Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Atrial conduction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 577 records · Page 32Linked to original sources

[Diagnostic problems in the sinus node syndrome].

The sick sinus syndrome includes numerous arrhythmias due to various functional disorders of the sinus node, the atria and the A-V junctional tissue. These disturbances of impulse formation and conduction involve many diagnostic problems. If clinical methods as ECG monitoring are of no help, provocative tests are indicated. The best indirect test of the sinus node activity is the measurement of the sinus node recovery time after overdrive suppression. In addition, the sinu-atrial conduction time, the conduction velocity within the right atrium, the A-V node and the His-Purkinje system can be measured. In patients with the sick sinus syndrome abnormalities of conduction in the specialized cardiac tissue are common in addition to sinus node dysfunction. The results of the provocative tests are important for drug therapy or pacemaker implantation.

Arrhythmias, Cardiac↗

Distribution of conduction system fibers in the developing and adult rabbit heart revealed by an antineurofilament antibody.

Using an immunological approach, we demonstrated previously that a neurofilament-like protein is expressed in rabbit heart conduction tissue myocytes, and we proposed that these specialized cardiac muscle cells are of neuroectodermal origin. In the present study, we used the expression of the neurofilament-like protein as a marker for identifying conduction tissue cells and studying their distribution in the developing heart. In 11-day-old rabbit embryos, myocytes expressing the neurofilament-like protein were localized at the atrioventricular and the sinoatrial junctions and had a ring-like distribution. At embryonic day 12, reactive myocytes were found also in the subendocardial layer of the dorsal ventricular wall, in continuity with labeled myocytes at the atrioventricular junction. Examination of older embryos and of neonatal and adult hearts revealed that the expression of the neurofilament-like protein was not restricted to myocytes of conduction tissue regions, but it was also detectable in myocytes of the sinoatrial ring bundle, in scattered myocytes localized in the left sinal horn wall, and in the right atrium in proximity to atrioventricular sulcus tissue. Thus, using an intracellular marker, we show that precursors of adult atrial conduction tissue are distributed at the sinoatrial and atrioventricular junctions; at variance, ventricular conduction tissue precursors do not have a ring-like distribution but are localized in the subendocardial layer, in continuity with the atrioventricular junctional myocytes.

Aging↗

The electrophysiological effects of flosequinan.

We have evaluated the acute electrophysiological effects of flosequinan in 18 patients with normal ventricular function. Following intravenous infusion of flosequinan 100 mg over 1 h, mean (SD) systolic blood pressure fell from 131 +/- 19 to 120 +/- 22 mmHg (P less than 0.02) and there was significant shortening of sinus cycle length (732 +/- 151 to 575 +/- 93 ms, P less than 0.001), AH interval (110 +/- 45 to 71 +/- 19 ms, P less than 0.01), QRS duration (98 +/- 28 to 91 +/- 26 ms, P less than 0.02) and QT interval (373 +/- 47 to 337 +/- 35 ms, P less than 0.001), but no change in sinus node recovery time, intra-atrial conduction time, HV interval or the corrected QTc interval. There was a reduction in both anterograde atrioventricular Wenckebach cycle length (299 +/- 53 to 259 +/- 52 ms, P less than 0.01) and retrograde ventriculoatrial Wenckebach cycle length (375 +/- 77 to 300 +/- 56 ms, P less than 0.01). There was no change in atrial or ventricular effective refractory period (ERP) but atrial functional refractory period (FRP) shortened (233 +/- 31 to 212 +/- 24 ms, P = 0.07) as did ventricular FRP (249 +/- 24 to 234 +/- 21 ms, P less than 0.01). Patients received an oral dose of flosequinan 50 mg 12 h later. By 24 h, sinus cycle length, QRS duration and the QT interval had all returned towards baseline values, but ventricular ERP had lengthened (199 +/- 22 to 215 +/- 26 ms, P less than 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Lipomatous hypertrophy of the interauricular septum. Morphological and electrocardiographical aspects].

The authors report a case of lipomatous hypertrophy of the interatrial septum diagnosed by echocardiography and confirmed by computerised tomography. The electrocardiogram showed an intra-atrial conduction defect considered to be virtually pathognomonic of this condition. The differential diagnosis and clinical implications of this abnormality, which is usually a fortuitous finding, are discussed in the light of recent publications. A precise diagnosis avoids confusion with other pathologies necessitating specific treatment such as intra-atrial thrombi and tumours.

