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L Santangelo

Publications and source records attributed to L Santangelo.

At least 37 records · Page 2Linked to original sources
PubMed1997

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.

Adult↗
PubMed1997

QTc and not QTc dispersion behavior affects the occurrence of ventricular extrasystole during exercise in infarcted 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; 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.

Aged↗
PubMed1997

Ventricular repolarization time indexes following anthracycline treatment.

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.

Adult↗
PubMed1997

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.

Adult↗
PubMed1997

[Electrophysiological analysis of atrioventricular and intraventricular conduction in bi- and tri-fascicular blocks].

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

Aged↗
PubMed1996

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.

Adult↗
PubMed1996

Ionic mechanisms of ischemia-related ventricular arrhythmias.

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).

Animals↗
PubMed1996

Correlation between late potentials duration and QTc dispersion: Is there a causal relationship?

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.

Action Potentials↗
PubMed1996

[The pharmacological treatment of supraventricular atrioventricular nodal reentry or accessory pathway reentry tachycardias: the usefulness of transesophageal electrophysiological study in the selection of therapy].

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).

Adolescent↗
PubMed1996

[An unusual case of ectopic atrial tachycardia: triggered activity as an arrhythmogenic mechanism].

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.

Adrenergic beta-Antagonists↗
PubMed1996

[Sotalol, propafenone, and flecainide: compared multiparametric analysis of ventricular repolarization in subjects without organic cardiopathy].

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).

Adolescent↗
PubMed1995

[Assessment of dispersion++ of ventricular recovery in patients with chronic obstructive pulmonary disease].

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.

Adult↗
PubMed1994

[Surgical treatment of incessant atrial tachycardia: description of a case].

A 50 year old woman with no evidence of structural heart disease was referred for ectopic incessant repetitive atrial tachycardia uncontrolled by medical therapy. Intracavitary and transesophageal simultaneous recordings revealed the earliest atrial electrical activity to be located in the left atrium. Intraoperative electrophysiologic mapping demonstrated that the site of earliest atrial activation was in a small diverticulum of the left atrial appendage. Excision of the appendage and isolation of left atrium was carried out with restoration of sinus rhythm. The patient was arrhythmia-free till 24 months later. Surgical treatment appears to be an effective therapeutic option for drug-resistant ectopic atrial tachycardia.

Electrocardiography↗
PubMed1994

[Double ventricular response to a single atrial stimulation caused by simultaneous anterograde conduction through two atrioventricular nodal pathways].

In a patient with atrioventricular nodal reentrant tachycardia, during programmed stimulation, an atrial extrastimulus induced a double ventricular response due to a single atrial depolarization, with simultaneous and delayed anterograde conduction through fast and slow pathways, and induced the tachycardia. Pacing-induced type I block involving both pathways put these pathways out of phase, so that the distal conduction system and the ventricle responded to both the fast and slow pathways anterograde impulses.

Atrioventricular Node↗
PubMed1993

[Linking in a phase-3 branch block: the electrocardiographic manifestations].

Two cases of phase 3 intraventricular block and linking phenomenon of type 1 and type 2 (or bigeminal rhythm linking) are presented. In the first case, complexes that follow the extrasystolic blocked beat are wide, although they are associated with relative long R-R cycle:type 1 linking. In the second case, bundle branch block and normal conduction alternate in bigeminal extrasystolic beats:type 2 linking. The linking phenomenon is due to concealed retrograde penetration of the bundle branch that is blocked in anterograde direction. It delays the cycle and the refractory period of the bundle branch. Therefore, in type 1 linking, the subsequent stimulus, although occurring with a long R-R cycle, is again blocked in the same bundle branch. In type 2 linking, the R-R cycle and refractory period, occurring after bundle branch block, are shorted because comprised between retrograde activation by extrastimulus and anterograde activation by subsequent sinus stimulus. The subsequent ectopic impulse, although premature, is normally conducted.

Adult↗
PubMed1993

[Evolution of pacing modes in patients with implanted pacemakers. Personal considerations on a case load of 171 patients].

In this study retrospectively analyse pacemaker-implantation activity carried out during the last 5 years at the Laboratory of Electrophysiology, affiliated with the Cattedra di Cardiologia of the University of Naples--II Ateneo. Evolution in pacing modes is considered with regard to the patient age, the underlying pathologies and the technical progress in the field. The study has been performed in our laboratory, which is fit up for electrophysiologic studies and implantation of either temporary or permanent pacemakers. Patients included in this study have been implanted in our laboratory either for urgency or for election. They have been retrospectively divided into two groups (age < 65 yrs, 129 patients, and age < 65 yrs, 42 patients); in addition the patients have been classified according to the pathology leading to the implantation: atrio-ventricular block (second degree or third degree), low frequency fibrillation, sick sinus syndrome and carotid sinus syndrome. 171 patients have been examined, of whom 129 > 65 yrs. and 42 < 65 yrs. As for the pacing indication, 54 were atrio-ventricular block (56.1%), 50 were sick sinus syndrome (31.6%), 20 low frequency fibrillation (11.7%), and 1 was carotid sinus syndrome (0.6%). The ratio between single- and dual-chamber pacemakers has been progressively changing: in 1987 we implanted 33 single-chamber and no dual-chamber pacemaker, compared to 7 single- and 23 dual-chamber pacemaker implanted in the last year. This trend is in good agreement with literature data.

Aged↗