Biomedical subjects
Publications and source records attributed to L M Rolnitzky.
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The a priori hypothesis that diltiazem would reduce the frequency and repetitiveness of ventricular arrhythmias was tested 3 months after myocardial infarction in patients participating in the Multicenter Diltiazem Postinfarction Trial. After 3 months of follow-up, 1,546 of the 2,466 patients enrolled had a 24-hour continuous electrocardiographic recording that contained greater than or equal to 12 hours of analyzable data. They were similar to the patients who survived 3 months but chose not to have a 24-hour electrocardiographic recording (i.e., they were representative of the entire group that survived 3 months). After 3 months of follow-up, there were no significant differences between the diltiazem and placebo groups in the prevalence of atrioventricular block, the frequency of atrial arrhythmias or the frequency or repetitiveness of ventricular arrhythmias. Heart rate was significantly lower (67 +/- 12 vs 71 +/- 12 beats/min) and there was a significantly greater proportion of patients with sinus pauses greater than or equal to 2 seconds in duration in the diltiazem group (6%) than in the placebo group (3%). Comparison with placebo revealed no evidence either for an anti- or proarrhythmic effect of diltiazem. There was no reduction in sudden or arrhythmic death attributable to diltiazem treatment; the fraction of total deaths that were arrhythmic by the Hinkle classification was 41% in the placebo group and 42% in the diltiazem group. It may be that the lack of effect of diltiazem on ventricular arrhythmias is partially responsible for its lack of effect on mortality after myocardial infarction.
This study examined the relations among beta-adrenergic blocker use, various correlates of left ventricular function and the chance of developing congestive heart failure in patients after myocardial infarction. The study was performed with the placebo group of the Multicenter Diltiazem Post-Infarction Trial. Ejection fraction data were available in 1,084 patients; of these, 557 were receiving a beta-blocker and 527 were not. In addition to ejection fraction, other correlates of left ventricular function included the presence or absence of pulmonary rales, chest X-ray film evidence of pulmonary congestion and the presence of an S3 gallop. Beta-blocker use was less frequent in patients with an ejection fraction less than 30%, rales, an S3 gallop and pulmonary congestion on chest X-ray film. Twenty-one percent of patients with an ejection fraction less than 30%, 42% of patients with rales, 28% of patients with an S3 gallop and 28% of patients with pulmonary congestion were receiving beta-blocker therapy. For every correlate of left ventricular function, the chance of developing congestive heart failure was greater in patients with diminished left ventricular function than in those without. For each level of left ventricular function, the chance of developing congestive heart failure requiring treatment was greater in patients not taking a beta-blocker.(ABSTRACT TRUNCATED AT 250 WORDS)
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In animals, baroreflex sensitivity is inversely related to the likelihood of ventricular fibrillation during myocardial ischemia. After myocardial infarction in human patients, reduced baroreflex sensitivity is associated with increased mortality. A reduced standard deviation of normal RR intervals over a 24 h period is also associated with reduced survival after myocardial infarction. Therefore, 32 normotensive men who had survived their first myocardial infarction were studied to define the relation between baroreflex sensitivity assessed with phenylephrine injection and three Holter electrocardiographic measures of tonic vagal activity: the percent of successive normal RR intervals greater than 50 ms, the root mean square successive difference of normal RR intervals and the power in the high frequency energy of the normal RR interval power spectrum. Correlations among the Holter measures of heart period variability were greater than or equal to 0.94, indicating that these measures are so strongly correlated that any one of them can be used to represent the others. Baroreflex sensitivity showed weaker correlations with the three Holter variables (0.57 to 0.63), indicating that the Holter measures did not accurately predict baroreflex sensitivity. Baroreflex sensitivity showed a stronger correlation with the three Holter variables during the night than during the day. Baroreflex sensitivity and tonic vagal activity reflected by Holter variables were reduced more in patients with inferior myocardial infarction than in those with anterior infarction. The relative utility of baroreflex sensitivity and Holter measures of tonic vagal activity in predicting sudden cardiac death after myocardial infarction needs to be evaluated in a large prospective study.
