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Anisotropic conduction characteristics in ischemia-reperfusion induced chronic myocardial infarction
H Kottkamp1, B Vogt, G Hindricks
1Hospital of the Westfälische-Wilhelms-University Münster, Department of Cardiology/Angiology, Münster, FRG.
Insights
Anisotropic conduction in myocardial infarction differs based on infarct morphology. Type II infarctions, with surviving epicardial fibers, create conditions for arrhythmias like functional conduction block and slow conduction.
Area of Science:
- Cardiovascular Research
- Cardiac Electrophysiology
- Myocardial Infarction
Background:
- Anisotropic properties of cardiac tissue are crucial for understanding ventricular tachycardia.
- Morphological variations in chronic myocardial infarctions and their impact on anisotropic conduction remain incompletely understood.
- Frequency-dependent characteristics of anisotropic conduction in myocardial infarction require further investigation.
Purpose of the Study:
- To investigate the characteristics of anisotropic conduction in situ within chronic myocardial infarctions induced by ischemia-reperfusion.
- To elucidate the differences in anisotropic conduction properties between distinct morphological types of myocardial infarction.
- To determine the frequency dependency of anisotropic conduction in the context of myocardial infarction.
Main Methods:
- Myocardial infarction was induced in dogs via coronary artery occlusion-reperfusion.
- Epicardial mapping was performed using a 240-electrode array on the border zone of infarctions.
- Electrical stimulation was applied at various cycle lengths and with extrastimuli to assess conduction properties.
Main Results:
- Two distinct epicardial morphologies (Type I and Type II) were identified in chronic myocardial infarctions.
- Longitudinal conduction velocity (theta L) decreased significantly with faster pacing in infarcted animals compared to controls.
- Type II infarctions exhibited functional conduction block and very slow conduction upon premature stimulation, unlike Type I.
Conclusions:
- Chronic myocardial infarctions present with varying epicardial morphologies affecting anisotropic conduction.
- Anisotropic conduction demonstrates frequency dependence in the longitudinal direction but not the transverse direction.
- Type II infarctions create electrophysiological conditions conducive to reentrant arrhythmias, including functional conduction block and slow conduction.
Objectives:
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.
Methods:
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.
Results:
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.
Conclusions:
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.