Malinowski Marcin, Proudfoot Alistair G, Langholz David, Eberhart Lenora, Brown Michael, Schubert Hans, Wodarek Jeremy, Timek Tomasz A
Meijer Heart and Vascular Institute at Spectrum Health, Grand Rapids, MI, USA.
Department of Cardiac Surgery, Medical University of Silesia, School of Medicine in Katowice, Katowice, Poland.
Interact Cardiovasc Thorac Surg. 2017 Jun 1;24(6):905-910. doi: 10.1093/icvts/ivx012.
Functional tricuspid regurgitation (FTR) is common in patients with advanced heart failure and frequently complicates left ventricular assist device implantation yet remains poorly understood. We set out to establish large animal model of FTR that could serve as a research platform to investigate the pathogenesis of FTR associated with end-stage heart failure.
: Through right thoracotomy, ten adult sheep underwent implantation of pacemaker with epicardial LV lead, five sonomicrometry crystals on the right ventricle, and left and right ventricular telemetry pressure sensors during a beating heart off-pump procedure. After 5 ± 1 days of recovery, baseline haemodynamic, echocardiographic and sonomicrometry data were collected. Animals were paced thereafter at a rate of 220-240 beats/min until the development of heart failure and concomitant tricuspid regurgitation.
: Three animals died during early recovery period and one during the pacing phase. Six surviving animals were paced for a mean of 14 ± 5 days. Cardiac function was significantly depressed compared to baseline, with LV ejection fraction falling from 69 ± 2% to 22 ± 4% ( P < 0.001) and RV fractional area change from 52 ± 11% to 25 ± 9% ( P = 0.005). All animals developed significant enlargement of tricuspid annulus (from 29.5 ± 1.6 to 36.5 ± 4.5 mm; P = 0.01) and right ventricle (from 21.9 ± 0.2 to 30.3 ± 0.6 mm; P = 0.03). Sonomicrometry derived contractility of RV free wall was depressed and at least moderate tricuspid insufficiency developed in all animals.
: Biventricular dysfunction, tricuspid annular dilatation and significant FTR were observed in our model of ovine tachycardia induced cardiomyopathy. This animal model reflects the clinical situation of end-stage heart failure patients presenting for mechanical support.
功能性三尖瓣反流（FTR）在晚期心力衰竭患者中很常见，并且经常使左心室辅助装置植入术复杂化，但人们对其仍知之甚少。我们着手建立FTR的大型动物模型，该模型可作为研究与终末期心力衰竭相关的FTR发病机制的研究平台。
通过右胸切开术，在10只成年绵羊心跳不停跳的情况下，植入带有心外膜左心室导线的起搏器、右心室的5个超声心动图晶体以及左、右心室遥测压力传感器。恢复5±1天后，收集基线血流动力学、超声心动图和超声心动图数据。此后，以220 - 240次/分钟的速率对动物进行起搏，直至发生心力衰竭和伴随的三尖瓣反流。
3只动物在早期恢复期死亡，1只在起搏阶段死亡。6只存活的动物平均起搏14±5天。与基线相比，心功能明显下降，左心室射血分数从69±2%降至22±4%（P < 0.001），右心室面积变化分数从52±11%降至25±9%（P = 0.005）。所有动物的三尖瓣环均显著扩大（从29.5±1.6增加到36.5±4.5毫米；P = 0.01），右心室也显著扩大（从21.9±0.2增加到30.3±0.6毫米；P = 0.03）。超声心动图测得的右心室游离壁收缩力下降，所有动物均出现至少中度的三尖瓣关闭不全。
在我们的绵羊心动过速诱导性心肌病模型中观察到双心室功能障碍、三尖瓣环扩张和显著的FTR。该动物模型反映了寻求机械支持的终末期心力衰竭患者的临床情况。
