SUMMARY The distribution of cardiac muscle cell disorganization in different regions of the left ventricular wall was studied quantitatively in 52 patients with hypertrophic cardiomyopathy. Cellular disorganization in the ventricular septum was both common and extensive (mean area of septal tissue section disorganized, 35 i 4%). Disorganization was also substantial (24 ± 3%) in the left ventricular free wall of these patients, although less marked than in the ventricular septum (p < 0.05). Anterior left ventricular free wall disorganization was particularly extensive (32 ± 4%) and did not differ significantly from that present in the ventricular septum. Marked cardiac muscle cell disorganization (> 5% of the tissue section) was diffusely distributed in the ventricular septum and left ventricular free wall in 33 of the 52 patients (63%).Particularly marked left ventricular free wall and combined free wall and septal disorganization was present in 14 patients without functional limitation in whom sudden death occurred early in life (< 25 years of age) and was the initial manifestation of cardiac disease. In contrast, although abnormally arranged cardiac muscle cells were identified in the left ventricular free wall in 47% of patients with other congenital or acquired heart diseases or normal hearts, this disorganization was usually limited in extent (mean area of section disorganized, 2 0.5%).Hence, in a large population of patients with hypertrophic cardiomyopathy, cellular disorganization was widely distributed throughout both the ventricular septum and left ventricular free wall. No definitive conclusions can be made regarding the significance of this distribution of cellular disorganization; however, our data suggest that this pattern may represent a diffuse cardiomyopathic process and be a determinant of clinical outcome in certain patients with hypertrophic cardiomyopathy.HYPERTROPHIC CARDIOMYOPATHY is a disease of cardiac muscle that is characterized by a hypertrophied, nondilated left ventricle' and, in most patients, asymmetric septal hypertrophy.2`6 Marked disorganization of cardiac muscle cells in the ventricular septum7-10 has also been shown by quantitative histologic analysis to be a highly specific and sensitive anatomic hallmark of hypertrophic cardiomyopathy.1' '3 Qualitative histologic studies have shown that cellular disorganization may also be present in the left ventricular free wall of patients with hypertrophic cardiomyopathy.?' ' In this study, we quantitated, for the first time, the extent of cellular disorganization in both the ventricular septum and left ventricular free wall of patients with hypertrophic cardiomyopathy compared with patients with other forms of cardiac hypertrophy; we also determined whether the distribution and extent of the cellular disorganization in patients with hypertrophic cardiomyopathy has significance with regard to clinical course or hemodynamic state.
We conclude that the RR interval scattergram makes it possible to differentiate between aberrant ventricular conduction and ventricular ectopy in atrial fibrillation, and thus, it is a useful noninvasive clinical tool.
The effect of alcohol on variant angina was studied in six patients who had a history of chest pain occurring with alcohol ingestion. On alcohol testing, Holter ECG monitoring was performed and a 12-lead ECG was recorded at the time of chest pain. In five, chest pain with ST elevation occurred 5.5 to 17.5 h after the ingestion of alcohol (100 to 150 ml as ethanol). These showed recurrent ST elevation on Holter ECG, most episodes being asymptomatic. Results of provocation testing were reproducible in all four patients in whom tests were repeated and ST elevation occurred in the same leads. No complications were observed. The Holter ECG revealed a higher heart rate after alcohol ingestion. The plasma level of alcohol was zero when angina occurred and plasma epinephrine, norepinephrine and serotonin were unchanged following alcohol ingestion. Alcohol ingestion may be a useful method of provoking variant angina, particularly in those who have a history of angina related to alcohol ingestion.
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