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Wave Duration (wave + duration)

Distribution by Scientific Domains
Medical Sciences89%
2 Other Domains11%

Kinds of Wave Duration

  • p wave duration
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    Selected Abstracts

    P Wave Duration and Morphology Predict Atrial Fibrillation Recurrence in Patients with Sinus Node Dysfunction and Atrial-Based Pacemaker

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 11 2002
    ANTONIO DE SISTI
    DE SISTI, A., et al.: P Wave Duration and Morphology Predict Atrial Fibrillation Recurrence in Patients with Sinus Node Dysfunction and Atrial-Based Pacemaker. P wave duration and morphology have never been systematically evaluated as markers of AF in patients with a conventional indication to pacing. This study correlated sinus P wave duration and morphology and the incidence of AF in patients with sinus node dysfunction (SND), previous history of AF before implant, and atrial-based pacemaker. Included were 140 patients (86 men, 54 women; mean age 71.8 ± 10.4 years) with recurrent paroxysmal AF and who received a DDD (128 patients) or AAI (12 patients) pacemaker for SND. Forty-nine patients had structural heart disease. Sinus P wave duration and morphology was evaluated in leads II, III. Twenty-two patients had an abnormal P wave morphology, diphasic (+/-) in 5 and notched (+/+) in 17. The basic pacemaker rate was programmed between 60 and 70 beats/min. Rate responsive function was activated in 65 patients. During a follow-up of 27.6 ± 17.8 months, AF was documented in 87 patients. Forty-four patients developed permanent AF, following at least one episode of paroxysmal AF in 26 cases. Statistical analysis used Cox model regression. Univariate predictors of AF (P < 0.10) were drugs (mean: 2 ± 1.4) and DC shock before pacing (16/140 patients), P wave duration (mean 112.5 ± 24.6 ms), basic pacemaker rate (mean 68 ± 5 beats/min), and drugs in the follow-up (mean 1.2 ± 0.94). Multivariate analysis showed that P wave duration (b = 0.013, s.e. = 0.004; P = 0.003), and drugs before pacing (b = 0.2; s.e.= 0.08; P < 0.01) resulted in a significant independent predictor of AF. Actuarial incidence of patients free of AF at 30 months was 35%: 56% in patients with a P wave < 120 ms, and 13% in those with P wave , 120 ms (P < 0.01 by Score test). Univariate predictors of permanent AF were drugs and DC shock before pacing, left atrial size (mean 39 ± 6 mm), P wave duration, abnormal P wave morphology (22/140 patients), and drugs in the follow-up. Multivariate analysis showed that P wave morphology was the most important predictor of permanent AF (b = - 0.56, s.e.= 0.2; P = 0.008). Incidence of patients free of permanent AF at 30 months was 69%: 74% in patients with normal P wave, compared to 28% in the case of abnormal P wave morphology (P < 0.01). P wave duration and morphology are good markers of postpacing AF recurrence in patients with SND and an atrial-based pacemaker. This observation suggests that intra- and interatrial conduction disturbances be extensively evaluated before implantation, and the indication for atrial resynchronization procedures be reevaluated. [source]

    Acute Cardiac Effects of Nicotine in Healthy Young Adults

    ECHOCARDIOGRAPHY, Issue 6 2002
    Catherine D. Jolma M.D.
    Background: Nicotine is known to have many physiologic effects. The influence of nicotine delivered in chewing gum upon cardiac hemodynamics and conduction has not been well-characterized. Methods: We studied the effects of nicotine in nonsmoking adults (6 male, 5 female; ages 23,36 years) using a double-blind, randomized, cross-over study. Subjects chewed nicotine gum (4 mg) or placebo. After 20 minutes (approximate time to peak nicotine levels), echocardiograms and signal-averaged electrocardiograms (SAECG) were obtained. After 40 minutes, subjects were again given nicotine gum or placebo in cross-over fashion. Standard echocardiographic measurements were made from two-dimensional images. We then calculated end-systolic wall stress (ESWS), shortening fraction (SF), systemic vascular resistance (SVR), velocity for circumferential fiber shortening corrected for heart rate (Vcfc), stroke volume, and cardiac output. P wave and QRS duration were measured from SAECG. Results: Significant differences (P < 0.05) from control or placebo were found for ESWS, mean blood pressure, cardiac output, SVR, heart rate, and P wave duration. No significant changes were seen in left ventricular ejection time (LVET), LV dimensions, SF, contractility (Vcfc), or QRS duration. Conclusions: These results suggest that nicotine chewing gum increases afterload and cardiac output. Cardiac contractility does not change acutely in response to nicotine gum. Heart rate and P wave duration are increased by chewing nicotine gum. [source]

