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J T Bigger

Publications and source records attributed to J T Bigger.

At least 19 recordsLinked to original sources
PubMed1995

Computer-assisted mapping of infarcted and viable regions of gross cardiac sections following experimental myocardial infarction.

We have developed a computer-assisted method that creates digital maps of the viable and infarcted regions of tetrazolium-stained gross cardiac sections. Here we describe and test the method, using a canine occlusion-reperfusion infarction model. Quantitative image analysis showed that the method accurately recorded differences between infarcted and viable regions at a spatial resolution of 5-20 pixels per mm2. Microscopic analysis of tissue samples taken from the sections showed that the maps were accurate. In 15 of 15 cases the histology of the samples matched that predicted by the maps. A comparison of infarct area measurements derived from the maps showed that the method was reproducible. The average intraoperator standard deviation was +/- 8% of a slice's infarcted area and the average interoperator standard deviation was +/- 20%. We conclude that the method creates accurate, detailed, and reproducible maps of the infarcted and viable regions of tetrazolium-stained cardiac sections.

Animals↗
PubMed1995

Temporal stability of heart period variability during a resting baseline and in response to psychological challenge.

Central to the psychophysiologic reactivity hypothesis of the etiology of coronary artery disease is the assumption that reactivity is an individual characteristic that is stable over time. Although heart rate (HR) and blood pressure reactivity appear to meet this criterion, temporal stability of cardiac autonomic control as measured by analysis of heart period variability (HPV) has not been assessed. In this study, we tested the stability of HPV, measured in both the time and frequency domain, during a quiet, resting baseline and in response to 5-min mental arithmetic and reaction time tasks, in 20 normal subjects measured in three testing sessions during a 9-month period. Stability, assessed by the intraclass correlation coefficient (ICC), was excellent for resting baseline measures of HR and HPV, with ICCs of 0.68-0.86. However, HR and HPV reactivity to either arithmetic or reaction time tasks generally was less stable, with ICCs of 0.17-0.73, in contrast to results of previous studies demonstrating long-term stability of HR responses to psychological challenge. Stability of aggregated reactivity scores was only slightly improved. Whether for individual tasks or aggregated measures, reactivity of total and low-frequency measures of HPV was moderately stable but stability of high-frequency HPV reactivity was poor.

Adult↗
PubMed1994

Predicting mortality after myocardial infarction from the response of RR variability to antiarrhythmic drug therapy.

OBJECTIVES: This study was designed to test the hypothesis that antiarrhythmic drugs that decrease RR variability will predict all-cause mortality during follow-up after myocardial infarction. BACKGROUND: RR variability, a noninvasive indicator of autonomic nervous system activity, predicts death after acute myocardial infarction independently of other risk predictors and changes substantially in response to some drugs. A previous study in patients with chronic heart disease and frequent ventricular premature complexes reported that flecainide decreased vagal modulation of RR intervals but amiodarone did not. The investigators of that study speculated that changes in RR variability during antiarrhythmic drug therapy predict an increased mortality rate during long-term drug treatment. To explore this hypothesis further, we compared the effects of encainide and flecainide, which increase long-term mortality substantially, on RR variability with the effects of placebo and moricizine, which have no significant effect on mortality during long-term treatment of unsustained ventricular arrhythmias after myocardial infarction. METHODS: The 24-h power spectral density was computed from the baseline electrocardiographic recordings and drug evaluation tapes, and six frequency domain measures of RR variability were calculated: ultra-low frequency (< 0.0033 Hz), very low frequency (0.0033 to < 0.04 Hz), low frequency (0.04 to < 0.15 Hz) and high frequency power (0.15 to < 0.40 Hz), plus total power (< 0.40 Hz) and the ratio of low to high frequency power. Changes in power spectral measures were related to drug treatment and to mortality. RESULTS: In the placebo group, values for RR interval and RR variability increased because of recovery from the effects of acute myocardial infarction. Contrasting placebo treatment with all three active antiarrhythmic drug treatments taken together showed that of all the measures of RR variability, only NN50, pNN50 and low frequency power changed significantly during drug treatment (Bonferroni adjusted p value < 0.025); these variables all decreased during drug therapy. Contrasting encainide and flecainide with moricizine, we found that the encainide and flecainide groups taken together showed a larger decrease in dLF than moricizine, but the difference was of borderline significance (Bonferroni adjusted p value < 0.08). Survival was significantly worse in the groups treated with encainide and flecainide than in the groups treated with placebo or moricizine (relative risk > 2.0, adjusted p < 0.05). The antiarrhythmic drug-induced change in measures of RR variability was not a significant predictor of all-cause mortality during a year of follow-up after myocardial infarction. CONCLUSIONS: Encainide, flecainide and moricizine all caused a decrease in RR variability in patients studied approximately 1 month after acute myocardial infarction. Encainide and flecainide caused a significant increase in mortality rates; placebo and moricizine did not. Baseline measurements of RR variability also predicted all-cause mortality after myocardial infarction. The decrease in RR variability produced by the three antiarrhythmic drugs did not predict mortality during follow-up.

