A semi-automatic algorithm for reducing the time spent on routine follow-up of cardioverter defibrillators.

BACKGROUND: The routine follow-up of cardioverter defibrillators (CD) is a time-consuming procedure. AIM of the STUDY and METHODS: The present study was a prospective randomized cross-over evaluation on the clinical usefulness of a specific semi-automatic software algorithm (Quick Check) for CD follow-up, available in CPI Guidant systems (CD and programmer). Time-saving, while ensuring all the required data and patient safety, was evaluated in a large group of patients (105), recruited in different centers. In the same session and under a physician's supervision all patients underwent a follow-up with the aid of Quick Check or a standard follow-up, in a randomized sequence. Each patient served as his own control. RESULTS: In the overall population of 105 patients, the time spent for follow-up was reduced by Quick Check from 186+/-105 sec to 106+/-67 sec (p<0.0001) (43% reduction). The reduction in time spent for follow-up with Quick Check was the same (43% reduction) in patients with detected episodes (n=38) (from 241+/-144 sec to 138+/-95 sec (p<0.0001)) and in patients without detected episodes (n=67) (from 154+/-52 sec to 88+/-34 sec (p<0. 0001)). No adverse events or deletion of potentially useful data was detected by the supervising physician. CONCLUSIONS: Use of a specific software algorithm for routine follow-up of implanted CDs allows a significant shortening of the time spent on routine follow-up, thus reducing costs. The supervision of a physician is a guarantee of patient safety.

Development of heart failure in bradycardic sick sinus syndrome.

Mounting evidence shows that elevated resting sinus rate is an independent predictor of cardiovascular morbidity and mortality in the general population, in elderly subjects, and in patients with myocardial infarction or hypertension. Therefore, a rather slow sinus rate appears to be a protecting factor acting through several mechanisms. The present contribution focuses on the relationship between sinus rate and heart failure. Its major objectives are to discuss whether in patients with heart failure a rather slow heart rate is advisable and whether a sinus bradycardia secondary to sinus node dysfunction can facilitate the development of heart failure. It has been reported that among patients with left ventricular dysfunction, increased sinus rate was a predictor of cardiovascular death at univariate analysis; however, a multivariate analysis to verify whether sinus rate was an independent predictor of mortality was not performed. Randomized trials carried out by utilizing beta-blockers or amiodarone in patients with heart failure showed that heart rate reduction by these drugs was a marker of their ability to reduce mortality. However, beta-blockers and amiodarone have additional pharmacological effects which interfere with the disease substrate. So, at present, though the results of these trials show that a rather slow sinus rate is advisable, we do not know whether in patients with heart failure sinus rate represents an independent predictor of mortality as in patients with myocardial infarction or hypertension and whether the reduction of sinus rate per se is beneficial. The results of the recent randomized THEOPACE trial showed, for the first time, that in a patient population with symptomatic sinus bradycardia (sinus rate < 50 b/min), an increase in heart rate, induced by DDD pacing or oral theophylline, reduced the incidence of overt heart failure. Therefore, sinus bradycardia seems to play a role in the genesis of heart failure. In a post-hoc analysis of the results of this trial it emerged that in the control (not treated) group, the subjects with sinus bradycardia more prone to develop heart failure were those of old age, about 80 years, with organic heart disease and severe chronotropic incompetence. However, this conclusion needs further validation.

Atrioventricular nodal versus atrioventricular supraventricular reentrant tachycardias: characterization by an integrated Doppler electrophysiological hemodynamic study.

During reentrant supraventricular tachycardias involving the atrioventricular node (AVN-SVT) or an AV bypass tract (AV-SVT), atrial pressure increases. While in AVN-SVT this increase relates to atrial contraction during ventricular systole, the mechanism remains unclear in AV-SVT. This study sought to clarify this mechanism. During 11 AVN-SVTs and 9 AV-SVTs, anterograde flow through the AV valves and retrograde flow in the pulmonary and hepatic veins were studied by pulsed-wave (PW) Doppler measuring the time interval between the ECG-R wave and (1) the end of venous retrograde flows, and (2) the beginning of valvular anterograde flows. The positive or negative difference between these two time intervals guided recognizing the atrial contraction against open or closed AV valves. Intracavitary pressures and cardiac index were also measured. During AVN-SVTs, venous retrograde flows always ended before the anterograde valvular flows, indicating atrial contraction against closed AV valves. During AV-SVTs, pulmonary retrograde flow ended before the beginning of mitral anterograde flow in five cases, began before but ended during the anterograde flow in three cases, and overlapped to the anterograde flow in one case. A corresponding behavior was observed at the right side of the heart. In both SVTs, atrial pressures increased and end-diastolic ventricular pressure and cardiac index decreased similarly. During AVN-SVT, the atrial contraction always occurs against closed AV valves, and during AV-SVT it generally occurs against totally or partially closed AV valves, explaining similar atrial pressure and cardiac index changes in both SVTs.

