Patients with conventional SC-ICD indication were randomized to DC-ICD, SC-ICD, or a DC-ICD programmed as an SC-ICD (SC-simulated) and followed for 16 months. Patients in the DC and SC-simulated groups crossed over after 8 months. The primary endpoint was a composite of CSAE: all-cause mortality; invasive intervention; hospitalization (>24 h) for cardiovascular causes; inappropriate shocks (two or more episodes); and sustained symptomatic AT lasting >48 h. The outcome variable was a pre-specified score that corrected for clinical severity and follow-up duration. Three hundred and thirty-four patients were analysed (DC-ICD, n = 112; SC-ICD, n = 111; SC-simulated, n = 111). The mean left ventricular ejection fraction was 0.36 ± 0.13, 69% were in functional class ≥II. CSAE occurred in 65 DC-ICD, 82 SC-ICD, and 84 SC-simulated patients. The outcome variable was 33% lower in the DC-ICD group (OR 0.31; 95% CI 0.14–0.67; P = 0.0028). Mortality was 4% in DC, 9% in SC, and 10% in SC-simulated.

In patients with a standard SC-ICD indication, DC-ICD was associated with less CSAE when compared with SC-ICD.

Thirty-one patients experiencing device recalls answered questions regarding their knowledge about the recall and their decision whether to replace the device. Fifty patients whose devices were not recalled reported demographic data. In both groups, psychological factors were assessed. No significant differences were found for psychological factors. Most patients reported being informed of their recall by their physician. Most estimated the risk of device failure to be low or very low, but they overestimated the fail rate. Thirty-six per cent of patients reported feeling anxious about the recall.

No significant differences existed in psychological factors and QOL between patients whose ICDs were recalled compared with those whose devices were not. The majority of patients whose ICDs are the subject of an FDA advisory/recall have a realistic understanding of the risks of device failure. Prompt information, support, and reassurance provided by healthcare professionals may allay patient distress.

Surviving patients (n = 610) who received an ICD in our institution since 1989 completed the Short Form Health Survey (SF-36) and the Hospital Anxiety and Depression Scale. Mean age was 62.4 years with 18% females. In a multivariate logistic regression analysis, symptomatic heart failure was the most important correlate of impaired QOL (SF-36) across all eight subscales [odds ratios (ORs) ranging from 5.21 to 22.53)], whereas psychotropic medication, age, comorbidity, amiodarone, and ICD shocks all correlated to a lesser extent. Symptomatic heart failure was also the most dominant correlate of anxiety [OR 5.15 (3.08–8.63), P < 0.001] and depression [OR 6.82 (3.77–12.39), P < 0.001]. Implantable cardioverter-defibrillator shocks correlated less yet significantly with anxiety [OR 2.21 (1.32–3.72) P < 0.01] and depression [OR 2.00 (1.06–3.80), P < 0.05].

Symptomatic heart failure was the single most important clinical correlate of impaired QOL, anxiety, and depression, with ICD shocks playing only a secondary role. This suggests that comorbidity rather than ICD therapy per se influences patients' device acceptance, supporting the increasing use of prophylactic ICD implantation.

We examined consecutive patients in whom CRT was implanted disregarding the atrial rhythm. Atrial fibrillation was defined as either current or earlier AF, response to CRT was defined as a decrease in the left ventricular end-systolic volume of ≥10% after 6 months. Total atrial conduction time (TACT), a measure to predict the risk of developing AF, was determined by echocardiography. We included 114 patients, of whom 56 (49%) were known with AF (23 current AF and 33 earlier AF). The other 58 patients had no history of AF. After 6 months, response in current and earlier AF and that in SR patients was comparable (56, 58 and 55%, respectively). In AF patients, multivariate analysis revealed a shorter TACT at baseline [odds ratio (OR) 16.7 (1.5–185.3), P = 0.02] and an interventricular mechanical delay (IVMD) >40 ms [OR 10.4 (1.0–110.9), P = 0.05] as predictors for response. Non-responders more frequently suffered from new-onset AF (P = 0.02).

