Nicholas Twidale

Effects on Cardiac Performance of Atrioventricular Node Catheter Ablation Using Radiofrequency Current for Drug‐Refractory Atrial Arrhythmias

Patients with atrial fibrillation or atrial flutter (AF) are candidates for radiofrequency (RF) catheter ablation of the atrioventricular (AV) node with the aim being to control heart rate. As patients wilh AF can have markedly impaired ventricular function, information concerning the hemodynamic effects of AV node ablation using RF current would be valuable. Fourteen consecutive patients (mean age 65 ± 3 years) with drug‐resistant AF underwent AV node catheter ablation with RF current and had permanent pacemaker implantation. The mean left ventricular ejection fraction (FFJ by two‐dimensional echoeardiography immediately before ablation was 42 ± 3% (range 14%–54%) and their mean exercise time was 4.4 ± 0.4 minutes. Complete AV block was achieved in all 14 patients with 6 ± 2 RF applications (range 1–18). There was no evidence of any acute cardiodepressant effect associated with delivery of RF current, and EF 3 days after ablation was 44 ± 4%. By 6 weeks after ablation, the left ventricular EF was significantly improved compared to baseline (47 ± 4% postablation vs 42 ± 3% preahlation; P < 0.05), and this modest increase in EF was accompanied by an improvement in exercise time (5.4 ± 0.4 min). In conclusion, delivery of RF current for AV node catheter ablation in patients with AF and reduced ventricular function is not associated with any acute cardiodepressant effect. On the contrary, improved control of rapid heart rate following successful AV node ablation is associated with a modest and progressive improvement in cardiac performance.

Morning increase in the time of onset of sustained ventricular tachycardia

Abstract A morning increase in the occurrence of cardiac events has recently been described in patients with coronary artery disease who present with acute myocardial infarction, sudden cardiac death and unstable angina. 1 Almost all of these reports have demonstrated that these events are more likely to occur between 6 a.m. and noon than during other times of the day. Several mechanisms have been postulated to explain this phenomenon, including increased platelet aggregation, 2 elevated plasma catecholamines, 3 increased coronary artery tone 4 or other factors either acting alone or in combination. Patients with sustained ventricular tachycardia (VT) frequently have advanced structural heart disease, most often related to underlying coronary artery disease. Data from ambulatory electrocardiographic recordings of patients who have an out-of-hospital cardiac arrest without acute myocardial infarction show that the most common initial arrhythmia is monomorphic VT, which is frequently preceded by a period of acceleration of the sinus rate. 5 Therefore, we investigated if the time of onset of VT might show a similar pattern.

Predictors of outcome after radiofrequency catheter ablation of the atrioventricular node for atrial fibrillation and congestive heart failure

BACKGROUND Although radiofrequency catheter ablation of the atrioventricular (AV) node is an established treatment for atrial fibrillation (AF) with uncontrolled ventricular response, factors that predict clinical outcome in patients with associated congestive heart failure (CHF) are unknown. METHODS AND RESULTS AV node ablation and permanent pacemaker implantation was performed in 44 consecutive patients (mean age 71+/-10 years) with CHF and AF associated with uncontrolled ventricular response. Immediately before ablation, mean left ventricular ejection fraction (EF) measured by 2-dimensional echocardiogram was 34.6%+/-9.8%, mean exercise tolerance time was 2.6+/-1.8 minutes, and mean quality of life score was 62.3+/-19.7. Complete AV block was achieved in all 44 patients but was complicated by death in 1 patient from cardiogenic shock soon after ablation. By 1 month after ablation, EF increased to 43.8%+/-13.7% (P < .01), exercise tolerance time was 4.0+/-2.5 minutes (P < .01), and mean quality of life score decreased to 35.6+/-18.1 (P < .01). Improved cardiac performance (increase in EF > or = 9% over baseline EF) was detected in 20 (45%) of the patients. During a mean follow-up of 17+/-9 months, 5 patients died suddenly of presumed ventricular tachyarrhythmia and 4 others died of progressive CHF. Multivariate Cox survival analysis identified baseline EF < or = 30%, presence of significant mitral regurgitation (>2+) before ablation, and failure to exhibit improved cardiac performance by 1 month after ablation as the only independent predictors of death. CONCLUSIONS Baseline variables and failure of EF to improve soon after AV node ablation identifies patients with CHF and AF who have a high mortality rate. Adjunctive therapy to reduce sudden death and progressive heart failure should be evaluated in this subgroup.