Atrial and ventricular pressures in atrial flutter.

The hemodynamic effects of atrial flutter (AF) are unknown. The purpose of the present study was to investigate the changes in atrial and ventricular pressures after induction of AF. In 23 patients with paroxysmal AF (age 59 +/- 9 years), a hemodynamic study was performed both during sinus rhythm and after induction of the tachyarrhythmia. During AF, 13 patients showed a fixed 2:1 AV conduction and 10 patients showed variable conduction. Mean right and left atrial pressures increased (P < 0.001) and right and left ventricular end-diastolic pressures decreased (P < 0.001) after induction of AF. Both the increase in mean atrial pressures and the decrease in ventricular end-diastolic pressures were present either in the patients with fixed 2:1 AV (heart rate: 133 +/- 15 beats/min) or in those with variable conduction (heart rate 96 +/- 15 beats/min), but were more marked in the former. AF produces an impairment of atrial function, as evidenced by the increase in mean atrial pressures and reduction in ventricular end-diastolic pressures in the absence of an elevated heart rate. The mechanisms responsible for the increase in mean atrial pressures are unknown; however, atrial contractions against closed AV valves seem to play an important role.

Short-term hemodynamic effects of DDD pacing from ventricular apex, right ventricular outflow tract and proximal septum.

Recently, short-term hemodynamic benefits of right ventricular outflow tract (RVOT) or proximal septum (His bundle area) pacing have been reported in comparison with traditional apical stimulation in preliminary investigations. The purpose of the present study was to compare the hemodynamics obtained during DDD pacing from ventricular apex, RVOT and proximal septum in patients with normal left ventricular function. A simultaneous hemodynamic and Doppler-echocardiographic study was performed in 21 patients (age 67 +/- 7 years) with sick-sinus syndrome (8 pts) or 2nd-3rd degree atrioventricular (AV) block (13 pts). The three stimulation sites were randomized and pacing was applied at an identical rate (84 +/- 5 beats/min) and at a constant AV delay (150 ms). Electrocardiographic, hemodynamic and Doppler-echocardiographic investigations were performed during stimulation from each site. The QRS duration did not show significant differences during DDD pacing from ventricular apex, RVOT and proximal septum. The hemodynamic measurements (systemic pressures, mean pulmonary wedge pressure, pulmonary pressures, right ventricular end-diastolic pressure, mean right atrial pressure, cardiac index, systemic vascular resistance and arteriovenous O2 difference) did not show significant differences during pacing from the three sites. Moreover, no significant differences were observed for the Doppler-echocardiographic measurements of systolic function (aortic stroke distance, left ventricular ejection fraction) and diastolic function (isovolumetric relaxion time, mitral E/A ratio, deceleration rate of the E wave). The results suggest that in patients with normal left ventricular function DDD pacing from RVOT or proximal septum does not improve cardiac function with regard to apical pacing.

Effects of intravenous propranolol on cardiovascular hemodynamics during supraventricular tachycardia.

Hemodynamic variables were evaluated in 10 patients during supraventricular tachycardia before and after administration of intravenous propranolol. The drug markedly worsened the already compromised hemodynamic pattern of supraventricular tachycardia.

Hemodynamics of idiopathic paroxysmal atrial fibrillation.