Aged↗

Electrical, contractile and structural remodeling during atrial fibrillation.

The natural history of atrial fibrillation (AF) is characterized by a gradual worsening with time. The recent finding that AF itself produces changes in atrial function and structure has provided a possible explanation for the progressive nature of this arrhythmia. Electrical remodeling (shortening of atrial refractoriness) develops within the first days of AF and contributes to an increase in stability of AF. However, 'domestication of AF' must also depend on a 'second factor' since the persistence of AF continues to increase after electrical remodeling has been completed. Atrial contractile remodeling (loss of contractility) leads to a reduced atrial transport function after cardioversion of AF. An important clinical consequence is that during several days after restoration of sinus rhythm, the risk of atrial thrombus formation is still high. In addition, the reduction of atrial contractility during AF may enhance atrial dilatation which may add to the persistence of AF. Tachycardia-induced structural remodeling takes place in a different time domain (weeks to months). Myolysis probably contributes to the loss of atrial contractile force. Although it might explain the loss of efficacy of pharmacological cardioversion and the development of permanent AF, the role of structural remodeling in the progression of AF is still unclear. Atrial structural remodeling also occurs as a result of heart failure and other underlying cardiovascular diseases. The associated atrial fibrosis might explain intra-atrial conduction disturbances and the susceptibility for AF. Thus, both AF itself and the underlying heart disease are responsible for the development of the arrhythmogenic substrate. New strategies for prevention and termination of AF should be build on our knowledge of the mechanisms and time course of AF-induced atrial remodeling.

Animals↗

Ethmozine: electrophysiology, hemodynamics, and antiarrhythmic efficacy in patients with life-threatening ventricular arrhythmias.

Thirteen patients with drug-resistant, life-threatening ventricular arrhythmias and inducible sustained ventricular tachycardia (VT) at electrophysiologic study received moricizine HC1 (ethmozine), 10 mg/kg/day orally. Eight patients underwent electrophysiologic study before and after drug administration; the arrhythmia became noninducible in one. In five other patients, spontaneous sustained VT occurred after 1 to 5 days of drug therapy, and one patient had a worsening of arrhythmias on ethmozine. Ethmozine prolonged infranodal conduction time (HV interval) (51.4 +/- 13.8 msec to 69.3 +/- 17.7 msec [mean +/- SD]), PR interval (201 +/- 28.1 msec to 244 +/- 62.2 msec), and QRS interval (123 +/- 27 msec to 147 +/- 32 msec). Ventricular refractory periods were not consistently affected, and only the one patient who became noninducible had an increase in effective ventricular refractory period (280 to 310 msec). The drug had no significant effect on sinus cycle length or sinus node recovery time, atrial conduction or refractoriness, or atrioventricular nodal refractoriness. Ethmozine had no effect on radionuclide ejection fraction (25.5 +/- 12.7% to 28.2 +/- 13.8%) or cardiac index (2.4 +/- 0.7 to 3.0 +/- 0.6 ml/min/m2) and caused no significant changes in mean aortic, right atrial, pulmonary arterial, or pulmonary capillary wedge pressures. Although the drug is well tolerated and produces no untoward hemodynamic effects, ethmozine is relatively ineffective in patients with sustained VT refractory to conventional antiarrhythmic agents.

Adult↗

Atrial amyloidosis: an arrhythmogenic substrate for persistent atrial fibrillation.

BACKGROUND: Structural changes, like atrial fibrosis, may increase the likelihood of atrial fibrillation (AF) occurring in response to triggering events. The influence of isolated atrial amyloidosis (IAA) is largely unknown. METHODS AND RESULTS: Right atrial appendages (1 or 2 entire cross sections) were obtained from 245 patients undergoing open-heart surgery. Atrial amyloid was identified by Congo red staining and classified by immunohistochemistry. Amyloid was found in 40 (16.3%) of 245 patients, and all deposits were immunoreactive for atrial natriuretic peptide (ANP). Thirty-eight (15.5%) patients suffered from persistent AF. The presence of amyloid correlated with age and P-wave duration and was related to sex, valve diseases, and the presence of AF (P<0.01). The association between atrial amyloid, AF, and P-wave duration was independent of age and sex. According to multiple logistic regression analysis, amyloid was the only age- and sex-independent predictor for the presence of AF. Atrial fibrosis was not a predictor for AF, and the amount of amyloid correlated inversely with the degree of interstitial fibrosis (P=0.001; r=-0.55). CONCLUSIONS: Our study provides evidence that IAA affects atrial conduction and increases the risk of AF. The occurrence of IAA depends on age leading to the formation of an amyloid nidus. The progression and consequences of IAA are then influenced by pathological conditions, such as valve diseases, that increase synthesis and secretion of ANP. The inverse correlation between IAA and atrial fibrosis suggests that these patients may not benefit from treatment with ACE inhibitors to reduce the amount of atrial fibrosis.

