The left atrium (LA) was mapped using the EnSite^TM system during an episode of induced or spontaneous AF in patients with paroxysmal AF. Sinus rhythm was restored with electrical cardioversion and maintained for 10 min before re-induction of AF and repeat mapping. Maps were compared examining the mean cycle length at identical vertices, provided the anatomical point had data on both maps. Complex fractionated atrial electrograms were considered stable if the compared electrogram was within 50 ms—delta to 120 ms + delta. Eleven patients were studied; 10 were included [3 female, mean age 59.5 years (32–76)]. Complex fractionated atrial electrograms were observed in all regions of the LA. Complex fractionated atrial electrograms were evenly distributed throughout the LA but most reproducible at the roof and antero-lateral wall. Complex fractionated atrial electrograms were highly conserved between two episodes of AF with 76.1 ± 11.8% of CFAE reproducible at delta of 20 ms.

Complex fractionated atrial electrograms are reproducible at the same anatomic site in a separate episode of AF.

Five patients (four women, one man, mean age 43 ± 16 years) with severe symptoms due to focal AT originating from a PV were studied. A single transseptal puncture was done. After confirmation of the diagnosis by conventional mapping, a 23 or 28 mm cryoballoon catheter was positioned in the PV of interest. Freezing was done for 300 s and repeated at least once before attempts to induce arrhythmia. All patients were successfully treated. Total procedure and fluoroscopy time was 138 ± 55 and 26 ± 21 min, respectively. During a follow-up of 10 ± 7 months no clinical recurrences occurred.

Cryoablation using a cryoballoon might be an easy and safe tool to treat ATs originating from the PV with reasonable procedure time.

One hundred and twenty-seven of 454 patients (69% male, 58% paroxysmal, age 60 ± 10 years, AF duration 8 ± 7 years) scheduled for AF ablation between February 2004 and May 2008 were treated with dofetilide. Patients had failed 1.9 ± 1.1 AADs. Anti-arrhythmic drugs were stopped five half-lives before ablation and 3 months for amiodarone. Patients were followed for 15 ± 7 months with routine and symptom-driven monitoring. Success was defined as no further AF and partial success as a 50% reduction in frequency/duration of AF episodes. Thirty-six patients started dofetilide 158 ± 167 days before ablation: 9 had no improvement, 16 experienced partial success, 8 had no further AF, and 2 improved enough to forgo ablation. Seventy-one patients started dofetilide immediately following ablation, of which 14 had no improvement, 22 experienced partial success, and 32 had no further AF. Twenty patients started dofetilide 119 ± 153 days post-ablation, of which four had no improvement, seven experienced partial success, and nine had no further AF. Six patients discontinued dofetilide during initiation for QT prolongation.

Dofetilide appears safe and effective in preventing AF in patients refractory to other AADs undergoing catheter ablation.

Five hundred and fifty-four patients from the AFT (n = 372) and PAFS (n = 182) were studied. The individual percentages of pacing, Atrial Sense Ventricular Pace (ASVP), Atrial Pace Ventricular Pace (APVP), and Atrial Pace Ventricular Sense (APVS) as well as total ventricular pacing during synchronous rhythm (VPinSR, %) were examined for an effect on AFB. Three hundred and twenty-one (AFT, age 64 ± 11, 55% male) and 79 (PAFS, age 71 ± 8, 54% male) patients had complete data for analysis. Increased VPinSR was weakly associated with an increased AFB (effect size—10% VPinSR increased AFB by only 0.03%) in AFT (P = 0.04) but not PAFS (P = 0.98) or the pooled analysis (P = 0.95). None of the synchronous paced modalities (ASVP, APVP, APVS) significantly increased AFB compared with sinus rhythm (Atrial Sense Ventricular Sense) (P = ns).

No pacing modality, atrial or ventricular, had a significant effect on AFB. On the basis of these data, the detrimental effect of high-frequency right ventricular pacing on AFB in paced PAF patients, unlike with persistent AF, appears to be minimal in the short term.