    Effects of intravenous lidocaine overdose on cardiac electrical activity and blood pressure in the horse

    EQUINE VETERINARY JOURNAL, Issue 5 2001
    G. A. MEYER
    Summary This study aimed to identify blood serum lidocaine concentrations in the horse which resulted in clinical signs of intoxication, and to document the effects of toxic levels on the cardiovascular and cardiopulmonary systems. Nineteen clinically normal mature horses of mixed breed, age and sex were observed. Lidocaine administration was initiated in each subject with an i.v. loading dose of 1.5 mg/kg bwt and followed by continuous infusion of 0.3 mg/kg bwt/min until clinical signs of intoxication were observed. Intoxication was defined as the development of skeletal muscle tremors. Prior to administration of lidocaine, blood samples for lidocaine analysis, heart rate, mean arterial blood pressure, systolic blood pressure, diastolic blood pressure, respiratory rate and electrocardiographic (ECG) data were collected. After recording baseline data, repeat data were collected at 5 min intervals until signs of intoxication were observed. The range of serum lidocaine concentrations at which the clinical signs of intoxication were observed was 1.85,4.53 ,g/ml (mean ± s.d. 3.24 ± 0.74 ,g/ml). Statistically significant changes in P wave duration, P-R interval, R-R interval and Q-T interval were observed in comparison to control values, as a result of lidocaine administration. These changes in ECG values did not fall outside published normal values and were not clinically significant. Heart rate, blood pressures and respiratory rates were unchanged from control values. This study establishes toxic serum lidocaine levels in the horse, and demonstrates that there were no clinically significant cardiovascular effects with serum lidocaine concentrations less than those required to produce signs of toxicity. [source]

    Preoperative Electrocardiographic Risk Assessment of Atrial Fibrillation After Coronary Artery Bypass Grafting

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2004
    Ph.D., YI GANG M.D.
    Introduction: This study evaluated the role of surface ECG in assessment of risk of new-onset atrial fibrillation (AF) after coronary artery bypass grafting surgery (CABG). Methods and Results: One hundred fifty-one patients (126 men and 25 women; age 65 ± 10 years) without a history of AF undergoing primary elective and isolated CABG were studied. Standard 12-lead ECGs and P wave signal-averaged ECG (PSAE) were recorded 24 hours before CABG using a MAC VU ECG recorder. In addition to routine ECG measurements, two P wave (P wave complexity ratio [pCR]; P wave morphology dispersion [PMD]) and six T wave morphology descriptors (total cosine R to T [TCRT]; T wave morphology dispersion of ascending and descending part of the T wave [aTMD and dTMD], and others), and three PSAE indices (filtered P wave duration [PD]; root mean square voltage of terminal 20 msec of averaged P wave [RMS20]; and integral of P wave [Pi]) were investigated. During a mean hospital stay of 7.3 ± 6.2 days after CABG, 40 (26%) patients developed AF (AF group) and 111 remained AF-free (no AF group). AF patients were older (69 ± 9 years vs 64 ± 10 years, P = 0.005). PD (135 ± 9 msec vs 133 ± 12 msec, P = NS) and RMS20 (4.5 ± 1.7 ,V vs 4.0 ± 1.6 ,V, P = NS) in AF were similar to that in no AF, whereas Pi was significantly increased in AF (757 ± 230 ,Vmsec vs 659 ± 206 ,Vmsec, P = 0.007). Both pCR (32 ± 11 vs 27 ± 10) and PMD (31.5 ± 14.0 vs 26.4 ± 12.3) were significantly greater in AF (P = 0.012 and 0.048, respectively). TCRT (0.028 ± 0.596 vs 0.310 ± 0.542, P = 0.009) and dTMD (0.63 ± 0.03 vs 0.64 ± 0.02, P = 0.004) were significantly reduced in AF compared with no AF. Measurements of aTMD and three other T wave descriptors were similar in AF and no AF. Significant variables by univariate analysis, including advanced age (P = 0.014), impaired left ventricular function (P = 0.02), greater Pi (P = 0.012), and lower TCRT (P = 0.007) or dTMD, were entered into multiple logistic regression models. Increased Pi (P = 0.038), reduced TCRT (P = 0.040), and lower dTMD (P = 0.014) predicted AF after CABG independently. In patients <70 years, a linear combination of increased pCR and lower TCRT separated AF and no AF with a sensitivity of 74% and specificity of 62% (P = 0.005). Conclusion: ECG assessment identifies patients vulnerable to AF after CABG. Combination of ECG parameters assessed preoperatively may play an important role in predicting new-onset AF after CABG. [source]

    Reversal of Electrical Remodeling After Cardioversion of Persistent Atrial Fibrillation

