Ventriculo-arterial coupling in pulmonary regurgitation following transannular patch repair of pulmonary stenosis.

IF 4.1 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
Rahi S Alipour Symakani, Wouter J van Genuchten, Lotte M Zandbergen, Alexander Hirsch, Piotr Alfred Wielopolski, Thierry Bové, Yannick J H J Taverne, Willem A Helbing, Beatrijs Bartelds, Daphne Merkus
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Abstract

Pulmonary regurgitation is a common consequence following the repair of tetralogy of Fallot and can lead to heart failure. Early detection of right ventricular dysfunction remains challenging, and current clinical markers have limited predictive value to identify which patients are at risk for heart failure and require interventions. This study aimed to investigate the potential of ventriculo-arterial coupling as a marker of early right ventricular dysfunction in a porcine model of chronic pulmonary regurgitation following transannular patch repair of neonatal pulmonary stenosis. Neonatal swine were subjected to pulmonary artery banding for 1 month to induce RV pressure overload, followed by transannular patch repair (rTAP, n=10) to create chronic pulmonary regurgitation, and were compared to Sham animals (n=6). Longitudinal hemodynamic assessments, including pressure-volume analysis and cardiac magnetic resonance imaging, were performed. VAC was defined as the ratio of end-systolic elastance to effective arterial elastance. Over the follow-up period of 4 months, VAC was preserved in the rTAP group. Effective arterial elastance was significantly lower in rTAP animals (P=0.001), while end-systolic elastance remained unchanged. Lower end-diastolic pulmonary artery pressures and increased early systolic ejection were observed in rTAP, correlating with higher VAC. Ventriculo-arterial coupling remains preserved in chronic pulmonary regurgitation due to decreased afterload, making it unsuitable as an early marker for right ventricular dysfunction. Low afterload, a consequence of diastolic emptying of the pulmonary artery into the right ventricle, may pseudo-normalize systolic function. Alternative markers e.g. focusing on diastolic function and atrio-ventricular interactions should be investigated.

经环形补片修复肺动脉狭窄后肺返流的心室-动脉耦合。
肺反流是法洛四联症修复后的常见后果,可导致心力衰竭。右室功能障碍的早期检测仍然具有挑战性,目前的临床标志物在识别哪些患者有心力衰竭风险和需要干预方面的预测价值有限。本研究旨在探讨新生儿肺狭窄经环补片修复后慢性肺反流猪模型中脑室-动脉耦合作为早期右心室功能障碍标志的潜力。对新生猪进行为期1个月的肺动脉绑扎,以诱导右心室压力过载,然后进行经环补片修复(rTAP, n=10),以造成慢性肺反流,并与假手术动物(n=6)进行比较。纵向血流动力学评估,包括压力-容量分析和心脏磁共振成像。VAC定义为收缩末期弹性与有效动脉弹性之比。在4个月的随访期间,rTAP组保留了VAC。rTAP动物的有效动脉弹性显著降低(P=0.001),而收缩末期弹性保持不变。rTAP患者舒张末期肺动脉压降低,早期收缩期射血增加,与较高的VAC相关。由于后负荷降低,慢性肺反流中仍保留了心室-动脉耦合,因此不适合作为右室功能障碍的早期标志。低后负荷是肺动脉舒张期排空进入右心室的结果,可能使收缩功能伪正常化。应该研究其他标志物,如专注于舒张功能和房室相互作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
9.60
自引率
10.40%
发文量
202
审稿时长
2-4 weeks
期刊介绍: The American Journal of Physiology-Heart and Circulatory Physiology publishes original investigations, reviews and perspectives on the physiology of the heart, vasculature, and lymphatics. These articles include experimental and theoretical studies of cardiovascular function at all levels of organization ranging from the intact and integrative animal and organ function to the cellular, subcellular, and molecular levels. The journal embraces new descriptions of these functions and their control systems, as well as their basis in biochemistry, biophysics, genetics, and cell biology. Preference is given to research that provides significant new mechanistic physiological insights that determine the performance of the normal and abnormal heart and circulation.
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