Causes of death of consecutive ICD recipients implanted over a 10 year period were analysed. Overall 822 patients (age 63 ± 11 years, 80% male, EF 34 ± 14%, secondary prevention 65%) were followed for 43 ± 30 months during which time 225 patients died (annual mortality 7.6%). Causes of death were cardiac arrhythmic in 16%, cardiac non-arrhythmic in 39%, non-cardiac vascular in 4%, non-cardiovascular in 27%, and unknown in 13%. Advanced age [relative risk (RR) 1.23 per decades, 95% confidence interval (CI) 1.06–1.43], NYHA class >II (RR 2.27, 95% CI 1.51–3.41), renal failure (RR 1.57, 95% CI 1.15–2.14), use of amiodarone (RR 2.56, 95% CI 1.91–3.43), digitalis (RR 1.87, 95% CI 1.40–2.49), diuretics (RR 1.89, 95% CI 1.35–2.66) were independent predictors of all-cause mortality. Predictors for arrhythmic mortality were NYHA class >II (RR 12, 95% CI 3.69–37.5), spontaneous or inducible VT as indication for ICD therapy (RR 2.53, 95% CI 1.06–6.05), and use of amiodarone (RR 3.95, 95% CI 2.02–7.75).

In this unselected group of ICD recipients, at least 16% of patients died from arrhythmic causes. Risk factors associated with arrhythmic mortality were a history of spontaneous or inducible VT, higher NYHA class, and amiodarone use.

Pubmed, Cochrane clinical trials database, and EMBASE were searched until December 2008. In addition, a manual search was performed using review articles, reference lists of papers, and abstracts from conference reports. Of the 90 initially identified studies, 11 observational studies with 3010 patients were analysed. The meta-analysis of these studies showed that CKD was associated with higher mortality risk (HR = 3.44, 95% CI 2.82–4.21, Z = 12.09, P < 0.001) while there were no significant differences between individual trials (P = 0.09, I² = 37.8%). A subgroup analysis which included the four studies that used estimated glomerular filtration rate (GFR) <60 mL/min/1.73 m² to define CKD showed a higher mortality in the CKD group as well (HR = 3.06, 95% CI 2.31–4.04, Z = 7.84, P < 0.001) without significant heterogeneity (P = 0.38, I² = 5.2%).

Our meta-analysis suggests that CKD is associated with increased mortality in patients who receive ICD therapy. Undoubtedly, prospective studies are needed in order to elucidate the impact of different stages of CKD in this setting. Given that the CKD prevalence is rapidly increasing, there is an imperative need for better risk stratification of ICD therapy candidates.

Subjects were 274 consecutive patients with non-ischaemic dilated cardiomyopathy who received ICD implantation. Estimated glomerular filtration rate (eGFR) was calculated using the modification of diet in renal disease formula. Renal dysfunction was defined as eGFR <60 mL/min/1.73 m². Differences in survival, appropriate ICD therapy and electrical storm in patients with and without renal dysfunction were compared. The effect of worsening renal function (decrease of eGFR of at least 15 mL/min/1.73 m² within 1 year) on appropriate ICD therapy was also evaluated. There was a higher incidence of appropriate ICD therapy in patients with eGFR <60 mL/min/1.73 m² than in those with eGFR ≥60 mL/min/1.73 m² (P = 0.0001). Patients with eGFR <60 mL/min/1.73 m² also showed a significantly higher rate of electrical storm (P = 0.003). Renal dysfunction with eGFR <60 mL/min/1.73 m² was an independent predictor of appropriate ICD therapy (HR 1.85, 95% CI 1.24–2.77, P = 0.003). Patients with worsening renal function within 1 year after implantation were at increased risk for appropriate ICD therapy (HR 2.50, 95% CI 1.39–4.52, P = 0.002).

Our results suggested that renal dysfunction is an independent risk factor for occurrence of life-threatening arrhythmia even in high-risk patients with non-ischaemic dilated cardiomyopathy.

Eighteen consecutive patients underwent contrast-enhanced, ECG-gated CT scanning. Coronary sinus, coronary veins, superior vena cava, the distal portion of the trachea, and of the two main bronchi were reconstructed. These images were then fused over the CS fluoroscopic angiogram. Registration accuracy was verified by assessing the overlap of CS borders both in the CT- and in the fluoroscopy-derived images. The mean distance between the centrelines of the CS was 0.73 mm, with a maximum distance of 2.22 mm. For the first-order branches, mean distance was 0.80 mm with a maximum distance of 2.64 mm. High Lin concordance correlation coefficients were computed (>0.95) for the CS and first-order branch diameters, although the Bland and Altman limits were large. The agreement between the number of vessels identified was moderate with = 0.43.

