External prolonged electrocardiogram monitoring in unexplained syncope and palpitations: results of the SYNARR-Flash study.

AIMS: SYNARR-Flash study (Monitoring of SYNcopes and/or sustained palpitations of suspected ARRhythmic origin) is an international, multicentre, observational, prospective trial designed to evaluate the role of external 4-week electrocardiogram (ECG) monitoring in clinical work-up of unexplained syncope and/or sustained palpitations of suspected arrhythmic origin. METHODS AND RESULTS: Consecutive patients were enrolled within 1 month after unexplained syncope or palpitations (index event) after being discharged from emergency room or hospitalization without a conclusive diagnosis. A 4-week ECG monitoring was obtained by external high-capacity loop recorder (SpiderFlash-T(®), Sorin) storing patient-activated and auto-triggered tracings. Diagnostic monitorings included (i) conclusive events with reoccurrence of syncope or palpitation with concomitant ECG recording (with/without arrhythmias) and (ii) events with asymptomatic predefined significant arrhythmias (sustained supraventricular or ventricular tachycardia, advanced atrio-ventricular block, sinus bradycardia <30 b.p.m., pauses >6 s). SYNARR-Flash study enrolled 395 patients (57.7% females, 56.9 ± 18.7 years, 28.1% with syncope, and 71.9% with palpitations) from 10 European centres. For syncope, the 4-week diagnostic yield was 24.5%, and predictors of diagnostic events were early start of recording (0-15 vs. >15 days after index event) (OR 6.2, 95% CI 1.3-29.6, P = 0.021) and previous history of supraventricular arrhythmias (OR 3.6, 95% CI 1.4-9.7, P = 0.018). For palpitations, the 4-week diagnostic yield was 71.6% and predictors of diagnostic events were history of recurrent palpitations (P < 0.001) and early start of recording (P = 0.001). CONCLUSION: The 4-week external ECG monitoring can be considered as first-line tool in the diagnostic work-up of syncope and palpitation. Early recorder use, history of supraventricular arrhythmia, and frequent previous events increased the likelihood of diagnostic events during the 4-week external ECG monitoring.

At the heart of the arterial baroreflex: a physiological basis for a new classification of carotid sinus hypersensitivity.

The aim of this review is to provide an update of the current knowledge of the physiological mechanisms underlying reflex syncope. Carotid sinus syncope will be used as the classical example of an autonomic reflex with relatively well-established afferent, central and efferent pathways. These pathways, as well as the pathophysiology of carotid sinus hypersensitivity (CSH) and the haemodynamic effects of cardiac standstill and vasodilatation will be discussed. We will demonstrate that continuous recordings of arterial pressure provide a better understanding of the cardiovascular mechanisms mediating arterial hypotension and cerebral hypoperfusion in patients with reflex syncope. Finally we will demonstrate that the current criteria to diagnose CSH are too lenient and that the conventional classification of carotid sinus syncope as cardioinhibitory, mixed and vasodepressor subtypes should be revised because isolated cardioinhibitory CSH (asystole without a fall in arterial pressure) does not occur. Instead, we suggest that all patients with CSH should be thought of as being 'mixed', between cardioinhibition and vasodepression. The proposed stricter set of criteria for CSH should be evaluated in future studies.

A2A adenosine receptor function in patients with vasovagal syncope.

AIMS: Adenosine is a possible mediator in vasovagal syncope (VVS) via the activation of its receptors. High expression of adenosine A2A receptors (A2AR) has been reported in VVS. The function of these over-expressed receptors in this population has never been evaluated. METHODS AND RESULTS: We used Adonis, a specific-made antibody with A2AR agonist properties, to evaluate binding parameters (i.e. dissociation constant KD) and cAMP production (i.e. EC50) by peripheral blood mononuclear cells of 16 VVS patients. Eight healthy volunteers served as controls. A2AR expression was higher in patients than controls; mean: 11.5 ± 1.2 vs. 7.7 ± 0.8 AU, P = 0.04. Also, KD values were higher in patients than controls: 2.1 ± 0.02 × 10(-7) vs. 5 ± 1 × 10(-8) M, P < 0.01 In controls, KD values were lower than EC50 (5 ± 1.7 × 10(-8) vs. 2.8 ± 0.4 10(-7) M, P < 0.01), but in patients, KD values did not differ from EC50: 2. ± 0.2 × 10(-7) vs. 2.5 ± 0.4 × 10(-7) M, P > 0.05. However, four patients had lower EC50 (3.5 ± 0.3 × 10(-8) M) than KD (2.9 ± 1.2 × 10(-7) M; KD/EC50 = 9.6), suggesting the presence of spare receptors. CONCLUSION: The function of A2AR of patients with VVS was preserved since their stimulation by Adonis led to cAMP production with an EC50 comparable with those in controls. However, their affinity was lower than those of controls. Our results suggest that A2AR are implicated in the physiopathology of VVS.