Failure to CRT is associated with new-onset AF. Total atrial activation time may be a parameter to predict response in AF patients.

A total of 200 consecutive HF patients (158 males, mean age 56 ± 13.5 years) with standard indications for cardiac resynchronization therapy (CRT) were evaluated prospectively. The prevalence of an interventricular mechanical delay ≥40 ms was lower in patients with pure right bundle branch block (RBBB) than that in those with RBBB plus left fascicular hemiblock (RBBB-LFH) and those with left bundle branch block (LBBB) (33 vs. 50 vs. 54%, P = 0.05). A maximal difference in peak myocardial systolic velocity among all 12 segments (Ts)>100 ms was found in 63% of the patients with LBBB, whereas it was present in 31% of the patients with pure RBBB and in 42% of those with RBBB-LFH (P < 0.001). A standard deviation of Ts (Ts-SD)>34 ms was present in 58% of the LBBB subjects, but in only 29% and 42% of the patients with pure RBBB and RBBB-LFH, respectively (P < 0.001). Intraventricular dyssynchrony, however, was not different in patients with pure RBBB and in those with RBBB-LFH in terms of maximal difference in Ts (P = 0.25) and Ts-SD (P = 0.17).

Although LBBB was more often associated with intraventricular dyssynchrony, ECG sign of additional left ventricular (LV) conduction delay is not a helpful tool for the identification of intra-LV mechanical dyssynchrony in HF patients with RBBB who would benefit from CRT.

We randomized 98 patients with atrioventricular block (AV-block) undergoing pacemaker implantation to positioning the ventricular lead in the high or mid septum (n = 53) or in the apex (n = 45) of the right ventricle. N-terminal pro-brain natriuetic peptide (BNP) levels, left ventricular ejection fraction (LVEF), and exercise capacity were analysed 3 days, 3 months, and 18 months after the implantation. The primary endpoints were the changes of these parameters from baseline to 18 months.

Changes of BNP levels, LVEF, and exercise capacity from baseline to 18 months were statistically not different between septal and apical stimulation. The clinical occurrence or deterioration of overt heart failure was similar in both treatment arms.

With regard to different parameters of congestive heart failure, a septal stimulation site is not superior to conventional apical pacing in unselected patients undergoing pacemaker implantation for AV-block.

Twelve consecutive patients with standard pacemaker indication (9 male, 74 ± 9 years) entered the study. Pacing leads were implanted in the right ventricular apex and directly in the His bundle, and were connected to different ports of the pacemaker. All patients first underwent 3 months of DHBP, followed by 3 months of RVAP. At the end of each 3-month period, myocardial perfusion was measured at rest using scintigraphy with Tc99m-SestaMIBI. The average values of perfusion were evaluated on a 20-segment basis. All patients also underwent clinical evaluation, echocardiography, and tissue Doppler imaging (TDI), to measure dyssynchrony, and a blood sample was taken for brain natriuretic peptide (BNP) assay. The perfusion score during DHBP pacing was significantly better than during RVAP (0.44 ± 0.5 vs. 0.71 ± 0.53, respectively; P = 0.011). None of the patients showed lower perfusion during DHBP than during RVAP. We found no significant difference in NYHA class, ventricular volumes, ejection fraction, or plasmatic BNP between DHBP and RVAP. However, mitral regurgitation (0.26 ± 0.21 vs. 0.37 ± 0.25; P < 0.001) and dyssynchrony (13.75 ± 4.28 vs. 22.02 ± 8.44; P = 0.008) were significantly less during DHBP than during RVAP.

Direct His bundle pacing is superior to RVAP in preserving the physiologic distribution of myocardial blood flow and reducing mitral regurgitation and left ventricular dyssynchrony.

