Is hospital admission for initiation of antiarrhythmic therapy with sotalol for atrial arrhythmias required? Yield of in-hospital monitoring and prediction of risk for significant arrhythmia complications.

OBJECTIVES: We sought to determine the yield of in-hospital monitoring for detection of significant arrhythmia complications in patients starting sotalol therapy for atrial arrhythmias and to identify factors that might predict safe outpatient initiation. BACKGROUND: The need for hospital admission during initiation of antiarrhythmic therapy has been questioned, particularly for sotalol, with which proarrhythmia may be dose related. METHODS: The records of 120 patients admitted to the hospital for initiation of sotalol therapy were retrospectively reviewed to determine the incidence of significant arrhythmia complications, defined as new or increased ventricular arrhythmias, significant bradycardia or excessive corrected QT (QTc) interval prolongation. RESULTS: Twenty-five patients (20.8%) experienced 35 complications, triggering therapy changes during the hospital period in 21 (17.5%). New or increased ventricular arrhythmias developed in 7 patients (5.8%) (torsade de pointes in 2), significant bradycardia in 20 (16.7%) (rate <40 beats/min in 13, pause >3.0 s in 4, third-degree atrioventricular block in 1, permanent pacemaker implantation in 3) and excessively prolonged QTc intervals in 8 (6.7%) (dosage reduced or discontinued in 6). Time to the earliest detection of complications was 2.1 +/- 2.5 (mean +/- SD) days after initiation of sotalol, with 22 of 25 patients meeting criteria for complications within 3 days of monitoring. Baseline electrocardiographic intervals or absence of heart disease failed to distinguish a low risk group. Multivariate analysis identified absence of a pacemaker as the only significant predictor of arrhythmia complications (p = 0.022). CONCLUSIONS: Because clinically significant complications can be detected with in-hospital monitoring in one of five patients starting sotalol therapy, hospital admission is warranted for initiation of sotalol. Patients without pacemakers are at higher risk for these complications.

Paradoxical failure of QT prolongation during cardioinhibitory neurocardiogenic syncope.

QT modulation was explored in 31 patients with cardioinhibitory neurocardiogenic syncope. Despite a marked in increase in RR intervals, the QT interval remained stable.

The role of pacing for the management of neurally mediated syncope: carotid sinus syndrome and vasovagal syncope.

The role of permanent cardiac pacing for the management of neurocardiogenic syncope is controversial; however, it does have a secondary role in appropriately selected individuals. Neurocardiogenic syncope includes vaso-vagal and enhanced antagonism of sympathetic-parasympathetic mechanisms. Differentiation of the so-called cardiac inhibitory, vasodepressor, and mixed forms of these disorders is frequently misleading when establishment of effective treatment strategies is attempted. Cardiac pacing can artificially restore near-normal heart rate and atrioventricular synchrony during a neurocardiogenic syncopal episode; however, cardiac pacing does not alter the peripheral vasodilatation, nor does it prevent the occurrence of the reflux response. Syncopal patients with carotid sinus hypersensitivity or vasovagal responses that include marked bradycardia and loss of atrioventricular synchrony can be supported by dual-chamber cardiac pacing in combination with other therapeutic interventions that diminish the severity of the reflex response. The conditions of patients with carotid sinus syndrome and carotid sinus hypersensitivity are frequently improved with cardiac pacing, and the conditions of elderly patients with vasovagal syncope are commonly improved with artificial pacing. The classic younger patient with malignant vasovagal syncope derives less benefit from artificial pacing; however, in carefully selected persons dual-chamber pacing combined with drug therapy and education decreases syncopal episodes and permits a return to normal activities.

Is absolute hypovolemia a risk factor for vasovagal response to head-up tilt?

To test the hypothesis that hypovolemia is associated with an increased incidence of vasovagal syncope during head-up tilt (HUT) 45 patients with history of syncope or presyncope were studied. Blood volume (radio-iodinated serum albumin) was determined, then subjects underwent a graded HUT (from 15 degrees-60 degrees HUT) with cuff blood pressure and ECG monitoring. All patients were kept on their own medications during evaluation. Thirty patients (12 male, 18 female, mean age 50 +/- 19 [SD] years) had hypovolemia, defined as blood volume < 90% of lab normal for corresponding sex, while 15 patients (7 male, 8 female, mean age 52 +/- 21 years) were normovolemic with blood volume ranging from 91%-110% of sex-matched normal subjects. The normovolemic patients served as controls. During HUT, a vasovagal response was elicited in 5 of the 30 hypovolemics and in 4 of the 15 normovolemic (16.7% and 26.7%, respectively, P = NS). In those who developed vasovagal response, the changes of heart rate and blood pressure during HUT were not significantly different between hypovolemics and normovolemics, neither at the endpoint (vasovagal response) nor immediately before the development of the vasovagal response. In patients with nonvasovagal events, four types of hemodynamic responses to tilt were observed: normal blood pressure response associated with normal heart rate increase, normal blood pressure response in association with accentuated increase in heart rate, orthostatic hypotension with normal acceleration of heart rate, and orthostatic hypotension with accelerated increase in heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Incidence and predictors of syncope in paced patients with sick sinus syndrome.

