Search

Aim of the study: To detect in adult patients late after repair of Tetralogy of Fallot (TOF) possible correlation between myocardial parameters assessed at rest by Tissue Doppler (TD) and cardiac performance during physical effort. Methods: Doppler echo, treadmill test and pulsed TD of both mitral and tricuspid annulus were performed in 25 healthy subjects and in 40 adult patients who had undergone surgery for TOF at a mean age of 1.4±0.5 years. Exclusion criteria were echocardiographic evidence of residual pulmonary, either stenosis or regurgitation. By use of TD, the following parameters were assessed: systolic peak velocities (Sm), pre-contraction time, contraction time, early ( E m ) and late ( A m ) diastolic velocities, E m / A m ratio, relaxation time. By treadmill test, we measured: maximal heart rate (HR), systolic blood pressure (SBP), rate-pressure product, maximal workload, time duration of the exercise. Results: the two groups were comparable for left ventricular measurements and for all transmitral and transtricuspid Doppler indexes, while tricuspid ring diameter was increased in TOF. TD analysis showed in TOF lower S m , E m and E m / A m ratio and prolonged PCT m and Rt m at tricuspid annulus level, despite comparable TD mitral annulus indexes. By treadmill test, TOF showed reduced time of exercise, number of METS reached and rate-pressure product. Multiple linear regression models evidenced in TOF independent positive association between tricuspid Em velocity and time of exercise ( p p p E m peak velocity of tricuspid annulus lower than 0.13 m/s showed 90% sensitivity and 93% specificity in identifying TOF patients unable to perform maximal exercise test. Conclusions: despite normal Doppler parameters, adult patients late after correction of TOF showed impaired right ventricular myocardial function. In these patients pulsed TD may be taken into account as a valuable supporting tool to predict the effort response and possibly to assess long-term follow-up of cardiac functional reserve.

Background: Basic research and animal experiments have shown electrophysiological changes during or after changes in mechanical loading. Electrical instability following mechanical stretch has been observed as development of after-depolarisation and dispersion of refractoriness and repolarisation. The aim of the present study was to evaluate the presence of the mechano-electrical feedback in humans, assessing the ventricular repolarisation changes following acute changes in left ventricular pressure. Material and methods: The study group comprised 30 consecutive patients (22 M and 8 F, aged 2 days–24 years) affected by severe congenital aortic stenosis and 30 patients (20 M and 10 F, aged 6 months–16 years) affected by severe coartaction of aorta. Ventricular repolarisation was evaluated before and after percutaneous balloon valvuloplasty and angioplasty in terms of absolute measures (JT, JTc, QT, QTc) and in terms of dispersion across the myocardium: QT and QTc dispersion (QTD, QTcD), JT and JTc dispersion (JTD and JTcD) and T-peak to T-end interval (Tp–Te). Results: Patients with severe aortic stenosis and patients with aortic coartaction showed a significant decrease in dispersion of ventricular repolarisation time indexes (QTD, QTcD, JTD, JTcD and Tp–Te) following valvuloplasty and angioplasty. Conclusions: Changes in hemodynamic loading can also produce electrophysiological effects in humans. Acute reduction in left ventricular pressure overload following balloon valvuloplasty and angioplasty, decreases electrical instability, as expressed by the reduction across the myocardium of the dispersion of ventricular repolarisation.

