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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.

Objective: To assess the effects of treatment with verapamil on regional and global left ventricular (LV) diastolic function in paediatric patients with hypertrophic cardiomyopathy (HCM)., Design: Twelve patients (age range 5.1 to 12.3 years, median 8.6) with HCM were evaluated during ongoing chronic oral treatment with verapamil (4 mg/kg/day) and four days after withdrawal of therapy. Twelve age- and body surface area-matched normal children served as controls. In an echocardiographic study, global LV diastolic function was evaluated by assessing isovolumic relaxation time (IVRT) and mitral flow indexes, including peak filling rate normalized to mitral stroke volume (PFR/SV). In addition, regional LV diastolic function was assessed by pulsed-wave Doppler tissue imaging at the subendocardial portion of the middle region of the anterior and posterior interventricular septum, and anterolateral and inferior walls to measure the peak velocities and the velocity-time integrals of myocardial excursion in both early diastole and atrial systole. In addition, as an index of diastolic asynchrony (AsyI), the variation in time to peak filling rate, measured as the time from the peak of the R wave on the electrocardiogram to the peak of the regional E wave, among the four myocardial regions was defined by subtracting the smallest value from the greatest and expressing the difference as a percentage of the smallest value., Results: Compared with the controls, patients with HCM without therapy showed a longer IVRT (P<0.01) and a decrease in PFR/SV (P<0.01) without a compensatory increase in filling during atrial systole. Oral administration of verapamil induced a significant shortening of the IVRT (P=0.003) and an increase in PFR/SV (P=0.02). Furthermore, patients with HCM without therapy showed a significantly longer time to peak filling rate (P<0.01) associated with a decreased peak velocity in early diastole without a concomitant increase in peak velocity during atrial systole in each of the myocardial regions. Furthermore, the AsyI was higher in the HCM group than in controls (19% versus 6%, respectively), and this index was inversely correlated with the PFR/SV (r=-0.86, P<0.001). The regional diastolic velocity of the myocardium at each of the four analyzed regions was not significantly different with verapamil, but the AsyI was significantly lower (P<0.05)., Conclusions: Children with HCM show abnormalities of both global and regional LV diastolic function. In these patients, chronic administration of verapamil plays a crucial role in the improvement in global LV filling and, as a consequence, in clinical manifestations. The beneficial effects of verapamil seem to be related to a reduction in diastolic asynchrony more than to significant changes in diastolic velocities of the myocardial fibres.

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<0.0001). Particularly, patients operated through a right ventricular approach showed higher values of QRS interval (P<0.0001) than those operated through a combined transatrial-transpulmonary approach. All the patients operated on for tetralogy of Fallot exhibit, with respect to control subjects, an inhomogeneous prolongation of ventricular repolarization across the myocardium, as showed 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, QTcD (P<0.0001), JTcD (P<0.0001), 'adjusted' QTcD (P<0.001) and Tp-Te interval (P<0.0001). A temporal and regional variation in the ventricular repolarization across the myocardium in patients with repaired tetralogy of Fallot, could create the pathophysiological substrate for an increased cardiac electrical instability. The presence of negative prognostic factors, relative to the surgical intervention or residual haemodynamic abnormalities, even if not influencing the arrhythmic substrate, invariably present, could determine 'trigger' conditions essential for the development of ventricular arrhythmias.

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, P = 0.026), a prior history of paroxysmal AF (SR vs. AF: 3.2% vs. 16.7%, P = 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, P = 0.001; three-vessel CAD (54.1% vs. 91.3%, P = 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 (P = 0.007) and a more severe CAD (P = 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.

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.

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.

An apparently healthy man of 26 years of age suddenly died. He was known to have had a small ventricular septal defect and complete right bundle branch block from early childhood. At post-mortem examination the small ventricular septal defect was found associated with an aneurysm of the membranous septum. Histological examination showed a normal atrioventricular node and bundle, adjacent to the aneurysm. There was fibrous interruption at the commencement of the right bundle branch, which was considered the basis of the bundle branch block. It was also considered that the right bundle branch block was of the hereditary type and that this, rather than the aneurysm of the membranous septum, was responsible for the unexpected death.

Study Population: Twenty patients without laboratory evidence of cardiac disease who underwent electrophysiological study because of recurrent ventricular tachyarrhythmias., Patients and Methods: 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., Results: 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, P < 0.001) values than those of patients in group B, despite shorter TaTe (71 +/- 10 ms versus 90 +/- 18 ms, P < 0.001) and TaTec (88 +/- 12 ms versus 110 +/- 12 ms, P < 0.001). 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)., Conclusions: 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.

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 degrees was considered the cut-off point for determining subjects with a considerable leftward QRSA deviation. Of the 27 Group A patients with a QRSA < -60 degrees, 38.5% developed an infrahisal second-degree atrioventricular (AV) block during incremental atrial stimulation (IAS) in comparison with 11.1% of those with QRSA > -60 degrees. Of the 9 Group B patients with a QRSA < -60 degrees, 44.4% exhibited severe impairment of infrahisal conduction at baseline and 66.6% developed an infrahisal second-degree AV block during IAS, whereas among the remaining 24 with a QRSA > -60 degrees, 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 < -60 degrees for the development of an infrahisal second-degree AV block during IAS, whereas the latter appeared the best noninvasive predictor in Group B with a slightly lesser predictive accuracy than HV > 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.

