COPD is a chronic debilitating condition that affects nearly 30 million adults in the United States and is responsible for > $38.8 billion of annual health-care costs, with more than one-half of that in direct expenditures.1 COPD also has many serious associated comorbidities, such as lung cancer and ischemic heart disease (IHD), that add to the enormous health burden of this condition.2 Its association with IHD deserves special attention because IHD is the leading cause of mortality in the United States. COPD and IHD share a common risk factor, cigarette smoking, and despite the widespread public health initiatives to curb smoking, ∼20% of US adults continue to smoke, collectively consuming 357 billion cigarettes per year.3 Moreover, large-scale epidemiologic studies have shown convincingly that, independent of cigarette smoking, COPD is a major risk factor for heart disease above and beyond the traditional risk factors such as hypercholesterolemia or hypertension.4 Although the exact cause is unknown, systemic inflammation, oxidative stress, and hypoxia have been implicated in this process. Of these factors, the greatest amount of evidence lies with systemic inflammation. It is now well established that the lungs of patients with COPD are chronically inflamed, leading to spillage of inflammatory mediators into the systemic circulation. Even with smoking cessation, lung and systemic inflammation persists in a disease severity-dependent manner.5 Notably, the inflammatory burden increases markedly during periods of exacerbation, and it is during these periods that patients with COPD have the highest risk of a cardiovascular event.6 Drugs that reduce the inflammatory process in COPD have been associated with improved cardiovascular outcomes in these patients.7,8 The pathway by which COPD contributes to IHD, however, remains incompletely defined.