Quantitative analysis of myocardial infarct structure in patients with ventricular tachycardia.

Abstract

To study whether myocardial infarction differs in patients with and without ventricular tachycardia, the hearts of 22 deceased patients with ventricular tachycardia and 21 deceased control patients were analyzed quantitatively. The hearts from the ventricular tachycardia group were heavier and more dilated than those from the control group. Histologic analysis of a representative cross section from each heart showed that the ventricular tachycardia group had larger, more solid infarcts than did the control group. The ventricular tachycardia group also had a greater area of spared subendocardium, more hydropic change of the spared subendocardium, and more "ribbon type" spared subendocardium, which was defined as spared subendocardium of uniform contour 1 mm thick or less. The ventricular tachycardia group was divided into a subacute subgroup (n = 14, dying c 10 weeks after infarction) and a chronic subgroup (n = 8, dying > 10 weeks after infarction). The infarcts of the subacute ventricular tachycardia group were more solid and had a greater amount of ribbon type spared subendocardium than those of the chronic ventricular tachycardia group. This information can serve as a baseline for the evaluation of animal preparations of tachycardia and, when combined with knowledge of the location of the arrhythmogenic region furnished by intraoperative mapping, should lead to better understanding of the anatomic substrate for ventricular tachycardia. Circulation 74, No. 6, 1266No. 6, -1279No. 6, , 1986 VENTRICULAR TACHYCARDIA is a common complication of myocardial infarction and is associated with increased morbidity and mortality. 1 Although the size of infarcts in patients with ventricular tachycardia has not previously been quantified morphometrically, arrhythmias have been reported to be associated with large creatine kinase infarct size index2 and with poor cardiac function,3 thus implicating large infarct size as a contributing factor for ventricular tachycardia. Although the mechanism by which a large infarct can lead to an arrhythmia is not definitely known, ventricular tachycardia occurring after the acute stage of an infarct is thought to be caused by reentry within the structurally altered tissue in or adjacent to the infarct. Laboratory between January 1975 and March 1985 were entered into the study if they (1) had a myocardial infarction, (2) had survived 10 days or longer after infarction, and (3) met the following criteria for either the ventricular tachycardia or the control group.The patients in the control group (group A) must have had no history of ventricular fibrillation or ventricular tachycardia lasting 10 beats or more after the first 48 hr after infarction and no history of ventricular tachycardia lasting 3 beats or more or coupled premature ventricular contractions after the first 4 days after infarction. The patients must have been hospitalized through at least day 10 after infarction and must have undergone some form of electrocardiographic monitoring such as routine heart monitoring i...

Characterization of the Peri-Infarct Zone by Contrast-Enhanced Cardiac Magnetic Resonance Imaging Is a Powerful Predictor of Post–Myocardial Infarction Mortality

“…Table 2 lists the univariable predictors of mortality with PϽ0. 10. When all of the clinical and imaging parameters associated with mortality on univariable analysis were considered in the multivariable model by stepwise forward selection, %MDE periphery and LV end-systolic volume index emerged as the 2 strongest independent predictors of allcause mortality (Table 2) and cardiovascular mortality.…”

“…5,6 Although dense, fibrous scars in the infarcted myocardium incapable of depolarization cannot alone cause arrhythmias, when surrounded by distorted bundles of surviving myocytes capable of depolarization in the infarct border zone, arrhythmogenic substrates for slow conduction and reentry phenomena may arise. [7][8][9][10][11][12][13] …”

A comparison of cardiac magnetic resonance imaging peri-infarct border zone quantification strategies for the prediction of ventricular tachyarrhythmia inducibility

“…Slow conduction, a required component of reentrant arrhythmias, is found in the border of healing infarcts [33,34]. In addition, areas of patchy infarct that may provide the geometric substrate for reentry [15], as well as areas of mixed dead and viable myocardium [21] have all been identified in the peri-infarct zone.…”

“…Infarct size is a known determinant of the risk for occurrence of VT [15][16][17]. Recent human studies have demonstrated that infarct characterization by late gadolinium enhancement (LGE) on CMR is predictive of overall mortality [12] as well as inducibility of ventricular arrhythmia during electrophysiological study (EPS) [11,18].…”

Role of Cardiac Magnetic Resonance Imaging in the Management and Treatment of Ventricular Tachycardia in Patients With Structural Heart Disease

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