Atrial Electromechanical Delay Research Articles

Relationship between atrial septal aneurysms and atrial electromechanical delay

Atrial septal aneurysm (ASA) is a saccular deformity located in the atrial septum. Atrial arrhythmias are common in patients with ASA. Atrial electromechanical delay (AEMD) can be used to evaluate development of atrial arrhythmias in various settings. The aim of the study was to investigate the relationship between ASA, cardiac arrhythmias and AEMD. Seventy patients with ASA served as the study group (30 men; mean age, 33.6 ± 10.9 years) and 70 healthy volunteers served as the control group (34 men; mean age, 31.4 ± 7.8 years). ASAs were diagnosed by transthoracic echocardiography based on the criteria of a minimal aneurysmal base of ≥ 15 mm; and an excursion of ≥ 10 mm. Inter-AEMD and intra-AEMDs of both atrium were measured from parameters of tissue Doppler imaging. There was no significant difference between the study and control groups in terms of age, gender, left atrium diameter, and left ventricular ejection fraction. Inter-AEMD (50.7 ± 22.5 ms vs. 36.9 ± 12.0 ms) and intra-left AEMD (44.6 ± 17.4 ms vs. 30.7 ± 11.6 ms) were significantly higher in patients with ASA with respect to control group. Inter-AEMD (63.6 ± 20.1 ms vs. 45.1 ± 21.5 ms, P = 0.001), intra-left AEMD (55.3 ± 15.6 ms vs. 40.1 ± 16.2 ms, P = 0.001), diameter of the ASA (19.9 ± 3.6 mm vs. 17.1 ± 2.7 mm, P = 0.001) and P wave dispersion (18.5 ± 6.7 ms vs. 11.8 ± 7.3 ms, P = 0.001) were significantly greater in the subgroup with arrhythmias compared to the subgroup without arrhythmias. Inter-AEMD and intra-left AEMD were found to be significantly prolonged in patients with ASA. Being a non-invasive, inexpensive and simple technique AEMD may provide significant contributions to assess the risk for paroxysmal supraventricular arrhythmia in patients with ASA.

A Novel Echocardiographic Marker in Hypertensive Patients: Is Diastolic Dysfunction Associated With Atrial Electromechanical Abnormalities in Hypertension?

Atrial arrhythmias are common problems in hypertensive patients. Atrial electromechanical delay (AEMD) can be used to evaluate development of atrial arrhythmias. The authors aimed to assess inter- and intra-AEMD in hypertensive patients. The study population consisted of 200 medically treated hypertensive patients and 151 normotensive controls. Inter-AEMD and intra-left AEMD were measured from parameters of Doppler tissue imaging. There were 72 (36%) hypertensive patients with diastolic dysfunction, 128 (64%) patients without diastolic dysfunction, and 151 healthy controls. Inter-AEMD (59 ms [36-104 ms] vs 42 ms [36-68 ms] vs 46 ms [30-82 ms]) was significantly higher in hypertensive patients with diastolic dysfunction compared with patients without diastolic dysfunction and controls. Our data demonstrated that inter-AEMD is longer in hypertensive patients with diastolic dysfunction. It may be suggested that diastolic dysfunction is associated with atrial electromechanical abnormalities, which can be associated with atrial fibrillation in hypertension.

Assessment of atrial electromechanical delay by tissue Doppler echocardiography in patients with nonischemic dilated cardiomyopathy