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2004
    MERRITT H. RAITT M.D.
    Introduction: In animals, atrial fibrillation results in reversible atrial electrical remodeling manifested as shortening of the atrial effective refractory period, slowing of intra-atrial conduction, and prolongation of sinus node recovery time. There is limited information on changes in these parameters after cardioversion in patients with persistent atrial fibrillation. Methods and Results: Thirty-eight patients who had been in atrial fibrillation for 1 to 12 months underwent electrophysiologic testing 10 minutes and 1 hour after cardioversion. At 1 week, 19 patients still in sinus rhythm returned for repeat testing. Reverse remodeling of the effective refractory period was not uniform across the three atrial sites tested. At the lateral right atrium, there was a highly significant increase in the effective refractory period between 10 minutes and 1 hour after cardioversion (drive cycle length 400 ms: 204 ± 17 ms vs 211 ± 20 ms, drive cycle length 550 ms: 213 ± 18 ms vs 219 ± 23 ms, P < 0.001). The effective refractory period at the coronary sinus and distal coronary sinus did not change in the first hour but had increased by 1 week. The corrected sinus node recovery time did not change in the first hour but was shorter at 1 week (606 ± 311 ms vs 408 ± 160 ms, P = 0.009). P wave duration also was shorter at 1 week (135 ± 18 ms vs 129 ± 13 ms, P = 0.04) consistent with increasing atrial conduction velocity. Conclusion: The atrial effective refractory period increases, sinus node function improves, and atrial conduction velocity goes up in the first week after cardioversion of long-standing atrial fibrillation in humans. Reverse electrical remodeling of the effective refractory period occurs at different rates in different regions of the atrium. (J Cardiovasc Electrophysiol, Vol. 15, pp. 507-512, May 2004) [source]

    Demonstration of Electrical and Anatomic Connections Between Marshall Bundles and Left Atrium in Dogs: Implications on the Generation of P Waves on Surface Electrocardiogram

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2002
    CHIKAYA OMICHI M.D.
    Marshall Bundle and P Wave.Introduction: The muscle bundles within the ligament of Marshall (LOM) are electrically active. The importance of these muscle bundles (Marshall bundle [MB]) to atrial activation and the generation of the ECG P wave is unclear. Methods and Results: We used optical mapping techniques to study epicardial activation patterns in isolated perfused left atrium in four dogs. In another seven dogs, P waves were studied before and after in vivo radiofrequency (RF) ablation of the connection between coronary sinus (CS) and the LOM. Computerized mapping was performed before and after RF ablation. Optical mapping studies showed that CS pacing resulted in broad wavefronts propagating from the middle and distal LOM directly to the adjacent left atrium (LA). Serial sections showed direct connection between MB and LA near the orifice of the left superior pulmonary vein in two dogs. In vivo studies showed that MB potentials were recorded in three dogs. After ablation, the duration of P waves remained unchanged. In the other four dogs, MB potentials were not recorded. Computerized mapping showed that LA wavefronts propagated to the MB region via LA-MB connection and then excited the CS. After ablation, the activation of CS muscle sleeves is delayed, and P wave duration increased from 65.3 ± 14.9 msec to 70.5 ± 17.2 msec (P = 0.025). Conclusion: In about half of the normal dogs, MB provides an electrical conduit between LA free wall and CS. Severing MB alters the atrial activation and lengthens the P wave. MB contributes to generation of the P wave on surface ECG. [source]

    Can Simple Doppler Measurements Estimate Interatrial Conduction Time?

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1p2 2003
    DRAGOS COZMA
    COZMA, D., et al.: Can Simple Doppler Measurements Estimate Interatrial Conduction Time?Prolongation of the interatrial conduction time (ia-CT) is considered an important factor in the pathophysiology of atrial fibrillation (AF) and as a criterion to perform multisite atrial pacing. Measurement of ia-CT requires an electrophysiologic study. The aim of this study was to compare echocardiographic with electrophysiologic measurements to determine if they are correlated. Methods and Results: The study included 32 consecutive patients who underwent electrophysiologic studies. We measured ia-CT between the high right atrium and the distal coronary sinus. In all patients we measured P wave duration, left atrial diameter and area, and ia-CT by Doppler echocardiography was measured as the difference in time intervals between the QRS onset and the tricuspid A wave, and the QRS onset and the mitral A wave (DT). Ia-CT was statistically correlated with DT(r = 0.79, P < 0.0001), but not with P wave duration or left atrial dimensions. Conclusions: Measurement DT may be reliable to estimate ia-CT without invasive procedure. Accordingly, DT could be used as a simple selection criterion when considering patients for atrial resynchronization therapy. (PACE 2003; 26[Pt. II]:436,439) [source]

