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The purpose of this study was to evaluate the effects of atrioventricular junction radiofrequency ablation on the quality of life, exercise performance, and echocardiographic parameters in 23 patients with chronic, severely symptomatic, drug-refractory atrial fibrillation or flutter. Initially, patients were randomized to receive ablation plus pacemaker therapy (n = 12) or pacemaker therapy alone (n = 11). After 15 days, palpitations decreased by 92% and 37% (p = 0.004), rest dyspnea by 79% and 40% (p = NS), effort dyspnea by 65% and 30% (p = 0.03), exercise intolerance by 54% and 17% (p = 0.005), and asthenia by 67% and 31% (p = 0.02) in the 2 groups, respectively. At the end of this short-term study, control patients also underwent ablation therapy, and a 3-month intrapatient followup study was performed in 22 patients. New York Heart Association functional class ≥3 was present in 14 patients (64%) before, but in only 3 patients (14%) after ablation therapy (p = 0.002); specific activity scale functional class ≥3 was present in 9 patients (41%) before, but in only 5 (23%) after ablation therapy (p = NS). Exercise duration during standardized stress testing increased by a mean of 63 ± 93 seconds (15% increase) (p = 0.001). In the 9 patients with depressed left ventricular systolic function, echocardiographic fractional shortening increased by 34% (from 23 ± 5% to 31 ± 9%) (p = 0.003). In the remaining 13 patients with normal systolic function, fractional shortening decreased by 10% (from 40 ± 5% to 36 ± 6%) (p = 0.05). In conclusion, radiofrequency ablation of the atrioventricular junction ameliorates quality of life and physical performance; left ventricular systolic function improves in patients with depressed cardiac performance at initial evaluation.

In conclusion, in patients affected by syncope, chronic vasodilator therapy enhances susceptibility to vasovagal reaction during upright tilt testing and, possibly, during spontaneous syncope. The impaired baroreflex compensatory mechanism, which became unable to maintain a sufficient systemic and cerebral blood flow, and thus prevent initiation of the vasovagal reaction, may be hypothesized. Tilt testing may be used to identify patients with drug-related vasovagal syncope.

In conclusion, most of the carotid sinus syndrome patients who have syncopal recurrence despite pacing therapy have a positive response to head-up tilt testing, which suggests the presence of a more complex neurogenic disease.

We performed a prospective study in 35 untreated patients agedor = 45 years, who had a mean sinus rate at rest ofor = 50 beats/min and/or intermittent sinoatrial block, and symptoms attributable to sinus node dysfunction. The patients were followed up for up to 4 years (mean 17 +/- 15 months). During follow-up, 20 patients (57%) had cardiovascular events that required treatment: 8 had syncope (23%); 6 had overt heart failure (17%); 4 patients had chronic atrial fibrillation (11%); and 2 patients had poorly tolerated episodes of paroxysmal tachyarrhythmias (6%). Actuarial rates of occurrence of all events were 35%, 49%, and 63%, respectively, after 1, 2, and 4 years. At univariate analysis, ageor = 65 years, end-systolic left ventricular diameteror = 30 mm, end-diastolic left ventricular diameteror = 52 mm, and ejection fraction55% were predictors of cardiovascular events. At multivariate analysis, age, end-diastolic diameter, and ejection fraction remained independent predictors of events. Actuarial rates of occurrence of syncope were 16%, 31%, and 31%, respectively, after 1, 2, and 4 years. Both univariate and multivariate predictors of syncope were history of syncope and corrected sinus node recoveryor = 800 ms. A favorable outcome was observed in the remaining 43% of patients. Thus, clinical cardiovascular events occur in most untreated sick sinus syndrome patients during long-term follow-up, even though a favorable course can be expected in 43% of patients. The outcome can be partly predicted on initial evaluation. In the patients with a favorable outcome, treatment can safely be delayed.

