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The cardiomyopathies: an overview
  1. M J Davies
  1. St George's Hospital Medical School, Histopathology Department, London, UK
  1. Professor MJ Davies, St George's Hospital Medical School, Histopathology Department, Cranmer Terrace, London SW17 ORE, UK

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The recent revision (table 1) of the definition of a cardiomyopathy by the World Health Organization1 recognises that ventricular dysfunction can result from a failure to correct volume or pressure overload in valve disease or to control hypertension. Loss of myocardium caused by coronary artery disease also leads to severe ventricular dysfunction. All of these end stage conditions are categorised as specific cardiomyopathies. The second form of cardiomyopathy is caused by intrinsic disorders of the myocardium itself and is subdivided on the basis of the pathophysiology. Such a functional rather than an aetiological classification has drawbacks but reflects our current state of knowledge. The different functional abnormalities produce characteristic changes in ventricular shape easily recognised in short axis echocardiographic planes and by pathologists (fig 1).

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Table 1

The cardiomyopathies, as defined by the World Health Organization1

Figure 1

The morphological expression of the intrinsic cardiomyopathies as seen in short axis cuts across the right and left ventricle at mid septal level. Hypertrophic cardiomyopathy may be symmetric or asymmetric. HCM, hypertrophic cardiomyopathy; DCM, dilated cardiomyopathy; RCM, restrictive cardiomyopathy; ARVD, arrhythmogenic right ventricular dysplasia; EMF, endomyocardial fibrosis; OCM, obliterative cardiomyopathy,

Dilated cardiomyopathy

The pathophysiological entity dilated cardiomyopathy (DCM) is heterogeneous with regard both to its pathogenesis and its morphology. Common to the whole group is a poorly contracting dilated left ventricle with a normal or reduced left ventricular wall thickness. The lack of an increase in left ventricular wall thickness tends to mask a significant increase in left ventricular mass. In the terminal stages thrombus may develop in the apices of both ventricles. The histological changes within the myocardium are listed above. The individual myocytes are increased in length rather than in width and lose the normal number of intracellular contractile myofibrils, and thus appear empty and vacuolated on histology (fig 2). The degree of …

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