    P Wave Duration and Morphology Predict Atrial Fibrillation Recurrence in Patients with Sinus Node Dysfunction and Atrial-Based Pacemaker

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 11 2002
    ANTONIO DE SISTI
    DE SISTI, A., et al.: P Wave Duration and Morphology Predict Atrial Fibrillation Recurrence in Patients with Sinus Node Dysfunction and Atrial-Based Pacemaker. P wave duration and morphology have never been systematically evaluated as markers of AF in patients with a conventional indication to pacing. This study correlated sinus P wave duration and morphology and the incidence of AF in patients with sinus node dysfunction (SND), previous history of AF before implant, and atrial-based pacemaker. Included were 140 patients (86 men, 54 women; mean age 71.8 ± 10.4 years) with recurrent paroxysmal AF and who received a DDD (128 patients) or AAI (12 patients) pacemaker for SND. Forty-nine patients had structural heart disease. Sinus P wave duration and morphology was evaluated in leads II, III. Twenty-two patients had an abnormal P wave morphology, diphasic (+/-) in 5 and notched (+/+) in 17. The basic pacemaker rate was programmed between 60 and 70 beats/min. Rate responsive function was activated in 65 patients. During a follow-up of 27.6 ± 17.8 months, AF was documented in 87 patients. Forty-four patients developed permanent AF, following at least one episode of paroxysmal AF in 26 cases. Statistical analysis used Cox model regression. Univariate predictors of AF (P < 0.10) were drugs (mean: 2 ± 1.4) and DC shock before pacing (16/140 patients), P wave duration (mean 112.5 ± 24.6 ms), basic pacemaker rate (mean 68 ± 5 beats/min), and drugs in the follow-up (mean 1.2 ± 0.94). Multivariate analysis showed that P wave duration (b = 0.013, s.e. = 0.004; P = 0.003), and drugs before pacing (b = 0.2; s.e.= 0.08; P < 0.01) resulted in a significant independent predictor of AF. Actuarial incidence of patients free of AF at 30 months was 35%: 56% in patients with a P wave < 120 ms, and 13% in those with P wave , 120 ms (P < 0.01 by Score test). Univariate predictors of permanent AF were drugs and DC shock before pacing, left atrial size (mean 39 ± 6 mm), P wave duration, abnormal P wave morphology (22/140 patients), and drugs in the follow-up. Multivariate analysis showed that P wave morphology was the most important predictor of permanent AF (b = - 0.56, s.e.= 0.2; P = 0.008). Incidence of patients free of permanent AF at 30 months was 69%: 74% in patients with normal P wave, compared to 28% in the case of abnormal P wave morphology (P < 0.01). P wave duration and morphology are good markers of postpacing AF recurrence in patients with SND and an atrial-based pacemaker. This observation suggests that intra- and interatrial conduction disturbances be extensively evaluated before implantation, and the indication for atrial resynchronization procedures be reevaluated. [source]

    Effect of Different Pacing Protocols on the Induction of Atrial Fibrillation in a Transvenously Paced Sheep Model

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2001
    RIK WILLEMS
    WILLEMS, R. et al.: Effect of Different Pacing Protocols on the Induction of Atrial Fibrillation in a Transvenously Paced Sheep Model. In different animal models rapid atrial stimulation led to a shortening and maladaptation to rate of the atrial effective refractory period (AERP). This atrial electrical remodeling resulted in an increased vulnerability to atrial fibrillation (AF). These experimental findings formed the rationale for a stringent pursuit of sinus rhythm in patients with AF, since this would prevent or reverse atrial remodeling. This study tested the hypothesis that a reduction of arrhythmia burden would lead to a decreased vulnerability for AF. Different rapid atrial pacing protocols in a sheep model were used. During 15 weeks, 13 animals were continuously rapid paced and 7 animals were intermittently burst-paced, resulting in rapid atrial activation during 100% versus 33 ± 4% of the time, respectively. In the continuously paced group, 77% of the animals developed sustained AF (i.e., >1 hour) versus only 29% in the burst-paced group (P < 0.05). However, there was no difference in mean AERP shortening over time, nor maximal AERP shortening per animal, between both protocols. Minimal AERP was 103 ± 5 ms in the continuously paced group and 107 ± 5 in the burst-paced group (P = NS). Significant changes could be identified in effect on P wave duration, AVN function, and atrial dilation. Conduction slowing was more pronounced in the continuously paced group with a maximal P wave duration of 136 ± 4 ms in this group versus 116 ± 5 in the burst-paced group (P < 0.05). In the continuously paced group, the right atrial area significantly increased from 2.5 ± 0.1 cm2 at baseline to 4.2 ± 0.2 cm2. In the burst-paced group there was no significant atrial dilatation (from 2.6 ± 0.1 to 2.8 ± 0.1 cm2). In conclusion, limiting atrial arrhythmia burden slowed the development of sustained AF in this sheep model. This was not mediated by a decreased influence on atrial refractoriness but seemed to be dependent on smaller changes in atrial conduction and dimensions. [source]

