Abnormal cardiovascular regulation in the mitral valve prolapse syndrome.
Abnormal cardiovascular regulation in the mitral valve prolapse syndrome.
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二尖瓣脱垂综合征中的心血管调节异常。
DOI：
10.1016/0002-9149(83)90130-3
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Blomqvist,CG
中科院分区：
文献类型：
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作者：
Gaffney,FA;Bastian,BC;Lane,LB;Taylor,WF;Horton,J;Schutte,JE;Graham,RM;Pettinger,W;Blomqvist,CG
对二尖瓣脱垂综合征患者的研究表明，自主神经系统功能障碍，但缺乏对机制的准确定义。我们测量了23例同时有MVP超声心动图和声学征象的有症状的女性和17名正常对照组的仰卧和站立心率、血压、心输出量、氧耗、血儿茶酚胺和血容量。对结果的分析显示了两个不同的患者亚组：心率正常但血管收缩增加的患者(I组，n=10)和立位性心动过速(II组，n=13)。II组患者仰卧位心率为97±3，而I组为79±2，对照组为78±8。估计的总血量在第一组患者中最低，在第二组患者中居中，在对照组中最高(p<；0.05)。患者和对照组仰卧休息时的其他测量结果相似。站立5分钟后，患者的平均血浆肾上腺素水平、舒张压(81±2比74±3毫米汞柱，p<；0.05)、外周阻力(1,878±114比1,414±92，dynes S cm−5，p<；0.01)、动静脉血氧差(6.7±0.4比5.3±0.5%)、每搏输出量指数(26±2比33±2 ml/m2，p<；0.0 1)明显高于对照组。心输出量在II组患者中正常，但在I组患者中减少，他们表现出明显的血管收缩。没有病人有“高动力”循环状态的证据。至少在一些有症状的MVP患者中，出现了前向搏出量减少、血管收缩和血容量收缩的循环。
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 mmHg, 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/m2, 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.