A total number of 70 patients with paroxysmal AF and episodes ≤24 h were scanned on a 1.5-T-CMRI before and 6 months after PVI during sinus rhythm. End-diastolic volume, end-systolic volume, and LVEF were determined by epicardial and endocardial measurements. Patients were categorized into two groups regarding cardiac function as assessed by CMRI: group 1 patients (n = 18) with an LVEF < 50% and patients with an LVEF > 50% (group 2, n = 52). Group 1 patients demonstrated a significant lower success rate than patients of group 2 after a follow-up of 152 ± 40 days (50 vs. 73%, P < 0.05). Cardiac magnetic resonance imaging in group 1 patients demonstrated a significant improvement in cardiac function after AF ablation (41 ± 6 vs. 51 ± 12%, P = 0.004), whereas group 2 patients did not show significant differences (60 ± 6 vs. 59 ± 9%, P = 0.22) after a 6 months follow-up.

Pulmonary vein isolation improves cardiac function in patients with paroxysmal AF and impaired LVEF. These data suggest that an impaired LV function can be partially attributed to AF with short-lasting paroxysms.

A total of 106 cases (58 males, average age 66.0 ± 8.8 years) with paroxysmal AF were included for ablation. They were allocated randomly to two groups: CPVI group (n = 54) and CPVI + SVCI group (n = 52). All cases underwent the procedure successfully. Pulmonary vein isolation was achieved in all cases. The procedural time and fluoroscopic time were comparable between the two groups. The mean ablation time for SVC was 7.8 ± 2.7 min. Superior vena cava isolation was obtained in 50/52 cases. In the remaining two cases, SVCI was not achieved because of obviating diaphragmatic nerve injury. During a mean follow-up of 4 ± 2 months, 12 (22.2%) cases in the CPVI group and 10 (19.2%) cases in the CPVI + SVCI group had atrial tachyarrhythmias (ATa) recurrence (P = 0.70). Nine of 12 cases in the CPVI group and 8/10 cases in the CPVI + SVCI group underwent reablation (P = 0.86), and PV reconnection occurred in 7/9 cases in the CPVI group and in 8/8 cases in the CPVI + SVCI group. All PV reconnection was reisolated by gaps ablation. There was no SVC reconnection in the CPVI + SVCI group. In two cases without PV reconnection from the CPVI group, SVC-originated short run of atrial tachycardia was identified and eliminated by the SVCI. At the end of 12 months of follow-up, 50 cases (92.6%) in the CPVI group and 49 (94.2%) in the CPVI + SVC group were free of ATa recurrence (P = 0.73).

In our series of paroxysmal AF patients, empirically adding SVCI to CPVI did not significantly reduce the AF recurrence after ablation. Superior vena cava isolation may be useful, however, in selected patients in whom the SVC is identified as a trigger for AF. However, because of the preliminary property of the study and its relatively small sample size, the impact of SVCI on clinical results should be evaluated in a large series of patients.

Thirty-nine patients with ECG documented atrial fibrillation (AF) scheduled for coronary artery bypass grafting (CABG) with or without concomitant valve surgery were consecutively elected for epicardial RF ablation. Thirty-nine age- and gender-matched patients scheduled for CABG with or without concomitant valve surgery only and with documented AF served as controls. The follow-up after ablation was 32 ± 11 months. The percentage of patients in sinus rhythm (SR) at long-term follow-up was 62 vs. 33% (P = 0.03) after ablation and no ablation, respectively. SR at 3 months was highly predictive of that at 32 months (sensitivity 95%, positive predictive value 86%). Long-term SR was associated with better QoL, fewer symptoms, higher ejection fraction, and smaller left and right atria than AF.

SR at 3 months was highly predictive of long-term SR that was associated with clinical improvement when compared with patients still in AF. AF at 3 months did not preclude a later stabilization to SR.

A retrospective cohort study was designed. A group of marathon runners (n = 252) and a population-based sample of sedentary men (n = 305) recruited in 1990–92 and 1994–96, respectively, were contacted in 2002–03 and invited to attend an outpatient clinic to identify suggestive symptoms of having experienced an arrhythmia requiring medical attention. In those with suggestive symptoms of atrial fibrillation, medical records were reviewed. Finally, LAF was diagnosed on the basis of the presence of atrial fibrillation in an electrocardiographic recording. In the group of marathon runners, an echocardiogram was performed at inclusion and at the end of the study. The annual incidence rate of LAF among marathon runners and sedentary men was 0.43/100 and 0.11/100, respectively. Endurance sport practice was associated with a higher risk of incident LAF in the multivariate age- and blood pressure-adjusted Cox regression models (hazard ratio = 8.80; 95% confidence interval: 1.26–61.29). In the group of marathon runners, left atrial inferosuperior diameter and left atrial volume were both associated with a higher risk of incident LAF.