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A high degree of heart rate (HR) variability is found in persons with normal hearts, whereas low HR variability can be found in patients with severe coronary artery disease, congestive heart failure and diabetic neuropathy. Two weeks after acute myocardial infarction, low HR variability predicted reduced long-term survival even after adjusting for clinical risk indicators, left ventricular ejection fraction, HR and ventricular arrhythmias. The present study elucidated the causes of differences in HR and HR variability between patients with low and high HR variability. In a matched-pair study, 10 patients with low HR variability (24-hour standard deviation of N-N intervals less than 50 ms) were randomly selected. For each of these 10 patients, a control patient with high HR variability (24-hour standard deviation of N-N intervals greater than or equal to 100 ms), matched for age, left ventricular ejection fraction and rales in the coronary care unit was selected. Patients who were taking either digitalis or beta-adrenergic blocking drugs were excluded. Analysis of 24-hour electrocardiograms showed that for the low HR variability group compared with the high: (1) the daytime and nighttime average HR was faster; (2) the difference between daytime and nighttime HR was less; (3) the proportion of differences greater than 50 ms between successive N-N intervals was smaller; and (4) the number of HR "spikes" per day (increase in HR greater than or equal to 10 beats/min, lasting from 3 to 15 minutes) was less.(ABSTRACT TRUNCATED AT 250 WORDS)
A 24-hour continuous electrocardiographic recording was made 11 +/- 3 days after acute myocardial infarction (AMI) in 820 of the 867 participants in the Multicenter Post-Infarction Program. Ninety patients (11%) had unsustained ventricular tachycardia (VT) and 2 (0.2%) had sustained VT (more than 15 seconds). In 53 of the 92 patients (58%) with VT, only 1 episode of VT was in the recording. In 26 patients the longest episode of VT was 3 consecutive complexes (28%); in 56 patients (61%) it was 4 to 10 complexes; and in only 10 patients (11%) were there more than 10 consecutive complexes. The average rate of VT was 121 +/- 34 complexes per minute (range 75 to 240). Most episodes of VT started well after the T wave. Occurrence of VT was strongly related to the frequency of ventricular premature complexes in the 24-hour recording; 46% of the patients with at least 100 ventricular premature complexes per hour had VT. The 92 patients who had VT were compared to the 728 who did not with respect to relevant clinical characteristics. Several variables were significantly (p less than 0.05) more common in the VT group: age older than 60 years, previous AMI, history of angina pectoris, occurrence of VT or ventricular fibrillation in the coronary care unit, left ventricular ejection fraction less than 30%, rales greater than bibasilar in the coronary care unit, and use of antiarrhythmic drugs, digitalis or diuretics at the time of discharge from hospital. Based on Kaplan-Meier survival curves, the cumulative probability of surviving 3 years was 0.67 for patients with VT and 0.85 for patients without VT (p less than 0.001). There were no statistically significant associations between individual VT characteristics and mortality. However, patients with longer runs of VT tended to have a higher mortality rate, and both patients with sustained VT died in the first month after the index infarct. VT had a strong and statistically significant association (p less than 0.05) with all-cause and arrhythmic mortality independent of other risk variables that were associated with VT. Adjusted for other risk indicators, VT nearly doubled the risk of dying during an average follow-up of 31 months.
