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Ischemic focal ventricular tachycardia (VT) occurs in animals and humans. Angiotensin-converting enzyme inhibitors and receptor blockers reduce sudden death in patients with ischemic heart disease. In our dog model of coronary artery occlusion (CAO), we tested the hypothesis that angiotensin II (AGII) will selectively promote focal VT and that the specific AT2 blocker PD-123319 (PD), or AT1 blocker losartan, will affect this VT. Anesthetized dogs (n = 90) underwent CAO, followed by three-dimensional activation mapping of inducible VT. Dogs without VT in 1-3 h after CAO received AGII, and those with VT received either PD or losartan. Focal endocardium excised from ischemic sites was studied in vitro with standard microelectrode. Of 33 dogs with no inducible VT, AGII infusion resulted in sustained VT of only focal Purkinje origin in 13 (39%) compared with 0 of 20 dogs with saline. Of 26 dogs with inducible VT at baseline, given PD, reinduction was blocked in 8 of 10 (P < 0.05) focal VT, but only 1 of 15 with reentry. In contrast, of 11 dogs given losartan, reinduction of either mechanism was not blocked. In vitro triggered activity in Purkinje was blocked by PD in 13 of 19 (P < 0.05), but not by losartan in 8. Also, triggered activity was promoted by AGII, losartan, or the combination in 9 of 12 tissues. AGLI promotes only focal, mainly Purkinje ischemic VT. PD, but not losartan, preferentially blocked focal VT, which is likely due to triggered activity due to delayed afterdepolarizations in Purkinje. [ABSTRACT FROM AUTHOR]

This study for the first time systematically evaluated the site of origin of focal ventricular tachycardia (VT) induced 1–3 h after acute coronary artery ligation in dogs. We determined whether delayed afterdepolarizations (DADs) and triggered activity (TA) are more often recorded from ischemic endocardium excised from focal sites of VT origin. A total of 145 α-chloralose-anesthetized dogs were studied: in 54 dogs without inducible VT, normal or ischemic endocardium was investigated in vitro; in 91 dogs, inducible VT was studied by three-dimensional activation mapping, with in vitro study of 51 endocardial foci compared with 40 endocardial ischemic sites not of VT origin. Incidence of DADs (71% vs. 33%, P < 0.05) and TA (32% vs. 11%, P < 0.05) was greater in ischemic than in normal Purkinje tissues. Purkinje sites of origin of focal VT demonstrated the greatest frequency of DADs (92%, P < 0.05) and TA (75%, P < 0.05), with repetitive TA predominating. Similar results were obtained in endocardial sites of origin. Action potentials were mildly depolarized and prolonged in the focal sites of origin. These abnormalities were stable up to 2.5 h of recording. This study demonstrated that DADs and TA may underlie a majority of focal VTs in ischemic endocardium and Purkinje tissue. [ABSTRACT FROM AUTHOR]

Examines the effect of alpha[sub 2]-adrenergic agonists on inducible ischemic ventricular tachycardia (VT) of both canine Purkinje fiber and myocardial origin. Indication that pharmacological stimulation of postjunctional alpha[sub 2]-adrenoceptors on Purkinje fibers may selectively prevent induction of VT of Purkinje fiber origin in the ischemic canine ventricle.

Deals with a study which defined the relationship between ischemia-reperfusion-induced myocardial damage and the occurrence of ventricular tachycardia and fibrillation. Methods; Results; Discussion.

Aim and Methods: To analyze the relationship of Purkinje and endocardial focal VT versus epicardial reentry VT to varying ischemic size (IS), one hundred seven alpha chloralose anesthetized dogs were studied with 3-D mapping before and after coronary artery occlusion (CAO) with or without collateral ligation (LIG) to vary IS and distribution. IS was measured as % of all electrograms recorded which had voltage drop >45% with CAO. Mapping localized the origin of reproducibly induced VT. Results: VT was similar in the LIG (77%, n=65) and non-LIG groups (75%, n=42). IS was larger in the LIG group 51±3% vs 34±2% (p<0.05). Epicardial reentry was more prevalent in LIG (80%) than non-LIG (24%, p<0.01). However, focal VT dominated in non-LIG group (63%, p<0.05). Regardless of infarct size, Purkinje focal VT originated from sites with ischemia in Purkinje (50%) or muscle (25%) recorded on the same electrode as Purkinje, while the additional 25% were only adjacent to ischemia <10 mm away. Endocardial focal VT was similar. Dogs without focal VT had 50% fewer ischemic Purkinje sites (p<0.01). In vitro data confirmed action potentials from ischemic sites showing depolarization, triangulation and triggered activity compared to normal tissue. Conclusions: Infarct size plays a major role in mechanism of VT. Larger infarcts have more epicardial reentry; small infarcts facilitate focal VT because of ischemia in endocardium and Purkinje. [ABSTRACT FROM AUTHOR]