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.

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.

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, P<0.001, QTD (67+/-34 ms vs 40+/-15 ms, P<0.001), QTcD (77+/-36 ms vs 52+/-23 ms, P<0.001) 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.

The anthracyclines are antibiotics effective in the treatment of many malignancies. However, their usefulness is limited by the development of potentially acute or chronic cardiotoxicity. No definitive guidelines exist for monitoring cardiac function during and after anthracyclines although methods have been suggested. Electrocardiograms and echocardiograms are routinely utilized for noninvasive assessment of myocardial function. The aim of the 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 the risk for either arrhythmia or heart failure. Electrocardiographic parameters were compared in 27 cancer patients before and after chemotherapy including doxorubicin. The data of the present study show that after only a short period of treatment with doxorubicin there is a significant increase in ventricular recovery time indexes (QTc dispersion and 'Adjusted' QTc dispersion). The relation between the electrophysiological response to doxorubicin and the potential cardiotoxic effect of this drug remains to be established through prospective studies.

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.

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 interval > or = 200 msec; group B (14 patients), with RBBB, LAH with a PQ interval > or = 200 msec; group C (8 patients), with LBBB and a PQ < 200 msec; group D (15 patients), with RBBB, LAH and a PQ < 200 msec; group E (3 patients), with RBBB, LPH and a PQ < 200 msec. In group A, 31% presented a long AH interval (> 140 msec), while 85% showed an increased infra-his conduction time (HV > 55 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 HV > 55 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 value > 55 msec) in the above mentioned groups: 71.4% in case of LBBB, 20.7% in case of RBBB+LAH (p < 0.001). 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, p < 0.001) 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, p < 0.001), 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

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.

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.

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; P < 0.05; T1, 445 +/- 24 ms versus 410 +/- 8 ms; P < 0.05; T2, 427 +/- 17 ms versus 412 +/- 14 ms; P < 0.05), and group Bx (n = 16) (BS, 426 +/- 28 ms versus 409 +/- 15 ms; P < 0.05; T1, 445 +/- 24 ms versus 420 +/- 19 ms; P < 0.05; T2, 427 +/- 17 ms versus 410 +/- 17 ms; P < 0.05). Group Bx showed a significantly longer QTcm than group A only at BS (409 +/- 15 ms versus 395 +/- 19 ms; P < 0.05). 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 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.

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).

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 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).

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.

The prevalence of coronary artery disease is lower in women than in men. Ovarian estrogen is believed to decrease the risk of coronary heart disease. Today, there is an increasing demand for estrogen replacement not only for amelioration of menopausal subjective symptoms but also for the prophylactic action of estrogen against osteoporosis in postmenopausal women. Is generally agreed that estrogen replacement therapy reduces cardiovascular morbidity and mortality in postmenopausal women. Estrogen replacement therapy may protect against coronary heart disease by altering plasma lipoprotein concentrations, by increasing HDL cholesterol and decreasing LDL cholesterol, and thereby inhibiting progression of coronary artery atherosclerosis. Oral contraceptive can induce deterioration in glucose tolerance that has consistently been associated with insulin excess and insulin resistance. This situation can increase the coronary heart disease risk. New findings suggest that there may be independent cardioprotective effects of estrogen, such a direct inhibitory influence on thrombosis, vasospasm or atherogenesis, inhibiting atherosclerotic plaque formation in arterial walls.

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.

Low-dose estrogen replacement therapy should be recommended to post-menopausal women, especially if they suffer from circulatory disorders, because it significantly reduces cardiovascular risk. Low-dose estrogens favourably affects lipid profile, without causing a significant increase of thrombotic risk: atherosclerosis is therefore prevented. Estrogen can augment coronary flow by the relaxation of vascular smooth-muscular cells. Finally, estrogen can improve left ventricle systolic and diastolic function, delaying the physiological aging process.

The diagnosis of previous non-Q wave myocardial infarction by standard electrocardiographic investigation is uncertain, particularly in elderly patients because of concomitant disease. We have studied 31 elderly patients (aged 63-72 years) with a diagnosis of non-Q wave myocardial infarction between 1-6 months after this acute event. The patients underwent clinical-anamnestic examination, standard electrocardiography, vectorcardiography according to the Frank system and M-mode and 2-D echo-cardiography with continuous and pulsated Doppler. The ECG showed ST-T anomalies in 12 patients (38.7%) whereas the VCG showed anomalies of QRS-loop normal convexity in 27 patients (87%) and 16 of these (51.6%) showed bites criteria (duration > or = 10 msec, voltage > or = 0.1 mV, present at least on two planes). By echocardiography, regional hypo-akinesia was observed in 19 patients (61.3%). Although bites are not only present in myocardial infarction, they indicate an interruption of myocardial gradual electric activation, compatible with fibrous areas, and should be evaluated as a part of the clinical-anamnestic, laboratory and instrumental data.

