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Circulation, Vol 51, 1149-1166, Copyright © 1975 by American Heart Association

ARTICLES

De subitaneis mortibus. XII. Asymmetrical hypertrophy of the heart

TN James and TK Marshall

Subjects with asymmetrical hypertrophy of the heart are prone to sudden death. Neither the pathogenesis of the eccentric hypertrophy nor the mechanism of sudden death is fully understood. In this report we describe certain postmortem findings in the hearts of 22 subjects who died suddenly, silently and unexpectedly, and in whom the only significant abnormality at autopsy was asymmetrical hypertrophy of the heart. Deep clefts were present in the septum in seven hearts, the small coronary arteries were abnormally narrowed in ten, the sinus node was sclerosed by fibrosis in 12, there was variable narrowing of the atrioventricular (A-V) node artery in many and the His bundle was too thin in three. There were multiple cysts or channels in the central fibrous body and of the adjacent A-V node and His bundle in four hearts. Most of the hearts displayed a fetal dispersion of the A-V node and His bundle throughout the central fibrous body, but this was particularly conspicuous in 13 hearts. These abnormalities in all parts of the conduction system suggest a variety of possible mechanisms by which the heart could become electrically unstable but do not indicate that one single mechanism is at fault in all. They offer some explanation for the reported high incidence of atrial fibrillation in such patients, and why they fare so badly with this arrhythmia. While the pathogenesis of asymmetrical hypertrophy may in some part be attributable to narrowed small coronary arteries or to an abnormal sequence or speed of septal and ventricular activation or to mechanical deficiency caused by deep septal clefts, none of these features was universally present in our series. Both asymmetrical hypertrophy of the heart and the sudden death which so frequently accompanies it probably develop by a variety of pathogenetic mechanisms.

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