Vanderheyden Marc, Bartunek Jozef, Verstreken Sofie, Mortier Linda, Goethals Marc, de Bruyne Bernard
Cardiovascular Center, Onze Lieve Vrouw Ziekenhuis, Moorselbaan 164, 9300 Aalst, Belgium.
Eur J Echocardiogr. 2005 Jan;6(1):47-53. doi: 10.1016/j.euje.2004.06.006.
Impaired vasodilator myocardial blood flow response has been observed in dilated cardiomyopathy (DCMP). However, the mechanisms responsible for this blunted response are not clear. In the present study, we investigated whether the blunted vasodilator flow response is related to indices of left ventricular performance in patients with idiopathic dilated cardiomyopathy.
Eighteen DCMP patients and 12 healthy subjects (C) underwent transoesophageal echocardiography within 48 h from cardiac catheterization. Coronary flow velocity reserve (CFR) was measured in the proximal LAD as the ratio of the peak diastolic coronary flow velocity (Vd-M) after intravenous administration of adenosine to peak baseline diastolic flow velocity (Vd-R). Left ventricular (LV) mass index was positively correlated with baseline coronary diastolic velocity (r=0.415; p=0.043) and inversely correlated with coronary flow reserve (r=-0.570; p=0.003). The baseline coronary diastolic velocity was higher in DCMP vs C (56+/-13 cm/s vs 35+/-12 cm/s; p=0.04). In DCMP pts Vd-R positively correlated with end-diastolic wall stress (r=0.654; p=0.01). Vd increased in both C (96+/-32 cm/s; p<0.05 vs baseline) and DCMP patients (108+/-20 cm/s; p<0.01 vs baseline). The CFR was lower in DCMP patients vs C (1.93+/-0.78 vs 2.99+/-1.01; p=0.009). In DCMP pts CFR was negatively correlated with right atrial pressure (r=-0.595; p=0.015), LVEDP (r=-0.576; p=0.015), pulmonary capillary wedge pressure (PCWP: r=-0.772; p<0.001) and positively with ejection fraction (EF: r=0.683; p=0.003).
Pts with DCMP have lower CFR compared to controls. This blunted CFR is due to higher baseline coronary flow and reflects higher wall stress. The close relation between CFR and EF, PCWP and LVEDP suggests that not only a higher baseline Vd but also compressive forces due to left ventricular dysfunction might be responsible for the observed blunted adenosine-mediated coronary vasodilation.
在扩张型心肌病(DCMP)中已观察到血管舒张性心肌血流反应受损。然而,导致这种反应减弱的机制尚不清楚。在本研究中,我们调查了特发性扩张型心肌病患者血管舒张性血流反应减弱是否与左心室功能指标有关。
18例DCMP患者和12名健康受试者(C)在心脏导管插入术后48小时内接受经食管超声心动图检查。在左前降支近端测量冠状动脉血流储备(CFR),即静脉注射腺苷后舒张期冠状动脉血流峰值速度(Vd-M)与舒张期基线血流峰值速度(Vd-R)之比。左心室(LV)质量指数与基线冠状动脉舒张期速度呈正相关(r = 0.415;p = 0.043),与冠状动脉血流储备呈负相关(r = -0.570;p = 0.003)。DCMP患者的基线冠状动脉舒张期速度高于C组(56±13 cm/s对35±12 cm/s;p = 0.04)。在DCMP患者中,Vd-R与舒张末期壁应力呈正相关(r = 0.654;p = 0.01)。C组(96±32 cm/s;与基线相比p < 0.05)和DCMP患者(108±20 cm/s;与基线相比p < 0.01)的Vd均增加。DCMP患者的CFR低于C组(1.93±0.78对2.99±1.01;p = 0.009)。在DCMP患者中,CFR与右心房压力呈负相关(r = -0.595;p = 0.015),与左心室舒张末期压力(LVEDP:r = -0.576;p = 0.015)、肺毛细血管楔压(PCWP:r = -0.772;p < 0.001)呈负相关,与射血分数(EF:r = 0.683;p = 0.003)呈正相关。
与对照组相比,DCMP患者的CFR较低。这种CFR减弱是由于较高的基线冠状动脉血流,反映了较高的壁应力。CFR与EF、PCWP和LVEDP之间的密切关系表明,不仅较高的基线Vd,而且左心室功能障碍引起的压缩力可能是观察到的腺苷介导的冠状动脉舒张减弱的原因。