Department of Cardiovascular Medicine (C.C.J., A.S., V.R.V., D. Padmanabhan, S.J.A., B.A.B.), Mayo Clinic Rochester, MN.
Division of Cardiovascular Disease, Mayo Clinic Arizona (D. Pedrotty).
Circ Heart Fail. 2021 Feb;14(2):e007530. doi: 10.1161/CIRCHEARTFAILURE.120.007530. Epub 2021 Jan 22.
Heart failure with preserved ejection fraction is increasing in prevalence, but few effective treatments are available. Elevated left ventricular (LV) diastolic filling pressures represent a key therapeutic target. Pericardial restraint contributes to elevated LV end-diastolic pressure, and acute studies have shown that pericardiotomy attenuates the rise in LV end-diastolic pressure with volume loading. However, whether these acute effects are sustained chronically remains unknown.
Minimally invasive pericardiotomy was performed percutaneously using a novel device in a porcine model of heart failure with preserved ejection fraction. Hemodynamics were assessed at baseline and following volume loading with pericardium intact, acutely following pericardiotomy, and then again chronically after 4 weeks. Cardiac structure was assessed by magnetic resonance imaging.
The increase in LV end-diastolic pressure with volume loading was mitigated by 41% (95% CI, 27%-45%, <0.0001; ΔLV end-diastolic pressure reduced from +9±3 mm Hg to +5±3 mm Hg, =0.0003, 95% CI, -2.2 to -5.5). The effect was sustained at 4 weeks (+5±2 mm Hg, =0.28 versus acute). There was no statistically significant effect of pericardiotomy on ventricular remodeling compared with age-matched controls. None of the animals developed hemodynamic or pathological indicators of pericardial constriction or frank systolic dysfunction.
The acute hemodynamic benefits of pericardiotomy are sustained for at least 4 weeks in a swine model of heart failure with preserved ejection fraction, without excessive chamber remodeling, pericarditis, or clinically significant systolic dysfunction. These data support trials evaluating minimally invasive pericardiotomy as a novel treatment for heart failure with preserved ejection fraction in humans.
射血分数保留型心力衰竭的患病率正在增加,但可用的有效治疗方法很少。升高的左心室(LV)舒张充盈压代表了一个关键的治疗靶点。心包束缚有助于升高 LV 舒张末期压力,急性研究表明心包切开术可减轻容量负荷下 LV 舒张末期压力的升高。然而,这些急性效应是否能持续慢性尚不清楚。
在射血分数保留型心力衰竭的猪模型中,使用一种新型装置经皮进行微创心包切开术。在心包完整时评估基础血流动力学,并在急性心包切开术后和 4 周后再次评估容量负荷后的血流动力学。通过磁共振成像评估心脏结构。
心包切开术使 LV 舒张末期压力随容量负荷增加的幅度减少了 41%(95%CI,27%-45%,<0.0001;ΔLV 舒张末期压力从+9±3 mm Hg 降至+5±3 mm Hg,=0.0003,95%CI,-2.2 至-5.5)。该效果在 4 周时仍然存在(+5±2 mm Hg,=0.28 与急性)。与年龄匹配的对照组相比,心包切开术对心室重构没有统计学上的显著影响。没有动物出现心包限制或明显收缩功能障碍的血流动力学或病理学指标。
在射血分数保留型心力衰竭的猪模型中,心包切开术的急性血流动力学益处至少可持续 4 周,且不会出现过度的心室重构、心包炎或临床显著的收缩功能障碍。这些数据支持评估微创心包切开术作为治疗射血分数保留型心力衰竭的新方法的临床试验。