Myocardial fibrosis in patients with hypertrophic cardiomyopathy (HCM) may play an important role in the function and/or dimensions of the left ventricle. We present an autopsied case of HCM followed for 10 years. A 68-year-woman with HCM underwent trans-aortic myectomy of the interventricular septum in 1979. A significant amount of round cell infiltration, myocardial fibrosis and disarray were observed in the resected specimen. She experienced repeated admissions due to diabetes mellitus and congestive heart failure, and died of renal failure in 1989. An autopsy revealed extensive myocardial fibrosis and significant cell infiltration in the ventricular myocardium. The infiltrating cells were almost all lymphocytes, and the ratio of CD4 to CD8 was 3.8. This ratio was different from that of typical viral myocarditis. This case suggests that there may be an undefined inflammatory process causing fibrosis in HCM, in addition to the ischemia due to intramural small coronary artery stenosis.
The purpose of this study was to determine whether two-dimensional echocardiography (2DE) can differentiate ischemic myocardial disease (IMD) from dilated cardiomyopathy (DCM). The subjects consisted of six cases of IMD which showed left ventricular dilatation (LVDd greater than or equal to 60 mm) and diffuse abnormality of wall motion, but did not show obvious localized myocardial infarction or left ventricular aneurysm on 2DE, and 16 cases of DCM. Two cases of IMD had previous myocardial infarction, and five cases of DCM had cardiomegaly following myocarditis. A short-axis image of the left ventricle was recorded at the chordal and the papillary muscle levels. Each image was divided into 4 segments, which were comprised of the septum, anterior wall, lateral (posterolateral) wall, and posterior (posteromedial) wall. Regional wall motion abnormality with reference to systolic thickening was analyzed qualitatively in each segment. The results were as follows: In ECG findings in IMD group, only one case showed abnormal Q waves and five cases showed left ventricular hypertrophy (LVH) similar to intraventricular conduction defect. On the other hand, in DCM group seven cases showed abnormal Q waves and five cases showed LVH. Two cases of IMD had two-vessel disease and four three-vessel disease, respectively. Left ventricular ejection fraction by cine-angiography ranged from 0.10 to 0.39 (mean 0.24) in IMD group and from 0.22 to 0.42 (mean 0.36) in DCM group. Mean LVDd showed no significant difference between these two groups. Five cases of DCM showed marked left ventricular dilatation (LVDd greater than or equal to 75 mm), but there were no such cases in IMD group. B-B' step was recognized in only one case of IMD, though it was present in eight cases in DCM. In regional wall motion, incidence of asynergy such as akinesis or dyskinesis was higher in IMD group than in DCM group. Left ventricular asynergy was more serious in the posteromedial wall than the posterolateral wall at the same image in five cases of IMD. However, in 12 cases of DCM, the degree of asynergy was equal at the both walls. In conclusion, it is recommended to examine echocardiographically the extent of severe asynergy in the posteromedial and posterolateral walls in order to differentiate IMD from DCM.
In 30 of 1,002 consecutive patients who had left heart catheterization and cineangiography for evaluation of either ischemic heart disease or cardiomyopathy the electrocardiogram showed giant negative T waves (greater than 10 mm) associated with high QRS voltage (R wave greater than 26 mm in lead V5 or the sum of the S wave in lead V1 and the R wave in lead V5 35 mm or more) in the precordial leads despite absence of hypertension or significant coronary artery disease. In all 30 patients a characteristic spade-like configuration (concentric apical hypertrophy) was observed in the right anterior oblique ventriculogram at end-diastole as well as in the long axis two dimensional echocardiogram.
To clarify interrelationship between myocardial infarction and coronary thrombosis, Japanese autopsy hearts with myocardial infarction were morphologically studied. For prevention of myocardial infarction, this kind of basic study would be imperative for the internists and surgeons who are interested in coronary bypass surgery.The materials consisted of 215 cases with 244 myocardial infarctions which were divided into 129 men and 86 women. Five age groups were set: young (20-39 y-o), middle aged (40-59 y-o), old (60-69 y-o), older (70-79 y-o) and oldest (over 80 y-o). Grade of coronary sclerosis was macroscopically estimated according to WHO standard and coronary thrombosis was both macro- and micro-scopically diagnosed.The overall incidence of coronary thrombosis in the infarction was 53% and the incidence was higher in the massive necrosis (M) type infarction, to 70% in male and 63% in female. In the M type infarction, the highest incidence was recorded in the old male (84%) and in the older female (69%). The anterior infarction fairly matched thrombosis in the anterior descending branch, but the posterior one which was relatively increasing after 70 y-o, did not show such an intimate relation to thrombosis in the right coronary artery. This tendency was especially marked in the older female group. The thrombosis appeared in only 3/7 cases with the M type infarction within the initial 24 hours after the clinical signs started.Thrombosis on moderate stenosis in the left coronary stem and proximal anterior descending branch was noted in the middle aged male. The site of thrombosis in the Ad branch shifted distalwards and thrombosis just above and distal to the severe atherom atous stenosis became remarkable with advancing age. Thrombosis was predisposed at the median portion of the right coronary artery and circumflex branch with a shift both proximal- and distal- wards with aging.