Impaired regional subendocardial coronary flow reserve in conscious dogs with pacing-induced heart failure.
Impaired regional subendocardial coronary flow reserve in conscious dogs with pacing-induced heart failure.
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DOI：
10.1152/ajpheart.1993.265.3.h801
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发表时间：
1993-09
期刊：
影响因子：
--
通讯作者：
R. Shannon;K. Komamura;Y. Shen;S. Bishop;S. Vatner
中科院分区：
文献类型：
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作者：
R. Shannon;K. Komamura;Y. Shen;S. Bishop;S. Vatner
本研究的目的是检查清醒的，慢性仪器与起搏诱导的心力衰竭，严重的双心室心肌病没有显着的肥厚模型的狗的冠状动脉流量和血管扩张储备。12只狗进行了研究后，28天的快速右心室起搏，并与6个假手术对照。清醒的起搏诱导心力衰竭犬的左心室（LV）平均透壁血流明显减少，而心内膜-心外膜血流比无显著差异。在充血性心力衰竭（CHF）患者中，腺苷对冠状动脉血管的近最大舒张反应是心外膜下冠状动脉血流和血管舒张储备得以保留，但有证据表明心内膜下血流和血管舒张储备受损，心内膜-心外膜比值显著降低。心内膜下冠状动脉血流储备恢复，心内膜-心外膜比率正常化。因此，在CHF中，存在对LV的内膜下选择性的冠状动脉血流和血管舒张剂储备受损。在心力衰竭过程的这一点上，这种损害与结构变化无关，而是LV舒张末期压显著升高的结果。
The purpose of the present investigation was to examine coronary flow and vasodilator reserve in conscious, chronically instrumented dogs with pacing-induced heart failure, a model of severe biventricular cardiomyopathy devoid of significant hypertrophy. Twelve dogs were studied after 28 days of rapid right ventricular pacing and were compared with six sham-operated controls. Left ventricular (LV) average transmural flow was significantly less in conscious dogs with pacing-induced heart failure, whereas the endocardial-to-epicardial flow ratio was not significantly different. In response to near maximal coronary vasodilation with adenosine, subepicardial coronary flow and vasodilator reserve were preserved in congestive heart failure (CHF), yet there was evidence of impaired subendocardial flow and vasodilator reserve, and the endocardial-to-epicardial ratio was significantly less. When the markedly elevated LV end-diastolic pressure was normalized in heart failure, there was restoration of subendocardial coronary flow reserve and a normalization of the endocardial-to-epicardial ratio. Thus, in CHF, there is impaired coronary flow and vasodilator reserve that is selective to the subendocardium of the LV. At this point in the heart failure process, this impairment is not associated with structural changes but is a consequence of the marked elevation in LV end-diastolic pressure.