The term Wolff-Parkinson-White (WPW) syndrome refers to people with a ventricular pre-excitation (VPE) pattern on ECG who experience symptomatic bouts of tachycardia.1 Asymptomatic patients with VPE are better described as simply having a “VPE pattern”. Diagnostic assessment and treatment have been described in detail in patients with symptomatic WPW syndrome, but little information exists about the prognosis of VPE discovered on routine ECG in an asymptomatic person. Our study aimed to examine retrospectively the follow up of a cohort of children with asymptomatic VPE, referred during a 15 year period to our unit. From January 1985 to July 2001, 98 children (56 male/42 female) found incidentally to have a VPE on routine ECG were referred to our division. All patients underwent a complete evaluation. The patients were considered asymptomatic if they had no documented tachycardia and no history of palpitations. At recruitment, all the patients underwent clinical examination, ECG, echocardiogram, ECG Holter, and, when possible, exercise testing. Accessory pathway location was established by the use of ECG criteria according to Fitzpatrick’s algorithm.2 The start of the follow up period dated from the time when the first ECG with a δ wave was recorded. Intermittence of VPE was defined as reappearance after loss. Loss of VPE was defined as the absence of VPE for more than three consecutive controls. In the absence of symptoms, patients were seen in outpatient clinic at 6–12 month intervals. ### Electrophysiological study (EPS) The shortest cycle length showing pre-excitation was designated as the minimal cycle length that maintained 1:1 conduction over the accessory pathway. Programmed atrial stimulation at a basic cycle length of 600, 500, and 400 ms with the introduction of one and two extrastimuli was performed. The effective refractory period of the accessory pathway was the longest A1–A2 interval without VPE. If atrial fibrillation (AF) was …

Background: As the response of the myocardium to pressure overload is age-dependent, this study was designed to examine left ventricular (LV) remodeling, mechanics, and tissue characterization in children with moderate congenital aortic stenosis. Methods: We studied by echocardiography Doppler 22 patients (mean age 12.4 ± 5.6 years) with peak and mean transvalvular gradient of 63 ± 6 and 32 ± 4 mm Hg, respectively. In addition, 30 age- and body surface area-matched participants with structurally normal hearts were used as a control group. Sex- and age-specific cut-off levels for LV mass/height 2.7 and relative wall thickness were defined to assess LV geometry. As a load-independent index of myocardial contractility, the relation between the rate-corrected velocity of circumferential fiber shortening both at endocardium and midwall, and meridional end-systolic stress was assessed. In addition, LV diastolic function was also evaluated by the mitral flow indexes. Finally, ultrasonic tissue characterization of the LV myocardium was performed by calculating the magnitude of cyclic variation, which reflects the intramural contractile function, and the averaged myocardial intensity of integrated backscatter, which is directly related to the myocardium collagen content. Results: The endocardial velocity of circumferential fiber shortening endocardium and meridional end-systolic stress relationship was within the normal range (mean ± 2SD) in 18 of 22 patients (81.8%), and midwall velocity of circumferential fiber shortening at endocardium and meridional end-systolic stress was normal in all 22 patients. No mitral flow index of LV diastolic function was significantly different between aortic stenosis group and normal participants. In our study population, 16 of 22 patients (72.7%) showed normal LV geometry, 3 (13.6%) had a pattern of concentric remodeling, and 3 (13.6%) concentric hypertrophy. LV hypertrophy was not marked (left ventricular mass index [LVMI] 2.7 ) in any patient. Finally, compared with control participants our study population showed, both at interventricular septum and posterior wall, comparable values of cyclic variation integrated backscatter, but significantly higher values of averaged myocardial integrated backscatter intensity ( P Conclusions: In children with moderate congenital aortic stenosis, the total amount of myocardial collagen was increased despite normal LV myocardial contractility and diastolic function. Furthermore, LV remodeling was abnormal in only about a quarter of our patients and none had more than mild hypertrophy. Although the majority of these patients do not have markers now recognized to predict higher risk of cardiovascular events, the long-term significance of myocardial fibrosis and its response to treatment remain to be investigated. (J Am Soc Echocardiogr 2003;16:214-20.)

