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The relationship of blood pressure to cardiac hypertrophy: experimental studies in rats
T Morgan1, H Brunner, J F Aubert
1Department of Physiology, University of Melbourne, Victoria, Australia.
Insights
Intermittent high blood pressure can cause cardiac hypertrophy, a key risk factor for heart disease. This suggests cardiac wall stress, not just workload, triggers this condition.
Area of Science:
- Cardiology
- Physiology
Background:
- Cardiac hypertrophy is a significant predictor of patient morbidity and mortality.
- The precise interplay between blood pressure, hormones, and cardiac hypertrophy remains incompletely understood.
Purpose of the Study:
- To investigate whether intermittent elevations in blood pressure can induce left ventricular hypertrophy.
- To explore the role of acute blood pressure surges in cardiac remodeling.
Main Methods:
- Experimental induction of hypertension using intraperitoneal injections of angiotensin II, noradrenalin, and methoxamine.
- Acute blood pressure elevations of ≥60 mmHg for up to 1 hour, up to 4 times daily.
- Measurement of cardiac index at 2 and 4 weeks post-intervention.
Main Results:
- All experimental procedures resulted in an increased cardiac index.
- Some groups exhibited growth retardation, where cardiac weight did not increase despite cardiac index elevation.
- Combined high sodium intake and angiotensin II injections exacerbated left ventricular hypertrophy.
Conclusions:
- Acute, intermittent elevation of blood pressure is capable of causing left ventricular hypertrophy.
- Cardiac wall stress appears to be a more critical trigger for hypertrophy than 24-hour workload.
Abstract:
Cardiac hypertrophy is an independent predictor of morbidity and mortality. The exact relationship between blood pressure, hormones and cardiac hypertrophy is unclear. This study was undertaken to determine if intermittent elevation of blood pressure could cause left ventricular hypertrophy. Blood pressure was elevated intermittently by intraperitoneal injections of angiotensin II, noradrenalin and methoxamine. Blood pressure was acutely elevated by 60 mmHg or more for periods lasting up to 1 hour on up to 4 occasions each day. Cardiac index was measured 2 and 4 weeks after the experiment started. The cardiac index was increased by all procedures. The results were complicated by a retardation of growth in some experimental groups, meaning that the cardiac weight did not increase though the index did. In a study looking at the interaction of sodium and angiotensin II high sodium intake caused left ventricular hypertrophy and injections of angiotensin II caused further left ventricular hypertrophy. This study indicated that acute intermittent elevation of blood pressure could cause left ventricular hypertrophy and suggests that wall stress rather than 24 hour workload is the important triggering mechanism.