Fusion imaging processing of two different imaging modalities (CT and fluoroscopy) may be feasible and accurate for guiding CRT implantation as it allows constant comprehensive display of CS body and branches. Prospective studies are needed for assessing clinical implications.

The retrograde contrast venograms were retrospectively reviewed in 133 patients (age 68 ± 9 years, 101 males). The quantity and distribution of veins were recorded as well as the final lead position. There were no major differences in the distribution of LV lead positions between I and N [posterior vein, 14.0% (I) vs. 15.8% (N); posterolateral vein, 21.1 vs. 18.4%; lateral vein, 59.7 vs. 50.0%; anterolateral vein, 3.5 vs. 13.2%; P= NS]. Excluding the middle and great cardiac veins, in total only 59 of 133 patients had more than one suitable vein as potential targets for LV lead placement (I, 36.8% vs. N, 50.0%; P = 0.16).

Underlying aetiology does not affect the quantity and distribution of coronary veins available for LV lead placement. The limitations of venous anatomy restrict LV lead placement to a single vein with little scope for site selection in almost half of all the patients. Given these limitations, in many patients, prospective targeting of LV lead placement may require a direct surgical approach.

Intracardiac LV and RV dP/dt were measured with a 0.014-in. sensor-tipped pressure guidewire during pacing at nine different VV intervals ranging from +80 ms (LV pre-excitation) to –80 ms (RV pre-excitation) in 26 patients who received a biventricular pacemaker. No correlation was found between the optimal VV intervals identified by maximum LV dP/dt and RV dP/dt, which were identical in only seven cases (27%). Only when testing slightly broader intervals (±20 ms) was there a statistically significant correlation (P= 0.037) between the optimized VV intervals. In the majority of patients (58%) either LV or RV pre-excitation was superior to simultaneous pacing according to LV dP/dt_max measurements.

RV dP/dt_max failed to identify the optimal VV interval when compared with LV dP/dt_max and can therefore not be recommended for VV optimization in CRT patients.

In our institution from 2000 to 2004, all extractions requiring an ablative sheath were performed using the EDS system. In 2004, an excimer laser system was acquired, which became the first choice. Consecutive patients undergoing extraction requiring an ablative sheath (EDS or laser) were studied. From 2000 to 2007, 140 leads were extracted from 74 patients (EDS 31 and laser 43). Procedural success was non-significantly higher in the laser vs. the EDS group (95 vs. 87%). In the EDS group, one patient suffered tamponade requiring surgery; in the laser group, one patient suffered a significant pericardial effusion treated conservatively. There were no deaths. Procedure and fluoroscopy times were similar between groups. More patients were referred for primary surgical extraction in the EDS vs. the laser era (7 vs. 0, P = 0.003).

Lead extraction using an ablative sheath is safe and effective. In our small study, there were no significant differences between EDS and laser sheaths in terms of success, time, or safety.

This study is a retrospective analysis of the case records of all patients referred to our institution for transvenous lead extraction, according to class I or II Heart Rhythm Society indications. Over 7 years, 300 consecutive patients underwent procedures for transvenous removal of 518 leads. The most frequent indication for extraction was infection (74%). Complete removal of 502 (96.9%) leads and partial removal of 10 leads (1.9%) were achieved. Six leads (1.2%) could not be removed. All defibrillation coils and coronary sinus leads were successfully removed. There were no procedure-related deaths but only one major complication (0.3%).

Our experience shows that the proposed mechanical technique is very effective and associated with few serious complications, thus confirming previous findings. This approach may be reproduced in other settings with very satisfactory results.

Special autopsy was performed on 78 patients deceased in a hospital. Age at death was 77.9 ± 10.0, implantation-death interval 4.0 ± 3.3 years, ventricular leads n = 78, and atrial leads n = 21. Thrombi along leads in brachiocephalic vein/upper caval vein (BV/UCV) were found in 22 (7), in right atrium (RA) in 11 (8), and in right ventricle (RV) in 11 cases. Bipolar lead rings were fixed by fibrous tissue in 43 (4) cases. Connective tissue bridges and tunnels were found in BV/UCV in 44 (13), in RA in 17 (15), and in RV in 68 cases, with a length of 0.2–12.0 cm. Right ventricular leads in tricuspidal orifice were fixed by fibrous tissue in 11 and penetrating chordae in 25 cases. Main causes of death were: heart failure in 35, pulmonary embolism in 9, and myocardial infarction in 11 cases.

