Pathogenetic role of myocardial fiber disarray in the progression of cardiac fibrosis in normal hearts, hypertensive hearts and hearts with hypertrophic cardiomyopathy.

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Abstract
To define the pathogenetic role of myocardial fiber disarray in the progression of cardiac fibrosis, the percent area of fibrosis in tissue with disarray was compared with that in tissue without disarray. Thirty autopsied hearts, 10 from patients with hypertrophic cardiomyopathy, 10 from patients with hypertension and 10 from normal adults, were studied. The percent areas of fibrosis in tissues with and without disarray were significantly different(p < 0.01) among hearts with hypertrophic cardiomyopathy (12.6 .+-. 4.0 and 8.2 .+-. 3.3%), hypertensive hearts (6.6 .+-. 3.6 and 2.5 .+-. 1.4%) and normal hearts (2.8 .+-. 1.2 and 1.0 .+-. 0.4%). The percent area of fibrosis in tissue with disarray was greater than in that without disarray in all 3 groups and the ratios of these percentages were similar in the 3 groups: 2.9 .+-. 4.2 in hypertrophic cardiomyopathy 2.5 .+-. 1.7 in hypertensive hearts and 2.5 .+-. 1.8 in normal hearts. The conclusions are: 1) disarray promotes fibrosis to a similar degree, not only in hypertrophic cardiomyopathy, but also in hypertensive hearts and normal hearts; 2) the increased level of fibrosis in hearts with hypertrophic cardiomyopathy and in hypertensive hearts, together with widespread fibrosis in hearts with hypertrophic cardiomyopathy in particular cannot be explained by disarray alone.