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Background: Weight-stable obese subjects have an increased risk of arrhythmias and sudden death, even in the absence of cardiac dysfunction, and the risk of sudden cardiac death (SCD) with increasing weight is seen in both genders. The mechanism of unexplained deaths in obese patients is still unclear and may be related to ventricular repolarization abnormalities. The aim of this study is to determine the effect of severe obesity on spatial and transmural ventricular repolarization and to clarify the influence of bariatric surgery with a consequent substantial weight loss on arrhythmogenic substrate in the morbidly obese population. Methods: For the study, we enrolled 100 severely obese patients; 50 age-matched non-obese healthy subjects were also recruited as controls. All subjects underwent conventional 12-lead electrocardiography for analysis of spatial and transmural ventricular repolarization assessed by corrected QT dispersion (QTcd), corrected JT dispersion (JTc-d) and transmural dispersion of repolarization, (TDR). All subjects underwent bariatric surgery and were resubmitted to electrocardiographic, biochemical and anthropometric examination 12 months postoperatively. Results: Severely obese patients had greater values in QTc-d, JTc-d and TDR than the normal-weight controls. Bariatric surgery reduced significantly the QTcd value, JTc-d value and TDR value. There was a significant correlation between decrease of heterogeneity of repolarization indexes (QTd, JTd and TDR) and bariatric surgery-induced weight loss.Conclusions: In severely obese patients, surgicallyinduced weight loss is associated with significant decrease in the heterogeneity of ventricular repolarization. The reduction of spatial (QTc-d, JTc-d) and transmural dispersion of repolarization (TDR) may be of clinical significance, by reducing the risk of potentially fatal arrhythmias in morbidly obese subjects.

Epidemiological data have shown a "demographic revolution" in our society which induced a progressive increase in the elderly population, and coronary heart disease occurs more frequently in this group of subjects. Moreover, the presence of other pathologies entails specific diagnostic and therapeutic aspects in the elderly. In acute coronary syndromes percutaneous coronary angioplasty and thrombolytic agents are ever more employed despite the higher morbidity and mortality rates in the elderly. Chronic ischemic heart disease therapy, even if not different from that in younger patients, requires careful evaluation of the risk/benefit ratio. Epidemiological data have shown a "demographic revolution" in our society which induced a progressive increase in the elderly population, and coronary heart disease occurs more frequently in this group of subjects. Moreover, the presence of other pathologies entails specific diagnostic and therapeutic aspects in the elderly. In acute coronary syndromes percutaneous coronary angioplasty and thrombolytic agents are ever more employed despite the higher morbidity and mortality rates in the elderly. Chronic ischemic heart disease therapy, even if not different from that in younger patients, requires careful evaluation of the risk/benefit ratio.

Idiopathic left ventricular tachycardia is a rare arrhythmia whose electrophysiological basis is not yet well-defined. We report a case of idiopathic left ventricular tachycardia caused by a reentrant circuit limited exclusively to the two fascicles of the left bundle branch.

We have evaluated, at baseline and during incremental atrial pacing (AP), intracardiac conduction features of 53 patients with electrocardiographic diagnosis of bifascicular or trifascicular block, free from any pharmacological treatment potentially able to affect atrioventricular (AV) conduction system properties. The patients have been subdivided in the following groups: group A (13 patients), with LBBB and a PQ intervalor = 200 msec; group B (14 patients), with RBBB, LAH with a PQ intervalor = 200 msec; group C (8 patients), with LBBB and a PQ200 msec; group D (15 patients), with RBBB, LAH and a PQ200 msec; group E (3 patients), with RBBB, LPH and a PQ200 msec. In group A, 31% presented a long AH interval (140 msec), while 85% showed an increased infra-his conduction time (HV55 msec). During AP, only 38.5% maintained a 1:1 AV conduction ratio up to 140 bpm, while 30.8% developed an infra-his Mobitz 2 2nd degree AV block. 15.4% an infrahis 2:1 2nd degree AV block, 15.4% an AV nodal Mobitz 2 2nd degree AV block. In group B, 64% and 29% exhibited respectively an AV nodal and an infrahis conduction delay. During AP, 57.1% maintained a 1:1 AV conduction ratio up to 140 bpm, 14.3% developed an AV nodal Mobitz 1 2nd degree AV block, 14.3% an infrahis Mobitz 1 2nd degree AV block, 7.1% an AV nodal 2:1 2nd degree AV block, 7.1% an infrahis Mobitz 2 2nd degree AV block. In group C, no patient manifested a prolonged AH interval, while 50% exhibited a HV55 msec. 62.5% maintained a 1:1 AV conduction ratio up to 140 bpm, 25% developed an AV nodal Mobitz 1 2nd degree AV block and 12.5% an infrahis 2:1 2nd degree AV block. In group D, no patient showed an increased AH interval and only 13% presented a HV interval exceeding 55 msec. During AP, 86.7% maintained a 1:1 AV conduction ratio up to 140 bpm, 6.6% developed an AV nodal Mobitz 1 2nd degree AV block, 6.6% an infrahis 2:1 2nd degree AV block. In group E, no patient showed a prolonged AH interval, while 2/3 (66.6%) exhibited an infrahis conduction delay. During AP, 100% developed an infrahis 2:1 2nd degree AV block. Considering all patients with LBBB (groups A+C) and with RBBB+LAH (groups B+D), no differences were found in terms of PQ, PA and AH intervals, even though, concerning patients with a long PQ (group A vs group B), AH interval resulted significantly longer in patients with RBBB+LAH (121.85 +/- 36.4 msec vs 163.29 +/- 55.96 msec, p = 0.031). Infrahis conduction, independently from the measurement adopted (HVI interval: from the beginning of the His to the onset of the ventricular electrogram recorded at the His region; HV2 interval: from the beginning of the His to the onset of the surface QRS), resulted more compromised in patients with LBBB than in patients with RBBB+LAH (HVI: 75.24 +/- 40.23 msec vs 50.79 +/- 25.16 msec, p = 0.011; HV2: 77.24 +/- 38.12 msec vs 53.92 +/- 29.3 msec, p = 0.015). Such a difference became even more significant when comparing the percentage of patients with a prolonged HV interval (average value55 msec) in the above mentioned groups: 71.4% in case of LBBB, 20.7% in case of RBBB+LAH (p0.001). Regarding intraventricular conduction (IV), no statistically significant differences were found. In patients with RBBB+LAH, IV was not related to infrahis conduction time and PQ interval appeared more related to AH (r = 0.838, p0.001) than to HV (PQ-HV1: r = 0.381, p = 0.041, PQ-HV2: r = 0.474, p = 0.009). Conversely, in patients with LBBB infrahis and IV conduction appeared linearly related (HVI-V: r = 0.416, p = 0.06; HV2-V: r = 0.445, p = 0.043). As for PQ interval, it resulted more closely related to infrahis conduction (PQ-HVI: r = 0.626, p = 0.002; PQ-HV2: r = 0.674, p0.001), than to AH (r = 0.533, p = 0.013). In conclusion, infrahis conduction resulted more impaired in patients with LBBB. In this group, differently from patients with RBBB+LAH, infrahis conduction seems to affect the degree of IV conduction delay. (ABST