Long-term endurance sport practice is associated with a higher risk of symptomatic LAF in men. This risk is associated with a larger left atrial inferosuperior diameter and volume in physically active subjects.

We included 470 patients who underwent an electrophysiological study for paroxysmal, regular, and narrow-QRS complex tachycardia without pre-excitation in sinus rhythm. The ECG recordings were reviewed for the presence of the following: (i) pseudo r' deflection (V1) and/or pseudo s-wave (inferior leads), (ii) identifiable P-wave after the QRS complex, (iii) QRS alternans, and (iv) repolarization abnormalities during tachycardia. We performed a cross-validation method using the first 300 patients to develop a logistic model to predict the tachycardia diagnosis. The model was validated through the remaining 170 patients. The invasive study demonstrated AVNRT in 314 patients and AVRT in 156 patients. The presence of pseudo r' deflection and/or pseudo s-wave, a visible P-wave after the QRS complex, and QRS alternans were selected by a stepwise multiple logistic regression analysis as predictors for the diagnosis of AVNRT. The application of the model in the validation group showed a shrinkage prediction factor of 3%. Diagnostic probabilities for both tachycardia mechanisms depending on every combination of selected ECG criteria were >75% in 70% of the patients.

The presence of pseudo r' deflection and/or pseudo s-wave, an identifiable P-wave after the QRS, and QRS alternans during tachycardia permit us to derive a reliable logistic model to predict the mechanism of paroxysmal AVRT in patients without pre-excitation. Precise probabilities for a correct diagnosis associated with every combination of those classical ECG criteria are presented.

A six step regimen of oral therapy was used in 55 infants with SVT: (i) propafenone (P); (ii) flecainide (F); (iii) flecainide plus propranolol (FP); (iv) amiodarone (A); (v) amiodarone plus propranolol (AP); (vi) amiodarone plus flecainide plus propranolol (AFP). If one step was not successful, the patient was passed on to the next treatment step and so on. Transesophageal atrial pacing (TAP) was used to evaluate treatment efficacy and the evolution of SVT at the end of the first, second, and third year. Propafenone was successful in 32.7% of the patients, F in 14.5%, FP in 23.6%, A alone in 5.4%, and AP in 18.1%; only 7.2% reached step 6. At month 12, after therapy wash out, SVT recurred spontaneously in 2 patients (3.6%) and remained inducible in 25 (45.5%). Inducibility was significantly higher in patients treated with A. At 24 months, SVT was inducible or spontaneous in 86% of the cases and at 36 months in 87%. There were no recurrences using the treatment confirmed by TAP. No further predictor of SVT inducibility was identified.

Supraventricular tachycardia disappeared in ~50% of the patients during the first year of life and in another 20% thereafter. The necessity for A treatment is the only predictor of persistence of the re-entry circuit during the first year of life. Transesophageal atrial pacing is useful in guiding the medical treatment.

A total of 1627 PM recipients with AF at implantation were followed in a single-centre, longitudinal study for up to 35 years. Baseline factors affecting survival and long-term follow-up were analysed. A total of 7362 patient-years of follow-up (PM implanted between 1971 and 2000, followed until 31 December 31 2005) were analysed. Female PM recipients lived significantly longer than male (P = 0.025; mean survival 91.9 vs. 72.1 months) despite older age at time of inclusion. Mean survival times almost doubled for patients implanted in the last decade, with 139.8 months in the nineties vs. 66.8 months in the seventies and 75.7 months in the eighties (P < 0.001). Male gender, age at implantation, non-syncopal bradycardia, and decade of implantation influenced survival.

Life expectancy in AF patients after PM implantation has doubled within the last three decades, with a mean survival in the overall population of 7.6 years for women and 6.0 years for men. Survival is influenced by several simple baseline characteristics, which may help to identify patients with very long survival times.

