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Paroxysmal supraventricular tachycardia (PSVT) and atrial fibrillation (AF) are both supraventricular arrhythmias, but their mechanisms are completely different. This study determines the incidence of symptomatic AF in a group of patients followed closely during routine outpatient care for PSVT. Thirty-nine patients with PSVT were followed for up to 4 years using telephone transmission of the electrocardiogram to document symptomatic arrhythmias. The cumulative proportion of patients who had AF was calculated using the Kaplan-Meier life-table method. In addition, we examined the importance of clinical variables traditionally believed to influence the occurrence of AF. The cumulative proportion of patients who had AF during follow-up was 13% at 3 months, 16% at 6 months, 22% at 1 year and 29% at 2 years. In most patients the start of AF was documented during an attack of PSVT rather than de novo as another primary arrhythmia. PSVT occurred significantly earlier during an observation period without treatment in patients in whom AF developed (p = 0.03). The occurrence of AF was not related to age, number of years of PSVT, heart rate during tachycardia or coexistent heart disease.

We evaluated a simplified version of a previously developed QRS scoring system for estimating infarct size using observations of Q- and R-wave durations and R/Q and R/S amplitude ratios in the standard 12-lead ECG. Groups of subjects with a minimal likelihood of having myocardial infarcts and minimal likelihood of having common noninfarction sources of QRS modification were studied to establish the specificity of each of the 37 criteria. Only two criteria required modification to achieve 95% specificity. These 37 criteria form the basis of a 29-point QRS scoring system. A 98% specificity was achieved when a score of more than 2 points was required to identify a myocardial infarct. Fifty patients were studied to determine the intra- and interobserver agreement with this scoring system. Each criterion achieved at least 91% intra- and interobserver agreement. These impressive levels of specificity and observer agreement must be matched by high sensitivity of the scoring system and a good correlation between the point score and infarct size in patients with proven infarcts if the point score is to be useful for detecting and sizing infarcts. Sensitivity and correlation between point score and infarct size are evaluated in later studies in this series. The standard ECG is inexpensive and can be obtained repetitively and noninvasively; its QRS complex may be an important means of estimating the size, presence and location of myocardial infarcts.

This study correlated the location and size of posterolateral myocardial infarcts (Mls) measured anatomically with that estimated by quantitative criteria derived from the standard 12-lead ECG. Twenty patients were studied who had autopsy-proved, single, posterolateral Mls and no confounding factors of ventricular hypertrophy or bundle branch block in their ECG. Left ventricular anatomic Ml size ranged from 1 to 46%. No patient had a ≥ 0.04-second Q wave in any electrocardiographic lead and only 55% had a 0.03-second Q wave. A 29-point, simplified QRS scoring system consisting of 37 weighted criteria was applied to the ECG. Points were scored by the ECG in 85% of the patients (range 1 to 8 points). Ml was indicated by a wide variety of QRS criteria; 19 of the 37 criteria from 8 different electrocardiographic leads were met. The correlation coefficient between MI size measured anatomically and that estimated by the QRS score was 0.72. Each point represented approximately 4% Ml of the left ventricular wall.

This study correlated the location and size of posterolateral myocardial infarcts (Mls) measured anatomically with that estimated by quantitative criteria derived from the standard 12-lead ECG. Twenty patients were studied who had autopsy-proved, single, posterolateral Mls and no confounding factors of ventricular hypertrophy or bundle branch block in their ECG. Left ventricular anatomic Ml size ranged from 1 to 46%. No patient had a ≥ 0.04-second Q wave in any electrocardiographic lead and only 55% had a 0.03-second Q wave. A 29-point, simplified QRS scoring system consisting of 37 weighted criteria was applied to the ECG. Points were scored by the ECG in 85% of the patients (range 1 to 8 points). Ml was indicated by a wide variety of QRS criteria; 19 of the 37 criteria from 8 different electrocardiographic leads were met. The correlation coefficient between MI size measured anatomically and that estimated by the QRS score was 0.72. Each point represented approximately 4% Ml of the left ventricular wall.

The effects of the intensity of exercise training on cardiorespiratory variables were investigated in a consecutive series of men with recent (median 8 weeks) acute myocardial infarction. Forty-five patients were randomly assigned either to a high- (65 to 75% maximum oxygen consumption rate [VO2max]) or to a low-intensity (less than 45% VO2max) exercise group. Patients engaged in medically supervised aerobic training 3 sessions a week for 12 weeks. With training, mean VO2max significantly increased by 11% (2.09 to 2.31 liters/min) within the high group and by 14% (1.93 to 2.21 liters/min) within the low group. Differences between groups were not statistically significant. Both groups also had comparable changes in heart rate, blood pressure and double-product at submaximal and maximal workloads. Analysis of blood lipids revealed that both groups experienced a significant increase in high density lipoprotein cholesterol. There were no significant changes in total serum cholesterol or triglycerides. These findings suggest that within an unselected population of patients after acute myocardial infarction referred for cardiac rehabilitation, low- and high-intensity exercise training produces relatively similar changes in cardiorespiratory variables during the initial 3 months of exercise training.