Antiarrhythmic drugs are known to affect depolarization and repolarization time in a different fashion. The aim of the present study was to compare the effects of sotalol, flecainide and propafenone on some common (mean QT and QTc, mean JT and JTc), or uncommon (QTc dispersion, T-peak to T-end interval-Tp-Te) electrocardiographic parameters in order to evaluate the effects of these antiarrhythmic drugs on repolarization time. QTc dispersion, defined as the difference between maximum and minimum QTc calculated from the standard 12 ECG leads, and the average Tp-Te interval, reflect regional variation in ventricular repolarization. We have analyzed retrospectively the standard 12-lead electrocardiograms of 28 patients (15 females and 13 males, age 36.11 +/- 16 years, range 11-67 years), recorded in the free-drug state and at the steady state after oral treatment with sotalol (160 mg/ die), flecainide (200 mg/die) and propafenone (450 mg/die). These drugs were prescribed, separately, for the treatment of patients with supraventricular tachycardia without underlying structural heart disease. Sotalol treatment prolongs ventricular repolarization times (QT, p = 0.0001; JT, p = 0.0001 and JTc, p = 0.0001) in an homogeneous fashion, as showed by the significant decrease in QTc dispersion (p = 0.026) and Tp-Te interval (p = 0.011). On the contrary, flecainide treatment is associated with an increase in QTc dispersion (p = 0.039) and Tp-Te interval (p = 0.0001), mean QT (p = 0.0001), QTc (p = 0.0001) and QRS (p = 0.0001), with no significant changes in JT and JTc (NS). Propafenone treatment does not affect repolarization time indexes, affecting only depolarization time as expressed by an increase in QRS (p = 0.046).

Objectives The aim of the study was to compare the diagnostic yield and the costs of implantable loop recorder (ILR) with those of the conventional strategy in patients with unexplained palpitations. Background In patients with unexplained palpitations, especially in those with infrequent symptoms, the conventional strat-egy, including short-term ambulatory electrocardiogram (ECG) monitoring and electrophysiological study, some-times fails to establish a diagnosis. Methods We studied 50 patients with infrequent (*1 episode/month), sustained (*1 min) palpitations. Before enroll-ment, patients had a negative initial evaluation, including history, physical examination, and ECG. Patients were randomized either to conventional strategy (24-h Holter recording, a 4-week period of ambulatory ECG monitor-ing with an external recorder, and electrophysiological study) (n * 24) or to ILR implantation with 1-year moni-toring (n * 26). Hospital costs of the 2 strategies were calculated. Results A diagnosis was obtained in 5 patients in the conventional strategy group, and in 19 subjects in the ILR group (21% vs. 73%, p * 0.001). Despite the higher initial cost, the cost per diagnosis in the ILR group was lower than in the conventional strategy group (€3,056 * €363 vs. €6,768 * €6,672, p * 0.012). Conclusions In subjects without severe heart disease and with infrequent palpitations, ILR is a safe and more cost-effective diagnostic approach than conventional strategy.

BACKGROUND: Recent data have shown that obesity is an important potential risk factor for atrial fibrillation (AF). The mechanism of development of AF in obesity patients is still unclear and may be related to atrial refractoriness heterogeneity. The aim of our study was to determine the influence of bariatric surgery with a consequent substantial weight loss on P-wave dispersion in morbidly obese population. METHODS: We enrolled in this study 40 severe obese patients, and 40 age-matched non-obese healthy subjects were also recruited as controls. All subjects underwent conventional 12-lead electrocardiography for the analysis of P-wave dispersion. All subjects underwent bariatric surgery and were resubmitted to electrocardiography, biochemical, and anthropometric examination within 12 months after intervention. RESULTS: Severe obese patients had greater values in P-wave duration and dispersion than the normal weight controls. Bariatric surgery reduced significantly P-wave dispersion. There was a significant correlation between decrease of atrial refractoriness heterogeneity and bariatric-surgery-induced weight loss. CONCLUSIONS: In severe obese patients, surgically induced weight loss reduction is associated with significant decreased in P-wave dispersion. The reduction of the atrial refractoriness heterogeneity may be of clinical significance by reducing the risk of atrial fibrillation in morbidly obese subjects.

Aims In dilated cardiomyopathy (DCM), attenuation of left atrial (LA) booster pump function has been observed, and attributed both to altered LA loading conditions owing to left ventricular (LV) diastolic dysfunction and to LA involvement in the myopathic process. The aim of the present study was to detect LA systolic dysfunction in DCM using speckle-tracking two-dimensional strain echocardiography (2DSE), and to assess the effects of cardiac resynchronization therapy (CRT) on LA myocardial strain during 6 month follow-up. Methods and results A total of 90 patients (aged, 52.4+10.2 years) with either idiopathic (n = 47) or ischaemic (n = 43) DCM underwent standard Doppler echo and 2DSE analysis of atrial longitudinal strain in the basal segments of LA septum and LA lateral wall, and in LA roof. The two groups were comparable for clinical variables (NYHA class: III in 72.2%; IV in 27.8%). LV volumes, ejection fraction, stroke volume, and mitral valve effective regurgitant orifice were similar between the two groups. No significant differences were evidenced in Doppler transmitral inflow measurements. LA diameter and maximal volume were also similar between the two groups. Conversely, LA active emptying volume and fraction were both lower in patients with idiopathic DCM. Peak systolic myocardial atrial strain was significantly compromised in patients with idiopathic DCM compared with ischaemic DCM in all the analysed atrial segments (P , 0.001). At follow-up, 64 patients (71.1%) (37 idiopathic and 27 ischaemic) were responders, and 26 (28.9%) (10 idiopathic; 16 ischaemic) were non-responders to CRT (responder: decrease of LV end-systolic volume .15%). A significant improvement in LA systolic function was obtained only in patients with ischaemic DCM responders to CRT (P , 0.001). By multivariable analysis, in the overall population, it was found that ischaemic aetiology of DCM (b-cofficient = 0.62; P , 0.0001) and positive response to CRT (b-cofficient = 0.42; P , 0.01) were the only independent determinants of LA lateral wall systolic strain. Conclusions Two-dimensional strain represents a promising non-invasive technique to assess LA atrial myocardial function in patients with DCM. LA pump and reservoir function at baseline and after CRT are more depressed in idiopathic compared with ischaemic DCM patients. Future longitudinal studies are warranted to understand further the natural history of LA myocardial function, the extent of reversibility of LA dysfunction with CRT, and the possible prognostic impact of such indexes in patients with congestive heart failure.

Dabigatran is a novel target specific oral anticoagulant for stroke prevention in non valvular atrial fibrillation. Little is still known about its real-world effectiveness and safety in the italian population. Aim of our study was to evaluate the efficacy and safety of dabigatran in a large single-center cohort of "real-life" italian population with non-valvular AF and to compare the results with those obtained from the RE-LY trial and the Medicare study.We studied a prospective cohort of 2108 patients (1119 male; mean age 69.4 ± 9.4 years) who started the oral anticoagulant treatment with dabigatran 110 mg twice-daily (DAB 110; N = 1075; 51%) or 150 mg twice-daily (DAB 150; N = 1033; 49%). Follow-up data were obtained trough outpatients visits each 3-6 months for assessing the clinical status, adherence to treatment, occurrence of side effects and major cardiovascular complications.In DAB 150 group the mean age was 64.9 ± 8.8 years, 56.8% of patients was male. CHA2DS2Vasc Score was ≥ 3 in 94.3% and HAS-BLED was ≥ 3 in 59.7%. In DAB 110 group (N = 1075) the mean age was 73.9 ± 7.5 years; 49.5% of patients was male. CHA2DS2Vasc Score was ≥ 3 in 73.4% and HAS-BLED was ≥ 3 in 87.4% of DAB 110 patients. One patient taking Dabigatran 110 mg bid had ischemic stroke without significantly neurological sequelae. In both groups, no patient experienced hemorrhagic stroke during the follow-up period. 147 patients (6.9%) of MonaldiCare population reported adverse effects from treatment with dabigatran, of whom 121 patients (5.7%) discontinued therapy. We reported one case of subarachnoid hemorrhage (0.05%) in a patient with high thrombo-embolic and high hemorrhagic risk score who was taking dabigatran 150 mg bid and one case (0.05%) of bladder bleeding in a patient who was taking dabigatran 110 mg bid. No major gastrointestinal bleeding was observed in the MonaldiCare population.MonaldiCare registry showed a safety profile of both dosages of dabigatran regarding major of fatal bleeding in a "real life" single center italian population at high thromboembolic and hemorrhagic risk. The majority of MonaldiCare patients tolerated dabigatran treatment without significant side effects. The efficacy of dabigatran was demonstrated by very low prevalence of ictus/TIA, also when patients underwent electrical AF cardioversion independently of the transesophageal examination.