Background Atrial electromechanical delay (AEMD) calculated from tissue Doppler imaging (TDI) echocardiography can be an alternative to invasive electrophysiologic studies. We investigated whether the AEMD obtained from TDI is prolonged in patients with nonischemic dilated cardiomyopathy (DCM). Methods Fifty-five patients with nonischemic DCM (23 men/32 women; age, 43.9 ± 14.8 years) and 55 controls (20 men/35 women; age, 41.3 ± 13.4 years) were included in this study. Atrial electromechanical delay (the time interval from the onset of P wave on electrocardiogram to the beginning of late diastolic wave [Am wave] on TDI) was calculated from the lateral and septal mitral annulus, and lateral tricuspid annulus (PA lateral, PA septum, and PA tricuspid, respectively). P-wave dispersion was calculated from the 12-lead electrocardiogram. Results PA lateral and PA septum duration were significantly longer in patients with nonischemic DCM than the controls (78.4 ± 19.7 versus 53.8 ± 6.6 and 55.2 ± 16.3 versus 40.5 ± 6.2, P < .0001 for both; respectively). However, PA tricuspid duration was statistically similar between the 2 groups (36.4 ± 10.9 versus 37.2 ± 5.7, P ≥ .05). P-wave dispersion was significantly higher in nonischemic DCM patients than the controls (53.0 ± 14.4 versus 37.5 ± 5.5, P < .0001). PA lateral was correlated with the left atrial maximal volume ( r = 0.64, P < .0001), P-wave dispersion ( r = 0.65, P < .0001), and log B-type natriuretic peptide (NT proBNP) ( r = 0.63, P < .0001). There was a statistically significant and negative correlation between the PA lateral and left ventricular ejection fraction ( r = −0.63, P < .0001) and E-wave deceleration time ( r = −0.34, P < .0001). Multivariate analysis revealed that left atrial maximal volume and log NT proBNP were the independent predictors of PA lateral ( P < .0001 and P = .003, respectively). Conclusion The AEMD was significantly prolonged in patients with nonischemic DCM. Left atrial enlargement and log NT proBNP were the independent predictors of this prolongation.

Assessment of Atrial Electromechanical Delay, Diastolic Functions, and Left Atrial Mechanical Functions in Patients with Type 1 Diabetes Mellitus

The aim of this study was to evaluate atrial electromechanical coupling obtained by tissue Doppler imaging (TDI), left and right ventricular diastolic functions, and left atrial (LA) mechanical functions in patients with type 1 diabetes mellitus (DM-1). A total of 43 patients with DM-1 (age 19.6 +/- 6.8 years) and 42 age- and gender-matched controls (age 19.5 +/- 6.4 years) were included. Atrial electromechanical coupling was measured with TDI and corrected for heart rate. P-wave dispersion (Pd) was calculated from the 12-lead electrocardiograms. Systolic and diastolic functions in both ventricles were assessed using conventional echocardiography and TDI. Myocardial performance index was calculated with TDI. LA maximal, minimal, and pre-systolic volumes were measured according to the biplane area-length method. LA mechanical function parameters were calculated. Intra- and interatrial electromechanical delays and Pd were significantly higher in patients with DM-1 compared with controls (P = .02, P < .0001, and P = 0.005, respectively). A-wave velocity and isovolumic relaxation time were higher and E/A ratio was lower in patients with DM-1 (P = .03, P = .03, and P = .003, respectively). According to TDI, systolic velocities and myocardial performance index values of both ventricles were comparable. Diastolic filling velocities of the left ventricle, including E(m) global, A(m) global, E(m)/A(m) ratio, and right ventricular A(m), were different between groups (P = .03, P = .02, P < .001, and P = .02, respectively). LA passive emptying fraction was decreased, and LA active emptying volume and LA active emptying fraction were increased in patients with DM-1 (P = .02, P = .001, and P < .0001, respectively). Interatrial electromechanical delay was positively correlated with the presence of DM-1, age, LA active emptying fraction, and Pd (P < .001, P = .007, P < .001, and P = .002, respectively), and was negatively correlated with E(m)/A(m) ratio and LA passive emptying fraction (P < .001 and P = .001, respectively). In multivariate analyses, age and DM-1 were independent predictors of interatrial electromechanical delay (P = .001 and P < .001, respectively). This study shows that intra- and interatrial electromechanical delays are prolonged diastolic functions of both ventricles and that LA mechanical functions are impaired in patients with DM-1. Age and the presence of DM-1 were independent factors of the interatrial electromechanical delay.

