Fibre-top atomic force microscope probe with optical near-field detection capabilities.

We present a fibre-top probe fabricated by carving a tipped cantilever on an optical fibre, with the tip machined in correspondence of the fibre core. When approached to an optical prism illuminated under total internal reflection conditions, the tip of the cantilever detects the optical tunnelling signal, while the light coupled from the opposite end of the fibre measures the deflection of the cantilever. Our results suggest that fibre-top technology can be used for the development of a new generation of hybrid probes that can combine atomic force microscopy with scanning near field optical microscopy.

Scanning probe nanoimprint lithography.

The present paper reports on a novel lithographic approach at the nanoscale level, which is based on scanning probe microscopy (SPM) and nanoimprint lithography (NIL). The experimental set-up consists of an atomic force microscope (AFM) operated via software specifically developed for the purpose. In particular, this software allows one to apply a predefined external load for a given lapse of time while monitoring in real-time the relative distance between the tip and the sample as well as the normal and lateral force during the embossing process. Additionally, we have employed AFM tips sculptured by means of focused ion beam in order to create indenting tools of the desired shape. Anti-sticking layers can also be used to functionalize the tips if one needs to investigate the effects of different treatments on the indentation and de-molding processes. The lithographic capabilities of this set-up are demonstrated on a polystyrene NIL-patterned sample, where imprinted features have been obtained upon using different normal load values for increasing time intervals, and on a thermoplastic polymer film, where the imprint process has been monitored in real-time.

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 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.

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.

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.

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.

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.

Sinus node function in hyperthyroid patients.

We have studied the electrophysiology of the sinus node and the role of the autonomic nervous system on sinus node function in 8 thyrotoxic patients of both sexes, 37.5 +/- 4.3 (mean +/- SE) yr old. The resting heart rate (RHR), the sino-atrial conduction time (SACT), and the sinus node recovery time (SNRT) were measured in the untreated condition (basal), after sympathetic blockade with propranolol 0.2 mg/kg body weight (BW) i.v. infusion, and after complete autonomic blockade with the additional administration of atropine 0.04 mg/kg BW i.v. bolus. 1) In the thyrotoxic patients the RHR was higher [117 +/- 6 beats per min (bpm)] than in 20 normal subjects (73 +/- 1 bpm, P less than 0.001), whereas the SACT and SNRT values were not different. 2) After sympathetic blockade with propranolol, the RHR decrement and SACT increase were greater in the hyperthyroid patients than in normal subjects, whereas there was no difference in SNRT values between the two groups. 3) In the thyrotoxic patients the complete autonomic blockade reestablished the electrophysiological parameters to values similar to those observed in basal condition. In conclusion, in thyrotoxic patients the intrinsic activity of the sinus node is increased. It appears that this is a direct consequence of thyroid hormone excess, rather than an effect of extrinsic influences exerted by the autonomic nervous system on sinus node activity.

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.

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.

A controlled trial of acute and long-term medical therapy in tilt-induced neurally mediated syncope.

To study the efficacy of medical treatment for preventing syncopal recurrences in patients affected by tilt-induced neurally mediated syncope, a randomized placebo-treatment prospective study was performed in 30 patients (10 men and 20 women, mean age 42 +/- 21 years) who had syncope reproduced in 2 consecutive head-up tilt-table tests without pharmacologic intervention (n = 20) or during isoproterenol infusion (n = 10). Patients were randomly assigned to 2 groups: 15 to placebo, and 15 to drug therapy (determined on the basis of serial pharmacologic tilting tests). Therapy was either atenolol (n = 7), dihydroergotamine (n = 2), domperidone (n = 2), cafedrine (n = 1), or elastic compression stockings, alone or in association with drugs (n = 3). During a mean of 10 +/- 7 months of follow-up, syncope recurred in 3 patients (20%) in the treatment group and in 4 (27%) in the placebo group; actuarial rates of absence of syncopal recurrences after 20 months were 70 and 67%, respectively. Thus, the outcome of either treated or untreated patients was favorable (with a low recurrence rate of syncope), and the usefulness of tilting-guided medical therapy remains uncertain.

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.

The natural course of untreated sick sinus syndrome and identification of the variables predictive of unfavorable outcome.

We performed a prospective study in 35 untreated patients aged > or = 45 years, who had a mean sinus rate at rest of < or = 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, age > or = 65 years, end-systolic left ventricular diameter > or = 30 mm, end-diastolic left ventricular diameter > or = 52 mm, and ejection fraction < 55% 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 recovery > or = 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.

Neurally mediated syncope detected by carotid sinus massage and head-up tilt test in sick sinus syndrome.

It is generally accepted that a positive response to carotid sinus massage (CSM) or head-up tilt (HUT) in patients affected by syncope suggests a reflex cause of the syncope. To study the role of the autonomic nervous system in causing syncope in the sick sinus syndrome (SSS), CSM and HUT were performed in 35 consecutive patients (20 men, mean age 70 +/- 9 years) with syncope and SSS. Results were compared with those in 35 patients affected by syncope that, despite careful cardiovascular and neurologic examination, were of uncertain origin (21 men; mean age 68 +/- 9 years) and with those of 35 subjects without syncope (20 men; mean age 69 +/- 10). All patients underwent CSM in the supine and standing positions for 10 seconds and HUT to 60 degrees for 60 minutes. In the patients with SSS, the full reproduction of spontaneous symptoms by CSM occurred in 21 (60%) and by HUT, in 19 (54%). At least 1 test was positive in 28 patients (80%): cardioinhibitory or mixed responses in 69%, vasodepressor responses in 11%. The percentages of positive tests in the patients with syncope of uncertain origin were similar to or slightly less than those of patients with SSS (CSM 63%, HUT 26%, overall 74%) with cardioinhibitory or mixed responses in 54% and vasodepressor in 20% (p less than 0.05). In control subjects, syncope was induced by CSM in 1 (3%) and by HUT in 2 (6%); overall positivity was 9%. In conclusion, in most patients affected by syncope and SSS, an abnormal neural reflex probably plays a major role in causing syncope.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of atrioventricular junction radiofrequency ablation in patients with chronic atrial fibrillation and flutter on quality of life and cardiac performance.

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 follow-up study was performed in 22 patients. New York Heart Association functional class > or = 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 > or = 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).(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanisms of syncope caused by transient bradycardia and the diagnostic value of electrophysiologic testing and cardiovascular reflexivity maneuvers.

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.

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.