    Electrophysiologicai Characteristics of the Atrium in Sinus Node Dysfunction With and Without Postpacing Atrial Fihriliation

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 3 2000
    ANTONIO DE SISTI
    DE SISTI, A., ET AL.: Electrophysiologicai Characteristics of the Atrium in Sinus Node Dysfunction With and Without Postpacing Atrial Fibrillation . In patients with sinus node dysfunction (SND) with or without associated paroxysmal atrial fibrillation (AF), the effectiveness of atrial pacing in reducing the incidence of AF is not definitive. In addition, despite several studies involving large populations of implanted patients, little attention has been paid to the electrophysioiogicai (EP) atrial substrate and the effect of permanent atrial pacing. The aim of this study is to correlate EP data and the risk of AF after DDD device implantation. We reviewed FP data of 38 consecutive patients with SND. mean age 70 ± 8 years, who were investigated free of antiarrhythmic treatment, for the evaluation of the atrial substrate. We also considered as control group 25 subjects, mean age 63 ± 14 years, referred to our EP laboratory for unexplained syncope or various atrioventricular disturbances. Following pharmacological washout and at a drive cycle length of 600 ms. effective and functional refractory periods (ERP, FRP), Sl-Al and S2-A2 latency, Al and A2 conduction duration, and latent vulnerability index (EHP/A2) were measured. AF induction was tested with up to three extrastimuli at paced cycle lengths of 600 and 400 ms in 20 patients. Induction of sustained AF (> 30 seconds) was considered as the endpoint. P wave duration on the surface ECG in lead II/Vl was also measured. DDD pacing mode was chosen in all patients with the minimal atrial rate programmed between 60 and 75 beats/min (mean 64 ± 4 beats/min). After implantation, the patients were followed-up for 29 ± 17 months and clinically documented occurrence of AF was determined. When comparing patients with SND and subjects of the control group, we did not find any significant statistical differences in terms of ERP (237 ± 33 vs 250 ± 29 ms), FRP (276 ± 30 vs 280 ± 32 ms) and Sl-Al (39 ± 16 vs 33 ± 11 ms) and S2-A2 latency (69 ± 24 vs 63 ± 25 ms). In contrast, we observed significant differences regarding Al (55 ± 19 vs 39 ± 13 ms; P < 0.001), A2 (95 ± 34 vs 57 ± 18 ms; P < 0.001) and P wave duration (104 ± 18 vs 94 ± 15 ms; P < 0.05), and ERP/A2 (2.8 ± 1.2 vs 4.8 ± 1.6; P < 0.001). When comparing patients with (n = 11) or without (n =27) postpacing AF occurrence, we did not find any difference with reference to ERP, FRP. Sl-Al, S2-A2, Al duration, or follow-up duration. In patients with postpacing AF occurrence, A2 was longer (116 ± 41 vs 87 ± 27 ms; P < 0.01), FRP/A2 lower (2.1 ± 0.4 vs 3.1 ± 1.4; P < 0.05), P wave more prolonged (116 ± 22 vs 99 ± 14 ms; P < 0.01), and preexisting AF history predominant (6/11 vs 5/27 patients; P < 0.05). No difference was observed between patients with (n = 8) and without (n = 12) AF induction during the EP study. In patients with SND, the atrial refractoriness appears normal and the most important abnormality concerns conduction slowing disturbances. Persistence of AF despite pacing stresses the importance of mechanisms responsible for AF not entirely brady-dependent. In this setting, more prolonged atrial conduction disturbances, responsible for a low vulnerability index, and a preexisting history of AF enable us to identify a high risk patient group for AF in the follow-up. sinus node dysfunction, atrial fibrillation, electrophysiologicai study, atrial pacing [source]

    Prevention of the Initiation of Atrial Fibrillation: Mechanism and Efficacy of Different Atrial Pacing Modes