We have found (i) thrombi on ventricular/atrial leads in 33/48%, (ii) bipolar lead rings fixed by fibrous tissue in 68/22%, (iii) connective tissue bridges or tunnels in ventricle/atrium in 87/71%, and (iv) ventricular leads fixed to valve or penetrating chordae in 46% of patients. We do recommend caution when extracting leads.

We included 1131 patients with inferior STEMI, who underwent primary PCI between 2000 and 2007 and of whom a pre-procedural 12-lead ECG was available, recorded immediately prior to PCI. The IRA was determined during emergency angiography. Coronary angiography confirmed the right coronary artery (RCA) as the IRA in 895 patients (79%) with inferior wall STEMI. Application of the ECG algorithm resulted in 624 true positive cases of acute RCA obstruction (sensitivity: 70%, 95% CI: 67 –73%) and 170 cases with true negative result (specificity: 72%, 95% CI: 66–77%). Sensitivity of >90% was established in patients with cumulative ST-segment deviation above median (>18.5 mm).

The conventional ECG algorithm showed a low sensitivity for the non-invasive diagnosis of RCA occlusion in an all-comer, inferior STEMI cohort undergoing primary PCI. Sensitivity was only sufficient in patients with extensive ST-segment deviation.

Patients with systolic heart failure [defined by a left ventricular ejection fraction (LVEF) <50%] were enrolled. Standard digitized 12-lead ECGs were used for analysis of T-wave morphology descriptors [lead dispersion, T-wave morphology dispersion, percentage of the loop area, percentage of the outer area, and the total cosine between QRS and T-wave (TCRT)]. A total of 650 patients with a mean age of 63 ± 14 years were enrolled and followed-up for 2.7 ± 1.8 years. The mean LVEF was 36 ± 9%. During this study, the total mortality rate was 32.7% and cardiovascular mortality rate was 22.3%. A stepwise backward Cox regression analysis showed that cardiovascular mortality was significantly associated with age (P < 0.001), diabetes mellitus (P = 0.022), haemoglobin (P = 0.001), LVEF (P = 0.001), and TCRT (P = 0.003). On the basis of a median TCRT of –0.473 as a cut-off point, a significant difference in cardiovascular mortality was observed from a Kaplan–Meier survival curve (P = 0.01). Total cosine between QRS and T-wave further stratified the risk of LVEF (P = 0.007), age (P = 0.001), haemoglobin (P < 0.001), and diabetes mellitus (P < 0.001) in cardiovascular mortality for these patients.

Total cosine between QRS and T-wave may provide further risk stratification for and therefore impact on the prognosis of patients with systolic heart failure.

Activation recovery intervals (ARI) and activation times (AT) were measured from unipolar electrograms at 10 sites along the apicobasal right ventricle (RV) in 14 patients with cardiomyopathy (LVEF < 40%). These measurements were made during control, dobutamine 2.5–5.0 µg/kg/min, and a recontrol phase while maintaining constant heart rates with atrial pacing. Dispersion of repolarization was calculated from the total recovery time (TRT, AT+ARI). Activation–repolarization coupling was assessed by linear regression of ARI and AT. Dispersion of repolarization across all 10 sites and between adjacent sites increased with dobutamine compared with control (whole DOR: range 15 ± 2 vs. 12 ± 2 ms, P = 0.06 and standard deviation 5.5 ± 0.9 vs. 4.3 ± 0.9 ms, P = 0.04; adjacent DOR: 5.9 ± 0.8 vs. 4.5 ± 0.6 ms, P = 0.04). This was associated with shallower ARI/AT slopes (–0.3 ± 0.2 vs. –0.8 ± 0.2, P = 0.05) and a decrease in ARI–AT correlation (R² 0.4 ± 0.1 vs. 0.6 ± 0.1, P = 0.05) with dobutamine compared with control.

Adrenergic stimulation increases apicobasal RV DOR and reduces coupling between activation and repolarization in patients with cardiomyopathy. This may provide a mechanism for the proarrhythmic potential of heightened adrenergic states in these patients.

