ST-segment elevation and ventricular fibrillation without coronary spasm by intracoronary injection of acetylcholine and/or ergonovine maleate in patients with Brugada syndrome

ST-segment elevation and ventricular fibrillation without coronary spasm by intracoronary injection of acetylcholine and/or ergonovine maleate in patients with Brugada syndrome
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DOI:
10.1016/s0735-1097(02)02494-4
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发表时间:
2002-11-20
影响因子:
24
通讯作者:
Kamakura, S
Kamakura, S
中科院分区:
医学1区
文献类型:
--
作者:
Noda, T;Shimizu, W;Kamakura, S

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目的 该研究检查了 Brugada 综合征患者是否对迷走神经刺激或缺血敏感。 背景 实验研究表明,显着的瞬态外向电流 (I-to) 介导的动作电位切迹以及随后心外膜(而非心内膜)动作电位圆顶的丢失,会引起 ST 段抬高和随后的心室颤动 (VF)。 方法 我们评估了冠状动脉痉挛、增强的频率在 27 名有症状的 Brugada 综合征患者和 30 名对照受试者中,V-1 至 V-3 导联 ST 段抬高(大于或等于 0.1 mV),并通过冠状动脉内注射乙酰胆碱 (ACh) 和/或马来酸麦角新碱 (EM) 诱导室颤。结果 27 名 Brugada 综合征患者中有 3 名 (11%) 诱发了冠状动脉痉挛,30 名对照受试者中有 13 名 (43%) 诱发了冠状动脉痉挛。 33 次右冠状动脉注射中有 11 次 (ACh: 6/11 [55%]; EM: 5/22 [23%]) 增强了 ST 段抬高,但没有冠状动脉痉挛,但 Brugada 综合征患者的任何左冠状动脉注射均未增强 ST 段抬高。 33 次右冠状动脉注射中的 3 次 (9%) 诱发心室颤动(ACh:2/11 [18%];EM:1/22 [5%]),但不是由任何左冠状动脉注射诱发。相比之下,在任何对照受试者中均未观察到 ST 段抬高或室颤。 结论 我们的结果支持这样的假设:轻度缺血和迷走神经影响与导致 Brugada 综合征的底物相加或协同作用,从而抬高 ST 段并促进室颤。这些观察结果表明,布鲁格达患者发生缺血性猝死的风险可能较高。 (C) 2002 年由美国心脏病学会基金会资助。
OBJECTIVES The study examined whether patients with Brugada syndrome are sensitive to vagal stimulation or ischemia.BACKGROUND Experimental studies have suggested that a prominent transient outward current (I-to)-mediated action potential notch and a subsequent loss of the action potential dome in the epicardium, but not in the endocardium, give rise to ST-segment elevation and subsequent ventricular fibrillation (VF).METHODS We evaluated the frequency of coronary spasm, augmentation (greater than or equal to0.1 mV) of ST-segment elevation in leads V-1 to V-3, and induction of VF by intracoronary injection of acetylcholine (ACh) and/or ergonovine maleate (EM) in 27 symptomatic patients with Brugada syndrome and 30 control subjects. RESULTS The coronary spasm was induced in 3 (11%) of the 27 patients with Brugada syndrome and in 13 (43%) of the 30 control subjects. ST-segment elevation was augmented by 11 (33%) of the 33 right coronary injections (ACh: 6/11 [55%]; EM: 5/22 [23%]), without coronary spasm, but not by any of the left coronary injections in patients with Brugada syndrome. Ventricular fibrillation was induced by 3 (9%) of the 33 right coronary injections (ACh: 2/11 [18%]; EM: 1/22 [5%]), but not by any of the left coronary injections. In contrast, neither ST-segment elevation nor VF was observed in any of the control subjects.CONCLUSIONS Our results support the hypothesis that mild ischemia and vagal influences act additively or synergistically with the substrate responsible for the Brugada syndrome to elevate the ST-segment and precipitate VF. These observations suggest that Brugada patients may be at a higher risk for ischemia-related sudden death. (C) 2002 by the American College of Cardiology Foundation.