PubMed · 6221742
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1982. [Rheumatic endocarditis (clinical reference)].. https://pubmed.ncbi.nlm.nih.gov/6221742/
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At the cellular and molecular level the transition to heart failure is a complex process that involves structural adaptation, not only of the heart, but of peripheral vasculature and renal tissues as well. Recent studies have suggested that autocrine, paracrine, and circulating biologically active mediators activate events that result in the concerted failure of adaptive mechanisms and the ultimate depression of cardiac myocyte function. Greater understanding of these local mechanisms in the future may lead to drug therapies that can selectively block these mechanisms and prevent the progression from compensation to overt heart failure.
M-mode echocardiograms of 202 cardiac patients were studied with respect to the pattern of left ventricular (LV) geometry. Patients with normal LV mass and volume were separated from those who had LV hypertrophy or enlargement on the basis of LV mass and volume indexed to body surface area. The relative wall thickness that is currently used to classify LV hypertrophy/enlargement was found to be inadequate for differentiating between concentric and eccentric types of LV hypertrophy. A new M-mode echocardiographic classification is therefore proposed that accurately separates the different types of LV enlargement; it also allows identification of patients who have chronically dilated left ventricles at the expense of thin walls and thus have normal LV mass.
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