Valentino Ducceschi

Risk factors for pacemaker implantation following aortic valve replacement: a single centre experience

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.

Perioperative clinical predictors of atrial fibrillation occurrence following coronary artery surgery

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.

Effect of blood gas derangement on QTc dispersion in severe chronic obstructive pulmonary disease: evidence of an electropathy?

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.

Autonomic nervous system imbalance and left ventricular systolic dysfunction as potential candidates for arrhythmogenesis in Becker muscular dystrophy

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.

Ventricular repolarization time indexes following anthracycline treatment

SummaryThe 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 nonivasive 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.

Usefulness of Doppler tissue imaging for the assessment of right and left ventricular myocardial function in patients with dual-chamber pacing

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.

Compared effects of sotalol, flecainide and propafenone on ventricular repolarization in patients free of underlying structural heart disease

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).

Intrahisian Conduction Disease and Junctional Ectopic Tachycardia

Junctional ectopic tachycardia (JET) is an uncommon arrhythmia that mainly affects pediatric patients. However, its clinical presentation may rarely occur in adulthood. Owing to its incessant nature, limited responsiveness to antiarrhythmic agents and poor prognosis, catheter ablation of the junctional focus is often required, even though this may be accompanied by the occurrence of complete atrioventricular block. We report the case of a 68‐year‐old man with episodes of sustained ventricular tachycardia and repetitive JET whose initiation was often anticipated by a sudden intrahisian conduction delay in the immediately preceding sinus beats.

Prognostic value of tissue Doppler-derived ventricular asynchrony in patients with left bundle branch block but not advanced heart failure

Objectives The aim of the present study was to evaluate the prognostic significance of tissue Doppler echocardiography (TDE)-derived ventricular asynchrony in patients with left bundle branch block (LBBB) but not advanced heart failure. Methods Fifty-five patients (mean age 66 ± 13 years; 33 male) with complete LBBB (QRS > 120 ms) hospitalized for an acute episode of decompensated heart failure and in New York Heart Association class II for at least 6 months before the study admission underwent standard Doppler echo and pulsed-wave TDE. Precontraction time (PCTm) from the beginning of Q wave of electrocardiogram to the onset of systolic myocardial velocity wave was evaluated in four different left ventricular (LV) basal myocardial segments (LV anterior, inferior, septal and lateral walls) and in one right ventricular (RV) lateral wall. Intraventricular activation delay (IntraV-del) was calculated by the difference of PCTm of each LV myocardial segment. Interventricular activation delay (InterV-del) was calculated by the difference of PCTm between the most delayed LV segment and RV lateral wall. Results The mean value of EF was 40 ± 9% and of InterV-del, IntraV-del was, respectively (97.4 ± 46.7 and 57.9 ± 35.5 ms). InterV-del was inversely related to EF (r = −0.68; P < 0001). During the follow-up (26 months, range 11–37 months) cardiac events were recorded in 23 (41%) patients: a worsening of heart failure (WHF) in 23 patients and cardiac death in ten patients. Cox proportional hazard multivariate analysis showed that age, and InterV-del [HR = 1.02 (P < 0.05) and 1.03 (P < 0005)] predicted mortality. A Receiver operating characteristic analysis showed that a cut-off value of InterV-del 100 ms (AUC = 0.86; P < 0001) predicted WHF and mortality with sensitivity and specificity of 75% and 90%; 81% and 84%, respectively. Conclusions TDE-derived interventricular asynchrony represents a prognostic indicator of major cardiac events at 2 years of follow-up in patients with LBBB but not advanced heart failure.

Increased dispersion of ventricular recovery time as a new repolarization abnormality in the Wolff-Parkinson-White syndrome

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.