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 3 2000
    WEN-CHUNG YU
    Several atrial pacing modes have been reported to be effective in the prevention of atrial fibrillation (AF); they included biatrial pacing, dual site right atrial pacing, Bachmann's bundle (BB) pacing, and coronary sinus pacing. However, the relative efficacy and electrophysiological mechanisms of these pacing modes in the prevention of AF are not clear. In 15 patients (age 54 ± 14 years) with paroxysmal AF, P wave duration, effective refractory period, and atrial conduction time were determined with six different atrial drive pacings, that were right atrial appendage (RAA), BB, right posterior interatrial septum (RPS), distal coronary sinus (DCS), RAA plus RPS simultaneously (DSA), and RAA plus DCS simultaneously (BiA). All these patients consistently had AF induced with early RAA extrastimulation coupling to RAA drive pacing. No patient had AF induced with RAA extrastimulation coupled to BB, RPS, or DCS drive pacing, but seven and eight patients had AF induced with RAA extrastimulation coupled to DSA and BiA drive pacing, respectively. The P wave duration was longest during RAA pacing, and became shorter during other atrial pacing modes. Analysis of electrophysiological change showed that early RAA extrastimulation coupled to RAA drive pacing caused the longest atrial conduction delay among these atrial pacing modes; BB, RPS, and DCS drive pacing caused a greater reduction of this conduction delay than DSA and BiA drive pacing. In addition, the effective refractory periods of RAA determined with BB, RPS, and DCS drive pacing were similar and longer than that determined with DSA and BiA drive pacing. In patients with paroxysmal AF, this arrhythmia was readily induced with RAA extrastimuli coupled to RAA drive pacing. BB, RPS, and DCS pacing were similar and more effective than DSA and BiA pacing in preventing AF. [source]

    Detailed ECG Analysis of Atrial Repolarization in Humans

    ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2009
    Fredrik Holmqvist M.D., Ph.D.
    Introduction: Data on human atrial repolarization are scarce since the QRS complex normally obscures its ECG trace. In the present study, consecutive patients with third-degree AV block were studied to better describe the human Ta wave. Methods and Results: Forty patients (mean age 75 years, 17 men) were included. All anti-arrhythmic drugs were discontinued before ECG recording. Standard 12-lead ECGs were recorded, transformed to orthogonal leads and studied using signal-averaged P wave analysis. The average P wave duration was 124 ± 16 ms. The PTa duration was 449 ± 55 ms (corrected PTa 512 ± 60 ms) and the Ta duration (P wave end to Ta wave end) was 323 ± 56 ms. The polarity of the Ta wave was opposite to that of the P wave in all leads. The Ta peaks were located at 196 ± 55 ms in Lead Y, 216 ± 50 ms in Lead X, and 335 ± 92 in Lead Z. No correlation was found between P wave duration and Ta duration, or between Ta peak amplitude and Ta duration. The morphology of the Ta wave was similar regardless of the interatrial conduction. Conclusions: The Ta wave has the opposite polarity, and the duration is generally two to three times that, of the P wave. Although the Ta peak may occasionally be located in the PQ interval during normal AV conduction, it is unlikely that enough information can be obtained from analysis of this segment to differentiate normal from abnormal atrial repolarization. Hence, an algorithm for QRST cancellation during sinus rhythm is needed to further improve analysis. [source]

    P-Wave Duration and Dispersion in Obese Subjects

    ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2008
    Feridun Kosar M.D.
    Background: Although previous studies have documented a variety of electrocardiogram (ECG) abnormalities in obesity, P-wave alterations, which represent an increased risk for atrial arrhythmia, have not been studied very well in these patients. The aim of the present study was to evaluate P-wave duration and P dispersion (Pd) in obese subjects, and to investigate the relationship between P-wave measurements, and the clinical and echocardiographic variables. Methods: The study population consisted of 52 obese and 30 normal weight control subjects. P-wave duration and P-wave dispersion were calculated on the 12-lead ECG. As echocardiographic variables, left atrial diameter (LAD), left ventricular end-diastolic, and end-systolic diameters (LVDD and LVSD), left ventricular ejection fraction (LVEF), interventricular septum thickness (IVST), left ventricular posterior wall thickness (LVPWT), and left ventricular mass (LVM) of the obese and the control subjects were measured by means of transthoracic echocardiography. Results: There were statistically significant differences between obese and controls as regards to Pmax (maximum P-wave duration) and Pd (P dispersion) (P < 0.001 and P < 0.001, respectively). Pmin (minimum P wave duration) was similar in both groups. Correlation analysis showed that Pd in the obese patients was related to any the clinical and echocardiographic parameters including BMI, LAD, LVDD, IVST, LVPWT, and LVM. Conclusion: Our data suggest that obesity affects P-wave dispersion and duration, and changes in P dispersion may be closely related to the clinical and the echocardiographic parameters such as BMI, LAD, IVST, LVPWT, and LVM. [source]

    Randomized Study of Early Intravenous Esmolol Versus Oral Beta-Blockers in Preventing Post-CABG Atrial Fibrillation in High Risk Patients Identified by Signal-Averaged ECG: Results of a Pilot Study

    ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2002
    Nomeda Balcetyte-Harris M.D.
    Background: Patients with prolonged signal-averaged ECG have four times higher risk for development of atrial fibrillation (AF) after coronary artery bypass surgery (CABG). Incidence of AF is reduced, but not eliminated by prophylaxis with beta-blockers. The limitations of prophylaxis with oral beta-blockers may be related to the delayed effect of oral therapy. We performed a pilot study of the efficacy of early intravenous esmolol and an oral beta-blocker regimen for prevention of postoperative AF. Methods: Fifty patients referred for CABG and considered to be at high risk for postoperative AF on the basis of prolonged signal-averaged ECG P wave duration > 140 ms were randomized to receive either a 24-hour infusion of esmolol 6,18 hours after CABG, at an average dose 67 ± 7 ,/kg/min, followed by oral beta-blockers versus oral beta-blockers only beginning on postoperative day 1. Results: Seven of 27 patients (26%) in the esmolol group and 6 of 23 patients (26%) in the oral beta-blocker group developed postoperative AF, P = NS. The mean time of onset of AF (2.7 ± 0.5 vs 2.7 ± 0.3 postoperative day, P = NS) and the median duration of AF (10 [2192] vs 7 [1.16] hours, P = NS) were similar between the two groups. Eleven (41%) patients treated with esmolol developed adverse events (hypotension: 8, bradycardia requiring temporary pacing: 2, left ventricular failure:1 patient) as compared to only one patient (4%) in the beta-blocker group who developed hypotension, P = 0.006. Conclusions: This randomized controlled pilot study suggests that intravenous esmolol is less well tolerated and offers no advantages to standard beta-blocker in preventing AF after CABG. A.N.E. 2002;7(2):86,91 [source]

    Scn3b knockout mice exhibit abnormal sino-atrial and cardiac conduction properties

    ACTA PHYSIOLOGICA, Issue 1 2010
    P. Hakim
    Abstract Aim:, In contrast to extensive reports on the roles of Nav1.5 , -subunits, there have been few studies associating the , -subunits with cardiac arrhythmogenesis. We investigated the sino-atrial and conduction properties in the hearts of Scn3b,/, mice. Methods:, The following properties were compared in the hearts of wild-type (WT) and Scn3b,/, mice: (1) mRNA expression levels of Scn3b, Scn1b and Scn5a in atrial tissue. (2) Expression of the ,3 protein in isolated cardiac myocytes. (3) Electrocardiographic recordings in intact anaesthetized preparations. (4) Bipolar electrogram recordings from the atria of spontaneously beating and electrically stimulated Langendorff-perfused hearts. Results:,Scn3b mRNA was expressed in the atria of WT but not Scn3b,/, hearts. This was in contrast to similar expression levels of Scn1b and Scn5a mRNA. Immunofluorescence experiments confirmed that the ,3 protein was expressed in WT and absent in Scn3b,/, cardiac myocytes. Lead I electrocardiograms from Scn3b,/, mice showed slower heart rates, longer P wave durations and prolonged PR intervals than WT hearts. Spontaneously beating Langendorff-perfused Scn3b,/, hearts demonstrated both abnormal atrial electrophysiological properties and evidence of partial or complete dissociation of atrial and ventricular activity. Atrial burst pacing protocols induced atrial tachycardia and fibrillation in all Scn3b,/, but hardly any WT hearts. Scn3b,/, hearts also demonstrated significantly longer sinus node recovery times than WT hearts. Conclusion:, These findings demonstrate, for the first time, that a deficiency in Scn3b results in significant atrial electrophysiological and intracardiac conduction abnormalities, complementing the changes in ventricular electrophysiology reported on an earlier occasion. [source]

    The generation of monthly gridded datasets for a range of climatic variables over the UK

    INTERNATIONAL JOURNAL OF CLIMATOLOGY, Issue 8 2005
    Matthew Perry
    Abstract Monthly or annual 5 km × 5 km gridded datasets covering the UK are generated for the 1961,2000 period, for 36 climatic parameters. As well as the usual elements of temperature, rainfall, sunshine, cloud, wind speed, and pressure, derived temperature variables (such as growing-season length, heating degree days, and heat and cold wave durations) and further precipitation variables (such as rainfall intensity, maximum consecutive dry days, and days of snow, hail and thunder) are analysed. The analysis process uses geographical information system capabilities to combine multiple regression with inverse-distance-weighted interpolation. Geographic and topographic factors, such as easting and northing, terrain height and shape, and urban and coastal effects, are incorporated either through normalization with regard to the 1961,90 average climate, or as independent variables in the regression. Local variations are then incorporated through the spatial interpolation of regression residuals. For each of the climatic parameters, the choice of model is based on verification statistics produced by excluding a random set of stations from the analysis for a selection of months, and comparing the observed values with the estimated values at each point. This gives some insight into the significance, direction, and seasonality of factors affecting different climate elements. It also gives a measure of the accuracy of the method at predicting values between station locations. The datasets are being used for the verification of climate modelling scenarios and are available via the Internet. © Crown Copyright 2005. Reproduced with the permission of Her Majesty's Stationery Office. Published by John Wiley & Sons, Ltd. [source]