Assessment of Atrial Conduction Time in Patients with Familial Mediterranean Fever

Increased inflammatory activity is known to be a pathophysiologic characteristic of atrial fibrillation. Familial Mediterranean fever (FMF) is a disease characterized by recurrent and sustained increased inflammatory activity. Atrial conduction abnormalities in these patients have not been investigated in terms of P-wave duration, P-wave dispersion (Pd), and atrial electromechanical delay measured by tissue Doppler echocardiography (TDE). We aimed to assess atrial conduction time in patients with FMF. A total of 33 patients with FMF (13 males/20 females, 28.4 +/- 12.5 years), and 33 controls (13 males/20 females, 28.5 +/- 12.1 years) were included. Atrial electromechanical coupling (PA) and intra- and interatrial electromechanical delay were measured with TDE. From the 12-lead electrocardiogram Pd was calculated. Atrial electromechanical coupling at the left lateral mitral annulus (PA lateral) was significantly higher in FMF patients (58.0 +/- 9.0 vs 51.0 +/- 5.8, P < 0.001). Interatrial (PA lateral-PA tricuspid) and intraatrial electromechanical delay (PA septum-PA tricuspid) were significantly longer in FMF patients (21.3 +/- 7.4 vs 12.9 +/- 4.6, P < 0.001 and 4.7 +/- 5.5 vs 2.1 +/- 1.7, P = 0.01, respectively). Also, Pd and maximum P-wave duration were significantly higher in FMF patients (42.8 +/- 7.9 vs 35.3 +/- 6.1, P < 0.001 and 98.6 +/- 9.0 vs 93.1 +/- 8.5, P = 0.01, respectively). A positive correlation was detected between interatrial electromechanical delay and Pd (r = 0.622, P < 0.001). Plasma level of C-reactive protein (CRP) correlated with interatrial electromechanical delay and Pd (r = 0.733, P < 0.001; and r = 0.427, P < 0.001, respectively). This study shows that atrial electromechanical delay and Pd are prolonged in FMF patients. Atrial electromechanical delay is closely associated with Pd and plasma level of CRP.

Atrial Function During Different Multisite Atrial Pacing Modalities in Patients With Bradycardia - Tachycardia Syndrome

Multisite atrial pacing (MAP) was introduced to improve atrial electrical synchrony and prevent recurrence of atrial fibrillation (AF). In the present study there were 57 patients with sinus node disease, AF recurrence and prolonged P-wave on ECG with 2 MAP modalities. In all patients 1 lead was implanted in the coronary sinus (CS) ostium area. In the right atrial appendage (RAA)+CS group (28 patients) the other atrial lead was in the RAA, and in the BB+CS group (29 patients) in the Bachmann's bundle (BB) region. Tissue Doppler was used to register the electromechanical delay (EMD) in the atrial walls and estimate the atrial contraction synchrony. Cardiac output and myocardial performance index did not differ during the 2 MAP modalities. During BB+CS, in comparison with RAA+CS pacing, the peak of the mitral atrial wave occurred earlier (P<0.01), the usual right-left atrial contraction sequence was reversed more frequently (P<0.004), all atrial EMDs except for the lateral left atrium (LA) were shorter (P<0.05), and LA synchrony was greater (P<0.001). In patients treated with MAP, implanting 1 of the atrial leads in the BB area instead of the RAA has no influence on global cardiac hemodynamics, but does result in earlier LA contraction, and reversal of the typical right-left atrial contraction sequence, as well as providing greater LA contraction synchrony.

Prediction of Atrial and Ventricular Electro-Mechanical Delays from Surface ECG for Optimization of Pacemaker AV Timing

Prediction of Atrial and Ventricular Electro-Mechanical Delays from Surface ECG for Optimization of Pacemaker AV Timing

Arrhythmogenesis in the Developing Heart During Anoxia‐Reoxygenation and Hypothermia‐Rewarming: An In Vitro Model