Late potentials are unaffected by radiofrequency catheter ablation in patients with ventricular tachycardia.

Reentrant ventricular tachycardia is dependent on an area of myofibers, embedded in scar tissue, which exhibit slow conduction. Late potentials recorded by signal‐averaged electrocardiography appear to correspond to these zones of slow conduction and frequently are present in patients with VT. We hypothesized that elimination of inducible VT by catheter‐mediated ablation of critical areas of slow conduction would alter late potentials. Four patients underwent catheter ablation in which radiofrequency current was delivered to zones of slow conduction exhibiting isolated mid‐diastolic potentials that could not be dissociated from the tachycardia. The four patients had developed VT (cycle length 382 ± 50 msec; mean ± SEM) 13–180 months after inferior myocardial infarction. Late potentials were present in each patient before catheter ablation was attempted. Although VT was not inducible in any patient immediately after ablation, late potentials were still present in all four patients and there was no significant difference in the QRS duration (136.5 ± 4.0 msec postablation; 135.7 ± 4.5 msec preablation), root mean square voltage in the terminal 40 msec of the QRS (10.0 ± 1.0 μV postablation; 5.9 ± 0.4 μV preablation). or in the duration of the low amplitude signal (69.2 ± 2.0 msec postablation; 62.7 ± 3.4 msec preablation). At follow‐up electrophysiology study performed 14 ± 7 days after ablation, one of the four patients had inducible VT. In conclusion, late potentials persist even after successful radiofrequency catheter ablation and do not appear to be useful for predicting results of follow‐up electrophysiology study.

Comparative hemodynamic effects of amiodarone, sotalol, and d-sotalol

The effects of intravenous boluses of amiodarone (5 mg/kg), racemic sotalol (enantiomeric ratio d/l-sotalol 1:1;1.5 mg/kg), and d-sotalol (0.75 mg/kg) on mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), total peripheral resistance (TPR), left ventricular end-diastolic pressure (LVEDP), and peak rate of change of left ventricular pressure (LV dp/dt) were assessed in conscious rabbits. Amiodarone and sotalol had a modest negative inotropic effect: amiodarone reduced peak LV dp/dt by 8 +/ 2% (mean +/- SEM) (p < 0.05) and sotalol by 6 +/- 2% (p < 0.05). These two drugs had quite different effects on CO as a result of differences in their actions on peripheral blood vessels: amiodarone caused a 13 +/- 3% (p < 0.05) increase in CO associated with a substantial vasodilatory effect (TPR reduced 25 +/- 3%; p < 0.01); sotalol did not produce any substantial change in either CO or TPR. Bolus intravenous injection of amiodarone was associated with a significant increase in HR (12 +/- 3%; p < 0.01), whereas sotalol reduced HR by 7 +/- 1% (p < 0.05). In contrast, administration of the dextro-rotatory optical isomer, d-sotalol, produced no significant change in peak LV dp/dt, LVEDP, CO, TPR, or HR. These results confirm that amiodarone and racemic sotalol have a comparatively weak cardiodepressant action. The experiments also show that the reduction in cardiac performance associated with racemic sotalol is mediated predominantly through the beta-adrenoreceptor blocking action of the levo-rotatory isomer (l-sotalol) rather than any substantial cardiodepressant effect of the dextro-rotatory isomer.

Plasma atrial natriuretic polypeptide concentrations during and after reversion of paroxysmal supraventricular tachycardias.