Adult↗

Effects of pacing site on QRS morphology in Wolff-Parkinson-White syndrome, with special reference to 'pseudo-tachycardia-dependent block in accessory pathway and 'atrial gap'.

In a patient with a Wolff-Parkinson-White (WPW) syndrome type A mid-right atrial stimulation at a rate of 73/min produced a lesser degree of ventricular pre-excitation than when a slower sinus rhythm was present. This paradoxical effect was not related to tachycardia-dependent block in the accessory pathway because pre-excitation again increased at faster pacing rates. It was partly the result of a (proportionally) greater prolongation of intra-atrial conduction time to the accessory pathway than to the atrioventricular node and partly of a faster atrioventricular nodal conduction time. The latter, in turn, could be attributed either to later-than-normal arrival of excitation at the atrioventricular node, at a time when this structure was more recovered, or to a change in the site or mode of entry into the atrioventricular node. A gap in the atria was present because at a St1-St2 interval shorter than that which A2 had been blocked in the accessory pathway conduction was again possible, but with longer A1-A2 intervals. Finally, at similar, short, coupling intervals the impulse penetrated the atrioventricular node from the mid-right atrium but not from the coronary sinus. The unusual findings in this case support a recent assumption that in patients with WPW type A atrial stimulation should be performed from the coronary sinus to minimize the potential sources of error which can be produced by intra-atrial delay.

Atrioventricular Node↗

Electrical remodeling of the atrium in an anatomic model of atrial flutter: relationship between substrate and triggers for conversion to atrial fibrillation.

BACKGROUND: Atrial flutter (AFL) and atrial fibrillation (AF) frequently coexist, yet the specific relationship between these arrhythmias, and particularly whether sustained AFL leads to AF, is unknown. METHODS AND RESULTS: We investigated the electrophysiological consequences of chronic AFL using an ovine anatomic right atrial Y-lesion model. AFL was induced in 7 animals, and 4 remained in sinus rhythm (controls). Sheep were monitored for spontaneous conversion of AFL to AF. Six of 7 sheep sustained AFL for 28 days. In 1 of 7 sheep, spontaneous conversion of AFL to AF occurred on day 5. AFL produced a highly significant fall in right and left atrial refractoriness (AERP, P<0.001), with 74+/-10% of the reduction occurring by day 3. Right atrial conduction velocity also fell significantly (baseline 89+/-9 cm/s versus day 28 64+/-14 cm/s, P<0.001) but over a slower time course. AERP and conduction velocity changes coincided with a characteristic biphasic decrease and increase in the AFL cycle length. The excitable gap (percent of AFL cycle length) increased from 13+/-3% at baseline to 46+/-8% by day 28 (P<0.001). Sustained AF (>30 seconds) was not inducible at baseline but after 28 days of AFL could be induced in 6 of 6 sheep by critically timed single or multiple extrastimuli delivered either in sinus rhythm or AFL. There was no significant change in any parameter in control sheep. CONCLUSIONS: In this model, AFL produced electrical remodeling and the substrate for sustained AF. However, spontaneous conversion to AF was uncommon, and the development of AF was dependent on specific triggers.

Animals↗

Sinus node function in patients with Brugada-type ECG.