UNLABELLED: In spite of a normal pacemaker function, syncope still occurs in some patients with sick sinus syndrome (SSS). Causes often remain unknown. To identify predictors and etiologies of this bothersome symptom, we studied 507 patients who received atrial, ventricular, and dual-chamber pacemakers for SSS. During a mean follow-up of 62 +/- 38 months, actuarial incidence of syncope was 3% at 1 year, 8% at 5 years, and 13% at 10 years. Causes were vasovagal (18%), orthostatic hypotension (25.5%), rapid atrial tachyarrhythmias (11.5%), ventricular tachycardia (5%), acute myocardial ischemia (2.5%), and pacemaker/lead malfunction (6.5%). In 13 patients (29.5%), syncope remained unexplained. The only preimplant predictor for syncope was syncope as primary indication for pacemaker implant. Electrocardiographic correlation with bradycardia was not a predictor of relief of syncope during the follow-up. IN CONCLUSION: (1) syncope in paced patients with SSS has multiple etiologies and may be multifactorial; (2) the only predictor of syncope after pacemaker implant is the occurrence of preimplant syncope as the main indication for pacing; (3) extensive Holter monitoring is not useful to document bradycardiac origin of syncope nor to predict its recurrence; (4) SSS probably overlaps with other entities such as autonomic dysfunction, vasovagal syncope, carotid sinus hypersensitivity, and venous pooling, which would provide an explanation for recurrent syncope in patients with normal pacemaker function.

Vasovagal syncope: diagnostic role of head-up tilt test in patients with positive ocular compression test.

We investigated the relative merits of the ocular compression test and the head-up tilt test to aid differentiation of syncope and seizures in young patients. Sixteen patients (10 males and 6 females) with a mean age of 14 +/- 4.7 (SD) years (range 7-22 years) underwent graded head-up tilt (15 degrees, 30 degrees, and 45 degrees for 2 minutes each, then 60 degrees for 20 minutes) following positive ocular compression testing defined as precipitation of asystole for at least 3 seconds (mean 5 seconds +/- 2 seconds, range 3-12 seconds). Each patient presented with recurrent unexplained loss of consciousness (mean number of episodes 30 +/- 45, mean duration of illness 52 +/- 40 months), and seven patients were receiving anticonvulsant medications, three of these had normal EEGs. Eleven patients (69%) developed vasovagal syncope during head-up tilt, reproducing their clinical episodes (systolic blood pressure decreased from 105 +/- 10 mmHg to 84 +/- 13 mmHg, diastolic blood pressure from 75 +/- 9 to 22 +/- 25 mmHg, and heart rate from 89 +/- 13 beats/min to 37 +/- 20 beats/min). Asystole occurred in two patients during vasovagal syncope lasting 11 seconds in one and 16 seconds in the other, and, it was associated with myoclonic movements in both (convulsive syncope). Based on these findings, and given the perceived potential hazards of the ocular compression test, the head-up tilt test may be a safer procedure that adds useful information to the diagnostic evaluation of these patients.

Potassium loading as adjunct treatment of repetitive ventricular arrhythmias.

To evaluate potassium supplementation as adjunct therapy for ventricular arrhythmias, consecutive normokalemic patients undergoing in-hospital antiarrhythmic therapy for ventricular tachycardia were randomly assigned to one of four groups: intravenous potassium chloride (Group I, 44 patients) v intravenous saline (Group II, 48 patients); and oral potassium chloride capsules (Group III 50 patients) v no additional treatment (Group IV, 47 patients). All groups underwent serial serum potassium determinations and 24-hour electrocardiographic monitoring. Analysis revealed no significant differences in ventricular ectopic activity among groups, and there was no significant association between serum potassium level and incidence of ventricular arrhythmias. We conclude that normokalemic patients undergoing antiarrhythmic therapy for ventricular tachycardia benefit little from concomitant short-term potassium supplementation.