Plasma concentrations of immunoreactive atrial natriuretic polypeptide were raised in 22 of 23 patients with paroxysmal supraventricular tachycardia and in all seven patients with atrial flutter. Plasma concentrations of atrial natriuretic polypeptide rose soon after the onset of supraventricular tachycardia. A sample taken 30 minutes after reversion to sinus rhythm (pharmacological or non-pharmacological) showed a significant fall in 19 of the 23 patients with paroxysmal supraventricular tachycardia and all seven patients with atrial flutter. Because atrial natriuretic polypeptide has powerful natriuretic and diuretic properties, an increase may contribute considerably to the polyuria that is often associated with episodes of supraventricular tachycardia.

Atrial natriuretic factor release during rapid ventricular pacing: Interplay between autonomic and hemodynamic stimulants

Plasma levels of atrial natriuretic factor (ANF) and norepinephrine are markedly elevated during episodes of ventricular tachycardia. Although atrial distention appears to be the major stimulus for ANF release, reflex changes in autonomic tone might also contribute. Plasma ANF and norepinephrine levels, sinus node cycle length, systolic blood pressure, and mean right atrial pressure were therefore assessed during rapid right ventricular pacing at 150 beats/min for 10 minutes. In five patients (group 1) observations were made without autonomic blockade, and another five patients (group 2) had ventricular pacing after cardiac autonomic blockade. In group 1 systolic blood pressure fell during ventricular pacing from 122 +/- 4 to 105 +/- 5 mm Hg (p < 0.02), norepinephrine levels increased from 195 +/- 26 to 411 +/- 71 pg/ml (p < 0.02), and sinus node cycle length decreased from 936 +/- 99 to 688 +/- 58 msec (p < 0.02). Right atrial pressure was elevated from 2.6 +/- 0.6 to 7.4 +/- 0.6 mm Hg (p < 0.02), and ANF levels increased from 161 +/- 23 to 240 +/- 26 pg/ml (p < 0.05). Whereas systolic blood pressure, norepinephrine, sinus cycle length, and right atrial pressure returned promptly to baseline levels when ventricular pacing was stopped, ANF levels continued to rise (296 +/- 37 pg/ml; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Ventricular Standstill Complicating Cardiac Catheterization

A patient is described in this paper who developed repeated episodes of venfricular stcindstill during left heart catheterization. The patient had a resting pattern of right bundle branch block with left anterior fascicular block; subsequent electrophysiology study was normal. Ventricular standstill during catheterization was apparentiy due to catheter‐related trauma of His bundle connections.

Concentrations of plasma atrial natriuretic factor during and after reversion of ventricular tachycardia.

Plasma concentrations of immunoreactive atrial natriuretic factor were considerably increased (mean 745 (376) pg/ml) in 15 patients during spontaneous ventricular tachycardia. There was no significant relation, however, between concentrations of plasma atrial natriuretic factor and systolic arterial blood pressure during tachycardia. Samples taken 30 minutes and 24 hours after reversion of ventricular tachycardia to sinus rhythm showed that, although plasma concentrations of atrial natriuretic factor had fallen significantly, they were still raised after 24 hours. Raised concentrations of atrial natriuretic factor during ventricular tachycardia did not seem to contribute significantly to the hypotension that is often associated with the arrhythmia.

Echocardiographic study of U wave inversion in the electrocardiograms of hypertensive patients

The prevalence of U wave inversion was evaluated in 58 adult patients with hypertension, and a possible mechanism for it was examined using M-mode echocardiographic indices. U wave inversion was the most common electrocardiographic abnormality, occurring in 34% of patients; voltage criteria for left ventricular hypertrophy were present in only 14% of patients, and ventricular strain pattern was not detected in any patient. Nonetheless, on echocardiography left ventricular posterior wall thickness was increased in 58% of patients. However, neither U wave inversion nor conventional voltage criteria for left ventricular hypertrophy was strongly predictive for this finding. The authors conclude that U wave inversion is a frequent finding in patients with hypertension, often occurring alone. Although it does not appear to be closely linked to the presence of left ventricular hypertrophy, it may relate to other, perhaps subtle, abnormalities of diastolic ventricular relaxation.