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To determine whether treatment with digitalis is associated with decreased survival after acute myocardial infarction (AMI), data from 504 patients who were enrolled in a postinfarction natural history study were analyzed. At the time of discharge, 229 patients (45%) were taking digitalis. After 3 years of follow-up, the cumulative survival rate for patients discharged on a regimen of digitalis was 66%, compared with 87% for those not treated (p less than 0.001). Univariate analysis showed that statistically significant differences existed between the 2 groups with respect to age, previous AMI, left ventricular failure in the coronary care unit, atrial fibrillation in the coronary care unit, peak creatine kinase levels, enlarged heart and pulmonary vascular congestion on the discharge chest x-ray, ventricular arrhythmias and treatment with diuretic, antiarrhythmic and beta-blocking drugs. Survival analysis using Cox's regression model showed that the association between digitalis and decreased survival was of borderline significance after adjustment for atrial fibrillation and left ventricular failure. Serum digoxin concentration was measured in 83% of the patients who took digitalis. Survival was inversely and significantly related to serum digoxin, i.e., the higher the serum digoxin concentration, the lower the long-term survival rate. After adjusting for atrial fibrillation and left ventricular failure, serum digoxin was not significantly related to survival. Taken together with the results of 3 other large, nonrandomized studies of digitalis treatment after AMI, this study suggests that digitalis treatment may have adverse effects on survival during follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)
Left ventricular (LV) dysfunction, ventricular arrhythmias, and ischemic jeopardy independently determine outcome after recovery from acute myocardial infarction. Because death and reinfarction are most common early after hospital discharge, predischarge assessment of risk is optimal. Noninvasive methods can adequately detect LV dysfunction and ventricular arrhythmias, but coronary angiography is needed to assess ischemic risk in several subsets of patients. Management should be guided by the magnitude and functional nature of risk factors.
We examined the relationships among ventricular arrhythmias, left ventricular dysfunction, and mortality after the occurrence of myocardial infarction in 766 patients who enrolled in a nine-hospital study and underwent two special tests. Frequency and repetitiveness of ventricular premature depolarizations (VPDs) were determined by computer analysis of predischarge 24 hr electrocardiographic recordings. The left ventricular ejection fraction (LVEF) was determined by radionuclide ventriculography and dichotomized at its optimal value of 30%. Frequency of VPDs was divided into three categories: (1) less than one per hour, (2) one to 2.9 per hour, and (3) three or more per hour. Repetitiveness of VPDs was also divided into three categories: (1) no repetitive VPDs, (2) paired VPDs, and (3) VPD runs. These variables were related, one at a time and jointly, to total mortality and to deaths caused by arrhythmias. The hazard ratios for dying in the higher or highest risk stratum vs the lower or lowest stratum for each variable (adjusted for the effects of the others) were: LVEF below 30%, 3.5; VPD runs, 1.9; and VPD frequency of three or more per hour, 2.0. There were no significant interactions among the three variables with respect to effects on the risk of mortality. There was a suggestion of an interaction between each risk variable and time after infarction. LVEF below 30% was a better predictor of early mortality (less than 6 months) and the presence of ventricular arrhythmias was a better predictor of late mortality (after 6 months).(ABSTRACT TRUNCATED AT 250 WORDS)
There is still no consensus on which arrhythmias should be treated in the 6- to 12-month high-risk period after acute myocardial infarction. To examine this question, we analyzed 24-hour ECG recordings in 430 patients who survived for at least 2 weeks after myocardial infarction and studied these patients for at least 1 year. During the year after infarction, 63 cardiac deaths occurred. High ventricular premature depolarization (VPD) frequency increased the risk of dying; 26% of the patients had greater than or equal to 10 VPDs/hr and were 2.6 times as likely to die within a year as those with lower frequencies. Repetitive VPDs (pairs or ventricular tachycardia) also were strongly associated with mortality. Thirty-one percent had repetitive VPDs, and these patients were 3.2 times as likely to die as those who lacked this characteristic. Frequent or repetitive VPDs were strongly associated with many other important postinfarction risk factors (e.g., left ventricular dysfunction or digitalis treatment). Nevertheless, frequent or repetitive VPDs contributed significantly to death in the first year after infarction independent of other risk factors; about 90% of these arrhythmias can be controlled satisfactorily with antiarrhythmic drugs. As yet, no definitive trial has been conducted to show whether controlling frequent or repetitive VPDs will significantly reduce the mortality in the first year after infarction. The principal design features for such a trial are discussed.
