Abnormal cardiovascular regulation in the mitral valve prolapse syndrome

Abstract

Studies of patients with mitral valve prolapse syndrome have suggested autonomic nervous system dysfunction, but a precise definition of mechanisms is lacking. We measured supine and standing heart rate, blood pressure, cardiac output, oxygen consumption, plasma catecholamines, and blood volume in 23 symptomatic women with both echocardiographic and phonographic signs of MVP and in 17 normal control subjects. An analysis of the results revealed 2 distinct subgroups of patients: those with normal heart rates but increased vasoconstriction (Group I, n = 10) and those with orthostatic tachycardia (Group II, n = 13). Group II patients had heart rates at rest supine of 97 ± 3 compared with 79 ± 2 in Group I patients and 78 ± 8 in control subjects. Estimated total blood volumes were lowest in Group I patients, intermediate in Group II patients, and highest in control subjects (p<0.05). Other measurements at rest supine were similar in patients and controls. After standing for 5 minutes, patients had a higher mean plasma epinephrine value, diastolic blood pressure (81 ± 2 versus 74 ± 3 mm Hg, p < 0.05), and peripheral resistance (1,878 ± 114 versus 1,414 ± 92, dynes s cm −5, p < 0.01), wider arteriovenous oxygen difference (6.7 ± 0.4 versus 5.3 ± 0.5 vol%), and lower stroke volume index (26 ± 2 versus 33 ± 2 ml/m 2, p < 0.01) than did the control subjects. Cardiac output was normal in Group II patients but reduced in Group I patients, who demonstrated marked vasoconstriction. No patient had evidence of a “hyperkinetic” circulatory state. A cycle of decreased forward stroke volume, vasoconstriction, and blood volume contraction appears to be present in at least some symptomatic patients with MVP.