Background. Left ventricular endocardial reentry is the conventional concept underlying surgery for ventricular tachycardia (VT). We assessed the incidences of patterns showing complete reentry circuits at either the subendocardial or subepicardial level and of patterns in which left ventricular endocardial mapping could only in part account for a reentrant mechanism.Methods and Results. We retrospectively analyzed epicardial and left ventricular endocardial isochronal maps of 47 VTs induced in 28 patients with chronic myocardial infarction (inferior, 14 patients; anteroseptal, 14 patients). Electrograms were recorded intraoperatively from 128 sites with epicardial sock and transatrial left ventricular endocardial balloon electrode arrays. Given the methodology used in this study, the mapping characteristics of the tachycardias suggested five types of activation patterns: 1) complete (90% or more ofVT cycle length) subendocardial reentry circuits in seven VTs (15%) and seven patients (25%), 2) complete subepicardial reentry circuits in four VTs (9%o) and four patients (14%), 3) incompletely mapped circuits with a left ventricular endocardial breakthrough preceding the epicardial breakthrough in 25 VTs (53%) and 21 patients (75%), 4) incompletely mapped circuits with a left ventricular epicardial breakthrough preceding the endocardial breakthrough in three VTs (6%) and three patients (11%), and 5) a right ventricular epicardial breakthrough preceding the left ventricular endocardial breakthrough in eight VTs (17%) and seven patients (25%). After surgery, one type 3 VT and three type 5 VTs were reinducible. Thus, left ventricular endocardial reentry substrates (types 1 and 3) accounted for 68% of VTs, but substrates involving subepicardial (types 2 and 4) and deep septal layers (type 5) accounted for 32%

These results offer a solid basis for a more precise interpretation of a wide range of electrophysiological data and provide a framework for future investigations of surface ECG reflections of endocardial and epicardial activation patterns recorded in patients with chronic myocardial infarction.

Presynaptic supersensitivity was demonstrated in isolated rat atria and perfused hearts 2 h after an intravenous injection of 6-hydroxydopamine (6-OH-DA), 100 mg/kg. This coincided with a maximum depletion of cardiac endogenous noradrenaline, a disappearance of the fluorescence of terminal adrenergic nerve fibers in the atrial myocardium, and an abolished chronotropic response to tyramine. The chronotropic response to dopamine was also significantly diminished. Maximal supersensitivity to the chronotropic effect of noradrenaline was observed 72 h after the injection of 6-OH-DA. Two weeks after the administration of 6-OH-DA, supersensitivity to noradrenaline was less marked, and the response to tyramine was restored. These changes corresponded to an increasing noradrenaline content in the heart and to the reappearance of histofluorescent fibers in the atria.