Anti-Arrhythmia Agents↗
PubMed1992

Correlations among time and frequency domain measures of heart period variability two weeks after acute myocardial infarction.

Seven hundred fifteen participants from a multicenter natural history study of acute myocardial infarction were studied (1) to determine the correlations among time and frequency domain measures of heart period variability, (2) to determine the correlations between the measures of heart period variability and previously established post-infarction risk predictors, and (3) to determine the predictive value of time domain measures of heart period variability for death during follow-up after acute myocardial infarction. Twenty-four hour electrocardiographic recordings obtained 11 +/- 3 days after acute myocardial infarction were analyzed and 11 measures of heart period variability were computed. Each of 4 bands in the heart period power spectrum had 1 or 2 corresponding variables in the time domain that correlated with it so strongly (r greater than or equal to 0.90) that the variables were essentially equivalent: ultra low frequency power with SDNN* and SDANN index,* very low frequency power and low-frequency power with SDNN index,* and high-frequency power with r-MSSD* and pNN50.* As expected from theoretical considerations, SDNN and the square root of total power were almost perfectly correlated. Correlations between the time and frequency domain measures of heart period variability and previously identified postinfarction risk predictors, e.g., left ventricular ejection fraction and ventricular arrhythmias, are remarkably weak. Time domain measures of heart period variability, especially those that measure ultra low or low-frequency power, are strongly and independently associated with death during follow-up. * Defined in Table II.

Electrocardiography, Ambulatory↗
PubMed1992

Stability over time of heart period variability in patients with previous myocardial infarction and ventricular arrhythmias. The CAPS and ESVEM investigators.

To determine the reproducibility of frequency domain measures of heart period variability in patients with previous myocardial infarction, 2 random samples of 40 patients each (1 from the Cardiac Arrhythmia Pilot Study [CAPS] [unsustained ventricular arrhythmias], and 1 from the Electrophysiologic Studies Versus Electrocardiographic Monitoring [ESVEM] [sustained ventricular arrhythmias] trial) were studied. For each patient, two 24-hour continuous electrocardiographic recordings were analyzed, and the average normal RR interval, total power and 4 components of total power were calculated. Group means and standard deviations for each sample were virtually identical for the pairs of 24-hour recordings. Furthermore, measurements for individual patients were stable from day to day, as measured by the intraclass correlation coefficients and the standard errors of measurement. Reproducibility of heart period variability measurements is excellent in patients with previous myocardial infarction and ventricular arrhythmias, and is comparable to the high stability previously found in a small group of normal subjects. The stability of measures of heart period variability facilitates distinguishing real changes due to progression or regression of cardiac disease or to drug effects from apparent changes due to random variation.

Adult↗
PubMed1992

The correlation between heart period variability and mean period length.

Heart rate variability and heart period variability are important indicators of the functioning of the autonomic nervous system and are strong predictors of survival after myocardial infarction. The standard deviation of a patient's series of normal heart periods (consecutive normal RR intervals) is positively and, in some populations, strongly correlated with the mean period length. This phenomenon has led some investigators to use the coefficient of variation as their measure of variability, because it correlates less strongly with the mean period length. Using data from a multicentre post-infarction natural history study, we show that the standard deviation of the instantaneous heart rates has, like the coefficient of variation, only a modest correlation with the mean period length. Unlike the coefficient of variation, however, this standard deviation is derivable from established statistical principles. We show further that the coefficient of variation, the standard deviation of heart rates, and the standard deviation of heart periods are approximately equally strong predictors of survival after myocardial infarction.