Factors facilitating and hindering the implementation of the European Society of Cardiology Syncope Guidelines at the Emergency Department: A nationwide qualitative study.

AIMS: Syncope care is often fragmented and inefficient. Structuring syncope care through implementation of guidelines and Syncope Units has been shown to improve diagnostic yield, reduce costs and improve quality of life. We implemented the European Society of Cardiology (ESC) 2018 syncope guidelines at the Emergency Departments (ED) and established Syncope Units in five Dutch hospitals. We evaluated the implementation process by identifying factors that hinder ('barriers') and facilitate ('facilitators') the implementation. METHODS AND RESULTS: We conducted, recorded and transcribed semi-structured interviews with 19 specialists and residents involved in syncope care from neurology, cardiology, internal medicine and emergency medicine. Two researchers independently classified the reported barriers and facilitators, according to the framework of qualitative research (Flottorp), which distinguished several separate fields ('levels'). Software package Atlas.ti was used for analysis. We identified 31 barriers and 22 facilitators. Most barriers occurred on the level of the individual health care professional (e.g. inexperienced residents having to work with the guideline at the ED) and the organizational context (e.g. specialists not relinquishing preceding procedures). Participants reported most facilitators at the level of innovation (e.g. structured work-flow at the ED). The multidisciplinary Syncope Unit was welcomed as useful solution to a perceived need in clinical practice. CONCLUSION: Implementing ESC syncope guidelines at the ED and establishing Syncope Units facilitated a structured multidisciplinary work-up for syncope patients. Most identified barriers related to the individual health care professional and the organizational context. Future implementation of the multidisciplinary guideline should be tailored to address these barriers.

Update in the treatment of neurally-mediated syncope.

Syncope is a transient, self-limited loss of consciousness, usually leading to falling. The underlying mechanism is a transient global cerebral hypoperfusion. Since there are many causes of syncope, a specific treatment cannot be administered without knowing of the exact mechanism responsible of loss of consciousness. Drugs are ineffective. The main therapeutic innovations of the most recent years are isometric counter-pressure maneuvres, lower limb compression bandage and therapy guided by implantable loop recorder in patients with recurrent suspected neurally-mediated syncope.

Dual-chamber pacing in the treatment of neurally mediated tilt-positive cardioinhibitory syncope : pacemaker versus no therapy: a multicenter randomized study. The Vasovagal Syncope International Study (VASIS) Investigators.

BACKGROUND-This study was performed to compare implantation of a DDI pacemaker with rate hysteresis with no implant in respect to syncopal recurrences in patients with severe cardioinhibitory tilt-positive neurally mediated syncope. METHODS AND RESULTS-Forty-two patients from 18 European centers were randomized to receive a DDI pacemaker programmed to 80 bpm with hysteresis of 45 bpm (19 patients) or no pacemaker (23 patients). Inclusion criteria were >/=3 syncopes over the last 2 years and a positive cardioinhibitory (Vasovagal Syncope International Study types 2A and 2B) response to tilt testing. The median number of previous syncopal episodes was 6; asystolic response to tilt testing was present in 36 patients (86%) (mean asystole, 13.9+/-10.2 seconds). All patients were followed up for a minimum of 1.0 years and a maximum of 6.7 years (mean, 3.7+/-2.2). One patient (5%) in the pacemaker arm experienced recurrence of syncope compared with 14 patients (61%) in the no-pacemaker arm (P=0.0006). In the no-pacemaker arm, the median time to first syncopal recurrence was 5 months, with a rate of 0.44 per year. On repeated tilt testing performed within 15 days after enrollment, positive responses were observed in 59% of patients with pacemakers and in 61% of patients without pacemakers (P=NS). CONCLUSIONS-In a limited, select group of patients with tilt-positive cardioinhibitory syncope, DDI pacing with hysteresis reduced the likelihood of syncope. The benefit of the therapy was maintained over the long term. Even in untreated patients, the syncopal recurrence burden was low. A negative result of tilt testing was not a useful means to evaluate therapy efficacy.

Mechanism of syncope in patients with isolated syncope and in patients with tilt-positive syncope.

