Can inhaled steroids mend a broken heart in chronic obstructive pulmonary disease?

I t has been recognised for several decades that individuals with reduced forced expiratory volume in one second (FEV1) are at increased risk of cardiovascular events, including myocardial infarction, stroke and arrhythmias [1–3]. Since reduced FEV1 and cardiovascular disease often share a common risk factor, cigarette smoking, many had ascribed the above relationship to the confounding effects of smoking. However, a closer examination of the epidemiological data reveals some salient but subtle features that suggest a far more complex reality. First, many of the large epidemiologic studies, which established reduced FEV1 as a risk factor for cardiovas-cular events, had carefully controlled for the effects of cigarette smoking using sophisticated and well-accepted statistical methods and had excluded at baseline those individuals with overt cardiovascular disease [4]. Secondly, these studies demonstrated that even among lifetime nonsmokers, reduced FEV1 was a determinant of cardiovascular disease [3, 5, 6]. Thirdly, the relationship was dose-dependent, such that individuals with the most severe reduction in FEV1 had the highest risk of cardiovascular events, while those with the least amount of impairment in FEV1 had the lowest risk regardless of the smoking status [4]. Taken together, these data indicated that the relationship between reduced FEV1 and cardiovascu-lar disease could not be entirely explained by the effects of cigarette smoking; they implied other causative pathways. Two decades of epidemiological research have also revealed that the contribution of reduced FEV1 to cardiovascular events is nontrivial. In fact, it is quite large. In one population-based study, HOLE et al. [3] showed when the lowest quintile of FEV1 (,73–75% of predicted) was compared with the highest quintile, the population-attributable risk for deaths related to ischemic heart disease was 26% in males and 24% in females, independent of the burden imposed by cigarette smoking. In other words, in this study, reduced FEV1 may have been responsible for at least 24–26% of all deaths related to ischemic heart disease. Remarkably, the magnitude of the cardiovas-cular mortality burden attributed to reduced FEV1 was similar to that imposed by hypercholesterolemia, which had a population attributable risk of ,21–25% [3]. Other studies have shown that in addition to baseline FEV1, rapid decline in FEV1, a hallmark of chronic obstructive pulmonary disease (COPD), is another risk factor for cardio-vascular events. In the Malmo ''Men Born in 1914'' Study, for instance, the cardiovascular event rate among smokers in the high, middle and low thirds with regard to the …