The hemodynamics of induced atrial fibrillation (AF) was investigated in 15 patients (ages 58 +/- 11 years) with paroxysmal AF presenting without organic heart disease or hypertension. A hemodynamic study was performed both during sinus rhythm and after the induction of AF. The mean heart rate increased from 73 +/- 11 to 128 +/- 18 beats/min (P < 0.001) after AF. Systolic and mean aortic pressures did not significantly change, and diastolic aortic pressure increased (78 +/- 11 vs 89 +/- 12 mmHg, P < 0.01). Left ventricular end-diastolic pressure decreased during AF (9 +/- 3 vs 6 +/- 2.6 mmHg, P < 0.005), whereas mean pulmonary wedge pressure increased (8 +/- 2 vs 12 +/- 4 mmHg, P < 0.001). Systolic pulmonary arterial pressure did not show significant variations, and there was a slight but statistically significant increase in the diastolic and mean pulmonary arterial pressures (P < 0.01). The right ventricular end-diastolic pressure decreased during AF (5.6 +/- 2 vs 3.8 +/- 2 mmHg, P < 0.01), whereas mean right atrial pressure showed a trend toward an increase. Stroke volume markedly decreased (P < 0.001) while the cardiac index did not significantly change. Systemic vascular resistance, pulmonary arteriolar resistance, and the arteriovenous O2 difference showed no significant variations after the induction of AF. These results suggest that in subjects without organic heart disease, paroxysmal AF is well tolerated hemodynamically, and the rise in the atrial pressures during AF is not related to an increase in the ventricular end-diastolic pressure.

Hemodynamic effects of oral sotalol during both sinus rhythm and atrial fibrillation.

OBJECTIVES: This study investigated the hemodynamic effects of oral sotalol during both sinus rhythm and paroxysmal atrial fibrillation. BACKGROUND: The hemodynamic effects of most antiarrhythmic drugs have been characterized in subjects during sinus rhythm. However, there are no data concerning these effects on the paroxysmal tachyarrhythmias. METHODS: In 17 patients with paroxysmal atrial fibrillation and without heart failure (aged 62 +/- 11 years, ejection fraction 51 +/- 4%), an electrophysiologic-hemodynamic study was performed twice. In the first study, hemodynamic variables were evaluated both during sinus rhythm and after the induction of atrial fibrillation. Sotalol (160 or 240 mg/day) was administered for 6 to 7 days and the study was then repeated with the same methods. RESULTS: The drug significantly diminished heart rate during both sinus rhythm and atrial fibrillation. During sinus rhythm, sotalol did not change systemic pressures and significantly increased left and right ventricular end-diastolic, left and right atrial and pulmonary pressures. Cardiac index decreased, whereas stroke volume was unchanged after the drug. Ejection fraction and left ventricular end-diastolic and end-systolic volumes evaluated by echocardiography were unchanged after sotalol. During atrial fibrillation, the drug had less evident effects on cardiac function. Left ventricular end-diastolic, left atrial and pulmonary pressures did not increase significantly. CONCLUSIONS: The hemodynamic changes induced by oral sotalol appear to be mainly related to an involvement of ventricular distensibility; this effect is less evident during atrial fibrillation than during sinus rhythm. In patients with paroxysmal atrial fibrillation without heart failure treated with oral sotalol, a recurrence of the tachyarrhythmia is hemodynamically well tolerated.

Role of sinus node artery disease in sick sinus syndrome in inferior wall acute myocardial infarction.

This study was undertaken to evaluate a possible role of sinus node (SN) artery disease in the pathogenesis of sick sinus syndrome (SSS) in patients with an inferior wall acute myocardial infarction (AMI). Coronary angiography and electrophysiologic studies of the SN, both in the basal state and after pharmacologic autonomic blockade, were performed in 23 study patients (mean age 60 years) with SSS and a previous inferior wall AMI and in another 23 control patients (mean age 57 years) with normal sinus rate and a previous inferior AMI. Stenosis of the SN artery (or that proximal to its origin) greater than 50% was present in 13 study patients (56%) and in 8 control patients (34%) (p less than 0.05). In the study group, the intrinsic heart rate was abnormal in 5 of the 6 patients (83%) with severe SN artery stenosis (greater than or equal to 75% narrowing), in 3 of the 7 (43%) with moderate stenosis (50 to 75% narrowing) and in 3 of the 10 (30%) with insignificant stenosis (less than 50% narrowing). In the study group, the correlation between the SN measures (heart rate, corrected SN recovery time and sinoatrial conduction time) and the severity of SN artery stenosis was good after autonomic blockade (r between 0.59 and 0.64) and poor in the basal state. These data provide evidence for a role of SN artery disease in the pathogenesis of SSS in patients with an inferior wall AMI.