Although in patients with hypertrophic cardiomyopathy (HCM) pathologic studies seem to suggest a correlation between morphologic findings and arrhythmias, it has never been confirmed in the clinical setting.We sought to noninvasively assess the electrical and textural properties of the myocardium and to define their potential relationship in patients with HCM.We studied 48 patients: 22 with HCM (mean age: 22 +/- 5.1 years) and 26 age- and body surface area-matched healthy patients. They underwent a standard echocardiographic examination to assess left ventricular size and thickness. In addition, by integrated backscatter analysis, we assessed textural properties of left ventricular myocardium with calibrated averaged intensity (IB) and to assess functional properties of the myocardium with cyclic variation, both at the interventricular septum (IVS) and posterior wall. Finally, we studied ventricular late potentials (VLPs) by signal-averaged electrocardiography and performed a 24-hour electrocardiography Holter monitoring to respectively define electrical instability and ventricular arrhythmias.Compared with control patients, patients with HCM had, both at IVS and posterior wall, increased IB (-28.8 +/- 10 vs -35 +/- 4 dB [P =.007] and -29 +/- 8 vs -33 +/- 5 dB [P.035], respectively) and decreased cyclic variation (6.8 +/- 2.7 vs 10.3 +/- 2.3 dB [P.001] and 8.2 +/- 2.9 vs 11.4 +/- 2.1 dB [P.001], respectively). In all, 5 patients with HCM had positivity of VLPs, and 4 of them showed nonsustained ventricular tachycardia (nsVT) on the Holter monitoring. Compared with patients who had HCM without VLPs and nsVT, patients with positivity of VLPs and nsVT showed higher IB both at IVS (-15.8 +/- 8.4 vs -32.6 +/- 5.9 dB [P.001] and -16.6 +/- 9.5 vs -31.5 +/- 7.5 dB [P =.002], respectively) and at posterior wall (-19.08 +/- 8.42 vs -32.5 +/- 4.2 dB [P.001] and -22.4 +/- 4.6 vs -31 +/- 7.5 [P =.04], respectively). A multivariate analysis showed IB at IVS (P =.042; odds ratio = 1.19) and positivity of VLPs (P =.026; odds ratio = 3.67) as independent predictors of nsVT.Patients with HCM showed abnormal morphologic and electrical properties of the myocardium. The correlation between VLPs and IB at IVS and their relationship with nsVT suggests a link between textural and electrical nonhomogeneity of myocardial fibers, a potential substrate of nsVT in patients with HCM.

Ambrisentan, an oral endothelin-1-receptor antagonist (ERA) selective for the endothelin A, showed an improvement in WHO functional class, 6 minute walk distance, and time to clinical worsening relative to placebo in randomised, double-blind, placebo-controlled, multicenter, 12-week clinical trials (ARIES study 1 and 2, total n=394) [1]. At this time, the long-term effects of ambrisentan on haemodynamics have not been reported in a prospective study. The aim of this study was to evaluate prospectively the efficacy and safety of ambrisentan treatment in adult patients with pulmonary arterial hypertension by assessing its long term effects on clinical status, exercise capacity, and cardiopulmonary haemodynamics. This was a single-centre, open-label, single-arm, prospective study. All patients with PAH starting oral ambrisentan as first line therapy or combination therapy (based on recommendations of the current ESC/ERS guidelines on pulmonary hypertension) [2] were enrolled after obtaining the informed consent. Clinical status, resting transcutaneous oxygen saturation (SpO2), 6-minute walk distance, serology and right heart catheterization (RHC) were assessed at baseline (before starting ambrisentan therapy) and at 1 year follow-up. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [3]. Clinical status evaluation included medical history, assessment of WHO functional class, measurement of systemic arterial pressure, transcutaneous oxygen saturation (SpO2) and heart rate.

Aim: The aim of the study was to evaluate in 263 competitive athletes possible correlations between changes induced by different sport activities in left ventricular (LV) structure and cardiac response during maximal physical effort. Methods: A total of 160 top-level endurance athletes (ATE; swimmers, runners; 28±4 years; 98 male) and 103 strength-trained athletes (ATS; weight-lifters, body-builders; 27±5 years; male), selected on the basis of training protocol (dynamic vs. static exercise), underwent standard Doppler echocardiography, heart rate variability analysis and maximal exercise stress test by bicycle ergometry. M- and B-mode echocardiographic LV measurements were determined at rest, while the following functional indexes were assessed during effort: maximal heart rate (HR), maximal systolic blood pressure (SBP) and maximal workload (Watts reached by bicycle test). Results: The two groups were comparable for age and sex, but ATS at rest showed higher HR, SBP, and body surface area (BSA). By echo analysis, LV mass index and ejection fraction did not significantly differ between the two groups. However, ATS showed increased sum of wall thickness (septum+posterior wall), relative wall thickness and LV end-systolic stress, while LV stroke volume and LV end-diastolic diameter (P