A 3-stage infusion of diltiazem was tested in 8 subjects for up to 48 hours: a bolus injection (10 mg over 3 minutes), a rapid loading infusion (20 mg over 30 minutes) and a maintenance infusion (10 mg/hour to the end of the study). This regimen produced stable median plasma diltiazem concentrations of approximately 150 ng/ml. The median half-life of elimination for diltiazem was 206 minutes (range 144 to 452) and median total clearance was 980 ml/min (range 665 to 1,907). The PR interval lengthened 10 to 18% during the maintenance infusion in 7 subjects; in 1 subject atrioventricular nodal Wenckebach conduction was recorded during the rapid loading infusion. Systolic blood pressure decreased from 124 ± 7 mm Hg (mean ± standard deviation) during the control period to 121 ± 8 mm Hg during the rapid loading infusion (p = 0.03 compared with control) and to 117 ± 7 mm Hg (p = 0.04 compared with control) during the maintenance infusion. Heart rate did not change. PR interval and blood pressure returned to control levels within 4 hours after the infusion was stopped. Loading and maintenance infusion may be an attractive method of administering diltiazem when stable drug concentrations are required for prolonged periods.

Coronary heart disease (CHD) is a chronic, progressive disease widely prevalent in industrial societies, including the United States. More than 3,400 Americans suffer myocardial infarctions each day, incurring an annual estimated economic cost of $60 billion. A first step in the prevention of this disease has been the identification of characteristics, or risk factors, that are present in individuals prone to develop CHD. Epidemiological studies have found these factors to include a family history of heart disease, elevations in blood pressure and serum cholesterol, cigarette smoking, obesity, a sedentary lifestyle, and the Type A behavior pattern.

The ability of an independently developed QRS point score to estimate the size of infarcts predominantly within the anterior third of the left ventricular was evaluated by quantitative pathologic-electrocardiographic correlation. The study was limited to 21 patients with a single infarct documented by postmortem examination, for whom an appropriately timed standard 12 lead electrocardiogram was available that did not exhibit signs of left or right ventricular hypertrophy, left or right bundle branch block or anterior or posterior fascicular block. At necropsy the heart was cut into five to seven slices. The location and size of the infarct was quantitated by computer-assisted planimetry of the slices. The electrocardiogram of 19 (90 percent) of the patients exhibited either a Q wave or an R wave of no more than 20 ms in lead V2. The infarct in the two patients without this electrocardiographic finding was small, occupying 2 and 3 percent of the left ventricle, respectively. The percent infarction of the left ventricle correlated with the QRS point score (r=0.80). Thus in patients without complicating factors in the electrocardiogram and with a single infarct, the electrocardiogram provides a marker for infarction in the anterior third of the left ventricle and permits estimation of infarct size.

The purpose of this article is to investigate the occurrence of symptomatic paroxysmal supraventricular tachycardia (PSVT) in untreated patients and to assess factors that influenced its occurrence. We studied 34 patients with this arrhythmia during an observation period in which they received no antiarrhythmic drug therapy for up to 90 days. Recurrence of PSVT was documented by telephone transmission of the electrocardiogram. Each patient was allowed to have exactly one episode of tachycardia before being removed from the study. We measured how long patients remained free of their tachycardia (the tachycardia-free period) and heart rate during tachycardia. Twenty-nine of the 34 patients had an attack of symptomatic tachycardia within the 90-day observation period. The proportion of patients who had not had any symptomatic PSVT by each day of follow-up was calculated using the Kaplan-Meier method as follows: 75% by day 3, 50% by day 19, 25% by day 36, and 17% by day 90. Patients with any other heart or lung disease had significantly shorter tachycardia-free periods. The mean heart rate during spontaneous tachycardia was 203.5 +/- 34.9 beats per minute (range, 142 to 288 beats per minute). Patients with longer tachycardia-free periods had significantly faster heart rates during tachycardia.

• Seven hundred twenty-four consecutive patients admitted to a coronary care unit for chest pain underwent comparative evaluation of ECG and lactic dehydrogenase (LDH) and creatine kinase (CK) enzyme and isoenzyme patterns. Of the 724 patients, 419 (58%) had the myocardial component (MB) of CK detected; however, 69 (16%) of the latter had no abnormal elevation of total CK levels. This group with CK-MB but persistently normal total CK levels demonstrated fewer diagnostic QRS changes on ECG (17% vs 54%) and a lower incidence of LDH 1:2 inversion (28% vs 79%) than did the group with CK-MB and abnormally elevated total CK levels. However, no specific level of either total CK or CK-MB could segregate the patients with QRS or LDH level changes, which suggests that persistently normal levels of CK do not exclude the diagnosis of myocardial infarction. Evidence that myocardial necrosis can occur in the absence of an abnormal elevation of total CK levels is confirmed histologically in one patient. (Arch Intern Med1982;142:33-38)