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Pulmonary disease induced by cardiovascular drugs

INTRODUCTION

A number of cardiovascular drugs have the potential to induce lung disease, although the incidence of diffuse parenchymal lung disease associated with antiarrhythmic drugs is quite rare (table 1A-B). Amiodarone is a classic example of a drug that causes pulmonary toxicity. Four different types of injury have been identified: chronic interstitial pneumonitis; organizing pneumonia; acute respiratory distress syndrome; and a solitary lung mass.

This topic review will provide an overview of the lung diseases induced by various cardiovascular drugs. The clinical manifestations, diagnosis, and management of pulmonary toxicity due to amiodarone are discussed separately. (See "Amiodarone pulmonary toxicity".)

ANGIOTENSIN CONVERTING ENZYME INHIBITORS

All of the angiotensin converting enzyme (ACE) inhibitors may induce a dry, persistent, and often nocturnal cough (in 5 to 20 percent of patients). The cough may develop within hours of the first dose or weeks to months later. It is more common in women, non-smokers, and persons of Chinese origin. The cough typically resolves 1 to 4 weeks after discontinuation of the ACE inhibitor but in a subgroup of coughers, resolution may take several months [1]. One important caveat is that cough may be a symptom of heart failure, and a thorough history and examination is needed to ascertain whether the cough is truly related to the ACE inhibitor therapy. An increased incidence of cough does not appear to occur with the angiotensin II receptor antagonists such as losartan. (See "Major side effects of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers" and "Evaluation of subacute and chronic cough in adults".)

Angioedema may rarely be associated with ACE inhibitor therapy. Since ACE inhibitor-associated angioedema typically causes swelling of the mouth, lips, tongue, larynx, pharynx, and subglottic tissues, upper airway compromise may be the presenting sign. Unlike classical hereditary angioedema, C1 inhibitor level and function and thus the C4 levels are normal in ACE inhibitor-associated angioedema. (See "An overview of angioedema: Pathogenesis and causes", section on 'ACE inhibitors'.)

In addition, captopril and perindopril have rarely been associated with the development of diffuse interstitial pneumonitis. Both a hypersensitivity pneumonitis and an eosinophilic pneumonitis have been described [2-4]. The radiographic appearance is nonspecific, with bilateral patchy alveolar opacities being the most frequent finding. Therapy consists of drug withdrawal.

              

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Literature review current through: Aug 2014. | This topic last updated: Jan 18, 2013.
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