PATHOPHYSIOLOGIC SUBSTRATE FOR SUSTAINED VENTRICULAR-TACHYCARDIA IN CORONARY-ARTERY DISEASE

Sustained ventricular tachycardia (VT) in the presence of coronary art ery disease (CAD) is almost always associated with prior infarction. I ts mechanism is reentrant excitation and it can be initiated >95% of t he time. Disrupted and delayed endocardial activation and prolonged, f ragmented electrograms recorded during sinus rhythm distinguish patien ts with VT from those with normal ventricles and those of prior infarc tion without VT. The extent of abnormalities of activation and number of abnormal, fragmented and late electrograms are greatest in patients with sustained VT. These abnormalities are associated with scar tissu e separating the viable myocytes. Fragmented electrograms are due to d iscontinuous activation due to nonuniform anisotropy caused by the sca r tissue. Patients with CAD demonstrate depressed excitability and pro longed relative refractory periods tie, an upward shift in the strengt h-interval curve) at sites of infarction but effective refractory peri ods measured at 10 mA comparable to normals and dispersion of refracto ry periods. However the associated abnormalities of conduction and act ivation produce an abnormal dispersion of recovery. Intraoperative map ping of patients with CAD has shown that most of the abnormalities of endocardial activation and conduction are in the subendocardial layers and subendocardial resection of these areas cures VT and abolishes de layed, fragmented electrograms and split potentials and normalizes the electrograms recorded from the subjacent tissue. This supports the hy pothesis that abnormalities of conduction are the critical pathophysio logic substrate of VT in CAD.