Review
Cardiac dysfunction during exacerbations of chronic obstructive pulmonary disease

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Summary

Chronic obstructive pulmonary disease (COPD) and cardiovascular disease often coexist, and acute cardiac events frequently occur during COPD exacerbations. Even when cardiac complications are not clinically apparent, biochemical evidence of cardiac dysfunction is often noted during exacerbations and portends poor prognosis. Diagnosis of cardiac disease in COPD can be difficult and necessitates a high degree of clinical suspicion. However, the additional strain of an exacerbation could be a pivotal moment, during which previously unsuspected cardiac dysfunction is exposed. In this Review, we present evidence about cardiac involvement in exacerbations of COPD, and discuss diagnostic challenges and treatment opportunities.

Introduction

Patients with chronic obstructive pulmonary disease (COPD) often have cardiovascular comorbidities.1 Patients with cardiovascular complications tend to have more symptoms and higher mortality than do patients with COPD alone.2 To distinguish symptoms of cardiac disease from those of COPD can be difficult, however, and cardiac disease is often unrecognised.3, 4 Exacerbations of COPD are characterised by symptomatic deterioration or increased use of health care; definitions do not ascribe cause, and primary cardiovascular instability precipitating acute deterioration in COPD symptoms is probably common.3 At one extreme, decompensated cardiac failure could be mistaken for COPD exacerbation.3, 5 But even without clinical signs of cardiac involvement, biochemical evidence of cardiac dysfunction is often present.6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19 Increased cardiac biomarkers during COPD exacerbations are associated with poor prognosis, but their wider implications are uncertain.6, 18, 19 In this Review, we examine the evidence for cardiac dysfunction during exacerbations of COPD and provide diagnostic, prognostic, and therapeutic perspectives.

Key messages

  • Diagnosed cardiac comorbidities are common patients with chronic obstructive pulmonary disease (COPD) and are associated with worse outlook. Prevalence might be underestimated because of underdiagnosis.

  • COPD exacerbations are often complicated by acute cardiac dysfunction, which can be difficult to recognise clinically.

  • Biochemical evidence of myocardial stretch (B-type natriuretic peptides) and myocardial injury (troponins) is often noted in exacerbations of COPD and is associated with increased mortality.

  • Results of observational studies suggest that cardiac treatments could improve outcomes from COPD exacerbations, but no prospective controlled trials have been done.

  • Further research into the pathogenesis and treatment of acute cardiac dysfunction in COPD exacerbations is urgently needed.

Section snippets

Epidemiology

COPD can be an important comorbidity in patients with cardiovascular disease: it is identified in 7–16% of patients with acute myocardial infarction and up to 52% of patients with heart failure (appendix). The presence of COPD is associated with an increased risk of readmission to hospital and long-term mortality.20 Patients with comorbid cardiac disease and COPD are less likely to be given β blockers for cardiac dysfunction or β agonists for airflow obstruction.21, 22

About 20% of patients with

Cardiac muscle injury

Biochemical evidence of cardiac injury during COPD exacerbations is common (table 2) and predicts both short-term and long-term mortality.6 Troponins are globular protein complexes bound to the actin filaments of myocytes that regulate contraction of skeletal and cardiac muscle. These proteins are released into the peripheral blood from cardiomyocytes after myocardial injury. Troponin measurements are mainly used to diagnose acute myocardial infarction, but, although they are specific for

Possible mechanisms of cardiac dysfunction

Several mechanisms could plausibly be implicated in provoking cardiac distress during COPD exacerbation (figure 1). Respiratory infections increase the risk of vascular events and are the most common precipitant of exacerbation.77 In a large prospective cohort of 20 101 exacerbations of COPD resulting in hospital admission (in which antibiotic prescription was a criterion to define exacerbation), myocardial infarction and stroke risk within the early period after admission were more than double

Recognition of cardiac dysfunction

Diagnosis of cardiac disease in COPD is difficult (figure 2). Electrocardiographic abnormalities are common in COPD exacerbations but under-recognised in clinical practice.4, 7 Additionally, recognition of an acute coronary syndrome is challenging because the traditional complex of chest pain, electrocardiographic changes, and increased troponin concentrations might be unreliable during an exacerbation of COPD. Many patients have electrocardiographic changes in the absence of acute cardiac

Treating cardiac disease in COPD exacerbations

Almost no evidence from clinical trials is available as a basis for management of cardiovascular disease during COPD exacerbations. In view of the prevalence and adverse consequences, cardiac involvement is an important topic for future research. Few existing COPD treatments reduce mortality from exacerbations and treatment of cardiovascular comorbidities could possibly have a greater effect on overall mortality than do specific respiratory treatments.

A particularly urgent question is whether

Conclusions

Accumulating evidence suggests that cardiac dysfunction during exacerbations of COPD is common and portends poor prognosis. The emphasis for treatment has been placed on optimisation of therapies for COPD itself—scant attention has been paid to the management of cardiovascular complications. However, convincing evidence suggests that a pulmonary exacerbation is often associated with cardiac exacerbations, but this co-occurrence is often not suspected and can be difficult to detect clinically

Search strategy and selection criteria

We searched PubMed with the terms “chronic obstructive pulmonary disease” or “COPD”, “exacerbation”, “cardiac failure” or “heart failure”, “myocardial infarction”, “troponin”, and “BNP” or “NT-proBNP” for original research and reviews published in any language on or before Sept 1, 2015. We did not do a systematic review, and used the most relevant results. Further studies were identified from the reference lists of reviewed papers. For foreign language studies, translations were used.

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