BACKGROUND: Because of its episodic behavior, the correlation of spontaneous syncope with an abnormal finding can be considered a reference standard. METHODS AND RESULTS: We inserted an implantable loop recorder in 111 patients with syncope, absence of significant structural heart disease, and a normal ECG; tilt-testing was negative in 82 (isolated syncope) and positive in 29 (tilt-positive). The patients had had >/=3 episodes of syncope in the previous 2 years and were followed up for 3 to 15 months. Results were similar in the isolated syncope group and the tilt-positive group: syncope recurred in 28 (34%) and 10 patients (34%), respectively, and electrocardiographic correlation was found in 24 (23%) and 8 (28%) patients, respectively. The most frequent finding, which was recorded in 46% and 62% of patients, respectively, was one or more prolonged asystolic pauses, mainly due to sinus arrest, preceded for a few minutes by progressive bradycardia or progressive tachycardia-bradycardia. Bradycardia without pauses was observed in 8% and 12% of cases, respectively. The remaining patients had normal sinus rhythm or sinus tachycardia, except for one, who had ectopic atrial tachycardia. In the tilt-positive group, an asystolic syncope was also recorded when the type of response to tilt-testing was vasodepressor or mixed. Presyncopal episodes were never characterized by asystolic pauses; normal sinus rhythm was the most frequent finding. CONCLUSIONS: Homogeneous findings were observed during syncope. In most patients, the likely cause was neurally-mediated, and the most frequent mechanism was a bradycardic reflex. In the other cases, a normal sinus rhythm was frequently recorded. Presyncope was not an accurate surrogate for syncope in establishing a diagnosis.

Mechanism of syncope in patients with bundle branch block and negative electrophysiological test.

BACKGROUND: In patients with syncope and bundle branch block (BBB), syncope is suspected to be attributable to a paroxysmal atrioventricular (AV) block, but little is known of its mechanism when electrophysiological study is negative. METHODS AND RESULTS: We applied an implantable loop recorder in 52 patients with BBB and negative conventional workup. During a follow-up of 3 to 15 months, syncope recurred in 22 patients (42%), the event being documented in 19 patients after a median of 48 days. The most frequent finding, recorded in 17 patients, was one or more prolonged asystolic pause mainly attributable to AV block; the remaining 2 patients had normal sinus rhythm or sinus tachycardia. The onset of the bradycardic episodes was always sudden but was sometimes preceded by ventricular premature beats. The median duration of the arrhythmic event was 47 seconds. An additional 3 patients developed nonsyncopal persistent III-degree AV block, and 2 patients had presyncope attributable to AV block with asystole. No patients suffered injury attributable to syncopal relapse. CONCLUSIONS: In patients with BBB and negative electrophysiological study, most syncopal recurrences have a homogeneous mechanism that is characterized by prolonged asystolic pauses, mainly attributable to sudden-onset paroxysmal AV block.

Clinical and genetic heterogeneity of right bundle branch block and ST-segment elevation syndrome: A prospective evaluation of 52 families.

BACKGROUND: The ECG pattern of right bundle branch block and ST-segment elevation in leads V(1) to V(3) (Brugada syndrome) is associated with high risk of sudden death in patients with a normal heart. Current management and prognosis are based on a single study suggesting a high mortality risk within 3 years for symptomatic and asymptomatic patients alike. As a consequence, aggressive management (implantable cardioverter defibrillator) is recommended for both groups. METHODS AND RESULTS: Sixty patients (45 males aged 40+/-15 years) with the typical ECG pattern were clinically evaluated. Events at follow-up were analyzed for patients with at least one episode of aborted sudden death or syncope of unknown origin before recognition of the syndrome (30 symptomatic patients) and for patients without previous history of events (30 asymptomatic patients). Prevalence of mutations of the cardiac sodium channel was 15%, demonstrating genetic heterogeneity. During a mean follow-up of 33+/-38 months, ventricular fibrillation occurred in 5 (16%) of 30 symptomatic patients and in none of the 30 asymptomatic patients. Programmed electrical stimulation was of limited value in identifying patients at risk (positive predictive value 50%, negative predictive value 46%). Pharmacological challenge with sodium channel blockers was unable to unmask most silent gene carriers (positive predictive value 35%). CONCLUSIONS: At variance with current views, asymptomatic patients are at lower risk for sudden death. Programmed electrical stimulation identifies only a fraction of individuals at risk, and sodium channel blockade fails to unmask most silent gene carriers. This novel evidence mandates a reappraisal of therapeutic management.