Objective: Atrial fibrillation (AF) is the most frequently encountered arrhythmic complication associated with coronary surgery. The aim of this paper was then to identify the clinical predictors of post-CABG AF occurrence. Methods: 150 consecutive patients were included in this study and divided into two groups according to the absence (SR group, 104 male and 22 female, age 58.4 ^ 8.8 years) or presence (AF group, 23 male and 1 female, age 65.4 ^ 6.3 years) of post-CABG AF. Forty-seven perioperative variables were considered. Results: After univariate analysis, advanced age (SR vs. AF: 58.4 ^ 8.8 vs. 65.4 ^ 6.3, P , 0:001), an increased BMI (SR vs. AF: 26.1 ^ 2.7 vs. 27.4 ^ 2.5, Pa 0:026), a prior history of paroxysmal AF (SR vs. AF: 3.2% vs. 16.7%, Pa 0:028), left atrial enlargement (SR vs. AF: 21.1% vs. 70.8%, P , 0:001) and a more severe coronary artery disease (CAD) (SR vs. AF: no. of diseased vessels: 2.42 ^ 0.7 vs. 2.91 ^ 0.3, Pa 0:001; three-vessel CAD (54.1% vs. 91.3%, Pa 0:002) were the only factors that statistically differed between the groups. Multivariate logistic regression analysis identified left atrial enlargement (P , 0:0001), a prior history of paroxysmal AF (Pa 0:007) and a more severe CAD (Pa 0:0047) to be independent correlates for AF. Conclusions: Post-CABG AF seems to require a well definite anatomical and electrical substrate that is generated by increased left atrial dimensions, a greater extension of coronary lesions and a possible electrical remodeling consequent to prior repetitive episodes of paroxysmal AF. q 1999 Published by Elsevier Science B.V. All rights reserved.

The authors present a case of coronary sinus spasm during left ventricular lead implantation for biventricular pacing relieved by direct infusion of nitroglycerin.

The anthracyclines, doxorubicin and daunorubicin, are antibiotics effective in the treatment of many malignancies. However, their usefulness is limited by the development of potentially fatal cardiotoxicity. Cardiac monitoring by a noninvasive test capable of identifying patients at high risk of cardiac damage, before the ejection fraction deteriorates would have clinical utility. Electrocardiograms and echocardiograms are routinely utilized for noninvasive assessment of myocardial function. However, of the ECG abnormalities described, none has been noted to be of consistent predictive value for cardiotoxicity. The aim of this study was to assess the effects of doxorubicin on ventricular repolarization time indexes, as they have been shown to be effective in the identification of electrical myocardial instability and, hence, in the identification of risk for either arrhythmia or heart failure. For this reason, electrocardiograms were compared in 35 cancer patients at the first presentation (drug-free state) and after 29.4 +/- 37.65 weeks of treatment with doxorubicin. The results of the present study showed that after only a short period of treatment with doxorubicin there was a significant increase in ventricular recovery time dispersion indexes (QTc, JT, and JTc dispersion, and their "adjusted" values). Thus, increased regional variation in ventricular repolarization could be, in the absence of a significant modification of the echocardiographic parameters, an early marker of an electropathy, due to the early cardiotoxic action of doxorubicin on myocardial cells, eventually leading to heart failure.

We evaluated the arrhythmic profile in a population of 20 Becker muscular dystrophy (BMD) patients searching for possible correlations between the severity of the arrhythmic events, the cardiac autonomic balance (assessed by heart rate variability analysis in the time domain) and the degree of left ventricular systolic impairment. A population of 14 male healthy individuals served as the control group. BMD subjects exhibited lower values of SDNN (P=0.013), SDANN index (P=0.008) and 24-h mean heart rate (P=0.002). The total number of premature ventricular beats (totPVB) and the number of PVB out of 1000 heartbeats (PVB/1000) appeared also higher in BMD subjects (P=0.05 and P=0.046, respectively). No difference was found in terms of 24-h mean QTc and 24-h longest QT among the two groups. TotPVB and PVB/1000 were inversely related to both the ejection fraction (r= -0.620, P=0.004 and r= -0.517, P=0.019) and to the shortening fraction (r= -0.568, P=0.009 and r= -0.469, P=0.037). Twenty-four-h mean QTc was also inversely related to both the ejection fraction (r= -0.520, P=0.019) and the fractional shortening (r= -0.491, P=0.028). These data suggest that in BMD there is cardiac autonomic imbalance characterized by sympathetic predominance and an increased susceptibility to ventricular arrhythmias, even in the absence of overt cardiomyopathy. Furthermore, the severity of the arrhythmic profile in BMD appears closely related to the degree of left ventricular systolic dysfunction.

QTc interval dispersion (QTcd) analysis (difference between maximum and minimum QTc calculated from at least five of the standard 12 ECG leads) and signal-averaged electrocardiograms were performed on 23 patients referred to our coronary care unit because of acute myocardial infarction. Late potentials were considered positive if all three of the following criteria were satisfied: (1) total QRS duration (QRSd) > 114 ms; (2) duration of QRS under 40 muV (LAS 40) > 38 ms; (3) root mean square voltage of the last 40 ms of QRS (RMS 40) < 25 muV. Patients were divided into two groups according to the presence (group A, 9 patients) or absence of late potentials (group B, 14 patients). Group A patients showed a significantly higher QTcd (0.0652 +/- 0.0177 s vs. 0.0448 +/- 0.0201 s; P = 0.021) and a significantly longer mean QTcm (0.43117 +/- 0.01817 s vs. 0.40472 +/- 0.03013 s; P = 0.028) than group B patients. Among the three different parameters used to define the presence of late potentials, QTcd was significantly related to LAS 40 (r = 0.418, P = 0.047) and mean QT cm to QRSd (r = 0.497; P = 0.016). We also found a significant correlation between QTcd and mean QTcm (r = 0.426; P = 0.043). In conclusion, our data suggest that (1) the presence of late potentials is associated with a greater dishomogeneity of ventricular recovery time; (2) the longer the duration of late potentials, expressed by LAS 40, the greater the QTcd, suggesting that the dispersion of repolarization could be attributed to slowly conducting areas from which late potentials arise; (3) mean QTcm is not useful to identify these areas because it is more affected by total rather than by terminal QRS duration; (4) regional discrepancies of ventricular recovery time are connected with general repolarization duration.