Twenty mini-pigs underwent AV nodal cryoablation at –80°C without prior cryomapping. The duration of the cryoapplication following atrioventricular block (AVB) was randomized to 0, 10, 20, 40, or 60 s. Atrioventricular block was obtained in all animals after a median of 3 (1–8 interquartile range) applications. One week later, AV nodal conduction fully recovered in animals with application duration <10 s, whereas persistent AVB incidence increased as a function of time in animals with longer applications duration. Cryoablation application duration following AVB was the only independent predictor of persistent AVB (OR, 1.116; 95% CI, 1.013–1.229; P = 0.026). There was no difference in lesion location or size between animals with vs. those without persistent AVB at 1 week. However, animals randomized to longer application duration demonstrated higher degree of cell destruction and fibrotic content.

In this closed-chest pig model, there was a relation between cryoapplication duration following AVB at –80°C and recovery of conduction. A safety window of at least 10 s was observed in all cases.

In 22 patients (10 male, mean age 65 ± 6 years) with paroxysmal atrial fibrillation (PAF), a PVI during real-time PV spike registration and oesophageal temperature measurement was attempted. In 15 patients, a steerable sheath was used along with the HIFU-BC. In 67 of 83 PVs (81%), PVI was achieved exclusively using HIFU. Using the steerable sheath, the acute PVI rate rose from 50% (10/20 PVs) to 90% (57/63 PVs). In the latter, PVI was achieved with a single HIFU application in 60% (38/63 PVs) and mean sonication time of 11 ± 7 s. The mean procedure time was 166 ± 74 min including 58 ± 25 min of HIFU-BC left atrial indwelling time. In four patients, peri-procedural complications occurred (one transient ischaemic attack, one phrenic nerve palsy, and two vascular access complications). During a median follow-up of 342 days (range 272–378 days), 71% patients remained free of any AF/AT recurrence without antiarrhythmic drugs after a single procedure.

The novel defocused 12F HIFU-BC used in conjunction with a steerable sheath allows for very rapid PVI in patients with PAF. The enthusiasm for rapid PVI is still dampened by the potential risk of collateral damage.

We evaluated 99 pts, 66 male, mean age 54.4 ± 10.1 years, referred for CA because of drug resistant AF. All pts were submitted to 64-slice MDCT scan for electroanatomic mapping integration, pulmonary veins anatomy delineation, LA thrombi exclusion, and LA volume estimation. Complete isolation of all the PVs was always performed with eventual cavo-tricuspid isthmus ablation. For a mean follow-up period (Fup) of 16.7 ± 6.6 months, clinical success was assessed after a 3-month blanking period. Anti-arrhythmic drug therapy was discontinued or modified at the clinician's criteria. At the end of the Fup, 29 pts suspended anti-arrhythmic drug therapy and 26% were of oral anticoagulation. Univariate analysis showed that the probability of AF relapse after CA was higher in pts with non-paroxysmal forms of AF. The probability of relapse was significantly higher in pts with LA volumes greater than 100 mL when assessed by MDCT. We found that the LA volume of 145 mL was a good cut-off value for AF recurrence prediction. Patients with LA volumes greater than 145 mL had significantly higher recurrence rates of arrhythmia, even when adjusted for the effect of age, gender, body mass index, hypertension, and type of AF.

Left atrium volume estimated by MDCT may be useful to identify pts in whom successful AF ablation can be achieved with simpler ablation procedures, restricted to PV isolation.

An episode of AF was defined by mode switching on CRT devices with an atrial rate >200 for at least 30 s. Of the 101 patients thought to be persistently in sinus rhythm (SR), 27% were found to have significant paroxysms of AF, with the cumulative percentage of time in the ‘mode-switch mode’ (i.e. the AF burden) of 1.6 ± 0.9%. Mortality was 19.2% in patients with newly identified PAF with hospitalization and thrombo-embolism rates of 42.3 and 2.1%, respectively, compared with mortality of 10.4% with hospitalization and thrombo-embolism rates of 41.8 and 1.9%, respectively, in patients persistently in SR (P= NS).

Analysis of data from CRT devices in a population of CHF patients with severe left ventricular dysfunction shows that a significant proportion of those perceived to be persistently in SR have undiagnosed paroxysms of AF but with relatively low burden. These episodes appear to be associated with a trend towards increased mortality but no effects on hospitalization or thrombo-embolism rates.

