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Mounting evidence indicates that chronic obstructive pulmonary disease (COPD) is an independent risk factor for cardiovascular (CV) mortality. Data from several large trials such as the Lung Health Study, Towards a Revolution in COPD Health, Understanding Potential Long-term Impacts on Function with Tiotropium, European Respiratory Society Study on Chronic Obstructive Pulmonary Disease and Inhaled Steroids in Obstructive Lung Disease (ISOLDE) have shown that fatal CV events contribute to a major portion (between 22% and 39%) of the deaths in this population.1 Patients with COPD have greater mortality, rehospitalisation rates and poorer health status after a myocardial infarction (MI). Recent insights into the mechanisms that underlie this excess risk support a strong biological basis for heightened susceptibility to CV events, with mechanisms such as oxidative stress, endothelial dysfunction, arterial stiffness, increased inflammation and thrombotic predisposition being common themes.2 While a biological basis for inherent susceptibility of patients with COPD for CV events is indeed highly likely, inequities in their medical care resulting in substantial ‘gaps’ in treatment have also been suggested to contribute to the disproportionate mortality.3 ,4 While the reasons are likely multifactorial, at least one plausible explanation relates to differences in symptom presentations of acute coronary syndrome (ACS) in COPD, where patients may present with dyspnoea, rather than chest pain, obfuscating the diagnosis of MI and in turn delaying institution of appropriate management (eg, reperfusion therapies).3
In their Heart paper, Rothnie et al provide fascinating insights into the associations between COPD and excess mortality following a first MI using data from the Myocardial Ischaemia National Audit Project (MINAP), a national register for all MI and ACS admissions in the UK.5 MINAP records information on patient comorbidity, care processes and management …
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