Aged↗
PubMed1992

Predicting arrhythmic events after acute myocardial infarction using the signal-averaged electrocardiogram.

To determine if the signal-averaged (SA) electrocardiogram (ECG) predicts the occurrence of sustained ventricular arrhythmia and sudden death after acute myocardial infarction, 182 consecutive patients underwent systematic noninvasive testing, including the SAECG. Seventy-one patients (39%) had an abnormal SAECG. The presence of an abnormal SAECG was not related to underlying left ventricular dysfunction or any other clinical or measured variable. There were 16 end points (sustained ventricular arrhythmia or sudden cardiac death) during 14-month follow-up. The SAECG was a significant predictor of these events (p less than 0.02), and an abnormal SAECG conferred a 2.7-fold increase in risk. The risk associated with an abnormal SAECG was independent of both left ventricular function and ventricular arrhythmia on Holter ECG. The SAECG had excellent negative predictive accuracy (95%), but the positive predictive accuracy was low (15%). When the results of the SAECG were combined with the results of the Holter ECG, a group of very high-risk patients was identified; at 18 months, the presence of abnormal SAECG and Holter ECG was associated with a risk of 26% compared with only 4% if both tests were normal. Furthermore, all published studies with a similar design were pooled for meta-analysis. The meta-analysis revealed a sixfold increase in risk, independent of left ventricular function, and an eightfold increase in risk, independent of Holter results when the SAECG was abnormal. The SAECG is a noninvasive test that can rapidly and easily provide potent prognostic information regarding the risk of sustained ventricular arrhythmias for patients after myocardial infarction.

Aged↗
PubMed1992

Methods of implantable cardioverter-defibrillator-pacemaker insertion to avoid interactions.

Experience with combined transvenous pacemaker and implantable cardioverter-defibrillator insertion in 21 patients is described. Special techniques are needed to avoid potentially lethal pacemaker-implantable cardioverter-defibrillator interaction. Separation between leads for the two devices should be maximized. The electrophysiologic criteria for successful device function can be met, even when some leads for both devices must be placed by a transvenous approach.

Arrhythmias, Cardiac↗
PubMed1992

Enrollment in clinical trials: institutional factors affecting enrollment in the cardiac arrhythmia suppression trial (CAST).

Recruitment and Enrollment Assessment in Clinical Trials (REACT), an NHLBI-sponsored substudy of the Cardiac Arrhythmia Suppression Trial (CAST), was conducted to assess factors associated with enrollment in clinical trials. We report on the relationships of institutional factors at CAST sites to patient enrollment. The proportion of CAST-eligible patients enrolling at each CAST site during the REACT study period was defined as the number of subjects enrolled divided by the sum of (1) the number enrolled plus (2) the number of eligibles who refused plus (3) the number of eligibles whose physicians refused to permit CAST personnel to attempt to enroll them. A questionnaire that included 78 questions regarding factors hypothesized to be associated with enrollment was completed between August 1988 and February 1990 by the nurse coordinators at all 112 CAST sites in the United States and Canada. Sixteen items were unanalyzable, and 37 of the remaining 62 were grouped into seven scales. The remaining items were analyzed individually. Enrollment proportions varied widely across the 112 CAST sites (mean 32.7% SD 22.6). Five variables or scales were included in the final multiple regression model (multiple R2 = .39). The most important of these was the proportion of eligible patients at a site cared for by medical staff other than private attending physicians (multiple R2 for this variable alone, .26). This proportion tended to be high in teaching hospitals. Other variables in this model that were associated with higher enrollment proportions included the number of days per week a nurse coordinator was present at the site, the number of nurse coordinator full-time equivalents at the site, fewer other clinical trials for which the nurse coordinator was responsible, and fewer perceived obstacles to enrollment. These findings indicate that enrollment was more successful at hospitals with higher proportions of eligible subjects cared for by fellows, housestaff, and service attending physicians and at institutions with the committed presence of a nurse-coordinator.

Arrhythmias, Cardiac↗
PubMed1992

Comparison of 24-hour parasympathetic activity in endurance-trained and untrained young men.