Transient bradycardia may be intrinsic because of sinus node or atrioventricular (AV) conduction abnormalities, or extrinsic because of abnormal vagal reflex. Twenty-five consecutive patients, referred to us for study of unexplained syncope, who, during electrocardiographic monitoring, had a documented episode of intermittent bradycardia that caused syncope, underwent a full electrophysiologic study, carotid sinus massage, and the head-up tilt test. A prolonged ventricular asystole (5 to 20 seconds) was documented during syncope in all patients: sinus arrest in 13, AV block in 7, sinus arrest plus AV block in 3, and asystolic pause during atrial fibrillation in 2. Abnormal electrophysiologic findings suggested the correct diagnosis in 6 patients (24%): block within the bundle of His in 5 and sick sinus syndrome in 1. An abnormal response to carotid sinus massage or to the head-up tilt test suggested a neurally mediated mechanism in 17 patients (68%). Overall, electrophysiologic study and vasovagal maneuvers were able to identify the mechanism of spontaneous syncope in 23 patients (92%). Thus, in patients affected by syncope due to transient bradycardia, the most likely mechanism of syncope is neurogenic, whereas it is cardiogenic only in a few instances. Electrophysiologic testing, carotid sinus massage, and the head-up tilt test can identify most of these patients. Conversely, when all these tests are negative, it is unlikely that transient bradycardia is the cause of syncope. Because of the different mechanisms involved, electrophysiologic study and vasovagal maneuvers are complementary diagnostic tools.

In conclusion, our results point out the importance of the vasodepressor reflex in patients with carotid sinus syndrome; it is present in most patients including those categorized as affected by the dominant cardioinhibitory form. The mechanism of vasodepression is complex, including a hemodynamic effect and suppression of sympathetic compensatory outflow.

The occurrence rate of spontaneous asystolic episodes during long-term follow-up in patients with abnormal asystolic responses induced by means of vasovagal maneuvers was evaluated. The heart rate of 23 patients (mean age 64 +/- 12 years; 6 women and 17 men) affected by neurally mediated syncope (mean 4.3 +/- 4.9 episodes) was continuously monitored by a specially designed implanted pacemaker able to detect and store in its memory all asystolic episodes lasting 3 to 6 or > 6 seconds. Asystolic, neurally mediated syncope was diagnosed when a reflex asystole of > 3 seconds was induced during carotid sinus massage (n = 22), eyeball compression test (n = 3) or head-up tilt test (n = 2). During a total of 357 months (mean 15 +/- 7) of monitoring, asystolic episodes occurred in 17 patients (74%): 1,765 episodes of 3- to 6-second (median 3) duration occurred in 14 patients, and 47 episodes of > 6-second (median 2) duration occurred in 11. The actuarial estimates of occurrence of asystolic episodes of > 3 and > 6 seconds were 82 and 53%, respectively, after 2 years of follow-up. Only 12 episodes of 3 to 6 seconds (0.7%), and 20 episodes of > 6 seconds (43%) resulted in presyncopal or syncopal symptoms. Thus, an asystolic response to vasovagal maneuvers predicts the occurrence of spontaneous asystolic episodes during follow-up. With few exceptions, spontaneous episodes are asymptomatic and their incidence is low.

The natural history of patients with severe carotid sinus syndrome, and the efficacy of permanent pacemaker treatment are not clearly known. A randomized treatment/nontreatment prospective study was performed in 60 patients affected by carotid sinus syndrome whose symptoms were judged to involve risk of major trauma or interfered with their daily activity. They were randomly assigned to 2 groups: 28 patients to no therapy (nonpacing group), and 32 to VVI (n = 18) or DDD (n = 14) pacemaker implant (pacing group). Syncope recurred in 16 patients (57%) of the nopacing group (mean follow-up 36 +/- 10 months) and in only 3 (9%) of the pacing group (mean follow-up 34 +/- 10 months) (p = 0.0002); moreover, 19 (68%) in the nonpacing group needed a secondary pacemaker implant because of the severity of symptoms. The actuarial rate of absence of syncopal recurrence after 1, 2, 3 and 4 years was 64, 54, 38 and 38%, respectively, for the nonpacing group, and 100, 97, 93 and 84%, respectively, for the pacing group (p = 0.0001). The actuarial rate of absence of minor symptoms after 1, 2, 3 and 4 years was 21, 14, 7 and 7%, respectively, for the nonpacing group and 66, 43, 27 and 27%, respectively, for the pacing group (p = 0.002). Reproducibility of carotid sinus reflex was tested after 15 +/- 8 months in 54 patients; an abnormal response to carotid sinus massage persisted in all 54. In conclusion, symptoms recur in most patients with untreated carotid sinus syndrome, and pacing is a useful therapy for preventing recurrences.