PubMed · 14950427
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J L HAMNER. 1952. General practice.. https://pubmed.ncbi.nlm.nih.gov/14950427/
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Arrhythmogenic right ventricular cardiomyopathy, also known as right ventricular dysplasia, is a genetically determined heart muscle disease associated with arrhythmia, heart failure, and sudden death. Autosomal dominant inheritance is typical. The identification of causative mutations in cell adhesion proteins has shed new light on its pathogenesis. Fibrofatty replacement of the myocardium, the hallmark pathologic feature, may be a response to injury caused by myocyte detachment. Sudden death is often the first manifestation in probands, emphasizing the importance of evaluating asymptomatic relatives for the disease. Standardized guidelines facilitate the clinical diagnosis of right ventricular dysplasia. However, familial studies have highlighted the need to broaden the diagnostic criteria, which are highly specific but lack sensitivity for early disease. Modifications have been proposed for the diagnosis of right ventricular dysplasia in relatives. Early right ventricular dysplasia is characterized by a "concealed phase" in which electrocardiographic and imaging abnormalities are often absent, but patients may nonetheless be at risk for arrhythmic events. Detection at this stage remains a clinical challenge, underscoring the potential value of mutation analysis in identifying affected persons. Serial evaluation of patients with suspected right ventricular dysplasia is recommended as clinical features may develop during the follow-up period. The onset of symptoms such as palpitation or syncope may herald an active phase of a previously quiescent disease, during which patients are at increased risk for sudden death. Greater awareness of right ventricular dysplasia among physicians and judicious use of implantable cardioverter-defibrillators may help to prevent unnecessary deaths.
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Atrial fibrillation (AF) is the most common sustained dysrhythmia in adults. It is ironic, then, that although mechanisms and effective treatments for most other supraventricular tachyarrhythmias have been discovered, AF remains incompletely understood and poorly treated. Nonetheless, our understanding of the pathophysiology of AF has improved in the last half-century, including some groundbreaking observations made in the last 10 years. Indeed, for some patients, the potential for cure now appears to be available. Because no unifying mechanism of AF has been proven, the aim of this review is to describe some of the common and important concepts behind current mechanistic theories of AF and how they contribute to our clinical understanding of AF.