OBJECTIVES: This study compares 24-h parasympathetic activity in aerobically trained and untrained healthy young men. BACKGROUND: Higher values of parasympathetic nervous system activity are associated with a low mortality rate in patients after myocardial infarction, but it remains uncertain what therapeutic interventions can be used to increase parasympathetic activity. Although it is thought that exercise training can increase parasympathetic activity, studies have reported conflicting results, perhaps because this variable was measured for only brief intervals and usually inferred from changes in reflex responses induced by pharmacologic blockade. METHODS: Parasympathetic activity was assessed noninvasively from 24-h ECG recordings by calculating high frequency (0.15 to 0.40 Hz) beat to beat heart period variability in eight endurance-trained men (maximal oxygen consumption greater than or equal to 55 ml/kg per min) and eight age-matched (mean = 29 yr) untrained men (maximal oxygen consumption less than or equal to 40 ml/kg per min). The data were analyzed separately for sleeping hours when parasympathetic activity is dominant and also for waking hours. RESULTS: The geometric mean of high frequency power was greater in the trained than in the untrained men during the day (852 vs. 177 ms2, p less than 0.005), during the night (1,874 vs. 427 ms2, p less than 0.005) and over the entire 24 h (1,165 vs. 276 ms2, p less than 0.001). CONCLUSIONS: Parasympathetic activity is substantially greater in trained than in untrained men, and this effect is present during both waking and sleeping hours. These data suggest that exercise training may increase parasympathetic activity over the entire day and may therefore prove to be a useful adjunct or alternative to drug therapy in lessening the derangements of autonomic balance found in many cardiovascular diseases.

Adult↗
PubMed1992

Prognostic significance of ventricular premature depolarizations measured 1 year after myocardial infarction in patients with early postinfarction asymptomatic ventricular arrhythmia.

OBJECTIVES: The objective of this study was to examine the relation between death and the frequency of premature ventricular depolarizations measured approximately 1 year after myocardial infarction. BACKGROUND: The reported association between premature ventricular depolarizations and death in the weeks after myocardial infarction is in part the basis for the use of antiarrhythmic drugs. Such an association has not been reported on for observations obtained at a much greater interval after myocardial infarction. METHODS: We examined the association between mortality and premature ventricular depolarization rates measured 1 year after myocardial infarction in patients with asymptomatic ventricular arrhythmia early (between 6 and 90 days, median 28) after infarction, as measured by 24-h ambulatory electrocardiographic recording. The study group consisted of 502 patients enrolled in the Cardiac Arrhythmia Pilot Study during 1983 to 1985. They were followed up during the course of the study and subsequently by a National Death Index search (average follow-up interval 1,080 days). RESULTS: Death was recorded for 87 patients through 1987. Because patients were admitted to the Cardiac Arrhythmia Pilot Study only if they had greater than or equal to 10 ventricular premature depolarizations/h, the arrhythmia rate measured at baseline (that is, early after infarction) was not expected to, and did not, predict mortality. In 360 patients ventricular premature depolarization rates were measured approximately 1 year from their index myocardial infarction while they were not receiving antiarrhythmic therapy. In these patients, who had survived 1 year after the index infarction, the rate of ventricular premature depolarizations/h measured 1 year after infarction was highly predictive of subsequent death (p less than 0.001). Recent heart failure and a history of diabetes mellitus were also strongly predictive of death. CONCLUSION: The prognostic value of ventricular premature depolarizations observed 1 year after a myocardial infarction may be significant even in a sample selected for frequent ventricular premature depolarizations observed early after the event.

Arrhythmias, Cardiac↗
PubMed1992

Proarrhythmic effects of procainamide and tocainide in a canine infarction model.

A canine model of myocardial infarction (MI) was used to study the type and frequency of ventricular antiarrhythmic and proarrhythmic effects due to procainamide and tocainide and the risk factors associated with development of proarrhythmia. An anterior MI was created by a 2-h occlusion of the left anterior descending artery (LAD) with complete reperfusion. Programmed ventricular stimulation was performed on two occasions after MI, on days 4-6 and on days 8-10, before drug and during antiarrhythmic drug infusion at three dose levels. The antiarrhythmic drugs were given in a randomized cross-over design. Only procainamide caused a dose-dependent increase in QRS, JTc, and right ventricular effective refractory period (ERP). Neither procainamide nor tocainide made sustained ventricular tachycardia (VT) noninducible, but procainamide slowed the tachycardia rate. Both drugs successfully made ventricular fibrillation (VF) noninducible: procainamide in 78% of trials and tocainide in 50% of trials. Proarrhythmia (development of inducible VT during drug when not present before drug or inability to terminate VT during drug administration) developed in 29% of dogs that received procainamide and 25% of dogs that received tocainide. There was no apparent correlation of QRS, JTc, and right ventricular ERP after drugs and proarrhythmia due to procainamide or tocainide. There was no significant difference in the size of MI between dogs with one or more proarrhythmic response to either drug and dogs that had no proarrhythmia. In this model, procainamide and tocainide had no antiarrhythmic efficacy for VT, but had moderate proarrhythmia potential that was unpredictable.