This prospective study of 100 patients evaluated the sensitivity and specificity of the repetitive ventricular response and ventricular tachycardia induced by programmed electrical stimulation for identifying patients with spontaneous ventricular tachyarrhythmias. The influence of underlying heart disease on such sensitivity and specificity was also evaluated. The repetitive ventricular response was sensitive (92 percent) for detecting patients with prior spontaneous ventricular tachyarrhythmias, but lacked specificity (57 percent); the rate of false positive responses was 43 percent. Inducible ventricular tachycardia was less sensitive (65 percent) but more specific (98 percent); the rate of false positive responses was only 3 percent. Among the 100 patients, 71 had heart disease, 29 did not. The presence of underlying heart disease had no significant effect on the sensitivity and specificity of repetitive ventricular responses or ventricular tachycardia induced by programmed stimulation; it did not increase the rate of false positive responses. It is concluded that (1) ventricular tachycardia induced with programmed ventricular stimulation is an excellent basis for guiding the management of clinically significant ventricular tachyarrhythmias, regardless of underlying heart disease; and (2) the repetitive ventricular response is not useful for this purpose because of its high rate of false positive responses among patients with or without significant heart disease.
A 24 hour electrocardiographic recording was performed before hospital discharge in 430 patients who survived the cardiac care unit phase of acute myocardial infarction. Fifty patients (11.6 percent) had ventricular tachycardia, that is, three or more consecutive ventricular complexes. In 25 (50 percent) of these 50 patients, there was only one episode of ventricular tachycardia and, in 15 patients (30 percent), the longest run of ventricular tachycardia was only three consecutive ventricular premature depolarizations. The average rate of tachycardia was 119/min. Tachycardia rarely started with R on T ventricular premature complexes (4 of 1,370 episodes in 50 patients). There was no difference between the groups with and without ventricular tachycardia with respect to age and sex, but the patients with tachycardia had a significantly greater prevalence of previous myocardial infarction, left ventricular failure in the cardiac care unit, atrial fibrillation, ventricular tachycardia or ventricular fibrillation in the cardiac care unit and significantly more frequent use of digitalis and diuretic and antiarrhythmic drugs at the time of hospital discharge. The group with tachycardia had a 38.0 percent 1 year mortality rate compared with the rate of 11.6 percent in the group without tachycardia. Ventricular tachycardia had a strong association with 1 year mortality (odds ratio = 4.7). Although ventricular tachycardia had a significantly association with many other postinfarction risk factors, it was still significantly associated with the 1 year mortality (p less than 0.05) when other important risk variables were controlled statistically using a multiple logistic regression model. The 36 month cumulative mortality rate was 54.0 percent in the group with ventricular tachycardia compared with 19.4 percent in the group without tachycardia.
We enrolled 250 patients with acute myocardial infarction after they had been discharged from the cardiac intensive care unit. Among 236 patients who performed a low-level exercise test just before hospital discharge, 52 (22%) had exercise-induced ST depression of at least 0.1 mV in ECG lead V5, 102 (43%) had ventricular arrhythmias, and 121 (51%) had an exercise capacity of shorter than 6 minutes. We used multiple logistic regression analysis to investigate the association of exercise variables with 1-year cardiac mortality. Exercise duration and ventricular premature depolarizations (VPDs) were significantly associated with 1-year mortality after acute myocardial infarction, both with and without control of the influence of other exercise variables statistically; the association of exercise-induced ST depression with 1-year cardiac mortality was not statistically significant. Standardized regression coefficients showed that the variables ranked in the following order in terms of predictive value: exercise duration, VPD frequency and ST depression. Jackknife techniques showed that multiple logistic regression using the three exercise variables was highly accurate in predicting 1-year mortality.