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  • Title: Mechanism of prolongation of pre-ejection period in the hypertrophied left ventricle with normal systolic function in unanesthetized hypertensive dogs.
    Author: Matsuno Y, Morioka S, Murakami Y, Kobayashi S, Moriyama K.
    Journal: Clin Cardiol; 1988 Oct; 11(10):702-6. PubMed ID: 3224453.
    Abstract:
    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 less than 0.05). Diastolic aortic pressure also increased significantly (80 +/- 12 to 118 +/- 24 mmHg) (p less than 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 less than 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/cm2, 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 less than 0.01) greater than the sham-operated dogs (5.7 +/- 0.8 vs. 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.(ABSTRACT TRUNCATED AT 250 WORDS)
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