All Danish patients were discharged following first-time atrial fibrillation and their pharmacotherapy was identified by individual-level-linkage of nationwide registers of hospitalization and drug dispensing from pharmacies. A total of 108 791 patients survived 30 days after discharge and were included. In 1995–1996, 7.4% of the patients received beta-blockers, increasing to 44.3% in 2003–2004. The corresponding figures for amiodarone were 2.9 and 5.4%. In contrast, use of nondihydropyridine calcium-channel blockers, digoxin, sotalol, and class 1C antiarrhythmics decreased from 20.6, 63.9, 21.3, and 4.0% in 1995–1996 to 12.6, 43.8, 4.2, and 1.3% in 2003–2004, respectively. Notably, patients receiving anticoagulants increased from 29.8 to 43.5%. Multivariate logistic regression analysis revealed females to be associated with more use of digoxin, but less use of amiodarone and oral anticoagulants than males. Patients above 80 years received less pharmacotherapy, apart from digoxin treatment that was more commonly used in elderly.

Pharmacotherapy of atrial fibrillation has changed towards increased beta-blocker use with a coincident decrease in the use of other rate-limiting drugs and sotalol. Treatment with amiodarone or class 1C antiarrhythmics remained very low. Oral anticoagulant therapy increased considerably, but women and elderly were apparently undertreated.

The Euro Heart Survey on AF enrolled 5333 patients with AF in 35 European countries in 2003 and 2004. This was a bottom-up cost study conducted for the five largest contributors in terms of patients enrolled. Quantities of resource use during the enrolment admission and during 1-year follow-up were inferred from survey data and multiplied by national unit costs in order to estimate per patient costs associated with AF for each country. Mean costs of inpatient admission of an AF patient were estimated at 1363, 5252, 2322, 6360, and 6445 and mean costs incurred on an annual basis at 1507, 3225, 1010, 2315, and 2328 in Greece, Italy, Poland, Spain, and the Netherlands, respectively. Inpatient care and interventional procedures were identified as the main drivers of costs, accounting for more than 70% of total annual costs in all five countries.

Estimates of the economic burden posed by AF are critical in light of the increasing importance of AF as a public health problem.

Atrioventricular node ablation and subsequent permanent pacing is a well-established therapy for patients with AF. Long-term right ventricular pacing may induce HF.

In 121 (45 with previous HF) patients with drug refractory AF, AV node ablation and implantation of a pacemaker was performed. At baseline and after a mean follow-up of 4.3 ± 3.3 years, New York Heart Association (NYHA) functional class for HF and left ventricular (LV) and atrial diameters were assessed. During and at the end of follow-up, hospitalizations for HF, mortality, and quality of life were assessed using the SF-36 and an AVN-specific questionnaire. No significant changes in NYHA functional class (87 vs. 77% in NYHA I/II at baseline vs. end of follow-up) and LV end diastolic diameter (51 ± 7 vs. 52 ± 8 mm) were observed. Left ventricular end systolic diameter decreased (from 37 ± 9 to 34 ± 7 mm, P = 0.03) and fractional shortening improved (from 28 ± 10 to 34 ± 9, P = 0.02) in all patients and in patients with previous HF, but not in patients without previous HF. Hospitalizations for HF occurred in 24 patients (20%), predominantly those with previous HF. All-cause mortality occurred in 31 (26%) patients. At the end of follow-up, quality of life was comparable with the control group.

Long-term outcome of AV node ablation and permanent pacing is good. Atrioventricular node ablation remains a treatment option for AF.

Thirty-nine patients subjected to PV isolation for paroxysmal AF were followed-up for at least 3 years according to a strict protocol. Fourteen patients (35.8%) had one, 19 patients (50%) had two, and 6 patients (15.4%) had three ablation procedures. At end of follow-up (42.2 ± 6.0 months), 17 patients (43.5%) were completely free of AF or other atrial arrhythmia, and 26 patients (66.6%) had symptomatic improvement. The long-term success rate was 21.4% for patients subjected to a single ablation procedure, 52.6% for patients subjected to two catheter ablation procedures, and 66.7% for patients who underwent three ablation procedures (P = 0.094). There was also a trend for patients who underwent a combination of different ablation procedures (ostial, antral, and/or circumferential) to have a higher AF-free survival when compared with patients subjected to the same procedure (P-value for log-rank test = 0.036).

