Mau James, Menzie Stuart, Huang Yifei, Ward Michael, Hunyor Stephen
Cardiac Technology Centre, Kolling Institute, St Leonards, Australia.
J Thorac Cardiovasc Surg. 2009 Jul;138(1):172-8. doi: 10.1016/j.jtcvs.2009.03.012.
Right ventricular failure manifests in 25% of left ventricular assist device recipients because of ventricular coupling mechanism disruption. Septal ischemia accentuates this process, but the effect of septal infarction has not been elucidated. Right ventricular response to incremental left ventricular unloading was studied in sheep with septal infarction.
Septal infarction was induced in 6 sheep using ethanol delivery into the main septal perforating artery. Six shams avoided ethanol. Load-independent and in-series right ventricular response to incremental (0%-100%) left ventricular unloading was measured 4 weeks later. Dimensions of whole heart, wall thickness, and chamber volumes were obtained using sonomicrometers. Selective perfusion with triphenyltetrazolium quantified septal damage.
Right ventricular preload-recruitable-stroke-work, contractility, and ejection fraction were lower at 75% and 100% left ventricular unloading in sham compared with infarcted animals (75%: 26.3 +/- 3.4, 0.70 +/- 0.15, and 23.9 +/- 4.6 vs 37 +/- 2.6 erg *10;3, 0.99 +/- 0.18 mm Hg/mL, and 35.5% +/- 3.4%, all P < . 01, 100%: 24.8 +/- 4.5, 0.67 +/- 0.14, and 23.8 +/- 5.8 vs 36.0 +/- 4.6 erg *10;3, 0.90 +/- 0.09 mm Hg/mL, and 32.7% +/- 11.0%, all P < . 01). Central venous pressure was higher at 75% and 100% unloading in sham compared with infarcted animals (75%: 8.6 +/- 1.0 vs 4.5 +/- 1.0, 100%: 12.4 +/- 0.8 vs 3.4 +/- 1.0 mm Hg, all P < . 01). Right ventricular cardiac output was less in shams with 100% unloading (1.2 +/- 0.2 L/min vs 2.1 +/- 0.3 L/min, P < . 01). End-diastolic and end-systolic right ventricular short-axis dimension at 75% and 100% unloading was greater in sham compared with infarcted animals (75%: 34.4 +/- 5.5 mm and 29.1 +/- 5.5 mm vs 25.6 +/- 4.7 mm and 20.5 +/- 4.0 mm; 100%: 37.6 +/- 6.6 mm and 29.9 +/- 5.9 mm vs 25.5 +/- 3.9 mm and 21.1 +/- 3.8 mm, all P < .01). Prolonged diastolic relaxation (Tau) in infarcted animals was normalized with 75% and 100% unloading.
High-level (>or=75%) left ventricular unloading causes right ventricular dilatation and compromised function. Chronic septal damage, however, confers protection by preserving right ventricular dimensions.
由于心室耦合机制破坏,25%的左心室辅助装置接受者会出现右心室衰竭。室间隔缺血会加剧这一过程,但室间隔梗死的影响尚未阐明。本研究在患有室间隔梗死的绵羊中,研究了右心室对左心室逐渐卸载的反应。
对6只绵羊通过向室间隔主要穿支动脉注入乙醇诱导室间隔梗死。6只假手术组绵羊不注入乙醇。4周后测量右心室在左心室逐渐卸载(0%-100%)时与负荷无关的和串联的反应。使用超声微测仪获取全心尺寸、壁厚和腔室容积。用三苯基四氮唑进行选择性灌注以量化室间隔损伤。
与梗死动物相比,假手术组在左心室卸载75%和100%时,右心室前负荷可募集搏功、收缩性和射血分数较低(75%时:26.3±3.4、0.70±0.15和23.9±4.6,对比37±2.6尔格×10³、0.99±0.18毫米汞柱/毫升和35.5%±3.4%,所有P<.01;100%时:24.8±4.5、0.67±0.14和23.8±5.8,对比36.0±4.6尔格×10³、0.90±0.09毫米汞柱/毫升和32.7%±11.0%,所有P<.01)。与梗死动物相比,假手术组在卸载75%和100%时中心静脉压更高(75%时:8.6±1.0对比4.5±1.0,100%时:12.4±0.8对比3.4±1.0毫米汞柱,所有P<.01)。假手术组在100%卸载时右心室心输出量较少(1.2±0.2升/分钟对比2.1±0.3升/分钟,P<.01)。与梗死动物相比,假手术组在卸载75%和100%时舒张末期和收缩末期右心室短轴尺寸更大(75%时:34.4±5.5毫米和29.1±5.5毫米对比25.6±4.7毫米和20.5±4.0毫米;100%时:37.6±6.6毫米和29.9±5.9毫米对比25.5±3.9毫米和21.1±3.8毫米,所有P<.01)。梗死动物中延长的心舒张期松弛时间(Tau)在75%和100%卸载时恢复正常。
高水平(≥75%)的左心室卸载会导致右心室扩张和功能受损。然而,慢性室间隔损伤通过维持右心室尺寸提供保护。