Nitenberg Alain, Durand Eric, Delatour Bertrand, Sdiri Wissem, Raha Saliha, Lafont Antoine
Service de Physiologie et d'Explorations Fonctionnelles, CHU Jean Verdier, Assistance Publique-Hôpitaux de Paris, Université Paris 13, Bondy, France.
J Invasive Cardiol. 2007 Sep;19(9):390-4.
The aim of this study was to compare the ability of intracoronary adenosine (ADE) and postocclusion hyperemia (PH) to cause maximal hyperemia in humans.
The current clinical standard for induction of maximal coronary hyperemia is intracoronary ADE. However, animal studies have shown that maximal hyperemia was not achieved by ADE and that PH yielded a higher hyperemic response.
In 10 stable patients with coronary artery stenosis > or = 80%, basal and peak coronary blood flow velocity (intracoronary Doppler) were measured before and after coronary angioplasty (PTCA), both after an intracoronary bolus of 60 mcg ADE, and after 30-second occlusion of the coronary artery by a balloon angioplasty catheter. Coronary reserve was estimated through coronary flow reserve (CFR = peak-to-resting coronary blood flow velocity), and coronary resistance reserve (CRR = [resting aortic pressure/resting coronary flow velocity]/[aortic pressure at peak velocity/peak coronary flow velocity]).
Before PTCA, ADE and PH result in comparable CFR (1.79 +/- 0.65 vs. 1.95 +/- 0.52, respectively; p = 0.0846), but CRR was higher with PH (1.75 +/- 0.52 vs. 2.14 +/- 0.81, respectively; p = 0.0125). After PTCA, CFR and CRR were significantly lower with ADE than with PH (CFR = 2.53 +/- 0.58 vs. 3.31 +/- 0.67, respectively; p = 0.0001, and CRR = 2.58 +/- 0.49 vs. 3.46 +/- 0.79; p = 0.0004, respectively). Lastly, the higher the coronary reserve, the greater the differences between ADE and PH values.
Because intracoronary 60 mcg ADE elicits a lower hyperemic response than PH, intracoronary ADE represents a potential source of error in coronary reserve measurements, and may result in an underestimation of the physiological significance of a coronary artery stenosis.
本研究旨在比较冠状动脉内注射腺苷(ADE)和闭塞后充血(PH)在人体中诱发最大充血的能力。
目前诱导最大冠状动脉充血的临床标准是冠状动脉内注射ADE。然而,动物研究表明,ADE未能实现最大充血,而PH产生的充血反应更高。
对10例冠状动脉狭窄≥80%的稳定患者,在冠状动脉成形术(PTCA)前后、冠状动脉内推注60 mcg ADE后以及用球囊成形术导管对冠状动脉进行30秒闭塞后,测量基础和峰值冠状动脉血流速度(冠状动脉内多普勒)。通过冠状动脉血流储备(CFR = 峰值与静息冠状动脉血流速度之比)和冠状动脉阻力储备(CRR = [静息主动脉压/静息冠状动脉血流速度]/[峰值速度时的主动脉压/峰值冠状动脉血流速度])来评估冠状动脉储备。
PTCA前,ADE和PH导致的CFR相当(分别为1.79±0.65和1.95±0.52;p = 0.0846),但PH的CRR更高(分别为1.75±0.52和2.14±0.81;p = 0.0125)。PTCA后,ADE的CFR和CRR显著低于PH(CFR分别为2.53±0.58和3.31±0.67;p = 0.0001,CRR分别为2.58±0.49和3.46±0.79;p = 0.0004)。最后,冠状动脉储备越高,ADE和PH值之间的差异越大。
由于冠状动脉内60 mcg ADE引起的充血反应低于PH,冠状动脉内ADE是冠状动脉储备测量中潜在的误差来源,可能导致对冠状动脉狭窄生理意义的低估。