Animals↗
PubMed1992

Frequency domain measures of heart period variability and mortality after myocardial infarction.

BACKGROUND: We studied 715 patients 2 weeks after myocardial infarction to establish the associations between six frequency domain measures of heart period variability (HPV) and mortality during 4 years of follow-up. METHODS AND RESULTS: Each measure of HPV had a significant and at least moderately strong univariate association with all-cause mortality, cardiac death, and arrhythmic death. Power in the lower-frequency bands--ultra low frequency (ULF) and very low frequency (VLF) power--had stronger associations with all three mortality end points than power in the higher-frequency bands--low frequency (LF) and high frequency (HF) power. The 24-hour total power also had a significant and strong association with all three mortality end points. VLF power was the only variable that was more strongly associated with arrhythmic death than with cardiac death or all-cause mortality. In multivariate Cox regression models using a step-up approach to evaluate the independent associations between frequency domain measures of heart period variability and death of all causes, ULF power was selected first (i.e., was the single component with the strongest association). Adding VLF or LF power to the Cox regression model significantly improved the prediction of outcome. With both ULF and VLF power in the Cox regression model, the addition of the other two components, LF and HF power, singly or together, did not significantly improve the prediction of all-cause mortality. We explored the relation between the heart period variability measures and all-cause mortality, cardiac death, and arrhythmic death before and after adjusting for five previously established postinfarction risk predictors: age, New York Heart Association functional class, rales in the coronary care unit, left ventricular ejection fraction, and ventricular arrhythmias detected in a 24-hour Holter ECG recording. CONCLUSIONS: After adjustment for the five risk predictors, the association between mortality and total, ULF, and VLF power remained significant and strong, whereas LF and HF power were only moderately strongly associated with mortality. The tendency for VLF power to be more strongly associated with arrhythmic death than with all-cause or cardiac death was still evident after adjusting for the five covariates. Adding measures of HPV to previously known predictors of risk after myocardial infarction identifies small subgroups with a 2.5-year mortality risk of approximately 50%.

Aged↗
PubMed1992

The implantable defibrillator: an electronic bridge to cardiac transplantation.

BACKGROUND: Sudden cardiac death (SCD) is common among patients awaiting heart transplantation. Medical management of SCD may fail due to lack of efficacy or adverse side effects. The implantable cardioverter-defibrillator (ICD) may extend patient survival until a donor heart is available. METHODS AND RESULTS: We reviewed 16 patients listed for transplantation between November 1988 and October 1991 who underwent ICD implantation for ventricular arrhythmias refractory to medical management. Mean age was 51.4 +/- 11.4 years (range, 19-66 years), mean ejection fraction was 15.4 +/- 3.0% (range, 10-21%), and underlying cardiomyopathy was ischemic (12 patients), valvular (one patient), or dilated (three patients). There was no mortality from ICD insertion. Fourteen patients were discharged before transplantation, and two patients remained in the hospital until transplantation. Twelve patients underwent transplantation after a mean of 155.7 +/- 113.7 days (range, 3-319) on the transplant list. The ICD delivered shocks for tachyarrhythmia associated with near syncope in 15 of 16 patients. ICD shocks numbered > 10 in five patients, 5-9 in three patients, and 1-4 in seven patients. There was no morbidity or mortality attributed to patch electrode removal. CONCLUSIONS: We conclude that the ICD can be implanted with minimal morbidity in transplant candidates, allowing the patients to be ambulatory and to leave the hospital while awaiting heart transplantation. In patients at risk of SCD, the ICD is an effective electronic bridge to transplantation.

