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Low ventricular performance and high resistance in established hypertension in adults
1Department of Internal Medicine, Baogang Hospital, Shanghai Second Medical University, Shanghai, People's Republic of China.
Objective:
To investigate the relationship between left ventricular performance and sympathetic nervous activity.
Design:
We studied the alpha- and beta-adrenergic responsiveness of the subjects and assessed their left ventricular performance.
Methods:
Fifty-four adult established hypertensive patients, all with apparent left ventricular hypertrophy, and 36 age-matched normotensive controls were studied. Thirty-four of the hypertensive patients were within the +/- 2SD confidence area of fractional shortening/end-systolic stress relation of the normotensive controls and are denoted subgroup A; 19 patients were below the lower limit and are denoted subgroup B. Isoproterenol and neosynephrine injection tests were used to assess beta- and alpha-adrenergic responsiveness, respectively. Intravenous infusion tests using regitine and isoproterenol were performed in 16 patients to assess the effects of sympatho-adrenergic responsiveness on changes in left ventricular performance.
Results:
Afterload and left ventricular mass were similar in the two subgroups. Left ventricular performance and beta-adrenergic responsiveness in subgroup A were comparable with the corresponding levels in the normotensives, whereas in subgroup B both were markedly decreased. The regitine infusion test induced a fall of 25% in peripheral resistance from baseline, but no significant improvement in left ventricular performance. In contrast, isoproterenol infusion test resulted in striking improvements: left ventricular performance increased by 60%, afterload decreased by 48% and peripheral resistance fell by 50% from baseline.
Conclusion:
The diminished ventricular performance and high resistance observed in adult established hypertension may be due to synergic effects of significantly reduced beta-adrenergic responsiveness coupled with enhanced alpha-adrenergic responsiveness.