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To the Editor:
In their article, Cagliani et al. observed a 40% reduction of caveolin-3 in the myocardium of a single patient and concluded that this mutation affects skeletal muscle and myocardium differentially.1 The findings raise concerns.
Was cardiac involvement absent in the patients because there were no comprehensive cardiac investigations? At least history, clinical cardiologic examination, ECG, echocardiography, and 24-hour ECG are necessary to assess cardiac involvement. Only rudimentary data of these investigations were provided for Patients III-1, III-4, and IV-1. Since cardiac involvement may also develop during the disease course, it is important to regularly follow up. Reduced myocardial caveolin-3 in Patient III-1 may be independent of the underlying mutation and could be also influenced by coronary heart disease or extracorporal circulation during surgery. In rabbits, chronic myocardial hypoxia increased nitric oxide synthase and simultaneously reduced caveolin-3.2
Was myocardial biopsy taken from a region supplied by a stenosed or normal coronary artery? Was the microdeletion also detected in the myocardium? Possibly hyper-CK-emia …
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