Shy-Drager syndrome is a very rare disease affecting the autonomic nervous system. Usefulness of beta-adrenergic chronic therapy has already been focused in these cases. Ambulatory blood pressure monitoring may help to study the cardiocirculatory adaptation in Shy-Drager syndrome patients.

The authors carried out a perspective study to determine the frequency of silent ischemia (SI), in 50 consecutive patients with end stage renal failure, during dialysis by Holter monitoring. Twenty patients had SI. The number of cardiovascular risk factors, principally diabetes, smoking and the underlying renal disease was related to ischemic events. Dialysis may predispose to and facilitate the detection of myocardial ischemia by the simultaneous presence of hypotension, hypovolemia, hypoxia and tachycardia. Holter monitoring may allow the detection of ischemic events and the identification of a subgroup of dialytic patients with a high cardiovascular risk.

Thalassaemia major determines an impaired effort tolerance because of a condition of severe anaemia, progressive left ventricular dysfunction, pulmonary circulation compromise. The aim of our study is to evaluate haemodynamic response to exercise in thalassaemic patients without clinical features of heart failure. We have selected 13 patients affected by thalassaemia major (Thal+; 10-18 years). Each patient was transfused when haemoglobin values were < 9-9.5 g/dl and was treated with desferrioxamine (40 mg/kg sc) when serum ferritin values were > 2,000 ng/ml. Thal+ patients were compared with normal subjects (Thal- 10-16 years). No patient assumed hypotensive therapy, no had familiar history of hypertension. Both groups have undergone an ergometric stress test at the cycloergometer, with increase of 25 W every 2 min, up to the reaching of the maximum age-related heart rate, or up to muscle exhaustion or unbearable dyspnea, followed by a 10 min recovery phase. The following parameters were taken in consideration: systolic (SBP) and diastolic (DBP) blood pressure, heart rate (HR), the product of the heart rate by the systolic blood pressure (DP), at rest, at the maximum common work (MCW), at maximum stress and in the recovery phases. At rest, only DP showed significant differences between the two groups: in Thal+ patients higher than in Thal- (p = 0.045). At the MCW, Thal+ patients had SBP (p = 0.019), DBP (p = 0.01), HR (p = 0.035) and DP (p = 0.003) higher than Thal- patients. At maximum stress only DBP showed significant differences in Thal+ patients (p = 0.019), although Thal+ patients achieved lower levels of workload (p = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

In obesity, the systemic resistances (SR) are reduced while the blood volume is increased. The rise of cardiac output (CO), stress-induced, produces an increase in blood pressure (BP), as an hypertensive behavior of the stress-response. The aim of our study is to evaluate if, in obese subjects, the considerable increase of BP is more related to the rise of CO than to the rise of SR. For this reason we studied the behavior of BP through indexes derived from the ratio of SBP values at the 1st, 3rd, 5th, 10th minutes of the recovery by the SBP value at the acme of stress. These indexes are under neurovegetative control, and were shown to be impaired in hypertensive pts. The results of ergometric stress test (EST) of 37 obese subjects (Ob+) (27 males and 10 females, mean age 46.2 +/- 7.3 years), determined according to Lorentz's formula, was compared with the parameters deduced from the EST of 18 normal subjects (Ob-) (13 males and 5 females, mean age 36.7 +/- 8.5). The exercise showed an increase, more pronounced in Ob+ subjects, of SBP and DBP, and this also persisted in the recovery phase. Although BP was significantly higher in the Ob+group, the SBP indexes did not differ in the two groups. Then, from these data it can be deduced that, although during EST in obese subjects there is an absolute increase of BP and this persists in the recovery phase, the behavior of this parameter probably cannot be related to alteration of neurovegetative system as demonstrated by the normal SBP indexes.

A family history of hypertension can influence the behaviour of blood pressure during ergometric stress test (EST) in normotensive subjects, so that it is also used in the assessment of risk of hypertension. To evaluate the relationship between parental history and blood pressure values during exercise, 57 consecutive adolescents (aged 10-16 years) were studied. Out of them, 25 patients have not been considered because of the presence of organic pathologies of various nature that could interfere with the pressure behaviour. All patients underwent EST with a load increase of 25 W every 3 min until the maximal age-related heart rate. The patients were divided in 2 groups based on the presence (PH+ 13 patients, mean age 13 +/- 2 years) or on the absence (PH- 19 patients, mean age 13 +/- 2 years) of parental history of hypertension. No difference in body surface and maximum workload was observed between the 2 groups. Exercise test induced an increase in systolic blood pressure (SBP) both in PH- and PH+ patients, but no significant differences were found in any stage of the exercise in the 2 groups. Maximum heart rate (HR) was not different in the 2 groups and diastolic blood pressure (DBP) was substantially unchanged during exercise. The variation of SBP (delta SBP) between maximum stress and first, third, fifth and tenth min of the recovery phase were considered. Besides, 4 SBP indexes were deduced from the ratio of SBP values at the first, third, fifth and tenth min of the recovery by the SBP value at the acme of stress.(ABSTRACT TRUNCATED AT 250 WORDS)