Forty normotensive patients (mean age 12.3 ± 6.5 years) followed up after a successful repair of aortic coarctation (mean age at coarctectomy 5.1 ± 4.8 yrs) were studied by echo-Doppler to (1) evaluate left ventricular (LV) remodeling and endocardial and midwall mechanics, and (2) identify factors that might predispose to persistent abnormalities. Sex- and age-specific cutoff levels for LV mass/height2.7 and relative wall thickness were defined to assess LV geometry. To adjust for age- and growth-related changes in ventricular mechanics, all echocardiographic variables were expressed as a Z-score relative to the normal distribution. In addition, the smallest diameter of the aorta was assessed by magnetic resonance imaging and calculated as percent narrowing compared with the diameter of the aorta at the diaphragmatic level. In the study group, 24 of 40 patients (60%) had normal LV geometry. Among the 16 patients (40%) with abnormal LV geometry, 5 (12.5%) had a pattern of concentric remodeling and 11 (27.5%) an eccentric hypertrophy. LV hypertrophy was marked (LV mass index >51 g/m2.7) in 5 of these patients. No patient had a pattern of concentric hypertrophy. LV contractility was increased (Z-score >95th percentile) in 28 patients (70%) as assessed using the endocardial stress-velocity index. In contrast, LV contractility assessed using midwall stress-velocity index remained elevated (Z-score >95th percentile) in 15 patients (37.5%). The stepwise multiple logistic regression analysis was not able to detect any significant independent predictor of abnormal LV remodeling, including sex, age at surgical repair, length of postoperative follow-up, heart rate, body mass index, systolic and diastolic blood pressure, and smallest diameter of the aorta, as well as indexes of LV geometry (shape, mass, volume, mass/volume ratio) and function (preload, afterload, pump function, and myocardial contractility). Thus, normotensive patients after surgical repair of aortic coarctation may be in an LV hyperdynamic cardiovascular state (more frequent in those who have undergone late repair) and have multiple patterns of LV geometry.

The aim of the study was to evaluate by Doppler tissue imaging (DTI) the combined effects of atrio-ventricular (AV) delay and heart rate (HR) changes on global and segmental right (RV) and left (LV) ventricular diastolic function in 15 patients with dual-chamber pacemakers paced in the DDD mode. RV and LV inflow velocities and regional systolic and diastolic pulsed-wave (PW) DTI parameters were analyzed at four different pacing modes: (1) HR 70 beats/min, AV delay 125 ms; (2) HR 70 beats/min, AV delay 188 ms; (3) HR 89 beats/min, AV delay 125 ms; (4) HR 89 beats/min, AV delay 188 ms. For each pacing mode selected, RV diastolic filling velocities always prevailed over LV ones. As for RV and LV adaptation to the four different stimulation protocols, a higher paced rate and a prolonged AV delay caused across both the AV valves a decrease of E wave and of E/A ratios. The intersegmental comparison of PW-DTI parameters outlined that RV free wall exhibited significantly higher peak systolic (Sm) and early-diastolic (Em) wall velocities, and longer systolic ejection time. Considering separately RV and LV segmental physiology at the four programmed pacing modes, an increase in HR determined a progressive shortening of systolic ejection times in all the segments analyzed. Moreover, in each region the Em/Am ratio decreased with higher HR and longer AV delay. Conversely, Em encountered a progressive reduction in RV free wall, while remaining quite unchanged in all the LV regions. Both ventricles shared a similar pattern of global and regional adaptation to programmed HR and AV delay modifications, consisting in a progressive greater contribution of late diastole to ventricular filling at higher HR and more prolonged AV delay. However, at a regional level the right ventricle exhibited higher systolic and diastolic wall velocities than all left ventricular regions.

