Open AccessMechanism of prolongation of pre‐ejection period in the hypertrophied left ventricle with normal systolic function in unanesthetized hypertensive dogs
Author(s) -
Matsuno Y.,
Morioka S.,
Murakami Y.,
Kobayashi S.,
Moriyama K.
Publication year - 1988
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960111009
Subject(s) - medicine , preload , cardiology , ventricle , blood pressure , contractility , diastole , afterload , ejection fraction , heart rate , systole , hemodynamics , heart failure
To determine the mechanism for prolongation of pre‐ejection period (PEP) in the hypertensive heart with normal systolic function, cardiac catheterizations, echocardiograms, and electrocardiograms were performed at the baseline period (CS, control stage) and eight weeks (HS, hypertensive stage) after the induction of systemic hypertension by Page's method in unanesthetized dogs. Mean aortic blood pressure increased significantly (96 ± 12 to 137±26 mmHg) (p<0.05). Diastolic aortic pressure also increased significantly (80±12 to 118±24 mmHg) (p<0.01). Left ventricular (LV) PEP of HS was significantly prolonged (72±12 vs. 87±22 ms, CS vs. HS). The ratio of LV pre‐ejection period to ejection time (PEP/ET) also increased significantly (0.33 ±0.04 to 0.42 ±0.07) (p<0.05). LV end‐diastolic wall stress as an index of preload decreased significantly (7.7 ±2.5 vs. 5.9± 1.8 10 3 dynes/cm 2 , CS vs. HS). Heart rate, mean velocity of circumferential fiber shortening (VCF) and end‐systolic wall stress of HS did not change. That is, myocardial contractility in the hypertensive heart of HS most likely is not depressed. At autopsy, left ventricle to body weight ratio of HS was significantly (p<0.01) greater than the sham‐operated dogs (5.7±0.8vs. 4.3±0.5 g/kg). From these findings, there are two possible factors responsible for prolongation of PEP of HS. First, elevated diastolic aortic pressure may influence PEP. Second, the prolonged PEP is possibly caused by the decrease of preload. Boudoulas et al. reported that the abnormalities in systolic time intervals (STI) were equivalent in patient subgroups with high and low diastolic arterial pressure within hypertensive groups. Therefore, we conclude that the main factor to prolong PEP in the hypertensive heart with normal systolic function is possibly the decrease of preload rather than the depressed myocardial contractility or elevated diastolic aortic pressure.