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The double jeopardy of chronic obstructive pulmonary disease and myocardial infarction
  1. Shashank S Sinha and
  2. Hitinder S Gurm
  1. Division of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA
  1. Correspondence to Dr Hitinder S Gurm; hgurm{at}

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Despite several therapeutic advances in the last few decades, chronic obstructive pulmonary disease (COPD) is a burgeoning cause of morbidity and mortality worldwide and is the fourth leading cause of death globally.1 Yet a curious paradox persists. As the only common disease for which the prevalence and mortality rates continue to rise, COPD still remains as a remarkably underdiagnosed and undertreated disease.1 The worldwide prevalence may be underestimated for a host of reasons including missed diagnosis, delays in establishing the diagnosis, variable definitions of COPD and the lack of age-adjusted estimates. COPD is of more than academic interest to cardiologists. Patients with COPD are at an increased risk of an array of acute cardiovascular events, including myocardial infarction (MI) and have increased short-term and long-term mortality compared with their non-COPD counterparts.2 In fact, up to one-third of deaths in patients with COPD may be ascribed to cardiovascular disease.2 Cardiovascular mortality increases by 28% for every 10% decrement in forced expiratory volume in 1 s.2 Furthermore, it has been shown that patients with COPD are undertreated with standard, guideline-based post-MI pharmacotherapy. Finally, the presence of COPD is associated with worse long-term outcome in patients undergoing percutaneous coronary intervention (PCI) or coronary artery bypass graft.3 ,4

COPD and coronary artery disease share common risk factor profiles and potentially mechanistic pathways. Tobacco use and old age contribute to elevated risk for both of these disease entities. In a recent study analysing 25 857 patients with COPD in the Health Improvement Network database over a 2-year period, a COPD exacerbation was associated with over a twofold increased risk of MI during a 5-day period following the exacerbation.5 Notably, the risk returned to baseline within 5 days of treatment for the exacerbation.5 Although the exact pathogenesis remains to be …

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