Dromotropic effects of oral theophylline in patients with atrial fibrillation and a slow ventricular response.

Theophylline increases sinus rate, but as yet its use has not been investigated in patients with chronic atrioventricular conduction disturbances. Resting electrocardiogram, 24-h Holter recording and treadmill test were performed in 17 patients with chronic atrial fibrillation and a slow ventricular response not related to drugs (age: 75 +/- 8 years). Then slow-release theophylline was administered (700 mg daily) and after 5 days these investigations were repeated with the same methods. Theophylline increased mean resting heart rate (51 +/- 6 versus 67 +/- 13 beats.min-1, P less than 0.01), mean 24-h heart rate (51 +/- 6 versus 68 +/- 14 beats.min-1, P less than 0.01) and minimal 24-h heart rate (32 +/- 6 versus 42 +/- 11 beats.min-1, P less than 0.01). Cardiac pauses greater than 2.5 s were present in 13 patients during control recording; after theophylline they disappeared in 11 and markedly decreased in the remaining two. The longest R-R interval decreased in all patients (3218 +/- 943 versus 2121 +/- 518 ms, P less than 0.01). The daily number of wide QRS complexes increased in 16 out of 17 patients (428 +/- 752 versus 1146 +/- 1464 ms, P less than 0.01). Exercise heart rate, evaluated at the end of first and second stage, was higher after theophylline than during control test (P less than 0.01). These data suggest that oral theophylline can represent a valid therapy in most patients with atrial fibrillation and a slow ventricular response.

Relationship between the most proximal His bundle and the morphology of intracavitary pressure curves.

A precise localization of the most proximal His bundle (HB) is useful both for diagnostic and for therapeutic purposes, allowing the modification of atrioventricular (AV) nodal conduction. For selective diagnosis a bipolar lead is utilized; for therapy, a unipolar lead. The aim of the present study was to determine the relationship between the most proximal HB and the morphology of intracavitary pressure curves. In 15 patients (aged 64 +/- 10 years), both bipolar and unipolar H-V intervals were continuously recorded while gradually withdrawing the catheter, which detected the pressure at its tip, from the right ventricle to the atrium. The longest bipolar H-V was 55.5 +/- 13 ms and the shortest 44.5 +/- 11 ms (P less than 0.001); the longest unipolar H-V was 56.5 +/- 14 ms and the shortest 46.2 +/- 11 ms (P less than 0.001). During unipolar recording, H deflection was present in all patients at the same time as ventricular, transvalvular and atrial pressure curves; during bipolar recording, the H electrogram was not present in only one patient concomitantly with the atrial curve. During bipolar recording, the atrial H-V interval was greater than transvalvular H-V in nine patients (mean differences: 6 +/- 2 ms) and they were equal in five; with unipolar recording the atrial H-V interval was greater than transvalvular H-V in 13 patients (mean difference: 8 +/- 6 ms) and they were equal in two. In all patients, the H wave amplitude diminished from the transvalvular area to the atrial one.(ABSTRACT TRUNCATED AT 250 WORDS)

Intrinsic electrophysiologic properties of reentrant supraventricular tachycardia involving bypass tracts.

This study evaluates the effects of autonomic blockade (propranolol, 0.2 mg/kg, and atropine, 0.04 mg/kg) in 20 patients with paroxysmal supraventricular tachycardia (SVT). In 8 patients the SVT circuit involved a concealed atrioventricular bypass for retrograde conduction (group I) and in 12 a concealed atrio-His pathway (group II). Autonomic blockade did not significantly change atrial and ventricular refractory periods, whereas it prolonged atrioventricular nodal refractoriness without varying AH interval. The ventriculoatrial interval did not change in any patient. The H2A2 interval was unchanged in all but 2 group II patients. In both groups, the effective refractory period of the concealed bypass was prolonged by autonomic blockade. In the basal state, SVT was induced in all patients; after autonomic blockade, SVT was induced in 7 patients in group I (87%) and in 7 in group II (58%) (p less than 0.05). Cycle length of SVT was prolonged after autonomic blockade in 11 of these 14 patients. The variations were observed only in the anterograde conduction (Ae-H interval), whereas retrograde conduction (H-Ae interval) was unchanged in all patients. These data indicate that the autonomic system appears to facilitate induction of SVT in patients with concealed atrio-His bypass as well as shorten the cycle length of SVT in both groups of patients.

