Patients with hypertrophic cardiomyopathy and atrial fibrillation face a high stroke risk even without other CHA2DS2-VASc risk factors, supporting lifelong anticoagulation at the first evidence of atrial fibrillation.
Highlights the pathophysiological continuum in hypertrophic cardiomyopathy leading to diastolic dysfunction, left atrial dilatation, and atrial fibrillation.
Among the various non-ischaemic primary myocardial diseases recognized in humans, the most common is hypertrophic cardiomyopathy (HCM). Though first recognized more than 60 years ago because of the characteristic physical signs of its most dramatic form, idiopathic hypertrophic subaortic stenosis (IHSS),1 the rapid dissemination of the echocardiogram 10 years later soon led to the recognition that IHSS was merely a part of a continuum of genetically determined hypertrophic anomalies, often without outflow obstruction.2 The more characteristic haemodynamic abnormality is left ventricular diastolic dysfunction. This, in turn, can lead to left atrial dilatation which, if sufficiently severe, can contribute to the development of atrial fibrillation (AF).
Borer et al. (Wed,) conducted a editorial in Hypertrophic Cardiomyopathy and Atrial Fibrillation. Anticoagulation was evaluated. Patients with hypertrophic cardiomyopathy and atrial fibrillation face a high stroke risk even without other CHA2DS2-VASc risk factors, supporting lifelong anticoagulation at the first evidence of atrial fibrillation.
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