Faragli Alessandro, Alogna Alessio, Lee Chong Bin, Zhu Miry, Ghorbani Niky, Lo Muzio Francesco Paolo, Schnackenburg Bernhard, Stehning Christian, Kuehne Titus, Post Heiner, Goubergrits Leonid, Nagel Eike, Pieske Burkert, Kelle Sebastian, Kelm Marcus
Department of Internal Medicine and Cardiology, Deutsches Herzzentrum Berlin, Berlin, Germany.
Charité - Universitätsmedizin Berlin, Department of Internal Medicine and Cardiology, Campus Virchow-Klinikum, Berlin, Germany.
Front Cardiovasc Med. 2021 Jul 26;8:689255. doi: 10.3389/fcvm.2021.689255. eCollection 2021.
Myocardial efficiency should be maintained stable under light-to-moderate stress conditions, but ischemia puts the myocardium at risk for impaired functionality. Additionally, the measurement of such efficiency typically requires invasive heart catheterization and exposure to ionizing radiation. In this work, we aimed to non-invasively assess myocardial power and the resulting efficiency during pharmacological stress testing and ischemia induction. In a cohort of = 10 healthy Landrace pigs, dobutamine stress testing was performed, followed by verapamil-induced ischemia alongside cardiac magnetic resonance (CMR) imaging. External myocardial power, internal myocardial power, and myocardial efficiency were assessed non-invasively using geometrical and functional parameters from CMR volumetric as well as blood flow and pressure measurements. External myocardial power significantly increased under dobutamine stress [2.3 (1.6-3.1) W/m vs. 1.3 (1.1-1.6) W/m, = 0.005] and significantly decreased under verapamil-induced ischemia [0.8 (0.5-0.9) W/m, = 0.005]. Internal myocardial power [baseline: 5.9 (4.6-8.5) W/m] was not affected by dobutamine [7.5 (6.9-9.0) W/m, = 0.241] nor verapamil [5.8 (4.7-8.8) W/m, = 0.878]. Myocardial efficiency did not change from baseline to dobutamine [21% (15-27) vs. 31% (20-44), = 0.059] but decreased significantly during verapamil-induced ischemia [10% (8-13), = 0.005]. In healthy Landrace pigs, dobutamine stress increased external myocardial power, whereas myocardial efficiency was maintained stable. On the contrary, verapamil-induced ischemia substantially decreased external myocardial power and myocardial efficiency. Non-invasive CMR was able to quantify these efficiency losses and might be useful for future clinical studies evaluating the effects of therapeutic interventions on myocardial energetics.
在轻度至中度应激条件下,心肌效率应保持稳定,但缺血会使心肌面临功能受损的风险。此外,测量这种效率通常需要进行侵入性心脏导管插入术并暴露于电离辐射。在这项研究中,我们旨在在药物应激测试和缺血诱导过程中对心肌功率及其产生的效率进行非侵入性评估。在一组10头健康长白猪中,进行了多巴酚丁胺应激测试,随后在心脏磁共振(CMR)成像的同时进行维拉帕米诱导的缺血。使用CMR容积的几何和功能参数以及血流和压力测量值,对外部心肌功率、内部心肌功率和心肌效率进行非侵入性评估。在多巴酚丁胺应激下,外部心肌功率显著增加[2.3(1.6 - 3.1)W/m对1.3(1.1 - 1.6)W/m,P = 0.005],而在维拉帕米诱导的缺血下显著降低[0.8(0.5 - 0.9)W/m,P = 0.005]。内部心肌功率[基线:5.9(4.6 - 8.5)W/m]不受多巴酚丁胺[7.5(6.9 - 9.0)W/m,P = 0.241]或维拉帕米[5.8(4.7 - 8.8)W/m,P = 0.878]的影响。心肌效率从基线到多巴酚丁胺时没有变化[21%(15 - 27)对31%(20 - 44),P = 0.059],但在维拉帕米诱导的缺血期间显著降低[10%(8 - 13),P = 0.005]。在健康长白猪中,多巴酚丁胺应激增加了外部心肌功率,而心肌效率保持稳定。相反,维拉帕米诱导缺血显著降低了外部心肌功率和心肌效率。非侵入性CMR能够量化这些效率损失,可能对未来评估治疗干预对心肌能量学影响的临床研究有用。