Key result
Induction of systemic hypertension in unanesthetized dogs significantly increased LV chamber stroke work (p<0.05), whereas LV myocardial external work normalized for wall stress was not altered.
Why the study?
Does systemic hypertension alter external work and its control mechanism in concentric hypertrophied left ventricles in unanesthetized dogs?
Does systemic hypertension alter external work and its control mechanism in concentric hypertrophied left ventricles in unanesthetized dogs?
p-value: p=<0.05
In a canine model of systemic hypertension, concentric left ventricular hypertrophy maintains normal myocardial external work despite an increase in overall LV chamber external work.
Supports compensatory role of hypertrophy in canine hypertension; hypothesis-generating for human concentric LVH.
This study aimed to evaluate the change in external work and its control mechanism in the concentric hypertrophied heart induced by systemic hypertension. The calculated stroke work, myocardial contractility, afterload, and preload were examined in the baseline period (Control Stage, CS) and in the eighth week after the induction of perinephritic hypertension (Hypertensive Stage, HS) in unanesthetized dogs. These variables were examined with echocardiograms and high-fidelity left ventricular (LV) and ascending aortic pressures. Mean aortic pressure was significantly (p less than 0.05) elevated from 95 +/- 10 to 134 +/- 27 mmHg in HS. The ratio of end-diastolic wall thickness to radius significantly (p less than 0.05) increased in the HS. The calculated stroke work of the LV chamber was significantly (p less than 0.05) increased from 7022 +/- 1203 to 8860 +/- 1548 X 10(3) erg in HS while the stroke work normalized for wall thickness by calculating the wall stress was not altered (3069 +/- 1086 v.s. 2989 +/- 866 erg; CS v.s. HS) with no significant change in heart rate in HS. In the HS, the end-systolic wall stress (afterload) and the slope of end-systolic wall stress-dimension relationship (myocardial contractility) were unchanged while the end-diastolic wall stress (preload) slightly reduced. These results suggest that, in the concentric hypertrophied left ventricle induced by systemic hypertension, the LV myocardial external work is normal, whereas the LV chamber external work increases.(ABSTRACT TRUNCATED AT 250 WORDS)
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Matsuno et al. (1990) studied Systemic hypertension. Induction of perinephritic hypertension vs. Baseline period (Control Stage) was evaluated on Calculated stroke work of the left ventricular chamber (p=<0.05). Induction of systemic hypertension in unanesthetized dogs significantly increased LV chamber stroke work (p<0.05), whereas LV myocardial external work normalized for wall stress was not altered.
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