Left ventricular outflow tract (LVOT) obstruction due to anomalous tissue tag arising from the mitral valve is a rare congenital cardiac anomaly. It generally becomes symptomatic during the first decade of life as exercise intolerance, chest pain, or syncope at effort. To date, only a few cases of critical systemic obstruction due to isolated mitral valve anomaly in neonates have been reported. We report the case of a neonate who was a few hours old and was referred in severe clinical condition due to critical left ventricular outflow obstruction resulting from an anomalous tissue tag of mitral valve origin.

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.

Ventricular repolarization analysis has been shown to be effective in the identification of electrical myocardial instability leading to ventricular arrhythmias. The aim of the present study was to examine ventricular repolarization time indexes, in terms of both absolute measures and dispersion across the myocardium, in young patients with repaired tetralogy of Fallot (41 pts; 28M/13F, age 11.7+/-3.6 years), assessing, furthermore, the possible influence of known negative prognostic factors relative to the surgical operation and residual haemodynamic abnormalities. The data of the study group were compared with those of 33 aged-matched asymptomatic control subjects (22M/11F, age 11.7+/-2.3 years). Ventricular depolarisation, as expressed by QRS duration, resulted significantly longer in total Fallot group than in the Control group (P

Tetralogy of Fallot is the most common form of cyanotic congenital heart disease. Measurement of physical activity is usually performed as a routine part of the patient's cardiac evaluation. The aim of this study was to examine the exercise performance of young patients operated on for tetralogy of Fallot, assessing the possible influence of known negative prognostic factors related to the surgical repair. The study group comprised 41 consecutive patients (29 male and 12 female, ages 11.2 +/- 3.9 years, range 6-16 years) operated on for tetralogy of Fallot. Patients in the study group were divided in subgroups in relation to the age of surgical intervention (before or after 2 years of life), the surgical approach (combined transatrial/transpulmonary approach or right ventriculotomy), and the presence of aortopulmonary shunts prior to performing total correction. Their data were compared with those of 33 aged-matched asymptomatic control subjects (19 male and 14 female, ages 11.9 +/- 1.3 years, range 11-16 years). Blood pressure and heart rate measured at rest were similar between control and Fallot groups. A normal increase in systolic blood pressure was observed in response to exercise intensity for all subgroups. No significant difference between control and Fallot groups was found under conditions of mild or moderate exercise or for diastolic blood pressure at rest and in response to exercise. Lower maximal heart rate and systolic blood pressure values were recorded in all patients when compared with the control subjects. Significant differences in peak workload were detected between control and Fallot groups and between the control and each subgroup; however, no difference was found between subgroups. In conclusion, despite their very satisfactory clinical status, all patients showed a reduced peak workload, irrespective of the surgical approach, age at surgery, and aortopulmonary shunts prior to performing total correction.

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.

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).

Cardiac arrhythmias are common in patients with chronic obstructive pulmonary disease. Several factors may contribute to the development of arrhythmias in these patients including hypoxemia, hypercapnia, acid-base disturbances. The aim of the study was to assess QTc dispersion in patients with chronic obstructive pulmonary disease, who are at high risk of arrhythmias. Interlead QT variability as measured on the 12-lead electrocardiogram is not a technical artifact but probably reflects regional differences in ventricular repolarization. Increased dispersion of ventricular recovery time is believed to provide a substrate which supports serious ventricular arrhythmias. We showed that in patients with chronic obstructive pulmonary disease, free of underlying structural heart disease, the QTc dispersion is significant greater (p = 0.036) than in a control group, despite a similar value in mean QTc value. The data of the present study suggest that the determination of dispersion of repolarization times may be affected by metabolic changes occurring in patients with chronic obstructive pulmonary disease.