Aims To evaluate whether quantification of the extent of scarred left ventricular (LV) tissue by speckle-tracking strain echo (2DSE) can predict response to cardiac resynchronization therapy (CRT) in patients with ischaemic dilated cardiomyopathy (DCM). Methods and results Forty-five patients (58.3 ± 8.3 years; 24 males) with ischaemic DCM scheduled for CRT, and 25 controls were studied. A week before implantation all the patients underwent standard Doppler echo, 2DSE, and contrast-enhanced magnetic resonance (MR). Clinical and echocardiographic evaluation was repeated 6 months after CRT. The patients were considered as responders to CRT if LV end-systolic volume decreased by 15%. In DCM patients, LV ejection fraction was 29.2 ± 5.1%. By evaluating the 765 segments with MR, subendocardial infarct was identified in 17.0% and transmural infarct in 18.3%. With 2DSE, the average global longitudinal strain (GLS) was −23.1 ± 3.6% in controls and −15.1 ± 5.1% in DCM (P = 0.001). GLS showed a close correlation with total scar burden using MR (r = 0.64, P < 0.001). At follow-up, patients were subdivided into responders (n = 30; 66.7%) and non-responders (n = 15; 33.3%) to CRT. GLS was significantly different in non-responders than in responders (GLS: −10.4 ± 5.1 in non-responders vs. −18.4 ± 14% in responders, P < 0.001). In a multivariable analysis, GLS (P < 0.0001) and radial intraventricular dyssynchrony (P < 0.001) were powerful independent determinants of response to CRT. Conclusion GLS is strongly associated with total scar burden assessed by MR, and is an excellent independent predictor of response to CRT.

Aims: Cardiac resynchronization therapy (CRT) has become an attractive therapeutic option for patients with end-stage heart failure (HF). Currently, patients are selected for CRT on ECG and on echocardiographic criteria analysed at rest. Whether the physical effort may further increase myocardial dyssynchrony is not fully established. The aim of the study was to test by the use of Doppler myocardial imaging (DMI) if dynamic left ventricular (LV) dyssynchrony during physical effort may be a determinant of dynamic mitral regurgitation in patients with dilated cardiomyopathy and 'narrow' QRS. Methods and results: Sixty patients (62.3 ± 8.3 years) with idiopathic dilated cardiomyopathy and narrow QRS duration (< 120 ms) were selected. All the patients underwent standard Doppler echo, colour DMI, supine bicycle exercise stress echocardiography, and cardiopulmonary exercise testing. Cardiac synchronicity was assessed, at rest and at peak exercise, from measurements of time intervals (Ts) between the onset of the QRS complex and the peak myocardial systolic velocity, in a six-basal-six-mid-segmental model. Standard deviation of Ts of the 12 LV segments (Ts-SD-12) was also calculated. In baseline conditions, HF patients showed an LV ejection fraction of 30.1 ± 4%, and a significant electromechanical delay (Ts-SD-12 ≥ 34.4 ms) in 20 patients (33.3%). At peak of physical exercise, a significant electromechanical delay was detected in 35 patients (58.3%), whereas in 47 patients (78.3%) exercise-induced increase in mitral valve effective regurgitant orifice (ERO) was observed. By multivariable analysis, an independent positive association between changes in Ts-SD-12 and in mitral valve ERO (P < 0.0001), as well as an independent inverse correlation of the same changes in Ts-SD-12 with LV stroke volume (P < 0.0001) were detected. In addition, changes in Ts-SD-12 were also independent determinants of peak VO2 (P < 0.0001) during cardiopulmonary exercise testing. Conclusion: Colour DMI is an effective technique for assessing the severity of regional delay in activation of LV walls in HF patients with narrow QRS both at rest and during stress test. The increase in LV dyssynchrony during exercise strongly correlates with the increase in mitral regurgitation severity and with the impairment of LV stroke volume. © The European Society of Cardiology 2007. All rights reserved.

Becker’s muscular dystrophy (BMD) is an X linked recessive muscular dystrophy caused by dystrophin anomalies in striated muscles, with myocardial involvement1,2 and consequent dilated cardiomyopathy, rhythm and conduction disorders, and a high risk of sudden cardiac death.3,4 Heart rate variability (HRV) is a measure of the cyclical variations of beat-to-beat (RR) intervals that reflects cardiac autonomic function and sympathovagal balance.5,6 A predominance of sympathetic tone in cardiac activity induces tachycardia and reduced beat-to-beat variations, whereas parasympathetic nerve activity reduces heart rate and increases HRV.7 HRV is a well-correlated non-invasive parameter used to stratify arrhythmic risk in patients with chronic failure. In general, higher HRV is desirable, and lower HRV has been found to be a significant independent predictor of cardiac mortality and morbidity.8,9 The objective of our study was to evaluate the prognostic value of HRV for sudden death in a population of patients with BMD and dilated cardiomyopathy. The study population consisted in 30 men (mean age 44.2 (SD 12) years) with BMD and a variable stage of myocardial involvement. The control group consisted of 30 healthy men (age 39 (3.2) years). All patients included in study underwent physical …

Pacemaker lead extraction has been shown to be an effective and safe treatment in the case of infected permanent pacemaker leads. However, it can lead to potentially serious complications, usually occurring during the extraction procedure. This report describes a case of a 74-year-old male with a persistent superior vena cava thrombosis related to an infected permanent pacemaker lead transvenous extraction. Clinical and surgical management are discussed.

Aims The aim of our study was to evaluate the effect of cardiac resyncronization therapy on QT dispersion (QTd), JT dispersion (JTd), and transmural dispersion of repolarization (TDR), markers of heterogeneity of ventricular repolarization in a study population with severe heart failure. Methods and results Fifty patients (43 male, 7 female, age 60.2+3.1 years) suffering from congestive heart failure (n ¼ 39 NYHA class III; n ¼ 11 NYHA class IV) as a result of coronary artery disease (n ¼ 19)or of dilated cardiomyopathy (n ¼ 31), with sinus rhythm (SR), QRS duration .120 ms (mean QRS duration ¼ 156+21 ms), an ejection fraction ,35%, left ventricular end-diastolic diameter .55 mm, presence of atrioventricular asynchrony, intra- and inter-ventricular asynchrony, underwent permanent biventricular pacemaker implantation. A 12-lead standard electrocardiogram was performed at baseline, during right-, left-, and biventricular pacing (BiVP) and QTd, JTd, and TDR were assessed. BiVP significantly reduced QTd (73.93+19.4 ms during BiVP vs. 91+6.7 ms in SR, P ¼ 0.004), JTd (73.18+17.16 ms during BiVP vs. 100.72+39.04 at baseline, P ¼ 0.003), TDR (93.16+15.60 vs.101.55+19.08 at baseline, P , 0.004), compared with SR. Right ventricular endocardial pacing and left ventricular epicardial pacing both increased QTd (RVendoP 94+51 ms, P , 0.03; LVepiP 116+71 ms, P , 0.02), and TDR (RVendoP 108.13+19.94 ms, P , 0.002; LVepiP 114.71+26.1, P , 0.05). There was no effect on JTd during right and left ventricular stimulation. Conclusions BiVP causes a statistically significant reduction of ventricular heterogeneity of repolarization and has an electrophysiological anti-arrhythmic influence on the arrhythmogenic substrate of dilated cardiomyopathy.