Catheter ablation does not eliminate paroxysmal AF in up to 56% of patients in the long term, despite the use of two or three ablation procedures in two-thirds of them. However, it confers symptomatic improvement in 67% of treated patients.

Thirty patients with paroxysmal AF originating from the pulmonary veins (PVs) or superior vena cava (SVC) were enrolled. Frequency analysis was performed on the intracardiac electrograms recorded from various mapping sites in both atria sequentially with simultaneous surface electrogram recordings. The SVC–AF patients had a trend toward a higher DF in ECG lead V1 when compared with the PV–AF patients (7.35 ± 2.09 vs. 5.89 ± 0.79 Hz, P = 0.018). The mean dominant frequency (DF) of the LA mapping sites in the PV–AF patients was higher than that in the SVC–AF patients (7.06 ± 0.66 vs. 6.13 ± 0.96 Hz, P = 0.009), whereas the mean DF of the RA mapping sites was similar between the two groups (5.84 ± 0.80 vs. 6.26 ± 1.11 Hz, P = NS). The intra-class correlation coefficient (ICC) between the mean DF of the RA sites and V1 was higher (r = 0.21, P = 0.02) when compared with the mean DF of the LA sites (r = –0.007, P > 0.05). Furthermore, the maximal ICC was observed in the anterolateral RA free wall (r = 0.84, P < 0.001) and not the other anatomic sites of the RA and LA.

The fibrillatory activity observed in ECG lead V1 correlated primarily with the activity of the anterolateral RA free wall and thus may be useful for detecting the AF source if it is close to that area.

Blood samples were collected in patients with paroxysmal AF before and after PV isolation. Interleukin (IL)-6, IL-1β, TNF-, IL-8, IL-10, and IL-12, and stromal derived factor (SDF)-1 were measured by immunoassay. CD34+CD133+, CD117+, and endothelial progenitor cells (EPCs) were analysed by flow cytometry and culture assay. After ablation procedure, a rise in creatine kinase and troponin T levels indicated myocardial necrosis. Leukocyte counts and C-reactive protein and IL-6 levels increased significantly. Myocardial necrosis and inflammatory response correlated with an increase in IL-6 (P = 0.007). In contrast, SDF-1 levels decreased after RF ablation (P = 0.004). Yet, no significant changes were observed in IL-1β, TNF-, IL-8, IL 10, and IL-12 plasma levels or in the number of circulating CD34+CD133+ and CD117+ progenitor cells, whereas EPCs decreased by trend.

Although PV isolation by RF ablation in patients with paroxysmal AF induces a systemic inflammatory response associated with myocardial necrosis, no alterations in circulating progenitor cells were observed. Thus, isolated myocardial necrosis may not be sufficient to account for progenitor cell mobilization.

We performed a retrospective single centre study in a District General Hospital. The transthoracic echocardiogram reports of all patients with a discharge diagnosis of MI during a 6-month period were studied. We reviewed the notes of all patients with an estimated left ventricular ejection fraction (LVEF) of <35% and used UK national guidance to assess the incidence of potential ICD indications. Five hundred and forty-six patients had a discharge diagnosis of MI. Fifty had estimated LVEF <35% and 8–11 of these met the NICE post-MI primary prevention criteria for ICD implantation. This gives an estimated incidence based upon our local population of 29–39 patients/million/year. Most of these patients (64–88%) were identified purely by ECG criteria (QRS > 120 ms) and LVEF.

The latest published UK ICD data give a new implantation rate of ~40/million/year. Combining our results with published data for NICE secondary prevention indications gives a combined ICD indication incidence of ~105–115/million/year. This suggests there is currently significant under-provision of ICD therapy in the UK.