We assessed the feasibility of transthoracic three-dimensional reconstruction of the pulmonary valve and subpulmonary left ventricular outflow tract in two patients with transposition of great arteries, ventricular septal defect, and obstruction to the left ventricular outflow tract. Three dimensional reconstruction of the pulmonary valve could be displayed as ‘en face” through a three-dimensional generated “pulmotomy view,” allowing an overview of the pulmonary aspect of the valve from a surgeon's perspective. In similar fashion, reconstruction of the subpulmonary outflow tract could be displayed along its longitudinal axis as seen through a left ventriculotomy. Unique views could be obtained equivalent to surgical or autopsy dissections, allowing more complete understanding of the morphology and severity of left-sided obstructive lesions.

Objective: To identify perioperative clinical predictors of permanent pacemaker implantation following aortic valve replacement. Design and patients: Prospective cohort study on 276 patients submitted for aortic valve replacement: 267 patients (mean (SD) age, 57.5 (14) years) with no conduction disturbances, and nine patients (67.7 (5) years) with severe conduction disturbances requiring permanent pacing; 65 perioperative variables (38 preoperative, eight intraoperative, and 19 postoperative) were considered. Results: Nine patients (3.2%) had irreversible second or third degree atrioventricular (AV) block requiring permanent pacing. Risk factors for permanent pacing identified by univariate analysis were: preoperative: additional valvar disease, aortic regurgitation, myocardial infarction, pulmonary hypertension, anaemia, use of digitalis; intraoperative: cardiac arrest; postoperative: cardiac arrest, conduction disturbances, electrolytic imbalance, angiotensin converting enzyme inhibitor use. Multivariate logistic regression analysis identified preoperative aortic regurgitation (p < 0.005; odds ratio (OR) 6.6, 95% confidence interval (CI) 1.6 to 12.2), myocardial infarction (p < 0.0005; OR 15.2, 95% CI 6.3 to 19.9), pulmonary hypertension (p < 0.005; OR 12.5, 95% CI 3.2 to 18.3), and postoperative electrolyte imbalance (p < 0.01; OR 4.5, 95% CI 1.3 to 6.4). Conclusions: Irreversible AV block requiring permanent pacemaker implantation is an uncommon condition following aortic valve replacement. Previous aortic regurgitation, myocardial infarction, pulmonary hypertension, and postoperative electrolyte imbalance should be considered in order to identify patients at increased risk for advanced AV block.

Junctional ectopic tachycardia (JET) is a rare arrhythmia presenting either as a primary form1 or more often as a transient phenomenon immediately after heart surgery.2 Congenital JET usually occurs in the first six months of life as a persistent arrhythmia, associated in up to 60% of cases with cardiomegaly and/or heart failure.1 Congenital JET has been described in sporadic case reports or larger multicentre populations. The purpose of this study is to examine retrospectively the clinical presentation and outcome of a cohort of nine patients with congenital JET referred during a 20 year period time to a single unit and all medically treated. Nine patients (two male, seven female) suffering from persistent sustained JET were referred to our hospital between 1980 and 1999. All the patients underwent a complete medical history, physical examination, 12 lead ECG, 24 hour Holter recording, and echocardiogram. The diagnosis of JET was based on electrocardiographic evidence of a narrow complex tachycardia and atrioventricular dissociation. All the patients underwent medical treatment according to the following regimen: A Ic antiarrhythmic drug (propafenone or flecainide) was administered in combination with amiodarone when the latter proved ineffective alone in controlling the arrhythmia. This combination of drugs was also used in an attempt to reduce the dose of amiodarone, and prevent signs of …

"Sudden unexplained death (SUD) is a tragic event for both the family and community, particularly when it occurs in young individuals. Sudden cardiac death (SCD) represents the leading form of SUD and is defined as an unexpected event without an obvious extracardiac cause, occurring within 1hour after the onset of symptoms. In children, the main causes of SCD are inherited cardiac disorders, whereas coronary artery diseases (congenital or acquired), congenital heart diseases, and myocarditis are rare. The present review examines the current state of knowledge regarding SCD in children, discussing the epidemiology, clinical causes, and prevention strategies."