BACKGROUND: Some studies have shown that patients with Brugada syndrome (BS) have atrioventricular conduction disturbance, but their sinus node function has not been evaluated. METHODS AND RESULTS: The patients group consisted of 59 male patients and 1 female patient with BS. Supraventricular and ventricular programmed electrical stimulation (PES) was performed. Ventricular fibrillation (VF) or sustained polymorphic ventricular tachycardia was induced by ventricular PES in 26 patients with BS (VF group), but was not induced in the other 34 patients (non-VF group). Sinus node function and conduction of the atrioventricular (AV) node in the control group, non-VF group and VF group were evaluated. Sinus node function was attenuated and the His - ventricle interval was prolonged in the VF group (corrected sinus node recovery time: 452+/-126 ms (VF group), 324+/-146 ms (non-VF group), Sino-atrial conduction time: 179+/-60 ms (VF group), 127+/-60 ms (non-VF group), His-ventricle interval: 41+/-9 ms (VF group), 35+/-8 ms (non-VF group)). CONCLUSION: The function of both the sinus node and AV node are attenuated in patients with PES-induced VF.

Adult↗

Clinical implications of "pure" Hisian pacing in addition to para-Hisian pacing for the diagnosis of supraventricular tachycardia.

BACKGROUND: Para-Hisian pacing is an effective method of differentiating between pathways for retrograde conduction over the accessory pathway (AP) and over the atrioventricular node (AVN). When performing para-Hisian pacing, the pacing spike sometimes captures only the His bundle, which we named "pure" Hisian pacing (Hc). OBJECTIVE: We evaluated the significance of pure Hisian pacing for predicting the pathways of ventriculoatrial conduction. METHODS: In 62 patients with supraventricular tachycardia, both para-Hisian and pure Hisian pacing were carried out during the sinus rhythm, resulting in three different types of electrocardiographic complexes with wide (local ventricular myocardial capture), slightly narrow (both local myocardial and His bundle capture), and very narrow QRS widths (Hc). A change of atrial activation sequence as demonstrated by these pacing modes indicated the presence of multiple retrograde pathways. The diagnosis of retrograde pathways by para-Hisian pacing with or without Hc was evaluated. RESULTS: In 22 patients with AVN reentrant tachycardia, para-Hisian pacing alone was able to correctly predict ventriculo-atrial conduction exclusively through the AVN without requiring findings from Hc. In 40 AP patients, para-Hisian pacing showed a pattern of retrograde conduction through the AVN in six, through both the AVN and AP in 10, and through an AP in 24 patients. Four of these 24 patients were diagnosed as having multiple pathways (AP+AVN or dual APs) by the addition of Hc. CONCLUSION: Pure Hisian pacing can help disclose another pathway for retrograde conduction in AP patients, which is unpredicted by ordinary para-Hisian pacing.

Atrioventricular Node↗

Acute and chronic electrophysiological effects of pentisomide on the sinus and AV nodal function, noninvasive evaluation by a pacemaker with temporary pacing inhibition.

The acute and chronic electrophysiological effects on sinus function and AV nodal conduction of pentisomide (Pen), a new antiarrhythmic agent, were studied in ten patients with sick sinus syndrome (SSS) (group I) and in ten patients with normal sinus function (group II) using a permanent pacemaker with temporary pacing inhibition (Symbios 7005 Medtronic, Inc.). We measured noninvasively the corrected sinus node recovery time (CSNRT), the sino-atrial conduction time (SACT), according to Narula's method and the Wenckebach point before and after Pen administration, acutely and orally for 10 days. In group I intravenous injection (4 mg/kg) and oral administration (450 mg bid) of Pen significantly prolonged the CSNRT (+217% and +149%, respectively) and the SACT (+63% and +49%, respectively). In group II only the intravenous injection of Pen provoked a significant modification of CSNRT (+12%) and SACT (+14%). No modification in AV nodal conduction was noted in any patient. These results suggest that Pen must be used with caution in patients with sinus nodal dysfunction.

Aged↗

Frequency-dependent electrophysiological effect of ibutilide on human atrium and ventricle.

