Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dilated cardiomyopathy is a moderately common syndrome resulting from many causes, many of which are yet to be defined. The syndrome is relatively easy to diagnose in its late congestive stage if valvular abnormality, hypertensive disease, and gross myocardial infarction are absent. However, it should be suspected in patients with undiagnosed chest pain, in patients whose severe arrhythmia has no obvious cause, and in any patient with demonstrable ventricular dilatation or systolic malfunction. It may follow infections, especially viral ones and is found in many deficiency diseases, especially diabetes. Repeated episodes of angina due to epicardial disease may result in myocardial "stunning" with ultimate dilation and failure. Microvascular spasm or occlusion may be etiologically important. Dilated cardiomyopathy may be a manifestation of toxins, with ethanol being the most important. Immune mechanisms may play a major role, either independently or in connection with other factors. Early diagnosis may be made with the help of echocardiography, radionuclide angiography, and even coronary arteriography. Gallium scan may be helpful, and if positive myocardial biopsy is indicated. Therapy includes classic measures for congestive failure if it is present: cardiac glycosides, diuretics, antiarrhythmics, and anticoagulants. There is evidence that vasodilators, calcium channel blockers, and beta-adrenergic blockers may be helpful for both general and specific reasons, but these should be used with care. Prednisone and azathioprine may help if there is an inflammatory component. Cardiac replacement remains an ultimate measure.
 ...
PMID:Dilated cardiomyopathy: current concepts. 372 Feb 70

The origin of cardiomyopathies, a major cause of cardiac disability and death, has been largely unexplained. Pathologic features, common to all cardiomyopathies independent of origin, include ventricular hypertrophy and diffuse scarring with variable amounts of ventricular dilatation. This problem was studied experimentally in 2 models of congestive cardiomyopathy: the hereditary cardiomyopathic Syrian hamster and the hypertensive-diabetic rat. In both the genetic and the acquired disease models, there is focal myocytolytic necrosis followed by healing with focal scars, ventricular wall hypertrophy, ventricular dilatation with congestive heart failure and, ultimately, death. In view of the heterogeneous pathologic features of both diseases, silicone rubber perfusions have been used to study the microcirculation of the heart in these animals; microvascular spasm has been demonstrated early in the disease associated with small areas of myocytolytic necrosis that undergo subsequent fibrosis. Reactive hypertrophy then ensues as a compensatory response to this myocellular necrosis; it is the combination of cell loss and slowly decreasing contractility resulting from the reactive hypertrophy, which culminates in a cardiomyopathy. Administration of verapamil or prazosin to the cardiomyopathic Syrian hamster prevents microvascular spasm and development of cardiomyopathic changes in the myocardium. In view of these and other findings related to the anatomy and hyperreactivity of microcirculation, it is concluded that hypertrophic congestive cardiomyopathies may be caused by focal cell loss due to microvascular spasm and reperfusion injury, with the subsequent development of focal fibrosis and reactive hypertrophy in response to the myocardial necrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Microvascular spasm as a cause of cardiomyopathies and the calcium-blocking agent verapamil as potential primary therapy. 388 12