Bergström E, Pola K, Kjellström B, Töger J, Arvidsson P M, Carlsson M, Rådegran G, Arheden H, Ostenfeld E
Department of Clinical Sciences Lund, Clinical Physiology, Lund University, Skåne University Hospital, Lund, Sweden.
Department of Clinical Sciences Lund, Cardiology, Section of Heart Failure and Valvular Disease, Lund University, Skåne University Hospital, Lund, Sweden.
Physiol Rep. 2025 Sep;13(17):e70563. doi: 10.14814/phy2.70563.
Precapillary pulmonary hypertension (PH) is characterized by increased pulmonary vascular resistance (PVR), with progressively altered right (RV) and left ventricular (LV) hemodynamics and function. Kinetic energy (KE) from 4D flow cardiovascular magnetic resonance (CMR) is a measure of intracardiac hemodynamics. In this observational case-control study, we investigate physiological mechanisms influencing RV-KE and LV-KE in PH. Twenty PH patients and 12 healthy controls underwent CMR including cine images and 4D flow. LV contractility was derived from noninvasive pressure-volume loops, and PVR from right heart catheterization. RV-KE and LV-KE were computed for systole, early and late diastolic filling, and indexed to stroke volume (SV). Systolic RV-KE did not differ between patients and controls. In patients, systolic RV-KE was associated with RV-SV but not with PVR, suggesting that the RV may still be able to compensate for the increased afterload. Systolic LV-KE indexed to LV-SV, LV contractility, and heart rate were all higher in patients than controls, suggesting sympathetic upregulation as a possible driving mechanism behind increased systolic LV-KE. LV contractility was negatively associated with systolic LV-KE and LV-SV. Late filling KE was increased in both ventricles in patients, suggesting an enhanced importance of the atrial kick to the filling of both ventricles.
毛细血管前性肺动脉高压（PH）的特征是肺血管阻力（PVR）增加，右心室（RV）和左心室（LV）的血流动力学及功能逐渐改变。来自四维血流心血管磁共振成像（CMR）的动能（KE）是心内血流动力学的一种测量指标。在这项观察性病例对照研究中，我们探究了影响PH患者右心室动能（RV-KE）和左心室动能（LV-KE）的生理机制。20例PH患者和12名健康对照者接受了CMR检查，包括电影图像和四维血流检查。左心室收缩功能通过无创压力-容积环得出，PVR通过右心导管检查得出。计算出收缩期、舒张早期和晚期充盈期的RV-KE和LV-KE，并将其与每搏输出量（SV）进行指数化处理。患者和对照组的收缩期RV-KE没有差异。在患者中，收缩期RV-KE与RV-SV相关，但与PVR无关，这表明右心室可能仍能够代偿增加的后负荷。以LV-SV、左心室收缩功能和心率进行指数化处理的收缩期LV-KE在患者中均高于对照组，这表明交感神经上调可能是收缩期LV-KE增加背后的驱动机制。左心室收缩功能与收缩期LV-KE和LV-SV呈负相关。患者双侧心室的晚期充盈期KE均增加，这表明心房收缩对双侧心室充盈的重要性增强。
