Abstract

purpose: To evaluate whether impaired left ventricular filling determines the hemodynamic responses to isometric and orthostatic stress in a population with mild essential hypertension. patients and methods: The study population consisted of 32 patients with essential hypertension who were subdivided into those with preserved left ventricular filling (15 patients) and those with impaired left ventricular filling (17 patients). Echocardiograms were obtained before hemodynamic assessment was performed. Isometric stress and head-up tilt tests were done with a recovery period of at least 10 minutes between each to allow for blood pressure and heart rate to return to baseline. Hemodynamic reassessment was performed during the last minute of each test and at the end of the recovery period. Plasma epinephrine, norepinephrine, and dopamine levels were determined by radioenzymatic method. results: Isometric stress increased mean arterial pressure by 30% (p <0.0001) by an increase in cardiac output (p <0.0001) and total peripheral resistance (p <0.0001) associated with an increase in plasma catecholamine levels (p <0.0001). Patients with preserved left ventricular filling had an increase in arterial pressure predominantly through an elevation in cardiac output (17%, p <0.0001) associated with a small increase in plasma norepinephrine levels (p <0.05) and in peripheral resistance (11%, p <0.05). In contrast, patients with impaired left ventricular filling had an increase in arterial pressure mainly through an increase in peripheral resistance (25%, p <0.0001) that was associated with a 45% elevation in plasma norepinephrine levels (p <0.0001). Orthostatic stress (passive head-up tilt) caused an exaggerated decrease in stroke volume (p <0.01) and cardiac output (p <0.01) in patients with impaired left ventricular filling when compared with those with preserved diastolic function. conclusion: Impaired left ventricular filling blunts the response of the heart to isometric and orthostatic stress. As a consequence, hypertensive patients with impaired ventricular filling respond to these stressors with enhanced sympathetic stimulation and exaggerated vasoconstriction.

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