Anti-Arrhythmia Agents↗
PubMed1991

Stability over time of variables measuring heart rate variability in normal subjects.

Both time and frequency domain measures of heart rate (HR) variability have been used to assess autonomic tone in a variety of clinical conditions. Few studies in normal subjects have been performed to determine the stability of HR variability over time, or the correlation between and within time and frequency domain measures of HR variability. Fourteen normal subjects aged 20 to 55 years were studied with baseline and placebo 24-hour ambulatory electrocardiograms performed 3 to 65 days apart to assess the reproducibility of the following time domain measures of cycle length variability: the standard deviation of all normal cycle intervals; mean normal cycle interval; mean day normal cycle interval; night/day difference in mean normal cycle interval; root-mean-square successive cycle interval difference; percentage of differences between adjacent normal cycle length intervals that are greater than 50 ms computed over the entire 24-hour electrocardiographic recording (proportion of adjacent intervals greater than 50 ms); and the frequency domain measures of high (0.15 to 40 Hz), low (0.003 to 0.15) and total (0.003 to 0.40) power. The mean and standard deviations of these measures were virtually identical between placebo and baseline measurements and within the studied time range. Variables strongly dependent on vagal tone (high-frequency, low-frequency and total power, root-mean-square successive difference, and percentage of differences between adjacent normal cycle intervals greater than 50 ms computed over the entire 24-hour electrocardiographic recording) were highly correlated (r greater than 0.8). It is concluded that measures of HR variability are stable over short periods of time.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Time course of recovery of heart period variability after myocardial infarction.

Four components of the heart period power spectrum--ultra low frequency (less than 0.0033 Hz), very low frequency (0.0033 to less than 0.04 Hz), low frequency (0.04 to less than 0.15 Hz) and high frequency power (0.15 to 0.40 Hz)--plus total power (1.157 x 10(-5) to 0.4 Hz for a 24-h electrocardiographic [ECG] recording) all predict mortality after myocardial infarction. To determine the time course and magnitude of recovery for these measures of heart period variability, 68 patients in the Cardiac Arrhythmia Pilot Study (CAPS) placebo group who had 24-h ECG recordings at baseline, 3, 6 and 12 months after myocardial infarction were studied. The 24-h power spectral density was computed with use of fast Fourier transforms and divided into the four components listed previously. The values for the five frequency domain measures of heart period variability in the CAPS patients were similar to those found in 715 patients who participated in the Multicenter Post Infarction Program (MPIP), indicating that the CAPS sample is generally representative of postinfarction patients with respect to these measures. The values for the five measures were one third to one half of those found in 95 normal persons of similar age and gender. There was a substantial increase in all measures of heart period variability between the baseline 24-h ECG recording and the 3-month recording (p less than 0.001). Between 3 and 12 months, the values were quite stable for the group as a whole, as well as for individual patients (intraclass correlation coefficients greater than or equal to 0.66).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Effect of atenolol and diltiazem on heart period variability in normal persons.

Several time and frequency domain measures of heart period variability are reduced 1 to 2 weeks after myocardial infarction, and a reduced standard deviation of normal RR intervals over a 24 h period (SDNN) is associated with increased mortality. The predictive accuracy of heart period variability may be reduced by drugs used to treat patients after myocardial infarction. Accordingly, a randomized, three period, placebo-controlled, crossover (Latin square) design was used to determine the effect of atenolol and diltiazem on time and frequency measures of heart period variability calculated from 24 h continuous electrocardiographic recordings during treatment with atenolol, diltiazem and placebo in 18 normal volunteers. During atenolol treatment, the 24 h average normal RR (NN) interval increased 24% (p less than 0.001). The three measures of tonic vagal activity were significantly increased (p less than 0.001) during atenolol treatment: percent of successive normal RR intervals greater than 50 ms = 69%, root mean square successive difference of normal RR intervals = 61% and high frequency power in the heart period power spectrum = 84%. Low frequency power also increased 45% (p less than 0.01), indicating that this variable also is an indicator of tonic vagal activity over 24 h. Diltiazem had no significant effect on the 24 h average NN interval or on any measure of heart period variability. The decreased mortality rate after myocardial infarction associated with beta-adrenergic blocker but not calcium channel blocker therapy may be attributed in part to an increase in vagal tone caused by beta-blockers.

Adult↗