One hundred and seventy-one patients with persistent AF were randomized to receive candesartan 8 mg/day or placebo for 3–6 weeks before and candesartan 16 mg/day or placebo for 6 months after electrical cardioversion. P-SAECG was recorded in 114 patients (57 in each treatment group) after cardioversion and repeated in those with sinus rhythm at 1 and 6 weeks, and 3 and 6 months. Filtered P-wave duration (FPD), root-mean-squared (RMS) voltages of the terminal 40 ms of the filtered P-wave, RMS voltage of the entire filtered P-wave, and the integral of the voltages in the entire PD were analysed. No effects of candesartan were observed on any P-SAECG parameter at baseline. In the subgroup of patients in sinus rhythm after 6 months, FPD was significantly shorter both at baseline (151 ± 16 vs. 163 ± 16 ms) and at 6 months (143 ± 12 vs. 153 ± 15 ms) in the candesartan (n = 15) compared with the placebo group (n = 21).

Treatment with candesartan was associated with a shorter FPD in patients remaining in sinus rhythm for 6 months.

Detailed data relating to 1510 patients who received an implanted defibrillator and who were reported to a national pacemaker and implantable defibrillator registry in 2002 were examined and correlated with factors which have been suggested as affecting ICD implantation. None of the factors examined, which included factors related both to the need for ICD implantation and service provision, in addition to socio-economic deprivation, was found to correlate with regional ICD implantation rates.

There appears to have been no systematic planning of ICD services. Whether this has led to the marked regional variation and in inequity of service provision is not clear.

We conducted a telephone survey of 100 cardiologists and general physicians working at 30 different New Zealand hospitals who routinely manage patients with ischaemic heart disease and heart failure.

The majority of those surveyed (76%) rated their knowledge as satisfactory or better, although only 62% reported familiarity with international guidelines for ICD therapy. When asked to identify ICD indications 80% identified symptomatic or sustained ventricular arrhythmias and 73% left ventricular dysfunction. While 82% believed that the use of ICD therapy for secondary prevention was cost effective, only 53% believed they were cost effective for primary prevention. Lack of financial resource (88%), lack of local expertise (61%), lack of New Zealand guidelines (51%), and the referral process (43%) were seen as significant barriers to ICD referral by many participants. The majority of rural clinicians (71%) identified restricted access to investigations as a barrier to implantation, significantly higher than urban clinicians (18%, P = 0.001).

We have identified a number of potential barriers that will need to be addressed to raise the New Zealand ICD implantation rate.

We investigated the insulating properties of rubber and plastic gloves (double layer) within the first 60 min exposure (mimicking the maximum time of an explantation procedure) to saline (simulating the effects of body fluids on the gloves). For latex gloves, we measured an increase in voltage up to 68.1 V (P < 0.0001), for neoprene a maximum voltage of 5.3 V (P = 0.245), and for plastic a voltage of 2.3 V within the first hour. If the exposure time to fluid did not exceed 50 min, a double pair of intact gloves made of latex, neoprene, or plastic constituted such a large resistance that the resting voltage over the operating person would not exceed 50 V.

The use of intact medical gloves made of latex, neoprene, or plastic eliminates the potential electrical risk during explantation of an ICD. Two gloves on each hand offer sufficient protection. We will recommend the use of neoprene gloves.

Twenty-three subjects with unsuccessful transvenous coronary sinus lead placement underwent epicardial implantation. The subjects underwent clinical evaluation, cardiopulmonary exercise testing, and echocardiography before 3 and 6 months after. The results were compared with a control group (n = 35) who had received transvenous CRT. In both groups, there were significant improvements in all measures at 3 and 6 months. The improvement in peak VO₂ was delayed in the epicardial group compared with the transvenous group. At 6 months, the improvements seen in all variables showed no difference between the groups.

Epicardial lead placement is a viable option for patients with unsuccessful coronary sinus lead placement. The improvements in most variables were of a similar magnitude and over a similar time scale compared with transvenous placement. Improvements in peak VO₂ were delayed in the epicardial group, probably as a result of a prolonged recovery time.

