期刊论文详细信息
SHORT-TERM VASODILATOR EFFECT OF CAPTOPRIL IN PATIENTS WITH SEVERE MITRAL REGURGITATION IS PARASYMPATHETICALLY MEDIATED
Article
关键词: CONGESTIVE HEART-FAILURE;    CONVERTING-ENZYME-INHIBITION;    PRESSURE OVERLOAD HYPERTROPHY;    RENIN-ANGIOTENSIN SYSTEM;    DILATED CARDIOMYOPATHY;    NORMOTENSIVE MAN;    HYDRALAZINE;    ENALAPRILAT;    ACTIVATION;    REFLEX;   
DOI  :  10.1161/01.CIR.84.5.2049
来源: SCIE
【 摘 要 】

Background. Few data exist regarding the effects of angiotensin converting enzyme inhibitors in patients with regurgitant valvular lesions. We postulated an immediate improvement in cardiac performance with captopril in mitral regurgitation, which, in a hemodynamically compensated group of patients, might be mediated through parasympathetic vasodilation rather than through blockade of angiotensin converting enzyme. Methods and Results. Hemodynamics were examined before and 90 minutes after oral captopril (25-50 mg) in 18 patients (mean age, 31 years) with chronic, severe mitral regurgitation in New York Heart Association functional class II and III. One group of patients was given captopril alone (group 1, n = 9) and a second group was given captopril plus atropine 0.04 mg/kg i.v. (group 2, n = 9). Captopril alone (group 1) produced decreases in heart rate (90-81 beats/min, p < 0.001), mean arterial pressure (90-73 mm Hg, p < 0.001), systemic resistance (28-23 Wood units, p = 0.068), and pulmonary wedge pressure (19-14 mm Hg, p < 0.001). There was no improvement in either arteriovenous oxygen difference or thermodilution cardiac output; in fact, the latter slightly declined (3.45-3.35 l/min, p = 0.002). Pretreatment with atropine (group 2) diminished the effects of captopril on heart rate (107-103 beats/min, p = 0.065 for atropine effect by two-way ANOVA), mean arterial pressure (88-82 mm Hg, p = 0.01 for atropine effect), and systemic resistance (26-27 Wood units, p = 0.04 for atropine effect). Conclusions. In patients with chronic, severe mitral regurgitation, captopril reduced systemic arterial and left ventricular filling pressures but did not immediately augment cardiac output as expected. Furthermore, the modest systemic vasodilator effect of captopril was parasympathetically mediated.

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