Altun A, Kirdar C, Ozbay G
Cardiology Department, Faculty of Medicine, Trakya University, Edirne, Turkey.
Clin Cardiol. 1998 Oct;21(10):759-62. doi: 10.1002/clc.4960211012.
Advanced atrioventricular (AV) block is a frequent complication in patients with acute inferior myocardial infarction (AIMI). This conduction abnormality is associated with narrow QRS complex in conducted or junctional escape beats, suggesting that the site of block is the AV node; however, its pathophysiology has not been properly established.
This study investigated the effect of aminophylline in eight patients (5 men, 3 women, age range 51 to 78 years, mean 67.5 +/- 8.8 years) with atropine-resistant late advanced AV block during AIMI.
Advanced AV block was late in appearance in all patients, starting 2 to 5 days after AIMI, and consisted of second-degree Mobitz II type in two patients and of complete AV block in six patients; all patients had narrow QRS complexes. Before aminophylline administration, all patients had a temporary pacemaker installed which was switched off throughout the study. They were given intravenous atropine (1 mg) that was found to be ineffective. One-half h after atropine, the first aminophylline injection (240 mg) was given intravenously over 10 min. One h following the first injection, a second aminophylline dose (240 mg) was administered. Electrocardiographic rhythm strips were obtained before and after drug administration, and the type of AV block and atrial and ventricular rate were noted.
Aminophylline restored 1:1 conduction with first-degree AV block in six patients, Mobitz I AV block in one patient, and normal sinus rhythm in one patient. Mean atrial and ventricular rates before aminophylline were 104 +/- 16 beats/min and 57 +/- 9 beats/min, respectively, and after drug administration 95 +/- 25 beats/min and 89 +/- 17 beats/min, respectively, (p = 0.012).
These results indicate that aminophylline improves AV conduction in atropine-resistant late advanced AV block complicating AIMI.
进展性房室传导阻滞(AV阻滞)是急性下壁心肌梗死(AIMI)患者常见的并发症。这种传导异常与传导或交界性逸搏心律时QRS波群狭窄有关,提示阻滞部位在房室结;然而,其病理生理学尚未完全明确。
本研究调查了氨茶碱对8例AIMI期间出现阿托品抵抗的晚期进展性AV阻滞患者(5例男性,3例女性,年龄范围51至78岁,平均67.5±8.8岁)的影响。
所有患者的进展性AV阻滞均出现较晚,在AIMI后2至5天开始,其中2例为二度莫氏Ⅱ型,6例为完全性AV阻滞;所有患者的QRS波群均狭窄。在给予氨茶碱之前,所有患者均安装了临时起搏器,在整个研究过程中关闭。给予他们静脉注射阿托品(1mg),发现无效。阿托品注射后半小时,静脉注射第一剂氨茶碱(240mg),持续10分钟。第一次注射后1小时,给予第二剂氨茶碱(240mg)。在给药前后获取心电图节律条,并记录AV阻滞类型以及心房和心室率。
氨茶碱使6例患者恢复为一度AV阻滞的1:1传导,1例患者恢复为莫氏Ⅰ型AV阻滞,1例患者恢复为正常窦性心律。氨茶碱给药前平均心房率和心室率分别为104±16次/分钟和57±9次/分钟,给药后分别为95±25次/分钟和89±17次/分钟,(p = 0.012)。
这些结果表明,氨茶碱可改善AIMI合并阿托品抵抗的晚期进展性AV阻滞患者的房室传导。