Objective: The aim of our study was to evaluate the effect of cardiac resyncronization therapy (CRT) on QT dispersion (QTd), JT dispersion (JTd) and transmural dispersion of repolarization (TDR), markers of heterogeneity of ventricular repolarization in a study population with severe heart failure. Methods and Results: Fifty patients (43 male, 7 female, aged 60.2 ± 3.1 years) suffering from congestive heart failure (N = 39 NYHA class III; N = 11 NYHA class IV) as a result of coronary artery disease (N = 19) or of dilated cardiomyopathy (N = 31), sinus rhythm, QRS duration >130 ms (mean QRS duration >156 ± 21 ms), an ejection fraction < 35%, left ventricular end-diastolic diameter >55 mm, underwent permanent biventricular DDDR pacemaker implantation. A 12-lead standard electrocardiogram was performed at baseline, during right-, left-, and biventricular pacing and QTd, JTd and TDR were assessed. Biventricular pacing significantly reduced QTd (73.93 ± 19.4 ms during BiVP vs 91 ± 6.7 ms at sinus rhythm, p = 0.004), JTd (73.18 ± 17.16 ms during BiVP vs 100.72 ± 39.04 at baseline p = 0.003), TDR (93.16 ± 15.60 vs 101.55 ± 19.08 at baseline; p

Recent studies suggest that professional exposure to Extremely Low Frequency-Electro Magnetic Field (ELF-EMF) can increase the risk of sudden cardiac death. Aim of our work was to find predictive parameters of arrhythmic risk in a population of 28 railways drivers exposed to ELF-EMF. Our findings were that the exposure did not reduce HRV and did not increase the risk of arrhythmias.

Reactive oxygen species are produced during exercise. The antioxidants prevent or limit tissue damages by these species in physiological conditions. In particular, ascorbate and urate scavenge peroxynitrite, which can alter the function of many molecules, including the lecithin-cholesterol acyltransferase (LCAT) enzyme involved in reverse cholesterol transport. The aims of the present study were to compare the plasma antioxidant response to an ergometric test (ET) in hypertensive and healthy subjects, evaluate the exercise-dependent nitrosative stress in plasma, and assess whether the LCAT activity is altered by the exercise. Plasma samples, prepared before and after ET from hypertensive or healthy volunteers, were analysed for their levels of ascorbate, urate, alpha-tocopherol, retinol, nitrotyrosine, and LCAT activity. The alpha-tocopherol and retinol levels did not significantly change in both groups during exercise, while the ascorbate level changed displaying higher increase in controls (+38.8%) than in hypertensives (+17.2%). In these patients, during ET, the urate and nitrotyrosine levels changed more than in normotensives (+13.5 and +40.6% vs -3.1 and +25.2%, respectively). The antioxidants effectively prevented loss or reduction of LCAT activity, as it was similar in hypertensives and normotensives, and did not change after ET. The results demonstrate that exercise is associated with enhanced protein nitrosation, and suggest that the ascorbate or urate levels increase to limit oxidative damage.

Sudden cardiac death is a dramatic, undesirable event that can often result from cardiomyopathies. To investigate the validity of the QTdispersion (QTd) in revealing regional heterogeneity of repolarisation, with consequent possibility of sudden death,1 we evaluated ECGs of patients affected by Becker muscular dystrophy (BMD). This is an X linked recessive muscular dystrophy caused by dystrophin anomalies in striated muscles with myocardial involvement2–4 and consequent dilated cardiomyopathy, ventricular arrhythmias and, in 30% of cases, sudden cardiac death.5,6 The study was retrospective using the clinically validated database of ECGs and echocardiograms (echo recorded together with the ECG) from 30 BMD patients (mean (SD) age 25 (10) years) with variable stages of myocardial involvement, and 26 healthy, age matched controls. All subjects underwent a physical examination, blood analyses, and M mode and two dimensional echocardiography. The diagnosis of the type of muscular dystrophy in Becker patients was confirmed by DNA analysis (polymerase chain reaction) and by reduced dystrophin labelling from the immunohistochemical examination of biopsy samples. We excluded the ECGs from subjects with ST-T anomalies on the 12 lead ECG, and with sustained ventricular arrhythmias at 24 hour Holter monitoring, electrolyte …

The perioperative factors potentially associated with post-coronary artery bypass grafting (CABG) ventricular tachyarrhythmias (VT) onset have not been deeply investigated. Monomorphic or polymorphic ventricular tachycardia and ventricular fibrillation represent the most dreadful arrhythmic events that can complicate the postoperative course of CABG. As a consequence, the aim of our paper was to identify which perioperative variables might predict post-CABG VT occurrence. One hundred and fifty-two consecutive patients who underwent CABG surgery at our Institution were included in the study. Post-CABG VT occurred in 13 out of 152 patients (8.5%, six cases of monomorphic ventricular tachycardia and seven cases of ventricular fibrillation). At univariate analysis, VT patients were significantly younger (54.8±6.6 vs. 60.1±8.8, P=0.038), exhibited a more severe coronary artery disease (CAD) (number of diseased vessels 2.92±0.3 vs. 2.45±0.7, P=0.023, and percentage of patients with three-vessel CAD 91.7% vs. 57.3%, P=0.043) and received a greater number of CABGs than those remaining in sinus rhythm (SR) (percentage of patients receiving three or more CABGs 76.9% vs. 38.8%, P=0.018) Moreover, VT patients more frequently developed intra- or postoperative myocardial infarction (total CK>1000 76.9% vs. 38%, P=0.016 and MB-CK>normal range 72.7% vs. 30.7%, P=0.014), electrolyte derangement (84.6% vs. 45.6%, P=0.017) and a severe haemodynamic impairment (need for IABP 23% vs. 2.9%, P=0.009). At multivariate analysis, total CK>1000, postoperative electrolyte imbalance, the need for three or more CABGs and of IABP all were independent correlates for VT. In conclusion, post-CABG VT seem to be related to the preexistence of a severe underlying coronary artery disease along with perioperative triggering factors such as acute ischemia, electrolytic disorders and a sudden haemodynamic impairment.

Sustained ventricular tachyarrhythmias (VT), such as monomorphic or polymorphic ventricular tachycardia, and ventricular fibrillation, represent the most serious arrhythmic events that can complicate the postoperative course of coronary artery bypass grafting (CABG). The perioperative factors potentially associated with post-CABG sustained VT onset have not been thoroughly investigated. As a consequence, the aim of our study was to identify which perioperative variables might predict post-CABG VT occurrence. One hundred and fifty-two consecutive patients who underwent CABG surgery at our Institute were included in the study. Post-CABG VT occurred in 13 out of 152 patients (8.5%, six cases of monomorphic ventricular tachycardia and seven cases of ventricular fibrillation). Univariate analysis revealed that VT patients were significantly younger (54.8 +/- 6.6 vs 60.1 +/- 8.8, P = 0.038), exhibited more severe coronary artery disease (CAD) (no. of diseased vessels, 2.92 +/- 0.3 vs 2.45 +/- 0.7, P = 0.023; and percentage of patients with three-vessel CAD, 91.7 vs 57.3%, P = 0.043), and received a greater number of CABGs than those remaining in sinus rhythm (SR) (percentage of patients receiving three or more CABGs, 76.9 vs 38.8%, P = 0.018) Moreover, VT patients more frequently developed intra- or postoperative myocardial infarction (total CK > 1,000, 76.9 vs 38%, P = 0.016; and MB-CK > normal range, 72.7 vs 30.7%, P = 0.014), electrolyte derangement (84.6 vs 45.6%, P = 0.017), and a severe hemodynamic impairment (need for intra-aortic balloon pump (IABP), 23 vs 2.9%, P = 0.009). On multivariate analysis, total CK > 1,000, postoperative electrolyte imbalance, the need for three or more CABGs, and for IABP all were independent correlates for VT. In conclusion, post-CABG VT seem to be related to the preexistence of a severe underlying coronary artery disease along with perioperative triggering factors, such as acute ischemia, electrolytic disorders, and sudden hemodynamic impairment.