Fifty-two patients were included; 24 patients with atrioventricular nodal re-entry tachycardia (AVNRT), 13 patients with atrioventricular re-entry tachycardia (AVRT), and 15 patients with AT. Comparing the 37 non-AT patients with the 15 AT patients, there was a highly significant difference between the mean V–A interval difference, (delta V–A) 2.1 ± 1.8 ms (range 0–9 ms) vs. 79.1 ± 42 (range 22–267 ms) (P < 0.001), respectively. None of the patients in the non-AT group had a delta V–A > 10 ms. In contrast, all 15 patients with AT had a delta V–A interval >10 ms. Thus, the diagnostic accuracy of the delta V–A interval cut-off of >10 ms was 100%, with a 95% confidence interval of 93.1–100% for AT. In 11 (73%) of the 15 AT patients, the standard ventricular overdrive pacing manoeuvre was not possible. In 14 of the 15 patients (93%) in the AT group, standard atrial overdrive pacing showed variable V–A intervals, correctly diagnosing AT. In all 52 patients, this measurement was repeated during pacing from the other location. In five patients from the AT group, the result of the second attempt was different from the result of the first attempt.

We found that atrial differential pacing during paroxysmal SVT without termination of tachycardia and the finding of variable returning V–A interval was highly sensitive and specific for the diagnosis of AT. The manoeuvre can be easily performed in all patients with SVT and is highly reproducible. It is a useful adjunct to the currently available ventricular and atrial pacing manoeuvres.

The study enrolled patients with unexplained syncope who were consecutively referred to our Syncope Unit, either as outpatients or during hospitalization, in a 2-month period. The design of this observational study consists in three phases: a retrospective analysis of their clinical management in the 9 months prior to the first attendance at the Syncope Unit (phase one), their subsequent clinical management in the Syncope Unit (phase two) and a 9-month follow-up (phase three). The retrospective analysis of phase one showed that 25% of patients had already been hospitalized without diagnosis. After Syncope Unit evaluation, diagnosis was obtained in 82% of patients, with 15% of patients indicated to pacing. In the follow-up, 23% of patients experienced a syncopal recurrence. Our analysis indicated an 85% reduction of hospital costs in the follow-up period.

The clinical and economic analysis of the three phases of our study demonstrates that a Syncope Unit allows an improved management of patients with syncope.

Ninety-five consecutive patients received an implantable loop recorder to monitor recurrent syncope (n = 4.9±3.8) of unknown aetiology after cardiac investigations, including an electrophysiological study. Resting ECG was abnormal, suggesting an arrhythmic syncope, in 29 (30.5%) patients, while 21 (22.1%) patients had an underlying cardiac disease. During an average follow-up period of 10.2±5.2 months, 43 (45.2%) patients developed a new syncope associated in 27 of them (62.8%) with an arrhythmic event. Syncope was no more frequent in the subgroup of patients with cardiac conduction abnormalities on resting ECG, while the frequency of arrhythmic events was similar whether or not the ECG was normal. In the subgroup of patients with cardiac disease with normal left ventricular ejection fraction, the occurrence of syncope was less frequent, and the number of arrhythmic events was no greater in these patients.

Implantable loop recorder is a useful diagnostic tool for recurrent syncope of unknown aetiology.

In 69 consecutive patients who underwent biventricular (BIV) pacemaker implantation, we assessed the magnitude of intraventricular resynchronization achieved by means of simultaneous (BIV 0) and sequential BIV pacing (with an individually optimized VV interval value among +80 ms and –80 ms) using pulsed-wave tissue Doppler imaging techniques and in particular the measurement of the intra-LV electromechanical delay. The intra-LV delay was defined as the difference between the longest and the shortest activation time in the six basal segments of the LV. An abnormal intra-LV delay was defined as a value >41 ms. The intra-LV delay was 63 ± 28 ms baseline, decreased to 44 ± 26 ms with BIV 0 and to 26 ± 15 ms with optimized BIV (P = 0.001). BIV 0 determined the shortest delay in 28 (41%) patients (23 ± 12 ms). In 41 (59%) patients, a better resynchronization was achieved with optimized VV intervals (LV first in 32 and RV first in 5) or single-chamber pacing (LV in 3 and RV in 1). With BIV 0, the intra-LV delay remained abnormal in 41% and was longer than baseline in 30% of patients compared with 9 and 12% with optimized BIV, respectively (P = 0.001).