Role of autonomic reflexes in syncope associated with paroxysmal atrial fibrillation.

OBJECTIVES: The purpose of this study was to evaluate the role of autonomic reflexes in the genesis of syncope associated with the onset of paroxysmal atrial fibrillation. BACKGROUND: Syncope associated with paroxysmal atrial fibrillation has been interpreted as an ominous finding predictive of rapid ventricular rates. However, various mechanisms may be involved when heart rate is not particularly high. METHODS: Forty patients (age 60 +/- 14 years, 20 men, 20 women) with syncope and atrial fibrillation were compared with atrial fibrillation without syncope. Carotid sinus massage and head-up tilt testing (at 60 degrees for 60 min at baseline and during isoproterenol infusion) were performed during sinus rhythm. A positive response was defined as the induction of syncope. Atrial fibrillation was also induced on a tilt table at 60 degrees by means of short bursts of atrial pacing. RESULTS: Results of carotid sinus massage were positive in 15 (37%) of 40 patients but in no control subjects (p = 0.002). Head-up tilt test findings were positive in 25 (66%) of 38 patients and in 2 (12%) of 16 control subjects (p = 0.0004). The induction of atrial fibrillation in the upright position elicited syncope in 16 (42%) of 38 patients but in none of 16 control subjects (p = 0.001). At the beginning of atrial fibrillation, systolic blood pressure was lower in patients than in control subjects (88 +/- 32 vs. 127 +/- 32 mm Hg), whereas mean heart rate was similar (142 +/- 35 vs. 134 +/- 25 beats/min). The correlation between heart rate and systolic blood pressure was weak (r = 0.35), and in five patients syncope occurred at a heart rate < or = 130 beats/min. At the time of syncope, heart rate decreased (-12 +/- 21 beats/min) in patients with induced syncope, whereas it remained unchanged in patients without induced syncope (+1 +/- 17 beats/min, p = 0.04) or slightly increased in control subjects (+9 +/- 21 beats/min, p = 0.009). CONCLUSIONS: Patients with syncope associated with paroxysmal atrial fibrillation are predisposed to an abnormal neural response during both sinus rhythm and arrhythmia. In some patients the onset of atrial fibrillation triggers vasovagal syncope.

An abnormal neural reflex plays a role in causing syncope in sinus bradycardia.

OBJECTIVES: This study investigates the role of an abnormal neural reflex in causing syncope in patients with sinus bradycardia. BACKGROUND: Syncope is commonly considered an indication of severity in sinus bradycardia. However, the occurrence of syncope is unpredictable, and the prognosis appears to be similar in patients with and without syncope. METHODS: Head-up tilt testing (60 degrees for 60 min), carotid sinus massage in the supine and standing positions, 24-h Holter ambulatory electrocardiographic (ECG) recording and electrophysiologic study before and after pharmacologic autonomic blockade were performed in 25 patients with sinus bradycardia and syncope (group I, sinus rate < 50 beats/min, age 71 +/- 12 years) and 25 patients with sinus bradycardia and no neurologic symptoms (group II, sinus rate < 50 beats/min, age 67 +/- 16 years). RESULTS: Clinical characteristics and ambulatory ECG monitoring data were similar in the two study groups. A positive response (induction of syncope or presyncope with hypotension and/or bradycardia) was obtained by head-up tilt testing in 15 group I (60%) and in 3 group II (12%) patients (p < 0.001) and by carotid sinus massage in 11 group I (44%) and 6 group II (24%) patients (p = NS). Results of at least one test (head-up tilt testing or carotid sinus massage, or both) were positive in 19 group I (76%) and 9 group II (36%) patients (p < 0.01). Basal and intrinsic corrected sinus node recovery time did not differ significantly between the two groups. An abnormal intrinsic heart rate was present in 66% of group I and 26% of group II patients (p < 0.01). The different percentage of positive findings on head-up tilt testing and carotid sinus massage in the two groups was independent of the presence of intrinsic sinus node dysfunction. CONCLUSIONS: These results indicate that an abnormal neural reflex plays a role in causing syncope in patients with sinus bradycardia. This reflex seems to be unrelated to the severity of sinus node dysfunction, even if the latter could enhance the cardioinhibitory response.

Efficacy and safety of out-of-hospital self-administered single-dose oral drug treatment in the management of infrequent, well-tolerated paroxysmal supraventricular tachycardia.