The spatio-temporal pattern of arrhythmias in the embryonic/fetal heart subjected to a transient hypoxic or hypothermic stress remains to be established. Spontaneously beating hearts or isolated atria, ventricles, and conotruncus from 4-day-old chick embryos were subjected in vitro to 30-minute anoxia and 60-minute reoxygenation. Hearts were also submitted to 30-minute hypothermia (0-4 degrees C) and 60-minute rewarming. ECG disturbances and alterations of atrial and ventricular electromechanical delay (EMD) were systematically investigated. Baseline functional parameters were stable during at least 2 hours. Anoxia induced tachycardia, followed by bradycardia, atrial ectopy, first-, second-, and third-degree atrio-ventricular blocks and, finally, transient electromechanical arrest after 6.8 minutes, interquartile ranges (IQR) 3.1-16.2 (n = 8). Reoxygenation triggered also Wenckebach phenomenon and ventricular escape beats. At the onset of reoxygenation QT, PR, and ventricular EMD increased by 68%, 70%, and 250%, respectively, whereas atrial EMD was not altered. No fibrillations, no ventricular ectopic beats, and no electromechanical dissociation were observed. Arrhythmic activity of the isolated atria persisted throughout anoxia and upon reoxygenation, whereas activity of the isolated ventricles abruptly ceased after 5 minutes of anoxia and resumed after 5 minutes of reoxygenation. During hypothermia-rewarming, cardiac activity stopped at 17.9 degrees C, IQR 16.2-20.6 (n = 4) and resumed at the same temperature with no arrhythmias. All preparations fully recovered after 40 minutes of reoxygenation or rewarming. In the embryonic heart, arrhythmias mainly originated in the sinoatrial tissue and resembled those observed in the adult heart. Furthermore, oxygen readmission was by far more arrhythmogenic than rewarming and the chronotropic, dromotropic, and inotropic effects were fully reversible.

Doppler Tissue Evaluation of Intra-atrial and Interatrial Electromechanical Delay and Comparison with P-wave Dispersion in Patients with Mitral Stenosis

The aim of our study was to: (1) measure atrial electromechanical delay in patients with mitral stenosis (MS) and in a control group; (2) find the echocardiographic parameters that affect atrial electromechanical delay; and (3) examine the correlation between atrial electromechanical delay and P-wave dispersion (PWD). A total of 25 patients with pure MS (age 43 +/- 10 years; 18 women, 7 men) and 16 control subjects (age 41 +/- 8 years; 9 women, 7 men) were studied. Interatrial and intra-atrial electromechanical delay was measured with Doppler tissue echocardiography. From the 12-lead electrocardiograms, PWD was calculated. Interatrial electromechanical delay was 71.2 +/- 33 in the MS group and 40.5 +/- 21.0 in the control group (P = .01). In the MS group, PWD was 50 +/- 7 and in the control group it was 29 +/- 5 (P = .03). A positive correlation was detected between interatrial electromechanical delay and PWD (r = 0.6, P = .03). This study shows that interatrial electromechanical delay gets longer in MS and is correlated with PWD. Atrial electromechanical delay is related with left atrial size but not with severity of MS.

Ventricular but not atrial electro-mechanical delay of the embryonic heart is altered by anoxia-reoxygenation and improved by nitric oxide

Excitation-contraction coupling is modulated by nitric oxide (NO) which otherwise has either beneficial or detrimental effects on myocardial function during hypoxia-reoxygenation. This work aimed at characterizing the variations of electromechanical delay (EMD) induced by anoxia-reoxygenation within the developing heart and determining whether atrial and ventricular EMD are modulated by NO to the same extent. Hearts of 4 or 4.5-day-old chick embryos were excised and submitted in vitro to normoxia (45 min), anoxia (30 min) and reoxygenation (60 min). Electrocardiogram and atrial and ventricular contractions were simultaneously recorded throughout experiment. Anoxia-reoxygenation-induced chrono-, dromo-and inotropic disturbances and changes in EMD in atrium (EMDa) and ventricle (EMDv) were investigated in control hearts and in hearts exposed to 0.1, 1, 10, 50 and 100 microM of DETA-NONOate (a NO donating agent) or to 50 microM of L-NAME (a NOS inhibitor). Under normoxia, heart rate, PR interval, ventricular shortening velocity, EMDa and EMDv were similar in control, L-NAME-treated and DETA-NONOate-treated hearts. Under anoxia, cardiac activity became markedly erratic within less than 10 min in all groups. At the onset of reoxygenation, EMDv was increased by about 300% with respect to the preanoxic value while EMDa did not vary significatively. Compared to control conditions, L-NAME or DETA-NONOate had no influence on the negative chrono-, dromo- and inotropic effects induced by anoxia-reoxygenation. However, L-NAME prolonged EMDv during anoxia and delayed EMDv recovery during reoxygenation while 100 microM DETA-NONOate had the opposite effects. EMDa was neither affected by NOS inhibitor nor NO donor. At the end of reoxygenation, all the investigated parameters returned to their basal values. This work provides evidence that a NO-dependent pathway is involved in regulation of the ventricular excitation-contraction coupling in the anoxic-reoxygenated developing heart.