The study population consisted of 82 consecutive HF patients with standard CRT indications. Patients were classified as responders, if they were alive without cardiac decompensation and experienced ≥15% decrease in left ventricular end-systolic volume. Sixty-eight percent of the enrolled patients responded to CRT. When compared with non-responders, responders had a wider baseline QRS width (P = 0.001), more marked QRS shortening (QRS) immediately after CRT (P = 0.001), and a better improvement in aortic velocity time integral (VTI) 24 h after CRT (P = 0.02). Moreover, there was a trend towards a greater baseline intraventricular dyssynchrony in the responder group (P = 0.07). By multivariable logistic regression, the baseline QRS width (OR: 0.95, 95% CI: 0.90–0.97, P = 0.001), QRS (OR: 1.038, 95% CI: 1.012–1.064, P = 0.003), and acute aortic VTI (OR: 0.81, 95% CI: 0.68–0.96, P = 0.017) emerged as independent predictors of response to CRT. Receiver operating characteristic curve analysis identified a QRS width >145 ms, QRS >20 ms, and aortic VTI >14 cm to predict responders.

A positive response to CRT was observed in 68% of the patients. Cardiac resynchronization therapy response is predictable using simple electrocardiographic and echocardiographic data.

We analysed 12-lead resting ECGs of 4149 men and women aged 25–74 years from the population-based KORA Study. Computer-assisted analysis identified ECGs with J-point elevation in leads V1–V3 and QRS duration ≤150 ms. Positive ECGs were re-evaluated independently by expert cardiologists. Computer-assisted analysis identified 250/4149 ECGs, predominantly from male probands (206/250) who were younger (41.0 ± 11.9 vs. 52.1 ± 13.8 years, P < 0.0001) than males without the ECG sign. After expert review, not a single ECG showed a Brugada ECG pattern. A high percentage of ECGs were considered abnormal, the majority (73) showing left-ventricular hypertrophy. Manual analysis of a representative, randomly selected sample of 351 ECGs without computer-assisted pre-analysis revealed not a single Brugada ECG pattern. True Brugada patterns were reliably identified by screening of a control subset of patients.

Spontaneous Brugada ECG patterns are rare in the general population and may hence constitute a relevant biological signal. Computer-aided analysis can help to identify abnormal ECGs.

In four tertiary referral centres, 677 consecutive patients underwent an intravenous ajmaline challenge for diagnosis or exclusion of BS in accordance with the recommendations of the Brugada consensus conferences. Two hundred and sixty-two ajmaline challenges (39%) were positive. Male gender, familial BS, sudden cardiac arrest (SCA), first-degree AV-block, basal saddleback type ECG, and basal right bundle branch block were identified as predictors for a positive ajmaline challenge. A predictor for negative ajmaline test was the absence of ST-segment elevation at baseline. Six of 12 patients who had experienced SCA, and five of 25 patients with a familial sudden death exhibited a positive response to ajmaline. Only one patient (0.15%) developed sustained ventricular tachyarrhythmias (ventricular fibrillation) during ajmaline challenge, which was terminated by a single external defibrillator shock.

Ajmaline challenge is a safe procedure to unmask the electrocardiographic pattern of BS. Electrocardiographic and clinical parameters were identified to predict patients’ response to ajmaline. The results of this study guide the clinician in which setting an ajmaline challenge is an appropriate diagnostic step.

The investigators analysed the ONS mortality data for 2002–2005, inclusive. International classification of diseases-10 codes representing possible cardiac deaths were selected and divided into four classes; A1: definite cardiac deaths with no structural heart disease identified at post-mortem, A2: definite cardiac deaths with structural heart disease identified at post-mortem, A3: definite cardiac deaths with indeterminate cause, and B: possible cardiac deaths. Analysis of the data revealed an average of 419 (SD 16.5) definite cardiac deaths per annum (Class A1 + A2 + A3) equating to 1.8 per 100 000 per year (SD 0.08) or 8 deaths/week. There were also 433 (SD 6.2) deaths per year in class B which comprised primarily of deaths from drowning and epileptic seizures. The most prevalent causes were ischaemic heart disease (33.5%), cardiomyopathies (27%), sudden arrhythmic death syndrome (14%), myocarditis (11%), valvular heart disease (5%), and hypertensive cardiomyopathy (2%).

Our findings suggest that the number of cardiac and sudden deaths in the young identified is sufficiently high to command attention even without the inclusion of potential misclassifications (Class B). Awareness of such deaths among primary-care physicians, pathologists, and coroners should be raised to ensure that those at risk are identified and further tragedies are avoided.

