PATHOPHYSIOLOGY AND NATURAL HISTORY VENTRICULAR Quantitative analysis of myocardial infarct structure in patients with ventricular tachycardia

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, 1266-1279, 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.4 Previous studies point toward several different morphologic regions around the infarct as a possible site of reentry. Spared subendocardium between the infarct and the left ventricular cavity may contain at From the Departments of Pathology and Medicine, Duke University Medical Center, Durham, NC. Supported in part by SCOR grant HL 17670 from the NHLBI. Dr. Hackel is supported by Research Career Award HLB-K6-14188 from the U.S. Public Health Service. Address for correspondence: Raymond E. Ideker, M.D., Ph.D.. P.O. Box 3140, Duke University Medical Center, Durham, NC 27710. Received May 16, 1986; revision accepted Aug. 21, 1986. 1266 least part of the anatomic pathway for reentry,5 as indicated by the ability of surgical removal of this tissue to halt ventricular tachycardia.6 In animal preparations, ventricular tachycardia has been shown to arise from reentry in the patchy spared subepicardium over the infarct7 as well as intramurally by reentry involving the transmural extent of the infarcted region.' It has been reported that aneurysms with fibroelastosis coating the endocardium are associated with ventricular tachycardia, whereas aneurysms with thrombus and fibrosis without elastic tissue coating the endocardium are not.9 The purpose of this study was to analyze quantitatively the morphologic features of each of these regions of the infarcts in patients with and without a history of ventricular tachycardia. It is hoped that, in conjunction with electrophysiologic information gained by mapping, this information will lead to better understanding of the anatomic substrate of ventricular tachycardia and to the development of more exact preparations of postinfarction arrhythmias in animals. Materials and methods Patient selection. All deceased patients whose hearts were evaluated by the Duke University Cardiovascular Pathology CIRCULATION by gest on A ril 7, 2017 http://ciajournals.org/ D ow nladed from PATHOPHYSIOLOGY AND NATURAL HISTORY-VENTRICULAR ARRHYTHMIA 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 in the coronary care unit, telemetry, or Holter monitoring and had at least 10 ECGs recorded. Patients were excluded from the control group if they had unexplained sudden death. Patients with terminal ventricular tachycardia or ventricular fibrillation that was preceded by a subsequent infarction occurring within the last 48 hr of life were not excluded as controls. This acute subsequent myocardial infarct was not included in the quantitative histologic study described below. Patients admitted to the ventricular tachycardia group must have had at least one episode of ventricular tachycardia lasting 10 beats or more occurring 10 days or later after infarction. All but three of the patients in this group had runs of ventricular tachycardia lasting more than 30 sec. Patients were excluded if the only episodes of ventricular tachycardia occurred (1) within the last 24 hr of life, (2) less than 10 days since a subsequent acute myocardial infarction, major trauma, or surgery requiring general anesthesia, or (3) in the presence of other possible causes of ventricular tachycardia besides an infarct, such as pulmonary embolism, digitalis toxicity, cardiac catheterization, or insertion of a Swan-Ganz catheter. Based on the length of survival, the ventricular tachycardia group was subdivided into a subacute group (group B, dying within 10 weeks of infarction) and a chronic group (group C, dying 10 weeks or more after infarction). All patients from group C had ventricular tachycardia during or after week 10. Preparation of the hearts for study. All hearts were examined grossly by the standard protocol of the Duke Cardiovascular Pathology Laboratory, which includes the following procedures: injecting of coronary arteries with micropaque, B A photographing and x-ray photographing the whole heart, examining the coronary arteries every 5 mm and noting the degree of narrowing, cross sectioning the ventricles into five or six layers, and photographing and x-ray photographing the cross sections. By gross inspection, one of the middle cross sections that included representative portions of all the infarcts was selected for analysis. A tracing of the heart slice was made on clear plastic, and 24 radii were drawn on the tracings from the center of the left ventricle, evenly spaced every 15 degrees circumferentially. The radii were numbered 1 to 24 in a clockwise direction (base to apex orientation) with radius number 1 bisecting the septuml' (figure 1, A). These 24 numbered radii were used to determine the location of all subsequent measurements. The numbered radii were marked on the epicardial surface of the slice with India ink. Histologic slides of the entire circumference of the cross section were prepared with Masson or Mallory stain. With the marked epicardial surface as a guide, the numbered radii were reconstructed on the slides. Collection of gross data. The numbered radii were copied onto a photograph of each heart slice and the following measurements were made along each radius (figure 1, B): (1) radius of the left ventricular cavity (Rca), defined as the distance from the center of the left ventricle to the first cardiac tissue (mural thrombus excluded); (2) endocardial radius of the left ventricular wall (Rendo), defined as the distance from the center of the left ventricle to the endocardial surface of the left ventricular wall, excluding papillary muscle and trabeculae; (3) epicardial radius of the left ventricular wall (Repi), defined as the distance from the center of the left ventricle to the epicardial surface of the left ventricular wall; and (4) intraventricular space, defined as the space occupied by ventricular cavity or thrombus along a designated radius between papillary muscle or trabeculae and the left ventricular wall. The septum, excluding right ventricular trabeculae, was included as left ventricular wall. Measurements were rounded to the nearest 0.5 mm and adjusted to correct for magnification of the photograph. The presence of an aneurysm was noted for each heart. An aneurysm was defined as a portion of the left ventricular wall containing a myocardial infarct with two or more of the following characteristics: (1) transmural extent of infarction, (2) wall thinning, and (3) an outward bulge from the expected contour of