Ventricular Free Wall Weight Research Articles

Left ventricular hypertrophy: A cytometric study on 42 human hearts

A histocytometric study of 42 left ventricles was carried out. The cases consisted of normal hearts as well as a number of hypertrophic hearts which were progressively heavier in weight. The results of this study were analyzed by computer. We found an increase in myocardial cell size correlated with an increase in the ventricular free wall weight, up to a critical weight of 250 g. Beyond that critical weight, cellular hyperplasia was evident, followed by the further development of hypertrophy, in relation to the increase of ventricular weight. At the “critical weight” the progressive increase of cellular diameter, which is less than the theoretical value, abruptly ends and then decreases considerably. In contrast, this same phenomena is not seen for the cell length. The myocardial cell length shows a constant gradual increase always greater than the theoretical value regardless of ventricular weight. For this reason the cellular hyperplasia specifically presents an increase in cellular length beyond the increase in cellular diameter, which is reduced. A multiplication of myocardial nuclei beyond the critical weight was also observed. The results obtained are of physiopathological significance owing to modifications of the capillary network and the interstitial tissues. A histocytometric study of 42 left ventricles was carried out. The cases consisted of normal hearts as well as a number of hypertrophic hearts which were progressively heavier in weight. The results of this study were analyzed by computer. We found an increase in myocardial cell size correlated with an increase in the ventricular free wall weight, up to a critical weight of 250 g. Beyond that critical weight, cellular hyperplasia was evident, followed by the further development of hypertrophy, in relation to the increase of ventricular weight. At the “critical weight” the progressive increase of cellular diameter, which is less than the theoretical value, abruptly ends and then decreases considerably. In contrast, this same phenomena is not seen for the cell length. The myocardial cell length shows a constant gradual increase always greater than the theoretical value regardless of ventricular weight. For this reason the cellular hyperplasia specifically presents an increase in cellular length beyond the increase in cellular diameter, which is reduced. A multiplication of myocardial nuclei beyond the critical weight was also observed. The results obtained are of physiopathological significance owing to modifications of the capillary network and the interstitial tissues.

Gross anatomy associated with patterns called left posterior hemiblock.

From a compilation of 1411 gross dissections of the hearts from patients who had had recent electrocardiograms prior to death, 62 were found to have frontal QRS axes between +90 and +180°. Thirty-eight exhibited an S 1 Q 3 R 3 pattern-the second screening criterion basic to consideration for the label of left posterior hemiblock (LPH). Twenty-two of these also had right ventricular free wall weights in excess of 70 g. Two others exhibited inferior myocardial infarction only. Of the remaining 14, six afforded mild clinical suspicion of increased hemodynamic loading of the right heart but did not have increased right ventricular weights. Four had right bundle-branch block (RBBB), and only one had a prolonged P-R interval. The S 1 Q 3 R 3 pattern with right-axis deviation thus occurred in patients with or without right ventricular hypertrophy and with or without inferior wall myocardial infarction. Right bundle-branch block was a frequent occurrence in the spectrum of right-axis deviation (RAD) whether S 1 Q 3 R 3 was present or not. The scatter of the frequent associates of RAD-inferior myocardial lesions, right ventricular hypertrophy, a clinical history of right ventricular loading diseases, and RBBB—suggests three alternative ways of viewing the S 1 Q 3 R 3 pattern with RAD: (1) LPH is a cause of S 1 Q 3 R 3 with RAD. It is a manifestation of left ventricular myocardial disease, but it may be a result of overt infarction, or may be mimicked by right ventricular disease. (2) LPH is the cause of S 1 Q 3 R 3 with RAD. It is the means by which diverse etiologies produce a distinctive electrocardiographic pattern (including left ventricular myocardial deficits, right ventricular enlargement, or a small group of unknown causes). (3) LPH is an artifact of convenience. Patients with RAD may or may not have S 1 Q 3 R 3 ; they frequently have inferior wall myocardial infarction, right ventricular overload or enlargement, and RBBB.