Ectopic pacing at physiological rate improves postanoxic recovery of the developing heart.

Recently, rapid and transient cardiac pacing was shown to induce preconditioning in animal models. Whether the electrical stimulation per se or the concomitant myocardial ischemia affords such a protection remains unknown. We tested the hypothesis that chronic pacing of a cardiac preparation maintained in a normoxic condition can induce protection. Hearts of 4-day-old chick embryos were electrically paced in ovo over a 12-h period using asynchronous and intermittent ventricular stimulation (5 min on-10 min off) at 110% of the intrinsic rate. Sham (n = 6) and paced hearts (n = 6) were then excised, mounted in vitro, and subjected successively to 30 min of normoxia (20% O(2)), 30 min of anoxia (0% O(2)), and 60 min of reoxygenation (20% O(2)). Electrocardiogram and atrial and ventricular contractions were simultaneously recorded throughout the experiment. Reoxygenation-induced chrono-, dromo-, and inotropic disturbances, incidence of arrhythmias, and changes in electromechanical delay (EMD) in atria and ventricle were systematically investigated in sham and paced hearts. Under normoxia, the isolated heart beat spontaneously and regularly, and all baseline functional parameters were similar in sham and paced groups (means +/- SD): heart rate (190 +/- 36 beats/min), P-R interval (104 +/- 25 ms), mechanical atrioventricular propagation (20 +/- 4 mm/s), ventricular shortening velocity (1.7 +/- 1 mm/s), atrial EMD (17 +/- 4 ms), and ventricular EMD (16 +/- 2 ms). Under anoxia, cardiac function progressively collapsed, and sinoatrial activity finally stopped after approximately 9 min in both groups. During reoxygenation, paced hearts showed 1) a lower incidence of arrhythmias than sham hearts, 2) an increased rate of recovery of ventricular contractility compared with sham hearts, and 3) a faster return of ventricular EMD to basal value than sham hearts. However, recovery of heart rate, atrioventricular conduction, and atrial EMD was not improved by pacing. Activity of all hearts was fully restored at the end of reoxygenation. These findings suggest that chronic electrical stimulation of the ventricle at a near-physiological rate selectively alters some cellular functions within the heart and constitutes a nonischemic means to increase myocardial tolerance to a subsequent hypoxia-reoxygenation.

Disturbed atrioventricular electromechanical function long after mustard operation for transposition of great arteries: A potential contributing factor to atrial flutter

The objectives were to study atrial and ventricular electromechanical function in patients long after Mustard repair for transposition of great arteries and to identify possible causes and physiologic disturbances in those with recurrent atrial flutter. Electromechanical atrial and ventricular function was assessed in 22 patients (11 women) aged 27 +/- 5 years, 10 to 29 (mean 24) years after initial Mustard operation with electrocardiography and echocardiography. The study subjects involved 12 patients with documented atrial flutter and the remaining 10 without history of atrial arrhythmia served as controls. All patients were studied while in sinus rhythm. There was no difference in age, gender, or age at original Mustard surgery between the 2 patient groups. The P wave and QRS duration were significantly broader in patients compared with controls (128 +/- 14 ms vs 100 +/- 10 ms, P <.05 and 120 +/- 20 ms vs 93 +/- 6 ms, P <.01). Right ventricular end diastolic dimension was not different, whereas left ventricular fraction shortening was less (20% +/- 10% vs 35% +/- 12%, P <.01) in the patient group. Left and septal total ventricular long axes amplitude were significantly lower in patients compared with controls (1.4 +/- 0.4 cm vs 1.7 +/- 0.3 cm, P <.05 and 0.6 +/- 0.2 cm vs 1.0 +/- 0.3 cm, P <.01). Right-sided total long axis excursion was equally reduced in the 2 groups (1.0 +/- 0.3 cm). Septal and right-sided but not left-sided "a" wave was smaller in the patients (1.2 +/- 1 mm vs 3 +/- 1.2 mm, P <.001 and 1 +/- 1.3 mm vs 3 +/- 0.9 mm, P <.01). Right atrial electromechanical delay was significantly longer in patients with respect to controls (110 +/- 14 ms vs 84 +/- 25 ms, P <.001), but on the left there was no difference. The P wave duration correlated closely with right atrial electromechanical delay, r = 0.79, P <.003. Significant tricuspid regurgitation was found in 9 of 12 patients but none of the controls. Right ventricular dysfunction is present long after Mustard operation for transposition of great arteries whether flutter occurs. However, in patients with history of atrial flutter, evidence of left ventricular dysfunction, significant tricuspid regurgitation, impaired right atrial electrical and mechanical function, and reversed onset of atrial systole is also present. The consistent association of the disturbed atrial and ventricular electromechanical behavior suggests a multifactorial etiology for atrial arrhythmia.