Atrial fibrillation is the most common cardiac rhythm disorder associated with hospitalization. Two therapeutic options have been available: antiarrhythmic drug therapy, and external or internal electrical cardioversion. Electrical cardioversion of atrial fibrillation remains one of the most widely used and effective treatments for the restoration of normal sinus rhythm. However, many patients continue to receive an antiarrhythmic drug before and after cardioversion in an attempt either to cardiovert the arrhythmia chemically or to maintain sinus rhythm after successful cardioversion. Because some pharmacological agents can affect the cardioversion procedure for atrial fibrillation or flutter, and because many patients with such arrhythmias may require electrical cardioversion when they are taking antiarrhythmic drugs, the question of a possible effect of drug therapy on the efficacy and safety of electrical cardioversion of atrial fibrillation arises. Early reports of direct current cardioversion provoking potentially lethal ventricular arrhythmias raised suspicions of an arrhythmogenic role for digoxin antiarrhythmic therapy, and it is customary to withhold these drugs for 24 to 48 h before cardioversion is attempted. However, this complication is likely to arise only in patients who are close to, or actually manifesting, signs of drug toxicity. On the other hand, treatment with therapeutic concentrations of antiarrhythmic drugs before cardioversion may in some cases be associated with a significant reduction in the number of shocks and decreased energy required to restore sinus rhythm, a lower incidence of postshock arrhythmias and a reduced risk of early recurrence of atrial fibrillation.

Antiarrhythmic drugs are known to affect the depolarization and repolarization time in a different fashion. The aim of the present study was to compare the effects of Sotalol, Flecainide and Propafenone on some common (QT, QTc, JT, JTc) or uncommon (QTc dispersion, T-peak to T-end interval) electrocardiographic parameters in order to evaluate the effects of these antiarrhythmic drugs on ventricular repolarization time both in terms of absolute values and of dispersion across the myocardium. The analysis of these antiarrhythmic drug effects was performed on the standard 12-lead electrocardiograms of 31 patients (17F and 14M, age 38.1+/-17 years, range 11-67 years) in the free-drug state and at the steady state after oral treatment with Sotalol (160 mg daily), Flecainide (200 mg daily) and Propafenone (450 mg daily). These drugs were prescribed, separately, to all the 31 patients, free of underlying structural heart disease, for the treatment of their atrio-ventricular nodal re-entry tachycardia. Data of the present study show that Sotalol, over the range prescribed, significantly prolongs ventricular repolarization index QT (P=0.001), JT (P=0.0001) and JTc (P=0.0001) values in an homogeneous fashion, as shown by the significant decrease in QTcD (P=0.019) and Tp-Te (P=0.01). On the contrary, Flecainide treatment was associated with an increase in QTcD (P=0.029), Tp-Te (0.0001), QT (P=0.001), QTc (P=0.0001) and QRS (P=0.0001), with no significant changes in JT and JTc. Propafenone, over the range prescribed, did not affect repolarization time, resulting only in a prolongation of depolarization time as expressed by the increase of QRS (P=0.0001).

Background: Intraventricular conduction disturbances determine complete impairment of impulse propagation along the right or left bundle branch or the two left fascicles. Hypothesis: This study was undertaken to investigate the electrophysiologic significance of QRS axis (QRSA) orientation in bifascicular and trifascicular blocks. Methods: A group of 76 subjects, 43 with right bundle‐branch block (RBBB) and left anterior hemiblock (LAH) (Group A), and 33 with left bundle‐branch block (LBBB) (Group B) was submitted to electrophysiologic evaluation. Results: In Group A, QRSA was inversely related only to intraventricular conduction, while in Group B, QRSA inversely related to infrahisal conduction times. A value of ‐60°. Of the 9 Group B patients with a QRSA 60°, in only 8.3% were both infrahisal (HV1 and HV2) intervals dangerously prolonged, and 23.8% encountered an infrahisal second‐degree AV block during IAS. In Group A, atrioventricular conduction time >200 ms exhibited a better predictive accuracy than QRSA 80 ms. Conclusion: The degree of leftward QRSA deviation seems to reflect the entity of intraventricular conduction delay in patients with RBBB + LAH, while it appears to be directly related to infrahisal conduction prolongation in those with LBBB.

The aim of our study was to analyze the ventricular repolarization phase in patients with isolated aortic stenosis (AS) in order to search for possible abnormalities that might contribute to an explanation of the electrical instability peculiar to this valve disease. We selected a population of 39 patients with isolated AS (25 M and 14 F, mean age 60+/-16 yrs). As controls we considered a group of 31 age-matched healthy subjects 20 M and 11 F, mean age 55+/-14 yrs, P=NS. Disease severity was assessed by echocardiography, calculating the maximum and mean pressure gradients max and mean PG) and the functional valve orifice area. Various electrocardiographic intervals (QT, QT'c, JT, JTc) and indices (QT and QTc dispersion were adopted for a detailed non-invasive evaluation of the ventricular repolarization. In patients with AS, M-QT (391+/-45 ms vs 362+/-25 ms, P=0.002), M=QTc (431+/-29 ms vs 412+/-19 ms, P=0.003), M-JT (290+/-41 ms vs 265+/-26 ms, P=0.003, M-JTc 331+/-29 ms vs 302+/-19 ms, P0.001, QTD (67+/-34 ms vs 40+/-15 ms, P0.001), QTcD (77+/-36 ms vs 52+/-23 ms, P0.001) all resulted significantly greater than in controls. QTD and QTcD both resulted linearly related either to max PCi (r=0.388, P=0.018 and r=0.357, P=0.03) or to mean PG (r=0.513, P=0.004 and r=0.438, P=0.015), while M-JT and M-JTc turned out to be directly related only to mean PG (r=0.436, P=0.016 and r=0.483, P=0.007). Our findings suggest a prolonged duration of ventricular recovery and a greater dispersion of ventricular repolarization in patients with AS and might account for the electrical instability proper to this valve dysfunction. Besides, the existence of a linear direct relation between the severity of AS and the degree of inhomogeneity of left ventricular recovery, together with the correlation found among mean PCr and the total duration of the repolarization phase, expressed by the intervals JT and JTc, strongly suggest the hypothesis that in AS arrhythmogenic substrates development parallels the worsening of the valve defect.

Patients with dilated cardiomyopathy, ventricular volume or pressure overload, or dysynergistic ventricular contraction and relaxation are prone to develop severe ventricular arrhythmias. In these patients it has been suggested that the abnormal mechanics of contraction can disturb 'mechano-electric feedback', also known as 'contraction-excitation feedback', which is defined as the development of electrophysiological changes during or after changes in mechanical loading. This electrical instability, expressed by significant changes in ventricular repolarization and refractoriness and by the development of afterdepolarizations, has been variously reported in isolated tissues and isolated ventricles as well as in hearts in vivo. Furthermore, it is known that many patients with supraventricular tachycardia but otherwise structurally normal hearts can develop atrial fibrillation and that atrial arrhythmias frequently occur in the setting of acute or chronic increases in atrial size and pressure. It is possible that changes in atrial load directly alter the electrophysiological properties of the atrium by an analogue mechanism of contraction-excitation feedback. This paper reviews the literature concerning mechanoelectric feedback involvement in rhythm disorders, with the aim of investigating, through basic and clinical research, the clinical and therapeutic implications.

