g-Hsiung Chen

Clinicopathologic study of abnormal Q waves in Kawasaki disease (mucocutaneous lymph node syndrome): An infantile cardiac disease with myocarditis and myocardial infarction☆

Abstract A correlative study of abnormal Q waves and pathologic findings was performed on 15 hearts from children with Kawasaki disease. Gross pathologic study revealed acute angiitis with pericarditis, acute myocarditis and coronary heart disease as the result of angiitis. Three hearts in infants with abnormal Q waves in leads I and aVL and chest leads had gross transmural fibrosis in the anteroseptal-lateral walls of the left ventricle. Coagulation necrosis (acute myocardial infarction) or fibrosis, or both, in more than 30 percent of the wall thickness in the posterior ventricular wall was found in four of five hearts in infants with abnormal Q waves in leads II, III and aVF. Seven of the 15 infants had no abnormal Q waves, and only 2 of the 7 had myocardial damage in over 30 percent of the wall thickness. In 9 of the 15 hearts there were 11 gross areas of fibrosis; in these hearts there was a corresponding severe stenosis of more than 90 percent due to organization in the major coronary arteries supplying these areas. In three hearts with coagulation necrosis, the coronary occlusion was caused by fresh large thrombi. In the six hearts without sizable fibrosis, the grade of stenosis due to organization was less than 75 percent in each of the major coronary arteries. Coronary aneurysm due to angiitis was seen in 12 of the 15 hearts, and at autopsy fresh large thrombi were seen in each aneurysm. Ten of the 12 hearts exhibited sizable areas of myocardial damage. Three hearts without aneurysm manifested angiitis with mild stenosis of less than 25 percent, but there were no macroscopic fresh thrombi in any of the major coronary arteries. Thus, abnormal Q waves in children with Kawasaki disease almost always reflect myocardial damage in over 30 percent of the wall thickness of the left ventricle. Electrocardiograms are useful to determine the anterior or posterior localization of the damage. Nevertheless, the possibility of transmural and nontransmural areas of damage cannot be excluded in the absence of abnormal Q waves.

ECG pattern of left ventricular hypertrophy in nonobstructive hypertrophic cardiomyopathy: The significance of the mid-precordial changes

A review of electrocardiograms from 33 patients with nonobstructive hypertrophic cardiomyopathy was made. In 22 patients there was noted a high QRS voltage, depression of the ST segment, and inversion of the T wave, satisfying the diagnostic criteria of left ventricular hypertrophy with the abnormal changes not only extending to the midprecordial leads but showing the most striking abnormal changes in Lead V4 in 20 patients. The frontal plane electrical axis was normal (around 60 degrees), with the most remarkable changes in Lead II. In the VCG, the magnitude of the QRS loop was increased and directed anteriorly and to the left, and the T loop was deviated posteriorly and to the right opposite the QRS loop. The asymmetric septal and apical hypertrophy was noted on echocardiography and/or angiocardiography. The coronary arteries were normal without significant obstruction in selective coronary angiography. It was postulated that the asymmetric septal and apical hypertrophy was reflected in this ECG pattern. The recognition of this ECG pattern provides pertinent information in the clinical detection of nonobstructive HCM.

Anterior QRS loop in hypertrophic cardiomyopathy

Frank vectorcardiograms (VCGs) were reviewed in 45 patients with hypertrophic cardiomyopathy (HCM), 26 with obstruction and 19 without obstruction. Twelve of the 19 patients without obstruction and five of the 26 patients with obstruction were found to have predominantly anterior QRS loops. Fourteen patients had a large left anterior QRS loop with increased anterior and leftward force; the posterior and terminal rightward force were within the normal range, and the T loops were displaced posteriorly and to the right opposite to the QRS loop. Asymmetric septal and apical hypertrophy were noted echocardiographically and/or angiographically. Increased electrical force from the asymmetric hypertrophy of the septal and apical area is proposed to explain this large left anterior loop. Three patients had a QRS loop located anteriorly and to the right with electrocardiograms (ECGs) resembling those of posterolateral myocardial infarction or right ventricular hypertrophy. These finding suggest that (1) hypertrophic cardiomyopathy may be another cause of an anterior QRS loop; (2) the recognition of the large left anterior loop in the VCG in patients with a left ventricular hypertrophy pattern in the ECG is helpful in the diagnosis of HCM, especially the nonobstructive form; and (3) hypertrophic cardiomyopathy should be considered in the differential diagnosis of myocardial infarction or right ventricular hypertrophy.

Transient intraventricular conduction disturbances in hypertrophic obstructive cardiomyopathy.

ventricular septum, a 2.0 to 2.5 cm defect was demonstrated consistently in the left ventricular side of the septum (Fig. 1) and entered a large, irregularly defined space (aneurysm) communicating witb the right ventricular apex through an 0.5 cm defect in the right ventricular side of the septum (Fig. 2). The aneurysm showed maximal bulging into the right ventricle toward the end of ventricular diastole and became progressively smaller in ventricular systole. The changes resulted from the hypermobility of the thin right side of the septum. The left side of the septum was virtually immobile and no change occurred in the area of septal disruption. -mode echocardiograpby was confusing and nondiagnostic. The echocardiographic findings were confirmed at, surgery, at which time the aneurysm was plicated and the septal rupture into the right ventricle was repaired. The postoperative echocardiogram demonstrated no septal discontinuity and linear echo densities consistent with metallic sutures used to bnttress Teflon pledgets (Fig. 3). Recognition of a dissecting ventricular septal aneurysm following acute myocardial infarction is new and represents an extension of the capabilities of real-time ZDE. The potential now exists for early echocardiographic diagnosis of ventricular septai aneurysm prior to rupture which results in hemodynamic deterioration from ventricular shunting. Wood A: Perforation of the interventricular septum due to cardiac infarction. Br Heart J 6:191, 1944. Peel A: Dissecting aneurysm of the interventricular septum. Br Heart J 10:239, 1948. Scanlon d, Seward J, Tajik A: Visualization of ventricular septal rupture utilizing wide-angle two-dimensional echocardiography. Mayo Clin Proc 54:381, 1979. Farcot J, Boisante L, Rigaud M, Bardet J, Bourdarias J: Two-dimensional echocardiographic visualization of ventricular septal rupture after acute myocardial infarction. Am J Cardiol 45:370, 1980.