Most of the class III antiarrhythmic agents developed in recent years blocks the rapid component of delayed rectifier potassium current (IKr). IKr blocker shows reverse use-dependency and also may cause torsades de pointes at slower heart rate. Ibutilide fumarate, a novel class III antiarrhythmic agent, increases window Na(+) current at the action potential plateau phase. We studied the rate-dependent effect of ibutilide on the electrophysiological parameters of human atrium and ventricle. Franz catheter and a pacing catheter were placed closely in the high right atrium and right ventricular apex to record monophasic action potentials (MAP) during pacing at cycle length (PCL) of 600 ms and 350 ms in eight patients who underwent electrophysiological study. MAP duration of right atrium (RA-MAPD) and right ventricle (RV-MAPD), effective refractory period of RA and RV (RA-ERP and RV-ERP), intra-atrial conduction time (IACT) and intra-ventricular conduction time (IVCT) were measured before and after intravenous administration of ibutilide (0.01 mg/kg up to 1mg). A conduction time from RA pacing spike to distal coronary sinus potential was used to measure IACT, while QRS duration of surface ECG during RV pacing was used to measure IVCT. Ibutilide prolonged RA-MAPD by 60 ms at PCL 600 ms and by 53 ms at PCL 350 ms; RV-MAPD by 48 ms at PCL 600 ms and by 55 ms at PCL 350 ms. Ibutilide did not affected RA and RV-ERP/MAPD ratio, IACT, and IVCT. Ibutilide prolongs MAPD and ERP of human atrium and ventricle without reverse use-dependency.

Action Potentials↗

The signal-averaged P wave duration: a rapid and noninvasive marker of risk of atrial fibrillation.

OBJECTIVES: This study was undertaken to determine the ability of the signal-averaged electrocardiogram (ECG) to identify evidence of delayed atrial activation in patients with a history of atrial fibrillation. BACKGROUND: Atrial fibrillation is a reentrant rhythm and depends on atrial conduction delay for its development. The signal-averaging technique is useful for accurately measuring total cardiac activation times, including delayed low amplitude signals, and thus can help identify the substrate for reentrant arrhythmias. METHODS: Standard 12-lead and signal-averaged ECGs were recorded from 15 patients with a documented history of prior paroxysmal or chronic atrial fibrillation and 15 age- and disease-matched control subjects without a history of atrial fibrillation. Signal averaging was performed using an orthogonal lead system with the QRS complex as a trigger and the P wave as a template for the signal-averaging process. Total P wave duration was measured before and after filtering with a least squares fit filter. The P wave complexes on the three bipolar leads were combined into a vector combination of orthogonal leads. The total P wave duration of the individual unfiltered and filtered leads and the vector combination of filtered leads were calculated and used for analysis. RESULTS: The P wave duration by standard ECG was not significantly different in patients with a history of atrial fibrillation and control subjects. Signal-averaged P wave durations were measured from orthogonal leads before and after digital filtering. Mean unfiltered P wave duration was significantly longer in patients with a history of atrial fibrillation than in control subjects (132 +/- 22 vs. 114 +/- 14 ms [p < 0.03] in the X lead, 135 +/- 21 vs. 115 +/- 15 ms [p < 0.03] in the Y lead and 133 +/- 23 vs. 114 +/- 14 ms [p < 0.03] in the Z lead). Mean filtered P wave duration was also longer in patients with atrial fibrillation than in control subjects (151 +/- 23 vs. 130 +/- 19 ms [p < 0.01] in the X lead, 157 +/- 22 vs. 136 +/- 17 ms [p < 0.01] in the Y lead and 154 +/- 23 vs. 135 +/- 15 ms [p < 0.01] in the Z lead). After filtering, a vector composite of orthogonal leads was determined. Again, P wave duration in patients with a history of atrial fibrillation exceeded that in the control subjects (162 +/- 15 vs. 140 +/- 12 ms [p < 0.01]). Using the vector composite of filtered orthogonal leads, a P wave duration > or = 155 ms was associated with a sensitivity of 80%, a specificity of 93% and a positive predictive value of 92% for identifying patients with history of atrial fibrillation. CONCLUSIONS: A prolonged signal-averaged P wave duration may be a simple noninvasive marker of the risk for development of atrial fibrillation.

Aged↗

Large tip electrodes for successful elimination of atrial flutter resistant to conventional catheter ablation.

