatin had a favorable effect on lipoprotein levels during the 26-week trial period and significantly reduced cardiovascular event rates compared with placebo.

Despite the expected increased reduction in low-density lipoprotein cholesterol levels in patients receiving lovastatin (80 mg/d) compared with pravastatin (20 mg/d) (comparable dosages in terms of potency), Jungnickel and colleagues [3] found that pravastatin, not lovastatin, favorably affected coronary event rates in high-risk persons. The reasons may relate to chemical differences in the reductase inhibitors; lovastatin is lipophilic and pravastatin is hydrophilic [3]. Only further, well-designed comparison studies will resolve this issue.