Kottkamp H, Vogt B, Hindricks G, Shenasa M, Haverkamp W, Borggrefe M, Breithardt G
Hospital of the Westfälische-Wilhelms-University Münster, Department of Cardiology/Angiology, Münster, FRG.
Basic Res Cardiol. 1994 Mar-Apr;89(2):177-91. doi: 10.1007/BF00788736.
Anisotropic properties of cardiac tissue play an important role in initiation and perpetuation of ventricular tachycardia. However, anisotropic conduction properties in different morphologic types of chronic myocardial infarctions as well as frequency dependency still need to be elucidated. In the present study, the characteristics of anisotropic conduction were investigated in situ in the setting of ischemia-reperfusion induced chronic myocardial infarction.
Myocardial infarction was induced in 12 dogs by a percutaneous transcatheter left anterior descending coronary artery occlusion-reperfusion technique. Four additional dogs served as normal controls. After 14 to 20 days, epicardial mapping was performed using simultaneous unipolar recordings from 240 electrodes of a plaque electrode array placed on the epicardial border zone overlying the infarctions. Constant rate pacing with five cycle lengths (CL) ranging from 500 to 200 ms as well as programmed electrical stimulation (PES) with four basic cycle lengths (BCL) ranging from 430 to 300 ms and single extrastimuli (S2) were performed.
Two anatomically different patterns of epicardial surface morphology were analyzed, designated as type I and type II. In seven animals, there was a continuous thin layer of surviving epicardial muscle fibers overlying the infarction (type I). During pacing with CL of 500 vs 200 ms, conduction velocity longitudinal to fiber orientation (theta L) decreased significantly in the infarcted animals compared to control group (10.9% vs 5.2%, p < 0.05) whereas conduction velocity transverse to fiber axis (theta T) decreased to a similar degree in control and infarcted animals (6.9 vs 7.4%, n.s.). After premature stimulation, there was considerably greater reduction in theta L in infarcted animals than in controls (39.8% vs 31.5%, p < 0.05) whereas theta T decreased to a similar extend in infarcted and control animals (22.2% vs 21.4%, n.s.). During constant rate pacing and premature stimulation, no functional conduction block was induced in type I infarctions. In five animals, the transmural infarctions clearly extended to the epicardial surface, but continuous strands of surviving epicardial muscle fibers traversed the area of necrosis (type II). During PES with S2, functional conduction block and areas of very slow conduction were observed in each case.
In ischemia-reperfusion induced chronic myocardial infarctions, different epicardial patterns of morphology were observed. Anisotropic conduction was frequency dependent in the longitudinal but not in the transverse direction. In type I infarctions, functional conduction block was not inducible during PES whereas in type II infarctions, prerequisites for reentrant arrhythmias like functional conduction block and very slow conduction were induced in each case by single extrastimuli.
心脏组织的各向异性特性在室性心动过速的起始和持续中起重要作用。然而,不同形态类型的慢性心肌梗死中的各向异性传导特性以及频率依赖性仍有待阐明。在本研究中,在缺血再灌注诱导的慢性心肌梗死背景下对各向异性传导的特征进行了原位研究。
通过经皮经导管左前降支冠状动脉闭塞-再灌注技术在12只犬中诱导心肌梗死。另外4只犬作为正常对照。14至20天后,使用放置在梗死上方的心外膜边界区的斑块电极阵列的240个电极进行同步单极记录来进行心外膜标测。进行了五个周期长度(CL)范围从500至200 ms的恒率起搏以及四个基本周期长度(BCL)范围从430至300 ms的程控电刺激(PES)和单个期外刺激(S2)。
分析了两种解剖学上不同的心外膜表面形态模式,分别指定为I型和II型。在7只动物中,梗死上方有一层连续的存活心外膜肌纤维薄层(I型)。在CL为500 ms与200 ms起搏期间,与对照组相比,梗死动物中纵向于纤维方向的传导速度(θL)显著降低(10.9%对5.2%,p<0.05),而横向于纤维轴的传导速度(θT)在对照和梗死动物中降低程度相似(6.9对7.4%,无显著性差异)。过早刺激后,梗死动物中θL的降低比对照组大得多(39.8%对31.5%,p<0.05),而θT在梗死和对照动物中降低程度相似(22.2%对21.4%,无显著性差异)。在恒率起搏和过早刺激期间,I型梗死中未诱发功能性传导阻滞。在5只动物中,透壁梗死明显延伸至心外膜表面,但连续的存活心外膜肌纤维束穿过坏死区域(II型)。在带有S2的PES期间,每种情况下均观察到功能性传导阻滞和极慢传导区域。
在缺血再灌注诱导的慢性心肌梗死中,观察到不同的心外膜形态模式。各向异性传导在纵向是频率依赖性的,而在横向不是。在I型梗死中,PES期间不能诱发功能性传导阻滞,而在II型梗死中,单个期外刺激在每种情况下均诱发了折返性心律失常的先决条件,如功能性传导阻滞和极慢传导。