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Impaired peripheral vasoconstriction in response to alpha-adrenergic stimulation in patients with idiopathic
1Department of Internal Medicine, Institute of Clinical Medicine, University of Tsukuba, Ibaraki, Japan.
Insights
Patients with hypertrophic cardiomyopathy (HCM) show impaired vasoconstriction due to abnormal alpha-adrenergic receptor function. This finding helps explain exercise hypotension in HCM patients.
Area of Science:
- Cardiology
- Vascular Physiology
Background:
- Exercise hypotension is observed in hypertrophic cardiomyopathy (HCM) patients.
- This may stem from inadequate systemic vascular resistance increases during or post-exercise.
Purpose of the Study:
- To investigate the pathogenesis of limb vascular response abnormalities in idiopathic HCM patients.
- To assess peripheral vascular resistance regulation in HCM.
Main Methods:
- Intra-arterial infusions of acetylcholine, nitroglycerin, phenylephrine, and isoproterenol in 13 HCM patients and 9 controls.
- Forearm plethysmography to measure peripheral vascular resistance changes at rest and during infusions.
Main Results:
- Isoproterenol, acetylcholine, and nitroglycerin caused similar dose-related vasodilation in both groups.
- Phenylephrine infusions resulted in significantly lower percentage increases in vascular resistance in HCM patients compared to controls.
- Alpha-adrenergic mediated vasoconstriction was impaired in HCM patients' peripheral vasculature.
Conclusions:
- Peripheral vasoconstriction mediated by alpha-adrenergic receptors is impaired in patients with idiopathic HCM.
- This impairment may contribute to exercise hypotension in HCM.
Abstract:
Exercise hypotension has been documented in patients with hypertrophic cardiomyopathy (HCM). Some investigators reported that this is due to an inadequate increase of systemic vascular resistance during or after exercise. The aim of this study was to investigate the pathogenesis of limb vascular response abnormalities in patients with idiopathic HCM. Thirteen patients with HCM and 9 healthy controls were administered an endothelium-dependent dilator (acetylcholine), a direct smooth muscle dilator (nitroglycerin), an alpha-adrenergic stimulator (phenylephrine), and a beta-adrenergic stimulator (isoproterenol) by intra-arterial infusion. Peripheral vascular resistance was assessed by forearm plethysmography at rest and during each infusion to obtain the percentage change in vascular resistance. Isoproterenol, acetylcholine and nitroglycerin produced dose-related vasodilatation with no significant differences between HCM patients and healthy controls. The percentage increase in vascular resistance was significantly less in HCM patients than in healthy controls after phenylephrine infusions of 0.5 microg/min (155+/-38% vs 195+/-47%, mean+/-SD, p<0.05) and 1.0 microg/min (174+/-49% vs 238+/-65%, p<0.05). Vasoconstriction mediated by alpha-adrenergic receptors appeared to be impaired in the peripheral vasculature of patients with HCM.