OBJECTIVES: We tested the efficacy of two drug treatments, flecainide (F) and the combination ofdiltiazem and propranolol (D/P), administered as a single oral dose for termination of the arrhythmic episodes. BACKGROUND: Both prophylactic drug therapy and catheter ablation are questionable as first-line treatments in patients with infrequent and well-tolerated episodes of paroxysmal supraventricular tachycardia (SVT). METHODS: Among 42 eligible patients (13% of all screened for SVT) with infrequent (< or =5/year), well-tolerated and long-lasting episodes, 37 were enrolled and 33 had SVT inducible during electrophysiological study. In the latter, three treatments (placebo, F, and D/P) were administered in a random order 5 min after SVT induction on three different days. RESULTS: Conversion to sinus rhythm occurred within 2 h in 52%, 61%, and 94% of patients on placebo, F and D/P, respectively (p < 0.001). The conversion time was shorter after D/P (32 +/- 22 min) than after placebo (77 +/- 42 min, p < 0.001) or F (74 +/- 37 min, p < 0.001). Four patients (1 placebo, 1 D/P, and 2 F) had hypotension and four (3 D/P and 1 F) a sinus rate <50 beats/min following SVT interruption. Patients were discharged on a single oral dose of the most effective drug treatment (F or D/P) at time of acute testing. Twenty-six patients were discharged on D/P and five on F. During 17 +/- 12 months follow-up, the treatment was successful in 81% of D/P patients and in 80% of F patients, as all the arrhythmic episodes were interrupted out-of-hospital within 2 h. In the remaining patients, a failure occurred during one or more episodes because of drug ineffectiveness or drug unavailability. One patient had syncope after D/P ingestion. During follow-up, the percentage of patients calling for emergency room assistance was significantly reduced as compared to the year before enrollment (9% vs. 100%, p < 0.0001). CONCLUSIONS: The episodic treatment with oral D/P and F, as assessed during acute testing, appears effective in the management of selected patients with SVT. This therapeutic strategy minimizes the need for emergency room admissions during tachycardia recurrences.

Diagnostic value of history in patients with syncope with or without heart disease.

OBJECTIVES: We sought to establish what historical findings are predictive of the cause of syncope. BACKGROUND: The clinical features of the various types of syncope have not been systematically investigated. METHODS: Three hundred forty-one patients with syncope were prospectively evaluated. Each patient was interviewed using a standard questionnaire. A cause of syncope was assigned using standardized diagnostic criteria. RESULTS: A cardiac cause of syncope was established in 23% of the patients, a neurally mediated cause in 58% and a neurologic or psychiatric cause in 1%, and in the remaining 18%, the cause of syncope remained unexplained. In a preliminary analysis including age, gender and the presence of suspected or certain heart disease after the initial evaluation, only heart disease was an independent predictor of a cardiac cause of syncope (odds ratio 16, p = 0.00001), with a sensitivity of 95% and a specificity of 45%. In contrast, the absence of heart disease allowed us to exclude a cardiac cause of syncope in 97% of the patients. In patients with certain or suspected heart disease, the most specific predictors of a cardiac cause were syncope in the supine position or during effort, blurred vision and convulsive syncope. Significant and specific predictors of a neurally mediated cause were time between the first and last syncopal episode >4 years, abdominal discomfort before the loss of consciousness and nausea and diaphoresis during the recovery phase. In the patients without heart disease, palpitation was the only significant predictor of a cardiac cause. CONCLUSIONS: The presence of suspected or certain heart disease after the initial evaluation is a strong predictor of a cardiac cause of syncope. A few historical findings are useful to predict cardiac and neurally mediated syncope in patients with and without heart disease.

Systolic time intervals as possible predictors of pressure response to sustained beta-adrenergic blockade in arterial hypertension. A within-patient, placebo-controlled study.

