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Cardiac chamber weight was determined at necropsy in 323 men to develop correlative studies of electrocardiographic criteria for ventricular hypertrophy. Thirty recommended criteria for left ventricular (LV) hypertrophy, 10 for right ventricular (RV) hypertrophy, and combinations of both criteria for combined hypertrophy were evaluated. Four methods for electrocardiographic diagnosis of LV hypertrophy were derived: (1) a modification of the Romhilt-Estes point system; (2) the presence of any 1 of 3 criteria: (a) S V1 + R V5 or V6 greater than 35 mm, (b) left atrial abnormality, or (c) intrinsicoid deflection in lead V5 or V6 greater than or equal to 0.05 second; (3) a combination of any 2 criteria or of 1 criterion (above) plus at least 1 of the following 3 additional criteria: (a) left-axis deviation greater than -30 degrees, (b) QRS duration greater than 0.09 second, or (c) T-wave inversion in lead V6 of 1 mm or more; and (4) the use of a single criterion--left atrial abnormality. Sensitivity varied from 57 to 66% and specificity from 85 to 93% among these 4 methods. Myocardial infarction increased sensitivity of the foregoing methods, but the specificity was reduced. Method 2 is preferred for the electrocardiographic diagnosis of LV hypertrophy. Two methods were useful for right ventricular (RV) hypertrophy: (1) the use of any 1 of 4 criteria: (a) R/S ratio in lead V5 or V6 less than or equal to 1; (b) S V5 or V6 greater than or equal to 7 mm; (c) right-axis deviation of more than +90 degrees, or (d) P pulmonale; and (2) use of any 2 combinations of the foregoing criteria. Sensitivity ranged from 18 to 43% and specificity from 83 to 95%. Combined hypertrophy was best diagnosed using left atrial abnormality as the sole criteria of LV hypertrophy, plus any 1 of 3 criteria of RV hypertrophy: (a) R/S ratio in lead V5 or V6 less than or equal to 1, (b) S V5 or V6 greater than or equal to 7 mm, or (c) right axis deviation greater than +90 degrees.(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of aorto-coronary bypass surgery (ACBS) on ventricular arrhythmia was examined in 57 patients. Six-hour Holter monitoring was done on the day prior to and 3 mth after ACBS. None of the patients were on any antiarrhythmic drugs during these recordings. Ventricular arrhythmia was classified into three groups: Group I (45 patients) had an average of less than 10 premature ventricular contractions (PVCs) per hour, Group II (7 patients), 11-30 PVCs per hour and Group III (5 patients), greater than 30 PVCs per hour. There was no significant change in the number of patients in each group after ACBS. Complex PVCs were present in 8 patients preoperatively and in 9 patients after ACBS. The number of diseased vessels and the extent of left ventricular wall motion abnormality noted preoperatively, had no effect on ventricular arrhythmia following surgery. These data show that ACBS, when performed to relieve angina, does not have a significant effect on the prevalence of PVCs and does not prevent or reduce the occurrence of complex PVCs.

Most measurements establishing standard values for the normal electrocardiogram have been derived from a healthy population, whereas many electrocardiographic interpretations are necessary in hospitalized or seriously ill patients. Therefore, the characteristics of the electrocardiogram were described from 48 autopsied men known to be free of cardiopulmonary disease by clinical assessment and by a special cardiac examination using postmortem coronary angiography and a chamber partition technique. Highest values, mean and standard deviation, and the upper 97.5 percentile or lower 2.5 percentile when appropriate were noted for QRS voltage, QRS axis and duration, and intrinsicoid deflection in V5 or V6. Any ST-segment and T-wave changes were noted as well as left and right atrial abnormalities. Twenty-eight electrocardiographic criteria recommended to detect left ventricular hypertrophy and 10 recommended to detect right ventricular hypertrophy were evaluated for percentage of false-positive results and the 97.5 percentile value for each criterion was developed from the present data base. The data in this study can be used as a standard for comparing electrocardiographic variation in middle-aged men with specific relevance for electrocardiographic criteria of ventricular hypertrophy.

The sensitivity of 30 electrocardiographic criteria for left ventricular (LV) hypertrophy, isolated or combined, was examined to determine the relation to the underlying disease. Patients with coronary artery disease (CAD), systemic hypertension, valvular heart disease and cardiomyopathy were evaluated. A cardiac partition technique was used to define ventricular hypertrophy. Single electrocardiographic criteria often showed high sensitivity for 1 disease state, but not for others. Precordial voltage criteria were most sensitive for those with hypertensive and valvular disease. A QRS axis of more than −30 ° occurred most often in patients with CAD. Both left atrial abnormality and abnormal T-wave inversion of more than 1 mm in V6 occurred with a high sensitivity in general; however, T-wave inversion of more than 1 mm in V6 had a low sensitivity in cardiomyopathy. Methods using combinations of various electrocardiographic criteria improved sensitivity. Using these methods, sensitivity of the electrocardiogram for LV hypertrophy was excellent for patients with systemic hypertension and valvular heart disease and acceptable by usual standards for patients with CAD and cardiomyopathy. Because the use of a single criterion is often ineffective, methods using multiple electrocardiographic criteria to detect LV hypertrophy are recommended when the patients under study have diverse cardiac diseases.

Left atrial (LA) abnormality determined from precordial lead V1 was assessed by 2 observers as a criterion of left ventricular (LV) hypertrophy in the presence of right bundle branch block (BBS) in 23 patients. The presence of LV hypertrophy was confirmed from a postmortem cardiac partition technique and defined at 2 levels of confidence: probable and definite hypertrophy. Observers reliably differentiated between the hypertrophied and normal-sized ventricle in the presence of right BBB by using LA abnormality as an electrocardiographic criterion. When defined as definite hypertrophy, observer 1 correctly identified LV hypertrophy in 78% of the cases and observer 2 in 67% of the cases. False-positive results were present in 21% of cases by observer 1 and 14% by observer 2. Comparable results were achieved when a definition of probable hypertrophy was used. Observer performance of recognition of LA abnormality in this study was satisfactory with 91% agreement between observers. Our results are comparable and in some instances superior to conventional criteria commonly recommended to diagnose LV hypertrophy on the electrocardiogram without right BBB.

This study examined the hearts of 55 patients dying of chronic obstructive pulmonary disease, with and without cor pulmonale, quantitated histologically the degree of myocardial fibrosis in the left and right ventricle, and determined the relationship to associated disease states. Comparison has been made to a control group of 17 patients free of cardiopulmonary disease. Patients with associated and advanced ischemic heart disease, as proved by marked atherosclerosis and myocardial infarction, have significantly increased myocardial fibrosis throughout all layers of the left ventricular wall in comparison to control patients or patients with chronic obstructive pulmonary disease free of associated cardiac disease. Right ventricular fibrosis was not significantly increased; however, one case showed a marked degree of fibrosis related to myocardial infarction. Subdivision of patients with chronic obstructive pulmonary disease into groups with definite anatomic right ventricular hypertrophy, a clinical diagnosis of cor pulmonale, or with chronic hypoxemia failed to show any difference in the percentage of myocardial fibrosis of the ventricles among these groups. Increased fibrosis of the right or left ventricle in patients with chronic obstructive pulmonary disease, therefore, is not related to the degree of myocardial hypertrophy pathologically, the hypoxemic state, or clinical heart failure, but to ischemic heart disease with myocardial infarction.