Silent cortical strokes associated with atrial fibrillation.

To clarify whether silent cortical strokes (SCS) could be a predictor of symptomatic stroke in patients with atrial fibrillation (AF), 72 patients with AF (50 with chronic AF, 22 with paroxysmal AF) were studied. Patients with mitral stenosis, history of myocardial infarction, or dilated cardiomyopathy were excluded from this study. Using cranial magnetic resonance imaging (MRI), the patients were divided into those with SCS (23 patients, Group 1) and those without SCS (49 patients, Group 2). The incidence of symptomatic stroke was then compared between the two groups. Three patients (13%) in Group 1 developed symptomatic brain infarction; this is statistically significant (p < 0.05), compared with the patients in Group 2, none of whom experienced symptomatic stroke. We suggest that SCS is a predictor of symptomatic cerebral infarct in patients with AF. Therefore, it is thought to be important to diagnose SCS using cranial MRI or computed tomography and to keep patients with SCS under close surveillance.

Silent cerebral infarction associated with coronary artery disease.

To investigate the relationship of coronary artery disease and silent cerebral infarction, 50 patients who underwent coronary arteriography and cranial magnetic resonance imaging were studied. The patients were divided into three groups. The incidence of silent cerebral infarction (chiefly lacunar infarction) was significantly higher in patients with old myocardial infarction and in those with angina pectoris than in the control group (80, 78 and 29%, respectively, p < 0.05). Silent cerebral infarction is considered to be a risk factor for symptomatic cerebrovascular disease, so more attention should be focussed on the prevention of stroke in patients with coronary artery disease.

[Hypertrophic cardiomyopathy with left ventricular dilatation].

There is increasing interest in the notion that some patients with hypertrophic cardiomyopathy (HCM) progress to morphological and functional manifestations similar to those of dilated cardiomyopathy (DCM). From 165 consecutive patients with HCM, 20 patients with left ventricular dilatation (left ventricular end-diastolic diameter greater than or equal to 50 mm) were selected and designated as dilated HCM. The diagnosis of HCM was established in these patients either by detection of the classical form of HCM in family members, with 2-dimensional echocardiographic evidence of asymmetric septal hypertrophy (ASH; septal thickness greater than or equal to 15 mm and a ratio of septal to posterior wall thickness greater than or equal to 1.3); or by demonstrating myocardial fiber disarray in autopsy or biopsy samples. The clinical manifestations of these patients with dilated HCM were then compared with those of other forms of HCM without left ventricular dilatation; 1) 40 patients with hypertrophic obstructive cardiomyopathy (HOCM) who had resting intraventricular pressure gradients of 20 mmHg or more, 2) 80 patients with non-obstructive HCM, each of whom had ASH of the entire ventricular septum (typical ASH), and 3) 25 non-obstructive patients whose hypertrophy was localized to the apical region of the ventricular septum (apical ASH). Patients having apical hypertrophy with a spade-like configuration on the left ventriculogram were excluded from the study. Compared with HOCM and typical ASH groups, the patients with dilated HCM had family histories of significantly more frequent HCM and less frequent hypertension. The patients with dilated HCM also had significantly less fractional shortening (FS), decreased interventricular septal thickness, greater left ventricular end-diastolic pressure (LVEDP), and left ventricular dilatation. During the follow-up period (average: 3.5 years), seven patients (35%) with dilated HCM died; five from congestive heart failure (CHF), one suddenly, and one three days following mitral valve replacement. The other five patients had CHF at the time of their follow-up examination. The patients with apical ASH had clinical features similar to those of dilated HCM; a higher familial frequency, less marked septal hypertrophy, and higher LVEDP. They tended to develop left ventricular dilatation, associated with reduced fractional shortening, although left ventricular diameter at end-diastole did not exceed 50 mm. These findings suggested that dilated HCM is not a rare condition. It is observed in 12% of consecutive patients with HCM.(ABSTRACT TRUNCATED AT 400 WORDS)

[Hypertrophic cardiomyopathy manifesting different modes of illness: report of three cases].

Three cases of hypertrophic cardiomyopathy (HCM) which presented with different modes of appearance of left ventricular hypertrophy are reported. Case 1: A 24-year-old man had three relatives with HCM. At 13 years of age, he showed no electrocardiographic or echocardiographic abnormalities characteristic of HCM. During the ensuing 11 years, he developed asymmetric septal hypertrophy (ASH) and systolic anterior motion of the mitral valve (SAM), with right bundle branch block and T-wave inversion. Cardiac catheterization confirmed the diagnosis of hypertrophic obstructive cardiomyopathy by demonstrating an intraventricular pressure gradient of 25 mmHg. These observations indicate that this case developed abnormal hypertrophy during adolescence on the basis of genetic predisposition of an autosomal dominant trait. Case 2: A 51-year-old woman had three proven and three possibly affected relatives. At 35 years of age, she had a normal electrocardiogram, although the echocardiogram was not available. Now, 16 years later, she had developed ASH with abnormal Q-waves and was diagnosed as having non-obstructive HCM. These suggest that ASH can be manifested as late as during middle-age, even in those with genetic predisposition. Case 3: A 47-year-old woman was diagnosed as having hypertension and her blood pressure was 190/100 mmHg at 40 years of age, though she had no abnormal electrocardiographic findings and heart murmurs. Now, at 47 years of age, she had developed T-wave inversion, ASH, SAM, and an intraventricular pressure gradient of 50 mmHg. Thus, her ASH appeared during middle-age, and was probably provoked by hypertension, though a complete family survey could not be conducted. These three patients' findings indicate that there may be various modes of appearance of left ventricular hypertrophy in HCM. In the majority of patients with genetic predisposition, abnormal hypertrophy may develop during adolescence as in Case 1. In others, it may develop in middle-age, as it did in Case 2. The disease spectrum of HCM may additionally include those who develop abnormal hypertrophy during middle-age, following provocation by hypertension, as in Case 3.