Localization of slow conduction in a ventricular tachycardia circuit: Implications for catheter ablation

Characteristics and identification of sites of chagasic ventricular tachycardia by endocardial mapping

“…Both in sinus rhythm and during tachycardia, stimulation the site of origin, when performed in a slow conduction zone, has a long interval between the stimulus and the local electric activity or the QRS complex [27][28][29] . Using the ventricular stimulation technique through concealed entrainment, several authors showed, in patients with chronic ischemic heart disease, the participation of fractionated presystolic activity and mid-diastolic potential records with the slow circuit conduction region [6][7][8][9][30][31][32][33] .…”

Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction.

“…"1'4-21 At some sites, pacing entrains or resets the ventricular tachycardia with a stimulus to QRS (S-QRS) delay and without a change in QRS morphology. [14][15][16][17][18][19][20] This has been called by various authors entrainment with concealed fusion, concealed entrainment, and exact entrainment. Computer simulations and intraoperative mapping have shown that entrainment with concealed fusion can be due to depolarization of the pacing site within the reentry circuit with propagation of the stimulated orthodromic wave fronts along a path similar to that of the tachycardia wave fronts, whereas stimulated antidromic wave fronts collide in or near the circuit with orthodromic wave fronts and therefore do not depolarize surrounding myocardium to alter the QRS.1 '5"7 Entrainment with concealed fusion is consistent with pacing at a site in the reentry circuit but also may occur at some "bystander" sites that are adjacent to the reentry circuit but are not participating in the circuit itself.…”

An Uncommon Presentation for Cardiac Melanoma

“…One is based on reentry mechanism. [24][25][26][27] Data obtained from human and animal studies demonstrate that after myocardial infarction, asynchronous activation of muscle fibers follows the propagation of a slow activation wavefront through the scar area. 28 This area of slow conduction is the substrate for the reentry mechanism.…”