Cardiac Technology Centre, University of Sydney at Royal North Shore Hospital, Sydney, NSW, Australia.
J Thorac Cardiovasc Surg. 2011 Jul;142(1):209-15. doi: 10.1016/j.jtcvs.2010.05.057. Epub 2010 Dec 16.
Right ventricular (RV) function is compromised in 25% of left ventricular (LV) assist device recipients despite effective LV support. The risk of such dysfunction has been enhanced by an ischemic or undamaged interventricular septum; however, we found septal infarction to be paradoxically protective. We, therefore, evaluated the potential of nonsurround, nonuniform, biventricular-capable direct cardiac compression (DCC) (using the HeartPatch DCC) to overcome RV dysfunction in hearts with a normal or infarcted interventricular septum.
Ethanol ablation was used to create an interventricular septal infarction in 6 sheep, and 6 others served as the control sheep. The load-independent and in-series RV response to DCC was assessed using sonomicrometer heart dimension sensors. Triphenyltetrazolium perfusion delineated the septal damage.
LV DCC caused a greater increase of the RV preload recruitable stroke work in the control sheep than in the study sheep (190.6 ± 23.5 and 135.0 ± 40.8 erg*10^3, respectively, P < .001). In contrast, RV end-systolic elastance increased more in the septal-ablated sheep with RV DCC (17.29 ± 3.40 vs 9.88 ± 2.01 mm Hg/mL in the control sheep, P < .001). Abnormal RV diastolic function before device insertion in the septal-ablated sheep was normalized with both passive DCC placement and after activation (RV diastolic relaxation constant 23.5 ± 2.3 and 20.0 ± 2.1 ms, respectively, P < .001). Both biventricular and RV DCC actuation increased the RV systolic pressure more in the septal-ablated sheep than in the control sheep (37.9 ± 6.3 and 47.7 ± 4.6 mm Hg vs 29.7% ± 4.8% and 40.3% ± 8.3%, respectively, P < .001). In contrast, the RV end-systolic diameter decreased more during LV DCC (70.1% ± 15.9% vs 90.5% ± 5.0%, P < .001).
The HeartPatch DCC support of LV and RV function results from improvement of the systolic septal-lateral fractional change that is not influenced by septal infarction. The latter attenuated LV to RV device energy delivery during LV patch actuation but enhanced RV energy delivery during RV patch actuation. This DCC technique can provide effective support in high-risk RV failure situations arising from left ventricular assist device use.
尽管左心室辅助装置(LVAD)能有效支持左心室,但仍有 25%的患者出现右心室(RV)功能障碍。这种功能障碍的风险因缺血或未受损的室间隔而增加;然而,我们发现室间隔梗死具有保护作用。因此,我们评估了非环绕、非均匀、双心室能力的直接心脏压缩(DCC)(使用 HeartPatch DCC)在具有正常或梗死室间隔的心脏中克服 RV 功能障碍的潜力。
乙醇消融用于在 6 只绵羊中创建室间隔梗死,另外 6 只绵羊作为对照绵羊。使用超声心动图心尺寸传感器评估 DCC 对 RV 负荷独立和串联反应。三苯基四唑灌注描绘了间隔损伤。
与对照组绵羊相比,LVADCC 引起对照组绵羊 RV 前负荷可招徕工作的增加更大(190.6±23.5 和 135.0±40.8 erg*10^3,分别为 P<.001)。相比之下,在 RVADCC 的室间隔消融绵羊中,RV 收缩末期弹性增加更多(与对照组绵羊相比,分别为 17.29±3.40 和 9.88±2.01 mmHg/mL,P<.001)。在装置插入前,室间隔消融绵羊的 RV 舒张功能异常在被动 DCC 放置和激活后均得到正常化(RV 舒张松弛常数分别为 23.5±2.3 和 20.0±2.1 ms,P<.001)。双心室和 RV DCC 驱动在室间隔消融绵羊中引起的 RV 收缩压增加均大于对照组绵羊(37.9±6.3 和 47.7±4.6 mmHg 与 29.7%±4.8%和 40.3%±8.3%,分别为 P<.001)。相比之下,LVADCC 期间 RV 收缩末期直径下降更多(70.1%±15.9%与 90.5%±5.0%,P<.001)。
HeartPatch DCC 对 LV 和 RV 功能的支持源于改善收缩期间隔-外侧分数变化,而不受室间隔梗死的影响。后者在 LV 补丁驱动期间减弱了 LV 到 RV 的装置能量传递,但在 RV 补丁驱动期间增强了 RV 的能量传递。这种 DCC 技术可在因左心室辅助装置使用而导致的高危 RV 衰竭情况下提供有效支持。