Functional Valvular Incompetence in Decompensated Heart Failure: Noninvasive Monitoring and Response to Medical Management
Functional Valvular Incompetence in Decompensated Heart Failure: Noninvasive Monitoring and Response to Medical Management
复制标题
失代偿性心力衰竭的功能性瓣膜关闭不全：无创监测和医疗管理响应
DOI：
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发表时间：
2005
影响因子：
3.1
通讯作者：
K. Weber
中科院分区：
文献类型：
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作者：
P. Campos;I. D’Cruz;L. S. Johnson;A. Malhotra;K. Ramanathan;K. Weber
目的：我们假设功能性二尖瓣和三尖瓣关闭不全（分别为MR和TR）是缺血性或非缺血性心肌病伴收缩功能障碍的失代偿性心力衰竭（DF）心输出量减少的可逆原因。背景：DF定义为静息时心力衰竭的体征和症状，其根源在于继发于肾灌注受损的神经激素激活所转导的嗜盐状态。功能性MR和TR是全身血流减少的可逆原因。在优化医疗管理前后，可以无创监测它们对心输出量、胸腔积液量、心腔尺寸和瓣膜功能的影响。方法：14例男性受试者（66 ± 8岁），因缺血性（71%）或非缺血性（29%）心肌病继发射血分数降低（24 ± 5%），发生DF，临床表现为二尖瓣（MR）和三尖瓣（TR）关闭不全，在优化药物治疗恢复代偿性衰竭前和治疗后1周分别进行生物阻抗和超声心动图评估。结果：DF的药理消除伴随着体重的减轻（P < 0.01）。血流动力学改善包括心脏指数上升（2.1至2.6 L/min/m2; P < 0.01）和预测的肺动脉收缩压降低（58至35 mm Hg; P < 0.001），胸液含量（39至32千欧姆; P < 0.001）和全身血管阻力（1633至1209达因/秒/厘米5; P < 0.001）。功能性二尖瓣返流和TR的改善包括左心房和右心房面积的减少（分别为27至24 cm 2和26至23 cm 2; P < 0.001），MR和TR严重程度的彩色血流分级（P < 0.01）、二尖瓣返流容积（105 ~ 65 mL; P < 0.001）和有效MR开口尺寸（0.8 ~ 0.6 cm 2; P < 0.01）。结论：在DF中，功能性MR和TR导致心输出量减少、胸液含量增加和全身血管阻力增加，以及心房和瓣口尺寸增大，这些可以通过医疗管理来改善。生物阻抗和超声心动图提供了一系列无创评估血流动力学状态和瓣膜功能在这种情况下。
Objective:We hypothesized that functional mitral and tricuspid valvular incompetence (MR and TR, respectively) are reversible causes of reduced cardiac output in decompensated heart failure (DF) that accompanies systolic dysfunction in ischemic or nonischemic cardiomyopathy. Background:DF, defined as signs and symptoms of heart failure at rest, is rooted in a salt-avid state transduced by neurohormonal activation secondary to impaired renal perfusion. Functional MR and TR are reversible causes of reduced systemic blood flow. Their impact on cardiac output, thoracic fluid content, cardiac chamber dimensions, and valvular apparatus function can be monitored noninvasively, before and after optimized medical management. Methods:Fourteen male subjects (66 ± 8 years old) with reduced ejection fraction (24 ± 5%) secondary to ischemic (71%) or nonischemic (29%) cardiomyopathy, who developed DF with clinical evidence of mitral (MR) and tricuspid (TR) valvular incompetence, were each assessed by bioimpedance and echocardiography before and 1 week after optimized medical management restored compensated failure. Results:Pharmacologic elimination of DF was accompanied by a reduction in body weight (P < 0.01). Hemodynamic improvements included a rise in cardiac index (2.1 to 2.6 L/min/m2; P < 0.01) and a reduction in predicted pulmonary artery systolic pressure (58 to 35 mm Hg; P < 0.001), thoracic fluid content (39 to 32 kOhm; P < 0.001), and systemic vascular resistance (1633 to 1209 dynes/sec/cm5; P < 0.001). Improvements in functional MR and TR included reductions in left and right atrial areas (27 to 24 cm2 and 26 to 23 cm2, respectively; P < 0.001), color-flow grading of MR and TR severity (P < 0.01), mitral regurgitant volume (105 to 65 mL; P < 0.001), and effective MR orifice size (0.8 to 0.6 cm2; P < 0.01). Conclusions:In DF, functional MR and TR contribute to reduced cardiac output, increased thoracic fluid content, and systemic vascular resistance, together with enlarged atria and valvular orifice size, which can be improved by medical management. Bioimpedance and echocardiography provide for serial noninvasive assessments of hemodynamic status and valvular function in such cases.