A sub-optimal resynchronization is achieved with simultaneous BIV pacing in most patients. A tailored programming of the relative contribution of RV and LV pacing forms the prerequisite for improving CRT results.

Fifty-seven patients with systolic LV dysfunction underwent quantitative analysis of BNP, mitral regurgitation (MR), and dyssynchrony at rest and during exercise. None had inducible ischaemia on perfusion imaging. By multiple regression analysis, end-systolic volume index (P < 0.0001), effective regurgitant orifice (ERO) (P < 0.001), and E/Ea (P = 0.002) emerged as independent determinants of BNP at baseline (R² = 0.67). Exercise induced a significant rise in BNP levels (P < 0.0001). In multivariate analysis, a smaller change in systolic blood pressure (P = 0.04), a larger increase in ERO (P = 0.017), and in systolic dyssynchrony index (P = 0.006) during exercise emerged as independent determinants of exercise-induced increases in BNP (R² = 0.45).

MR severity, volume overload, and LV filling pressure are surrogates of BNP at rest. During exercise, changes in BNP reflect the presence of dynamic changes in both LV dyssynchrony and MR severity in the absence of inducible ischaemia.

We performed TWA assessment in three high-risk patients who previously had undergone implantation of both implantable cardioverter defibrillator and SCS to treat refractory angina. The test was performed after switching off the SCS and after 2 and 24 h stimulation at the default amplitude. The protocol was executed 2 months apart in order to assess the reproducibility of the results, collecting a total of 18 TWA reports. In all the three patients, we observed a significant reduction of TWA amplitude after 2 h stimulation. All the tests were classified as negative after 24 h stimulation with the nominal parameters.

Spinal cord stimulation results in a decrease in the TWA magnitude, and thus it seems to positively affect the arrhythmic substrate in a time-dependent manner.

Three ablation steps are required to obtain PIA electrical silence: electrical PV isolation, the creation of two lines of lesions between the two superior and inferior PVs and the abolition of residual electrical signals within the PIA. The endpoint was the electrical silence and the inability to pace in the PIA. The posterior inter-pulmonary-vein atrium silence was obtained in 42 AF patients (56 ± 9 years, four women). Recurrence of AF and atrial flutter was observed in 14 (33.3%) patients after the first procedure. Freedom from atrial arrhythmias after the second procedure was displayed by 94.4, 85.7, and 60.0% of patients with paroxysmal, persistent, and permanent AF, respectively. The left atrium (LA) volume was larger, and the percentages of the silent area of the LA surface and voltages were lower in patients with AF recurrence than in recurrence-free patients.

Posterior inter-pulmonary-vein atrium electrical silence can greatly decrease the AF recurrence. The clinical AF recurrence may be related to an enlarged LA, a low percentage of electrically silent area, and low voltage in the LA.

All patients undergoing pulmonary vein isolation (PVI) from May 2004 to October 2004 had troponin T levels measured 4 h following completion of the procedure. The first 30 patients also had a troponin T level measured 1 h prior to PVI to establish a baseline reference.

Sixty patients were studied, with 81.7% males and a mean age of 54.6 ± 9.9 years. No patient had underlying structural heart disease. The baseline troponin T level was normal (<0.01 µg/L) in all 30 patients. Post-procedure troponin T levels were elevated in all 60 patients compared with baseline (P < 0.05), with a mean level of 0.85 µg/L and a range of 0.26–1.57 µg/L after an average RF ablation time of 56 ± 15 min. All levels were above the reference range for diagnosis of acute myocardial infarction (>0.15 µg/L). Troponin T level was not related to the number of RF lesions, RF time, procedure time, or associated external cardioversion.

Troponin T elevations occurred in all patients undergoing PVI, to levels at least 20 times the normal concentration, into the range for diagnosis of acute myocardial infarction. Therefore, troponin T would not be specific for ischaemia in the setting of chest pain post-catheter ablation for AF.