Changes in contractility determine coronary haemodynamics in dyssynchronous left ventricular heart failure, not vice versa.
Changes in contractility determine coronary haemodynamics in dyssynchronous left ventricular heart failure, not vice versa.
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DOI：
10.1016/j.ijcha.2018.03.002
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发表时间：
2018-06
期刊：
影响因子：
--
通讯作者：
Perera D
中科院分区：
文献类型：
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作者：
Claridge S;Briceno N;Chen Z;De Silva K;Modi B;Jackson T;Behar JM;Niederer S;Rinaldi CA;Perera D
双心室起搏已被证明可急性增加心肌收缩力和冠状动脉流量，但因果关系尚不清楚。我们假设冠状动脉血流的变化是继发于心肌收缩力的变化。我们试图通过调节冠状动脉血流和心肌收缩力来研究这种关系。8例患者通过改变起搏位置改变了收缩力和舒张力。冠状动脉内注射腺苷可使冠状动脉自动调节功能暂时丧失。在不同的起搏设置下同时测量冠状动脉血流速度、冠状动脉压力和左心室压力数据，并进行充血和波强度分析。多部位起搏可有效改变左心室收缩力和舒张功能（pos. dp/dtmax −13%至+10%和负值。dp/dtmax −15%至+17%（与基线相比）。冠状动脉内腺苷降低了微血管阻力（362.5 mm Hg/s/m至156.7 mm Hg/s/m，p < 0.001），增加了LAD流速（22 cm/s vs 45 cm/s，p < 0.001），但没有急性改变收缩性或舒张性。主要的加速波，即后向扩张波的幅度，与收缩性和舒张性的程度成正比（r = 0.47，p < 0.01和r =-0.50，p < 0.01）。充血时灌注效率（加速波的比例）增加（76%静息vs 81%充血，p = 0.04）。灌注效率与静息时（r = 0.43和-0.50，p = 0.01）和充血时（r = 0.59和-0.6，p < 0.01）的收缩性和舒张性相关。腺苷急性增加收缩性心力衰竭患者的冠状动脉血流量并不增加收缩力。双心室起搏引起的冠状动脉血流变化可能是心肌收缩力增强的结果，而不是相反。
Biventricular pacing has been shown to increase both cardiac contractility and coronary flow acutely but the causal relationship is unclear. We hypothesised that changes in coronary flow are secondary to changes in cardiac contractility. We sought to examine this relationship by modulating coronary flow and cardiac contractility. Contractility and lusitropy were altered by varying the location of pacing in 8 patients. Coronary autoregulation was transiently disabled with intracoronary adenosine. Simultaneous coronary flow velocity, coronary pressure and left ventricular pressure data were measured in the different pacing settings with and without hyperaemia and wave intensity analysis performed. Multisite pacing was effective at altering left ventricular contractility and lusitropy (pos. dp/dtmax −13% to +10% and neg. dp/dtmax −15% to +17% compared to baseline). Intracoronary adenosine decreased microvascular resistance (362.5 mm Hg/s/m to 156.7 mm Hg/s/m, p < 0.001) and increased LAD flow velocity (22 cm/s vs 45 cm/s, p < 0.001) but did not acutely change contractility or lusitropy. The magnitude of the dominant accelerating wave, the Backward Expansion Wave, was proportional to the degree of contractility as well as lusitropy (r = 0.47, p < 0.01 and r = −0.50, p < 0.01). Perfusion efficiency (the proportion of accelerating waves) increased at hyperaemia (76% rest vs 81% hyperaemia, p = 0.04). Perfusion efficiency correlated with contractility and lusitropy at rest (r = 0.43 & −0.50 respectively, p = 0.01) and hyperaemia (r = 0.59 & −0.6, p < 0.01). Acutely increasing coronary flow with adenosine in patients with systolic heart failure does not increase contractility. Changes in coronary flow with biventricular pacing are likely to be a consequence of enhanced cardiac contractility from resynchronization and not vice versa.