Poor R wave progression in pure mitral stenosis. Correlation with hemodynamic data.

Poor R wave progression in the right precordial leads has frequently been reported in patients with pure mitral stenosis, but has never been investigated from clinical and hemodynamic points of view. In this work the clinical, electrocardiographic and hemodynamic data of 19 patients (mean age: 49 +/- 8.6 years), with pure mitral stenosis and poor R wave progression (study group) were compared with those of 19 subjects with pure mitral stenosis and normal R wave progression (control group). The age, sex distribution and duration of mitral valve disease were similar in the two groups; also clinical status, i.e. the distribution in the functional classes (NYHA), was similar in the two groups. Mitral valve area was similar in the two groups (1.3 +/- 0.5 vs 1.1 +/- 0.3 cm2), whereas wedge pressure, mean pulmonary artery pressure, systolic and diastolic right ventricle pressures and total pulmonary resistances showed significant lower values in patients with poor R wave progression compared to those with normal R wave progression (P less than 0.05). The hemodynamic variables of left ventricle and the cardiac index were similar in the two groups. In study group patients there was higher prevalence of vertical axis (P less than 0.05). These data indicate that in pure mitral stenosis, clinical status is similar in patients with poor R wave progression and in those with normal R wave progression, whereas in the former there is slighter hemodynamic involvement of the right ventricle.

Latent abnormalities of sinus node function in patients with organic heart disease and normal sinus node on clinical basis.

Sinus node (SN) function was analyzed in 22 patients (mean age: 46.2 +/- 12.9 years) with organic heart disease and normal SN on clinical basis (group I) and in 20 normal subjects (mean age: 43.9 +/- 15.6 years), (control group). Sinus cycle length (SCL), corrected sinus node recovery time (CSRT) and sinoatrial conduction time (SACT) were analyzed. After the control study, autonomic blockade (AB) was induced by i.v. propranolol (0.2 mg/Kg) and atropine (0.04 mg/Kg). Measurements of SCL, CSRT and SACT were then repeated. The mean SCL values were very similar in the two groups during the control state and after AB. There were no significant differences in SACTs between the two groups during the control state or after AB. On the contrary, the CSRT of group I was significantly longer than that of control group during the control state (344.8 +/- 78.9 versus 262.2 +/- 46.3 msec, P less than 0.001) and after AB (238.9 +/- 72.8 versus 166.8 +/- 39.3 msec, P less than 0.001). The analysis of real depression of SN automaticity (CSRT minus SACT) in the two groups shows that prolongation of CSRT in group I during the control study and after AB is related to an intrinsic abnormality of SN automaticity; on the contrary, no dysfunctions of the autonomic nervous system appear. These data indicate that the intrinsic abnormality of SN automaticity represents the earliest involvement of the SN in subjects with organic heart disease and normal SN on clinical basis, although this conclusion is speculative and requires experimental verification.

Effects of amiodarone on supraventricular tachycardia involving bypass tracts.

This study evaluates whether the electrophysiologic effects of i.v. amiodarone in patients with reentrant supraventricular tachycardia (SVT) can predict the efficacy of long-term oral therapy with this drug. The effects of oral and i.v. amiodarone were studied in 27 patients with SVT. In 14 the SVT circuit involved a concealed atrioventricular bypass for retrograde conduction (Group I), and in 13 a concealed atrio-His bypass (Group II). Intravenous amiodarone induced significant prolongation of the AH interval, the refractory periods of the atrium, atrioventricular node, His-Purkinje system and ventricular myocardium. The ventriculoatrial interval was slightly prolonged in Group I patients and did not change in Group II patients after i.v. administration of the drug. In both groups, the effective refractory period (ERP) of the concealed bypass was prolonged by i.v. amiodarone. During control state, SVT could be induced in all patients; after i.v. administration of the drug, SVT was presented in 6 patients in Group I and in 8 patients in Group II. In all cases, in which i.v. amiodarone prolonged the ERP of the concealed bypass to more than 350 ms, the drug always prevented SVT even when given orally. All but 2 patients--1 from Group I and 1 from Group II--remained asymptomatic after oral amiodarone. In the patient from Group I, SVT had been prevented by i.v. amiodarone, whereas in the patient from Group II SVT could not be induced by ventricular stimulation during the control state, but appeared after i.v. administration of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)