Junctional ectopic tachycardia (JET) is a rare type of supraventricular arrhythmia. Even if its management has improved in recent years, it remains a great challenge for the cardiologist. Two are the possible clinical presentations of this arrhythmia: as a primary idiopathic disorder during infancy, configuring the so called congenital JET, or more often as a transient phenomenon immediately after surgery for congenital heart disease, giving rise to the post-operative variety. The congenital form, firstly described as a distinct entity by Coumel et al. in 19761, usually occurs in the first six months of life presenting as a persistent sustained form, lasting up to 90% of the time. Its clinical presentation may be dramatic, being associated in up to 60% of cases with cardiomegaly and/or heart failure. Congenital JET is hampered by high mortality. Secondary dilated cardiomyopathy, ventricular fibrillation and sudden cardiac death have also been reported 2,3.

Sudden death is a possible occurrence for newborns younger than 1 year with severe aortic coarctation (CoA) before surgical correction. In our previous study, we showed a significant increase of QTc-D and JTc-D in newborns with isolated severe aortic coarctation, electrocardiographic parameters that clinical and experimental studies have suggested could reflect the physiological variability of regional and ventricular repolarization and could provide a substrate for life-threatening ventricular arrhythmias. The aim of the current study was to evaluate the effect of surgical repair of CoA on QTc-d, JTc-d in severe aortic coarctation newborns with no associated congenital cardiac malformations. The study included 30 newborns (18M; 70±12 h old) affected by severe congenital aortic coarctation, without associated cardiac malformations. All newborns underwent to classic extended end-to-end repair. Echocardiographic and electrocardiographic measurements were performed in each patient 24 h before and 24 h after the interventional procedure and at the end of the follow-up period, 1 month after the surgical correction. All patients at baseline, 24 h and one month after CoA surgical repair did not significantly differ in terms of heart rate, weight, height, and echocardiographic parameters. There were no statistically significant differences in QTc-D (111.7±47.4 vs 111.9±63.8 ms vs 108.5±55.4 ms; P=0.4) and JTc-D (98.1±41.3 vs 111.4±47.5 vs 105.1±33.4 ms; P=0.3) before, 24 h and 1 month after CoA surgical correction. In conclusions, our study did not show a statistically significant decrease in QTc-D and JTc-D, suggesting the hypothesis that the acute left ventricular afterload reduction, related to successful CoA surgical correction, may not reduce the ventricular electrical instability in the short-term follow-up.

This review has been focused on the new insights in the pathophysiology of mitral and aortic regurgitation and on the role of ACE-inhibitor therapy in children with chronic volume overload due to left-sided valvular lesions. Recent clinical studies show that these drugs have favorable effects when administered orally in chronic mitral and aortic regurgitation. Interestingly, the beneficial effects of ACE-inhibition regard the basic anatomic, hemodynamic and adaptive pathologic conditions related to volume overload, namely, the regurgitant orifice area and volume and ventricular remodeling. The heart is a plastic structure, constantly being altered in size, shape and composition in response to chronic volume overload. Thus, modulation of cardiac plasticity by ACE-inhibition raises the possibility of using new therapeutic strategies specifically designed to prevent and/or antagonize the mechanical disadvantages secondary to volume overload-induced cardiac remodeling. The beneficial effects of ACE-inhibition have also been observed in growing children with asymptomatic valvular regurgitation; thus, it appears that the unloading therapy has the potential of influencing the natural history of both mitral and aortic regurgitation and possibly delays surgical valve repair or replacement. These data justify early inhibition of the renin-angiotensin system in children with left ventricular volume overload due to mitral and aortic regurgitation.

Based on our previous experience in doxorubicin-treated patients, in whom we observed a significant increase of ventricular recovery time indexes, we analyzed these non- invasive parameters of myocardium electrical instability in forty-three 5-fluorouracil-treated patients, to test the hypothesis of a mechanoelectrical disarrangement occurring in 5-fluorouracil (5FU) cardiotoxicity. All patients enrolled were studied at the first presentation and following chemotherapy. The study showed the absence of any significant changes in recovery time indexes or in other electrocardiographic parameters. Our data suggest that 5FU does not interfere with electrical properties of myocardial fibers.

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.