The cardiovascular risk reduction associated with different statins for the prevention of cardiovascular disease and the cardiovascular risk increase associated with excess dietary intake of fat have been quantified. However, these relative risks have never been directly juxtaposed to determine whether an increase in relative risk by 1 activity could be neutralized by an opposing change in relative risk from a second activity. The investigators compared the increase in relative risk for cardiovascular disease associated with the total fat and trans fat content of fast foods against the relative risk decrease provided by daily statin consumption from a meta-analysis of statins in primary prevention of coronary artery disease (7 randomized controlled trials including 42,848 patients). The risk reduction associated with the daily consumption of most statins, with the exception of pravastatin, is more powerful than the risk increase caused by the daily extra fat intake associated with a 7-oz hamburger (Quarter Pounder) with cheese and a small milkshake. In conclusion, statin therapy can neutralize the cardiovascular risk caused by harmful diet choices. In other spheres of human activity, individuals choosing risky pursuits (motorcycling, smoking, driving) are advised or compelled to use measures to minimize the risk (safety equipment, filters, seatbelts). Likewise, some individuals eat unhealthily. Routine accessibility of statins in establishments providing unhealthy food might be a rational modern means to offset the cardiovascular risk. Fast food outlets already offer free condiments to supplement meals. A free statin-containing accompaniment would offer cardiovascular benefits, opposite to the effects of equally available salt, sugar, and high-fat condiments. Although no substitute for systematic lifestyle improvements, including healthy diet, regular exercise, weight loss, and smoking cessation, complimentary statin packets would add, at little cost, 1 positive choice to a panoply of negative ones.

Ferenczi EA, Asaria P, Hughes AD, Chaturvedi N, Francis DP.

Am J Cardiol. 2010 Aug 15;106(4):587-92.

Particulate matter (PM) air pollution is associated with an increased risk of cardiovascular morbidity and mortality. The focus of this review will be on the role that both acute and chronic exposure to PM plays in causing cardiovascular disease and on the latest major new findings and controversies in this field of research. Even short-term exposure to PM2.5 over a few hours can trigger myocardial infarctions, cardiac ischemia, arrhythmias, heart failure, stroke, exacerbation of peripheral arterial disease, and sudden death. Chronic exposure to moderately elevated levels also enhances the risk for developing a variety of cardiovascular diseases, possibly including hypertension and systemic atherosclerosis. Recent epidemiologic studies have furthered our understanding of the linkage between air pollutants and human health, with a multitude of plausible mechanistic explanations having been demonstrated experimentally during the past few years. Although a number of finer details relating to both the epidemiology and the mechanisms involved require more investigation, the overall weight of evidence is now sufficient to implicate PM exposure as a cause of cardiovascular disease. Without doubt, exposure to particulate matter can play a causal role in triggering a host of acute cardiovascular events via many mechanisms. Although long-term air pollution exposure has been shown to promote the development of atherosclerosis, the clinical significance of this relation requires more investigation.

1: Rev Environ Health. 2007 Apr-Jun;22(2):115-37.Links

Brook RD.

Division of Cardiovascular Medicine, University of Michigan, USA. robdbrok@umich.edu