Systolic time intervals (STI) were recorded at rest and during isometric exercise (IHG) in 20 hypertensive outpatients, WHO Stage 1 or 2. In a double-blind crossover study, slow-release metoprolol 200 mg once daily and matched placebo were given for 4 weeks each, at the end of a 2-week placebo washout. Blood pressure and STI were taken in the last day of washout and of either crossover period. Treatment decreased blood pressure and heart rate values at rest and on peak IHG; it didn't modify preejection period index (PEPI), left ventricular ejection time index (LVETI), and their ratio at rest, but decreased the ratio between diastolic blood pressure and PEPI (DBP/PEPI ratio) at rest and on peak IHG and lengthened the PEPI at peak IHG. Resting PEPI values on placebo treatment showed a negative correlation with systolic (r = -0.72) as well as diastolic (r = -0.80) pressure reduction on slow-release metoprolol as compared with placebo treatment. The PEP/LVET ratio at rest on placebo treatment showed a negative correlation with systolic (r = -0.78) as well as diastolic (r = -0.82) pressure reduction at rest on metoprolol compared with placebo treatment. Patients with a resting PEP/LVET ratio less than 0.43 showed a reduction in both systolic and diastolic pressure approximating or exceeding 20 mm Hg, whereas patients with a PEP/LVET ratio greater than 0.47 showed a decrease in systolic and diastolic blood pressure of less than 10 mm Hg. In patients with a PEP/LVET ratio of 0.43 to 0.47 (50% of the trial population), STI didn't show any correlation with the pressure response to beta-blockade. A positive correlation was found between the DBP/PEPI ratio at rest on placebo treatment and systolic (r = 0.56) as well as diastolic (r = 0.76) pressure reduction at rest on slow-release metoprolol compared with placebo treatment. Thus, STI appeared as promising predictors of the magnitude of blood pressure response to sustained beta-blocking therapy in mild-to-moderate essential hypertension, mostly in patients with a resting PEP/LVET ratio less then 0.43 or greater then 0.47.

Ablate and pace: palliating the symptoms?

Atrioventricular (AV) junction ablation (producing AV block) followed by pacemaker implantation is the most common nonpharmacologic treatment for patients affected by atrial fibrillation (AF) not controlled by antiarrhythmic drugs. In expert hands, the efficacy of producing complete AV block is usually >95% if a sequential right- and left-side approach is used; regression of AV block late after ablation (which requires a second procedure on a different day) occurs in <5% of cases. The clinical efficacy of ablate and pace therapy in controlling arrhythmic symptoms and improving overall quality of life is well established for patients with paroxysmal AF, although not yet for patients with persistent and permanent AF, owing to the lack of sufficient clinical studies. Ablation and pacing is clinically unsuccessful in a minority of cases. There have been little data available on long-term effects of this treatment on cardiac performance, morbidity, and survival. Although concern has arisen from some case reports, no evidence of adverse effect has ever been shown in controlled trials. Ablation and pacing does not seem to increase thromboembolic risk. We estimate that in Europe, about 396,000 patients with paroxysmal AF not controlled by drug therapy could therefore be candidates for ablate and pace therapy. Permanent forms of AF are even more frequent, but it is unknown how many are refractory to drug therapy. The recommended pacing mode is DDDR with mode switching for paroxysmal/persistent AF and VVIR for permanent AF.

A patient with syncopal ventricular tachycardia (noninducible on electrophysiologic study) and coronary artery disease.

The case of a 63-year-old patient with coronary artery disease presenting with syncopal sustained ventricular tachycardia is reported. He had very poor ventricular function, an extensive myocardial scar, and limited area of reversible ischemia. Coronary angiographic examination showed a left main equivalent coronary artery disease with critical stenosis. Although this patient should theoretically benefit from revascularization, we decided against this due to the high estimated perioperative mortality rate for coronary artery bypass grafting in such a patient. Therefore, we intensively treated myocardial ischemia and pump failure with digoxon, furosemide, dihydralazine, nitrates, and warfarin and prescribed a back-up defibrillator implant.

Long-term outcome of paced and nonpaced patients with severe carotid sinus syndrome.

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.

Progression of permanent atrial fibrillation after atrioventricular junction ablation and dual-chamber pacemaker implantation in patients with paroxysmal atrial tachyarrhythmias.

Among 63 patients affected by symptomatic drug refractory paroxysmal atrial fibrillation who had undergone atrioventricular junction ablation and dual-chamber pacemaker implantation, the actuarial estimate of progression of permanent atrial fibrillation was 22%, 40%, and 56% respectively, 1, 2, and 3 years after ablation. A stratification of the risk of development of permanent atrial fibrillation was obtained on the basis of several clinical variables.

Effects of left ventricular pacing on cardiac performance and on quality of life in patients with drug refractory heart failure.

We assessed the effects of left ventricular pacing on echocardiographic and clinical parameters in 13 consecutive patients with heart failure and bundle branch block by means of a controlled acute and medium-term evaluation. Left ventricular pacing induced a significant improvement in left ventricular ejection fraction, Minnesota Living with Heart Failure Questionnaire score, New York Heart Association class, and 6-minute walking test compared with sinus rhythm or right ventricular pacing.

Follow-up of asystolic episodes in patients with cardioinhibitory, neurally mediated syncope and VVI pacemaker.

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.