Analysis of vulnerability to reentry in acute myocardial ischemia using a realistic human heart model.

Electrophysiological alterations of the myocardium caused by acute ischemia constitute a pro-arrhythmic substrate for the generation of potentially lethal arrhythmias. Experimental evidence has shown that the main components of acute ischemia that induce these electrophysiological alterations are hyperkalemia, hypoxia (or anoxia in complete artery occlusion), and acidosis. However, the influence of each ischemic component on the likelihood of reentry is not completely established. Moreover, the role of the His-Purkinje system (HPS) in the initiation and maintenance of arrhythmias is not completely understood. In the present work, we investigate how the three components of ischemia affect the vulnerable window (VW) for reentry using computational simulations. In addition, we analyze the role of the HPS on arrhythmogenesis. A 3D biventricular/torso human model that includes a realistic geometry of the central and border ischemic zones with one of the most electrophysiologically detailed model of ischemia to date, as well as a realistic cardiac conduction system, were used to assess the VW for reentry. Four scenarios of ischemic severity corresponding to different minutes after coronary artery occlusion were simulated. Our results suggest that ischemic severity plays an important role in the generation of reentries. Indeed, this is the first 3D simulation study to show that ventricular arrhythmias could be generated under moderate ischemic conditions, but not in mild and severe ischemia. Moreover, our results show that anoxia is the ischemic component with the most significant effect on the width of the VW. Thus, a change in the level of anoxia from moderate to severe leads to a greater increment in the VW (40 ms), in comparison with the increment of 20 ms and 35 ms produced by the individual change in the level of hyperkalemia and acidosis, respectively. Finally, the HPS was a necessary element for the generation of approximately 17% of reentries obtained. The retrograde conduction from the myocardium to HPS in the ischemic region, conduction blocks in discrete sections of the HPS, and the degree of ischemia affecting Purkinje cells, are suggested as mechanisms that favor the generation of ventricular arrhythmias.

Catheter ablation of the parahisian accessory pathways from the aortic cusps-Experience of 20 cases-Improving the mapping strategy for better results.

INTRODUCTION: Catheter ablation of the parahisian accessory pathways (PHAP) has been established as the definitive therapy for this type of arrhythmia. However, the PHAP proximity to the normal atrioventricular conduction system makes the procedure technically challenging. Here, we have reported a case series of 20 patients with PHAP who underwent aortic access ablation to evaluate the safety and efficacy of this approach in the PHAP ablation. METHODS AND RESULTS: The ablation through the aortic cusps was the successful approach in 13 of 20 (65%) of the cases. In 11 patients, the aortic approach was the initial strategy for ablation, and the accessory pathway was eliminated in seven (63.6%) of them. The aortic approach followed a failed right-sided attempt in nine patients. In six (66.7%) patients, the ablation was successful with the aortic approach. The only independent predictor for the successful ablation with each approach was the earliest ventricular activation before delta wave (predelta time) and a right-sided earliest ventricular activation of more than 23 ms had high sensitivity and specificity for right-sided success. Systematically using the two strategies (right and left approaches), the ablation of the PHAP was successful in 18 (90%) patients. CONCLUSION: The aortic approach seems to be a safe and effective strategy for the ablation of PHAP. It can be used when the right-sided approach fails or even considered as an initial strategy when the predelta time is less than 23 ms in the right septal region. When combining the right- and left-sided approaches, the success rate is high. We believe that the retrograde aortic approach remains a key tool for this challenging ablation.

Mecanismos e dinâmica da progressão dos episódios de bloqueio atrioventricular 2: 1 para bloqueio atrioventricular de alto grau / Mechanisms and dynamics of episades of progression of 2:1 A-V block to high degree A-V

PURPOSE--To evaluate the mechanisms and dynamics of episodes of progression to high degree (HD) atrioventricular (AV) block (B) analyzed during incremental atrial pacing (St), in patients with previous 2:1 His-Purkinje (HP) AVB. METHODS--Data from 4 patients were analyzed. All of them with history of syncope and ECG exhibiting 2:1 AVB with wide QRS pattern. The AVB was in the HP system (HPS) in all. Every patient was submitted to electrophysiologic study with incremental atrial pacing, by which the conduction sequences and the AV conduction ratios (AVR) were analyzed. The basal (B) cycle length (CL) was defined as the shortest interval between two conducted beats (spontaneous or pacing-induced). The incremental atrial stimulation was performed beginning with CL 10 msec shorter than BCL until reaching 250 msec. RESULTS--Nineteen episodes of progression to HD-AVB were seen. A) With StCL between 31 and 26 of BCL, AVR were 3:1, 4:1 and 5:1, with only one blocking zone (BZ) in the HPS; B) with StCL between 24 and 22 of BCL, AVR were 5:1, 7:2, 9:2e11:3. In this situation a 2nd BZ ensues-on proximal, site of a decremental conduction, situated in the AV node (AVN) or in the HPS, and the other (distal level) always in HPS; C) with StCL between 24 and 16 of BCL, AVR were 5:1, 6:1, 10:2, 11:2 and 12:3. Here, these AVR were explained by postulating 3 BZ where 2 were in AVN and 1 in HPS, or inversely with 1 in AVN and 2 in HPS. The decremental conduction occurred in 1 or 2 out 3 BZ and an integral conduction (like 2:1 or 3:1) in the others. CONCLUSION--The BCL is the determinant of the AVR observed. As the StCL is shortened (< 26 BCL) a 2nd or 3rd BZ in the AVN or in the HPS ensues. These observations suggest that the mechanisms and dynamics of progression to HD-AVB apply only during incremental atrial pacing and there is a clear difference with what has been observed with the progression occurring exclusively at AV node.