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Reduced Systemic Vascular Resistance as Therapy for Severe Mitral Regurgitation of Valvular Origin

CHARLES W. HARSHAW, M.D.; WILLIAM GROSSMAN, M.D.; ALAN B. MUNRO, M.D.; and LAMBERT P. MCLAURIN, M.D.
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A preliminary report of this data has been presented at the American Heart Association meeting in Dallas, Texas, on 18 November 1974.

▸Requests for reprints should be addressed to William Grossman, M.D., Department of Medicine, University of North Carolina School of Medicine, Chapel Hill, NC 27514.


Chapel Hill, North Carolina


Ann Intern Med. 1975;83(3):312-316. doi:10.7326/0003-4819-83-3-312
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We examined the hemodynamic response to afterload reduction by sodium nitroprusside in 7 patients with severe mitral regurgitation of purely valvular origin. Lowering of systemic vascular resistance was associated with major reductions in pulmonary capillary mean (29 ± 2 to 13 ± 1 mm Hg) and left ventricular end diastolic (20 ± 3 to 9 ± 1 mm Hg) pressures, while substantial increases were noted in cardiac index (2.2 ± 0.5 to 3.1 ± 0.4 litres/min per m2 body surface area) and forward stroke volume (23 ± 4 to 34 ± 4 ml/beat/m2 body surface area). Angiographic calculations showed significant decreases in regurgitant volume (73 ± 19 to 55 ± 12 ml/beat/m 2 body surface area) and regurgitant fraction (0.70 ± 0.07 to 0.57 ± 0.06). No significant change occurred in left ventricular ejection fraction or heart rate, suggesting that the improved cardiac function was not due to a reflex increase in adrenergic stimulation. These observations support the concept that afterload reduction may be therapeutic in severe mitral regurgitation by reducing impedance to forward left ventricular output, thereby promoting greater forward and small regurgitant fractions of the total stroke volume.

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