Malignant ventricular arrhythmias have been reported in patients with repaired tetralogy of Fallot. The aim of this study was to examine ventricular repolarization time indexes, in terms of both absolute measures and dispersion across the myocardium, in young patients operated on for tetralogy of Fallot (32 patients; 19 males and 13 females, mean age 11.1 +/- 3.4 years); these electrocardiographic parameters have been shown to be effective in the identification of electrical myocardial instability and hence of risk for ventricular arrhythmias too. The electrocardiographic data of the study group were compared with those of 22 age-matched asymptomatic control subjects (14 males and 8 females, mean age 12 +/- 1.5 years). Furthermore it has also been investigated the possible influence on ventricular repolarization of known negative prognostic factors relative to the surgical approach, age at intervention, and presence of pulmonary obstruction and/or regurgitation. No patients in the study group revealed at the Holter recordings and/or at the exercise test severe ventricular arrhythmias. From the analysis of ventricular depolarization, expressed by QRS duration, emerged that it resulted significantly longer in total Fallot group (p < 0.0001), and in each subgroup (p < 0.05) compared to the control group. Particularly, patients operated through a right ventricular approach showed higher values of QRS interval (p < 0.05) than those operated through combined transatrial-transpulmonary approach. All patients operated on for tetralogy of Fallot showed, compared to control subjects, a non homogeneous prolongation of ventricular repolarization across the myocardium, as confirmed by the significant increase in the absolute indexes of ventricular repolarization, JTc (p < 0.001), QT (p < 0.0001) and QTc (p < 0.0001) with a concomitant prolongation of the indexes of dispersion of ventricular recovery time, QTc dispersion (p < 0.0001), JTc dispersion (p < 0.0001), "adjusted" QTc dispersion (p < 0.05) and T peak-T end interval (p < 0.0001). The non homogeneous ventricular repolarization across the myocardium, preceding the development of arrhythmic events, could be the effect of the right ventricular morphological and functional changes of tetralogy of Fallot predisposing to the development of ventricular reentry tachyarrhythmias.

We examined the effect of left ventricular filling on different combinations of programmable heart rate and atrioventricular delay in patients with dual-chamber pacemakers. Pacing mode with heart rates of 60 beats/min and 156 ms of atrioventricular delay induced a diastolic pattern that resembles more than others the one observed in healthy subjects in sinus rhythm.

Cardiac arrhythmias are common in patients with respiratory failure from chronic obstructive pulmonary disease (COPD). Several factors may be potentially arrhythmogenic in these patients, including hypoxemia and hypercapnia, acid-base disturbances, cor pulmonale and the use of digitalis, methylxanthines, and sympathomimetic drugs. The aim of this study was to examine the effect of hypoxemia and hypercapnia on QTc dispersion (QTcD) in COPD patients, and to evaluate the effect of a partial correction of one of these pro-arrhythmic factors, the hypoxemia, on Qtc dispersion, as QTcD has been proposed as a marker of heterogeneous repolarization and, hence of ventricular electrical instability. We showed that in 15 hypoxemic/hypercapnic COPD patients, compared to 20 controls, the QTcD was significantly higher (49.7 +/- 10.6 vs. 22.9 +/- 9.8 ms; P = 0.0001); furthermore, after only 24 h of oxygen therapy, and hence after a partial correction of hypoxemia, there was a significant reduction in QTcD in COPD patients (49.7 +/- 10.6 vs. 36.3 +/- 10.1 ms; P = 0.018). The data of the present study suggest that the increase in QTcD may be an early marker of a blood gas mediated electropathy in COPD patients.

Both a long QTc and a large QTc dispersion (QTcd) can predispose infarcted patients to ventricular arrhythmias. The former simply reflects a general prolongation of ventricular recovery time, whereas QTcd is useful for revealing regional inhomogeneities of ventricular repolarization. The aim of our study was to evaluate QTc and QTcd behavior during exercise in 50 patients (all men) with previous myocardial infarction, and its possible correlation with the occurrence of exercise-induced premature ventricular complexes (EIPVC). Our patients underwent ergometric stress test with a load increase of 25 W, every 2 min, until the maximal age-related heart rate or symptoms were obtained, followed by a 10-min recovery phase. QTc and QTcd measurement was performed at rest (BS) and during exercise at two progressively increasing heart rate steps: 100-115 beats/min (T1) and 116-130 beats/ min (T2). The patients were divided into two groups according to the absence (group A; n = 22) or presence (group B; n = 28) of EIPVC. In terms of QTcd, no significant difference was found between the two groups at BS, T1, and T2. As for the mean QTc (QTcm), it was significantly longer in group B at BS (416 +/- 22 ms versus 395 +/- 19 ms; P = 0.001) and at T1 (431 +/- 24 ms versus 410 +/- 8 ms; P = 0.0001). When group B was further differentiated into two subgroups-Bx and Bz-according to the severity of EIPVC, we noted that patients with the most severe arrhythmic response (group Bz; n = 12) showed a persisting, significantly longer QTcm than group A (BS, 426 +/- 28 ms versus 395 +/- 19 ms; P0.05; T1, 445 +/- 24 ms versus 410 +/- 8 ms; P0.05; T2, 427 +/- 17 ms versus 412 +/- 14 ms; P0.05), and group Bx (n = 16) (BS, 426 +/- 28 ms versus 409 +/- 15 ms; P0.05; T1, 445 +/- 24 ms versus 420 +/- 19 ms; P0.05; T2, 427 +/- 17 ms versus 410 +/- 17 ms; P0.05). Group Bx showed a significantly longer QTcm than group A only at BS (409 +/- 15 ms versus 395 +/- 19 ms; P0.05). No significant difference in QTcd was found between the three groups at BS, T1, and T2. We also noted that the relationship between QTcm and QTcd was modified by the exercise, changing from a trend of direct relation at BS, towards an inverse one during effort, which reached significance at T2 (r = -0.319; P = 0.037). Based on our data, EIPVC occurrence seems to be more affected by the total duration rather than by regional inhomogeneities of the ventricular recovery time. In those patients with the most severe arrhythmic response, the autonomic modifications generated by the exercise succeed in attenuating only the regional inhomogeneities, but do not eliminate the differences in total duration of the repolarization period.

