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Chronic Myocardial Infarction (chronic + myocardial_infarction)
Selected AbstractsMapping of Epicardial Activation in a Rabbit Model of Chronic Myocardial Infarction:JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2007Endocardial, Epicardial Pacing, Response to Atrial Introduction: This study examines the consequences of a large transmural apical infarct on the epicardial electrical activity in isolated rabbit hearts. Methods and Results: Hearts were isolated 8 weeks after coronary artery ligation. Membrane voltage from the epicardial surface of the left ventricle (LV) including the infarct was monitored using the voltage sensitive dye RH237. Optical action potentials were detected from the epicardial surface of the infarct; the signal amplitude was ,20% of those in the noninfarcted zone (NZ). Epicardial activation mapping of the LV free wall showed that during right atrial (RA) pacing, the activation sequence was not significantly different between infarcted and sham-operated groups. However, direct stimulation of the epicardium in the NZ revealed an area of slow conduction velocity (CV ,5 cm/s,1, ,10% of normal values) at the margin of the infarct zone (IZ). Within the IZ, CV was ,50% of normal. A prominent endocardial rim of myocardium in the infarct was not the source of epicardial optical signals because chemical ablation of the endocardium did not affect the epicardial activation pattern. Concluson: Therefore, remnant groups of myocytes in the mid-wall and epicardium of the infarct scar support normal electrical activation during RA pacing. Areas of delayed conduction emerge only on epicardial stimulation. [source] Excitable Gap in Canine Fibrillating Ventricular Myocardium: Effect of Subacute and Chronic Myocardial InfarctionJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2001TARESH TANEJA M.D. Excitable Gap in Infarcted Canine Myocardium.Introduction: The existence of an excitable gap during ventricular fibrillation (VF) has been suggested in several prior studies. However, the effects of myocardial infarction on the presence and duration of an excitable gap during VF have not been evaluated. Methods and Results: Electrophysiologic study was performed in normal dogs and in dogs with subacute and chronic infarction. Experimental infarction was produced by left anterior descending coronary ligation. The excitable gap was determined indirectly using either evaluation of intrinsic wavefronts during VF or from the shortest activation interval at individual sites using recordings from a 112- electrode plaque sutured to the epicardial surface of the left ventricle. The excitable gap also was correlated to local electrophysiologic and anatomic properties. The excitable gap using the wavefront propagation method and shortest activation method was significantly longer in subacute infarction dogs (48 ± 17 msec and 37 ± 18 msec, respectively) and chronic infarction dogs (41 ± 14 msec and 35 ± 14 msec, respectively) than normal dogs (32 ± 13 msec and 30 ± 11 msec, respectively; P < 0.05 normal vs subacute and chronic infarction dogs in both methods). The excitable gap occupied approximately 30% and 27% of the VF cycle length in all three groups using the wavefront propagation and shortest activation method, respectively. The excitable gap correlated better with local ventricular refractoriness determined using the wavefront propagation method than with the shortest activation method, but not at all with refractoriness determined using extrastimulus testing. Tissue necrosis was noted in subacute infarction dogs and fibrosis in chronic infarction dogs, but the gap was not highly correlated with anatomic changes. Conclusion: During VF, an excitable gap exists in both normal and infarcted canine ventricular myocardium. It is significantly longer in the presence of infarction. These finding have implications for understanding the pathophysiology of VF and targeting antiarrhythmic therapies. [source] Attenuation of infarct size in rats and dogs after myocardial infarction by low-energy laser irradiationLASERS IN SURGERY AND MEDICINE, Issue 3 2001Uri Oron PhD Abstract Background and Objective The aim of the present study was to investigate the possibility that low-energy laser irradiation attenuates infarct size formation after induction of chronic myocardial infarction (MI) in small and large experimental animals. Study Design/Materials and Methods Laser irradiation was applied to the infarcted area of rats and dogs at various power densities (2.5 to 20 mW/cm2) after occlusion of the coronary artery. Results In infarcted laser-irradiated rats that received laser irradiation immediately and 3 days after MI at energy densities of 2.5, 6, and 20 mW/cm2, there was a 14%, 62% (significant; P,<,0.05), and 2.8% reduction of infarct size (14 days after MI) relative to non,laser-irradiated rats, respectively. In dogs, a 49% (significant; P,<,0.01) reduction of infarct size was achieved. Conclusion The results of the present study indicate that delivery of low-energy laser irradiation to infarcted myocardium in rats and dogs has a profound effect on the infarct size after MI. Lasers Surg. Med. 28:204,211, 2001. © 2001 Wiley-Liss, Inc. [source] Effect of Underlying Heart Disease on the Frequency Content of Ventricular Fibrillation in the Dog HeartPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2000JASON T. JACOBSON Although prior studies have examined the frequency content of heal electro-gram characteristics during fibrillation, little is know about the effects of underlying heart disease on these parameters. This study was designed to compare the frequency content of local electrograms during VF in canine models of acute ischemia, subacute infarction, and chronic myocardial infarction (MI) to those in control animals to test the hypothesis that underlying heart disease can alter the basic characteristics of VF. VF was induced using burst pacing in three groups of mongrel dogs. Five dogs were evaluated 8 weeks after LAD occlusion MI, five were evaluated 5 days after experimental MI, and 5 had VF induced before (control) and immediately after LAD occlusion (ischemia). During VF, unipolar electrograms were recorded from 112 sites on the anterior LV and electrograms were evaluated 15 and 30 seconds after VF initiation in each group. Electrograms were analyzed by fast Fourier transform. No significant time dependent changes in VF characteristics were noted. The peak frequency was highest in control animals and 8-week MI, intermediate in 5-day MI, and lowest in acute ischemia (P < 0.01 for pairwise comparisons). In contrast, the fractional of energy within a bandwidth of 25% peak amplitude was highest in acute ischemia, (P < 0.001) and similar in the other three groups. Infarction decreased total energy by approximately 50%. In conclusion, the pressure of ischemia or infarction alters the frequency content of VF in a complex fashion. In addition to decreasing the peak frequency, the shape of the power spectral curve is altered in models of structural heart disease. These results suggest that the electrophysiological changes produced by infarction or ischemia alter the structural organization of ventricular fibrillation. [source] | ||||||||||