Retrospective review of all patients receiving a Medtronic® Reveal 9525/9526 for the investigation of unexplained syncope or pre-syncope in our centre between 1998 and 2008. All ILRs were programmed for a single manual activation with 40 min retrospective ECG recording. We identified all patients who subsequently underwent permanent pacemaker implantation and analysed the time delay between bradycardia onset and manual ILR activation. Five hundred and sixty-four patients underwent implantation of an ILR during the study period. Of these, 57 (10%) subsequently underwent the implantation of a pacemaker (31 male, median age 66 years, range 9–86 years). In this group, 35 of 57 (61%) bradycardia diagnoses were made in patients (18 male, median age 65 years, range 9–86 years) after manual activation of the ILR. The median time from bradycardia onset to ILR activation was 136 s (0–488 s). Nineteen recordings showed high-grade atrio-ventricular block and 16 sinus node disease.

Ten-year experience with the ILR confirms its utility in establishing a pacemaker indication as the cause for syncope or pre-syncope in 6% (34 of 564) of recipients following manual activation. This requires a recording loop of sufficient duration to reliably include both symptoms and activation.

We recorded a standard 12-lead surface ECG and a patient-activated ECG in direct succession in 508 consecutive patients enrolled in four centres. All ECGs were analysed by a single, blinded observer. ECGs were analysable in 505 (99.4%) patients (66% male, age 61 ± 15 years, and body mass index 27 ± 4). Analysis of the patient-activated ECG adequately detected a normal ECG (sensitivity 91% and specificity 95%), atrial fibrillation (AF) (sensitivity 99% and specificity 96%), and even T-wave abnormalities (sensitivity 90% and specificity 75%). Diagnostic accuracy for atrioventricular nodal block was moderate (sensitivity 79% and specificity 99%). Continuous parameters correlated well: (r² = 0.89 for heart rate, 0.83 for PR interval, 0.78 for QRS duration, and 0.89 for QTc).

Recordings made by this patient-operated ECG device allow to detect arrhythmias and other ECG changes with high accuracy compared with a standard ECG. It may help to improve accurate diagnosis of transient ECG changes such as paroxysmal AF in palpitations or other unexplained cardiac symptoms.

One hundred and fourteen patients with syncope completed a 48-item questionnaire derived from a generic measure of quality of life (the EQ-5D), the Syncope Functional Status Questionnaire, a depression scale (the CES-D) and historical symptoms. From these, clinical impact methodology was used to derive 12-item Impact of Syncope on Quality of Life (ISQL). The ISQL correlated with the number of syncopal spells in the previous year (r = 0.35), self-perceived health status (r = –0.55), the three scores from the SFSQ: [impairment (r = 0.77), fear and worry (r = 0.72), syncope dysfunction (r = 0.82), and depression (r = 0.62)], illustrating its convergent validity with these concepts. Known group differences were evident between patients who exhibited reduced quality of life on the EQ-5D and those who did not. There was no significant correlation between ISQL score and age or gender. ISQL score correlated better with the frequency of spells in the previous year than years prior to the previous year.

The ISQL is a brief valid measure of the impact of syncope on quality of life. It measures impairment, fear, depression, and physical limitations, and correlates with recent syncope frequency.

Thirty patients with ischaemic cardiomyopathy and prior dual chamber implantable cardioverter defibrillator implantation were enrolled. All patients underwent sequential MTWA testing using an exercise (E), atrial-paced (A), and atrioventricular-paced (AV) protocol. The number of indeterminate tests was lower during pacing (A: 17%; AV: 3%) compared with exercise (37%) (E vs. A: P = 0.015, E vs. AV: P = <0.001). When positive and indeterminate test results were grouped as non-negative, the concordance rates between E and A, E and AV, and A and AV were 60% ( = 0.17), 57% ( = 0.058), and 70% ( = 0.348), respectively. If indeterminate results were excluded, agreements were 60% ( = 0.19), 50% ( = 0.129) and 67% ( = 0.33), respectively.

Indeterminate test results are less common during pacing. However, there is a low concordance rate between test results using different protocols. This necessitates further study to determine the predictive value of each method in high risk patients with ischaemic cardiomyopathy.