The aim of this review is the utmost simplification of the cellular electrophysiologic background of ischemia-related arrhythmias. In the acute and subacute phase of myocardial infarction, arrhythmias can be caused by an abnormal impulse generation, abnormal automaticity or triggered activity caused by early or delayed afterdepolarizations (EAD and DAD), or by abnormalities of impulse conduction (i.e., reentry). This paper addresses therapeutic intervention aimed at preventing the depolarization of "pathologic" slow fibers, counteracting the inward calcium (Ca) influx that takes place through the L-type channels (Ca antagonists), or hyperpolarizing the diastolic membrane action potential, increasing potassium (K) efflux (K-channel openers) in arrhythmias generated by an abnormal automaticity (ectopic tachycardias or accelerated idioventricular rhythms). If the cause enhanced impulse generation is related to triggered activity, and since both EAD and DAD are dependent on calcium currents that can appear during a delayed repolarization, the therapeutic options are to shorten the repolarization phase through K-channel openers or Ca antagonists, or to suppress the inward currents directly responsible for the afterdepolarization with Ca blockers. Magnesium seems to represent a reasonable choice, as it is able to shorten the action potential duration and to function as a Ca antagonist. Abnormalities of impulse conduction (re-entry) account for the remainder of arrhythmias that occur in the acute and subacute phase of ischemia and for most dysrhythmias that develop during the chronic phase. Reentrant circuits due to ischemia are usually Na channel-dependent. Drug choice will depend on the length of the excitable gap: in case of a short gap (ventricular fibrillation, polymorphic ventricular tachycardia, etc.), the refractory period has been identified as the most vulnerable parameter, and therefore a correct therapeutic approach will be based on drugs able to prolong the effective refractory period (K-channel blockers, such as class III antiarrhythmic drugs); on the other hand, for those arrhythmias characterized by a long excitable gap (most of the monomorphic ventricular tachycardias), the most appropriate therapeutic intervention consists of depressing ventricular excit-ability and conduction by use of sodium-channel blockers such as mexiletine and lidocaine. Compared with other class I antiarrhythmic agents, these drugs minimally affect refractoriness and exhibit a use-dependent effect and a voltage dependent action (i.e., more pronounced on the ischemic tissue because of its partial depolarization).

The aim of our study was to assess whether the presence of ventricular preexcitation affects the spatial distribution of ventricular recovery time. Recent reports support the hypothesis that QT and QTc dispersions (QTd and QTcd) can be reliably adopted as a non-invasive parameter to estimate regional discrepancies of ventricular repolarization. The ECGs of 32 healthy subjects with Wolff-Parkinson-White syndrome and of 29 normal individuals have been analysed using a Digitizer (Calcomp 9000), in order to obtain, for each subject, a mean QRS (M-QRS), QT (M-QTe), QTc (M-QTec), JT (M-JT), JTc (M-JTc) from all the measured intervals of the 12 standard ECG leads. QRS, QT and QTc dispersions (QRSd, QTd, QTcd) were defined as the difference between the maximal and minimal QRS, QTe and Qtec values calculated in the various leads. We attained the following results: patients with WPW syndrome exhibited, with respect to controls, longer M-QRS (P < 0.001) and M-QTec (P < 0.001) values, despite similar M-QTe (P = NS), M-JT (P = NS) and M-JTc (P = NS). QRSd did not differ in the two groups(P = NS), while QTd and QTcd both resulted significantly greater in pre-excited subjects (P < 0.001). In the WPW group, QRSd was not related either to QTd (r = 0.325, P = NS) or to QTcd (r = 0.148, P = NS), while in the controls there was a significant relation between QRSd and both QTd (r = 0.522, P = 0.004) and QTcd (r = 0.379, P = 0.042). Our findings suggest that the presence of ventricular pre-excitation does not determine a prolongation of the mean ventricular recovery time, but increases regional discrepancies of the re-polarization process. This assumption is supported by the observation of greater values of QTd and QTcd associated with a similar QRSd.

We report a rare case of ectopic atrial tachycardia induced by ergometric stress test whose arrhythmogenic mechanism, after transesophageal electrophysiological study, seemed to be triggered activity. The patient was successfully treated with a beta-blocker (metoprolol), confirming the importance of autonomic modulation in the genesis of arrhythmias caused by afterdepolarizations.

Transesophageal atrial pacing is a diagnostic and therapeutic tool in patients with supraventricular reciprocating tachycardia (SVRT). The aim of the present study was to evaluate the effectiveness of transesophageal atrial pacing in the selection of the chronic treatment of SVRT. Between June 1993 and March 1995 we have performed transesophageal atrial pacing in 44 patients affected by atrioventricular nodal reentry tachycardia (AVNRT: n = 28) or atrioventricular reentrant tachycardia (AVRT) using a concealed or manifest bypass tract (n = 16). After a basal (free drug state) transesophageal atrial pacing, we performed serial electropharmacological tests during chronic treatment with sotalol (160 mg/die), flecainide (200 mg/die) and propafenone (450 mg/die). At the end of these tests, the patients were finally discharged with the drug that allowed a more difficult induction or a wider cycle length, and that showed a better clinical tolerance. At the end of the electropharmacological tests 53.6% of the patients affected by AVNRT were discharged with sotalol, 17.8% with propafenone and 28.6% with flecainide. The follow-up of these 28 patients is 11.4 +/- 1.7 months. In the 79.2% of the patients the drug is still effective (absence of whatever episode of SVRT in the follow-up period). In the AVRT group, at the end of the electropharmacological tests, 25% of the patients were discharged with sotalol, 6.25% with propafenone, and 68.75% with flecainide. The follow-up of these 16 patients is 11.7 +/- 1.8 months. In the 78.6% of the patients the drug is still effective (absence of episode of SVRT in the follow-up period).

The authors present a case of 36 year old male patient with idiopathic postural orthostatic tachycardia syndrome (POTS) diagnosed during head-up tilt testing. Power spectral analysis of heart rate variability (HRV) during the tilt test revealed that the ratio of low and high frequency powers (LF/HF) increased with the onset of orthostatic intolerance. This analysis confirmed in our patient a strong activation in sympathetic tone.

We present a case of a 55-year-old man with idiopathic dilated cardiomyopathy, ejection fraction (EF) of 27%, left bundle branch block with QRS duration of 160 ms, NYHA class III, and optimal medical therapy for at least 6 months who was referred to our division for cardiac resynchronization therapy (CRT) using a biventricular pacing device. During the operation, the coronary sinus branch cannulation failed using classical angioplasty guide wire techniques. The pacing lead was successfully implanted into the posterior target vein using a telescopic dual-catheter system. www.actabiomedica.it.

Twenty patients without laboratory evidence of cardiac disease who underwent electrophysiological study because of recurrent ventricular tachyarrhythmias.The study population was divided into two groups: group A (20 patients [six males and 14 females] mean age 42.2 +/- 13 years), with idiopathic ventricular tachycardia (VT), and group B (30 controls [10 males and 20 females] mean age 43.6 +/- 16 years). Noninvasive multiparametric analysis of the ventricular repolarization phase was performed on the standard 12-lead electrocardiogram by using a digitizer connected with a computerized system. The intervals JT, heart rate-corrected JT (JTc), JT apex (JTa), heart rate-corrected JTa (JTac), T apex T end (TaTe) and heart rate-corrected TaTe (TaTec) were measured and considered to be representative of the whole depolarization process. QT dispersions (QTeD) and QTc dispersions (QTecD) were calculated to assess the degree of spatial inhomogeneity of action potential duration.Patients in group A had higher JT (272 +/- 36 ms versus 265 +/- 25 ms, P = 0.01), JTc (336 +/- 28 ms versus 318 +/- 18 ms, P = 0.01), JTa (210 +/- 28 ms versus 185 +/- 28 ms, P = 0.001) and JTac (240 +/- 20 ms versus 215 +/- 13 ms, P0.001) values than those of patients in group B, despite shorter TaTe (71 +/- 10 ms versus 90 +/- 18 ms, P0.001) and TaTec (88 +/- 12 ms versus 110 +/- 12 ms, P0.001). Moreover, QTeD and QTecD were significantly longer in group A than in group B (55 +/- 18 ms versus 42 +/- 19 ms [P = 0.01] and 80 +/- 18 ms versus 55 +/- 28 ms [P = 0.001], respectively).Patients with idiopathic VT exhibit inhomogeneous prolongation of ventricular repolarization, due to a considerable increase in the initial part in association with a shorter terminal phase, as well as a greater dispersion of ventricular repolarization.