The most widely accepted criterion for successful radiofrequency catheter (RFC) ablation of typical atrial flutter is the development of bi-directional isthmus block. In a subset of patients, conventional RFC ablation fails to achieve this endpoint because deeper and wider lesions are required. We investigated the efficacy of a long 8-mm tip catheter in these cases. One hundred and seventy-four consecutive patients (137 male; 61 +/- 9 years) with recurrent typical atrial flutter underwent conventional RFC ablation first with a standard 4 mm tip catheter. In resistant cases (n = 52), ablation was continued using a large tip 8-mm catheter when the 4-mm tip catheter failed. Resistant atrial flutter was identified when 21 RFC pulses failed to reach the selected endpoint of bi-directional isthmus block or in cases of transient bi- directional block (at least 3 episodes). In 122 of the 174 patients (70%) conventional atrial flutter ablation was successfully performed with 13 +/- 5 RFC applications. In the remaining 52 subjects (30%), the ablation procedure was completed using the large tip electrode catheter. In 30 of these 52 patients (58%), the catheter was changed because of persistent intra-atrial conduction after 21 RFC pulses and in 22 (42%) because of intermittent conduction block after 11 +/- 5 applications. Using the large tip electrode catheter, the selected endpoint was achieved in all patients of both groups with 3 +/- 2 RFC pulses (power output of 50-60 W, pulse duration of 60 sec). No post-procedure complications were observed. After 15 +/- 5 months of follow-up, 16 patients (9%) had recurrence of atrial flutter. Five of the patients had been in the resistant group. In patients with atrial flutter resistant to conventional ablation therapy, the long tip (8-mm) catheter appears to be a safe and effective alternative to use of the conventional 4-mm tip catheter.

Atrial Flutter↗

[The effects of tolamolol on excito-conduction in men (author's transl)].

The electrophysiologic effects of tolamolol (UK-6558-01), a new beta-adrenergic blocking agent, were studied using the endocavitarian electrocardiography and the extrastimulus method. The drug was infused intravenously in the dose of 20 mg (0,23-0,36 mg per kilogram). Tolamolol resulted in: -- prolongation of sinus cycle length in 17 patients (P less than 0.001); -- prolongation of correct sinus node recovery time in 16 patients (P less than 0.001); -- there was no significant modification in intra-atrial conduction (P less than 0.3), while atrail effective refractory period was slightly lengthened (P less than 0.03); -- in A-V node conduction was prolonged in 17 patients (P less than 0.001) and the effective functional refractory periods were prolonged in all patients (P less than 0.001); -- a A-V block of 2 degrees grade appears in 17 patients at a more prolonged cycle length (P less than 0.001). Tolamolol had no effect on His-Purkinje system conduction time as well as the relative refractory period, measured before and after the drug in 2 patients. In 6 patients, during the induction of extrastimuli an "echo zone" appeared; after tolamolol its duration was reduced in 4 patients, in one unchanged and in one abolished. The therapeutical properties of this drug are discussed on the basis of such experimental data.

Adolescent↗

Intra-SA-nodal pacemaker shift: indirect evaluation in the open chest dog.

Thirteen open chest dogs with normal sinus node function were studied by premature stimulations with a constant relative prematurity--50% of the preceding sinus cycle length. These premature beats were induced in the lower part of the crista terminalis of the right atrium and to the roof of the left atrium. Significant linear correlations were found between the return cycle (A2A3) and the spontaneous cycle (A1A1) lengths, with a slope of +0.75 in the right atrium, +1.36 in the left atrium. The evaluation of sinus node function is disturbed by pacemaker shifts, both spontaneous and induced. Sinus node organisation may be assessed by stimulating standardised sites, by measuring intra-atrial conduction time, and by comparing A2A3 with A1A1 at constant relative prematurity during significant variations in A1A1 obtained with changes in vago-sympathetic tone.

Animals↗

Long-term effects of beta blocker therapy on P-wave duration and dispersion in congestive heart failure patients: a new effect?

Atrial fibrillation (AF) is associated with heart failure in approximately 20%-50% of patients with increased morbidity and mortality. P-wave maximum duration (PWM) and P-wave dispersion (PWD) are recent ECG markers and reflect increased risk of AF. The aim of our study was to investigate the long-term effects of metoprolol on atrial conduction abnormalities as estimated by PWM and PWD, which were calculated on 12-derivation surface ECG in heart failure patients. Forty-two NYHA class 3 to 4 patients (23 males, 19 females and aged 52.9 +/- 11.2) were enrolled in the study. At the end of the 6 months, PWM and PWD values were significantly decreased (for PWM: from 115.2 +/- 12.6 to 105.4 +/- 13.5; for PWD: from 39.3 +/- 9.1 to 28.6 +/- 10.5; P <.001 for both). Metoprolol treatment is associated with a decreased duration of PWM and PWD and this may reflect a reduction in the probability of atrial fibrillation in heart failure patients.

Adrenergic beta-Antagonists↗