    Aging-Related Increase to Inducible Atrial Fibrillation in the Rat Model

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2002
    HIDEKI HAYASHI M.D.
    Aging and Atrial Fibrillation.Introduction: Aging is associated with atrial interstitial fibrosis and increased incidence of atrial fibrillation (AF). We hypothesized that aged rats are suitable for study of aging-related AF and that partial atrial cellular uncoupling induced with heptanol in young rats mimics aging-related AF. Methods and Results: Interatrial conduction time and atrial response to burst atrial pacing were evaluated in 11 young (2,3 months) and 12 old (22,24 months) male rats (Fisher 344) in the Langendorff-perfused setting. At baseline, sustained (>30 sec) atrial tachycardia (AT) and AF were induced in 10 of 12 and in 7 of 12 old rats, respectively. No such arrhythmias could be induced in the young rats. Old rats had significantly (P < 0.01) longer interatrial conduction time and P wave durations than the young rats. Burst pacing failed to induce AT and AF in all 11 young rats studied. The effects of heptanol 2 to 10 ,M were studied in both groups. Heptanol 2 to 5 ,M promoted inducible AT in all 5 young rats studied; however, when its concentration was raised to 10 ,M, AT could no longer be induced in any of the 5 young rats. No AF could be induced in any of the 5 young rats at heptanol concentrations of 2 to 10 ,M. In the old rats, AF could still be induced during perfusion of 2 ,M heptanol. However, when its concentration was raised to 5 and 10 ,M, AF could not be induced in any of the 6 old rats studied. Optical mapping using a potentiometric dye showed a periodic single wavefront of activation during AT in both groups and 2 to 4 independent wavefronts propagating in different directions during AF in the old rats. Histology revealed a significant increase in interstitial atrial fibrosis (P < 0.01), atrial cell size (P < 0.05), and heart weight in old versus young rats. Fibrosis in the old rats was highly heterogeneous. Conclusion: The rat model is suitable for study of aging-related AF. Uniform partial atrial cellular uncoupling with heptanol perfusion in the young rats, although promoting inducible AT, does not mimic aging-related AF. The results suggest that heterogeneous atrial interstitial fibrosis and atrial cell hypertrophy might contribute to the aging-related increase in atrial conduction slowing, conduction block, and inducible AF in the old rat model. [source]

    P Wave Dispersion Predicts Recurrence of Paroxysmal Atrial Fibrillation in Patients with Atrioventricular Nodal Reentrant Tachycardia Treated with Radiofrequency Catheter Ablation

    ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2006
    Basri Amasyali M.D.
    Background: Paroxysmal atrial fibrillation (AF) recurs in up to one-third of patients with atrioventricular nodal reentrant tachycardia (AVNRT) treated with slow pathway ablation. Therefore, identification of patients at risk for recurrence of AF after slow pathway ablation is important because of the necessity for additional therapies. The purpose of this study was to determine whether successful slow pathway ablation influences P wave parameters and whether these parameters predict the recurrence of paroxysmal AF in patients with both AVNRT and paroxysmal AF after ablation. Methods: Thirty-six patients with AVNRT and documented paroxysmal AF (Group 1) were compared to 36 age-matched controls with AVNRT only (Group 2). P wave durations and P dispersion were measured before and after ablation. Results: No significant differences were observed between P wave parameters observed before and after ablation. Maximum P wave durations (Pmax) and P dispersion (Pdisp) were significantly higher in Group 1 than in Group 2 (P < 0.001 for both) whereas minimum P wave durations did not differ between groups, both before and after ablation. Ten patients (28%) in Group-1 had recurrence of AF during a mean follow-up of 34 ± 11 months. Univariate predictors of AF recurrence were Pdisp ,35.5 ms (P < 0.010), left atrial diameter >40 mm (P < 0.010), mitral or aortic calcification (P < 0.010), Pmax ,112 ms (P < 0.050), valvular heart disease (P < 0.050), and atrial vulnerability (induction of AF lasting >30 second) after ablation (P < 0.050). However, only Pdisp ,35.5 ms (P < 0.050) and left atrial diameter >40 mm (P < 0.010) were independent predictors of AF recurrences. Conclusion: This study suggests that P wave dispersion could identify patients with AVNRT susceptible to recurrence of AF after slow pathway ablation. [source]