Atrial electromechanical sequence in normal subjects and patients with DDD pacemakers.

To assess the effect of right atrial appendage pacing on atrial electromechanical interrelations in patients with DDD pacemakers. Prospective study by M mode echocardiogram, Doppler echocardiogram, and apexcardiogram, along with electrocardiogram and phonocardiogram. Tertiary cardiac referral centre. 20 patients with DDD pacemakers and 20 age matched normal controls. Age, RR interval, atrial size, left ventricular size, and fractional shortening were similar in the two groups. Atrial electromechanical delay (the time from the onset of P wave or atrial pacing spike on ECG to the onset of atrial contraction on M mode echogram) was 68 (SD 7) ms at the lateral site of right atrium, 82 (9) ms at the central fibrous body, 93 (11) ms at the lateral site of left atrium in normals. In patients with DDD pacing, however, this delay increased to 85 (22) ms, 117 (23) ms, and 138 (25) ms respectively (all P < 0.01). Interatrial mechanical delay (the time from the onset of right atrial motion to the onset of the left) increased from 25 (6) ms in normal controls to 53 (18) ms in patients (P < 0.01). Intra-atrial mechanical dispersion (the time from the earliest to the latest onset of regional atrial motion around the atrioventricular ring) in the right atrium increased from 6 (2) ms in normals to 19 (2) ms in patients (P < 0.01), but it remained unchanged in the left atrium (6 (2) ms in normal controls v 7 (2) ms in patients, P > 0.05). Peak atrial shortening rate was not different between the two groups. Differences of atrial electromechanical activity between the two groups were also reflected on Doppler echocardiogram and apexcardiogram. Right atrial appendage pacing disturbs the normal coordinate sequence of right atrial mechanical activity and leads to a striking and variable increase in intra-atrial conduction time as well as in interatrial conduction time. Left atrial contraction remains synchronous although the timing of the start of its contraction was delayed. These values can be determined in individual patients to allow optimal setting of DDD pacemakers.

912-40 Assessment of Atrial Electromechanical Sequence in Patients with DDD Pacemakers

To assess the effect of right atrial appendage pacing on atrial electromechanical sequence, we studied 20 patients (pts) with DDD pacemakers and 20 age-matched normals. Atrial motion was recorded in the anterior, lateral, posterior sites of mitral and tricuspid rings as well as central fibrous body (CFB) by 2D guided M-mode echo. Atrial electromechanical delay (EM-D), from onset of p wave or atrial pacing spike to that of atrial contraction was measured at each site; intraatrial dispersion, the time from earliest to latest onset of motion around each ring, and interatrial delay were measured. In normals, EM-D is 68 ± 7 ms at the lateral site of right atrium (RA), 81 ± 9 ms at the CFB, 94 ± 11 ms at the lateral site of left atrium (LA). In pts, EM-D at corresponding sites increased to 85 ± 22 ms, 117 ± 23 ms and 138 ± 25 ms respectively (all p &lt; 0.01). The interatrial delay increased from 26 ± 7 ms in normals to 53 ± 18 ms in pts (p &lt; 0.01). RA dispersion increased from 6 ± 2 ms in normals to 19 (2) in pts (p &lt; 0.01), but LA dispersion remained unchanged. Right atrial pacing disturbs the normal coordinate sequence of RA mechanical activity, leads to a striking and variable increase in interatrial conduct time. LA contraction remains synchronous. These values should be determined in individual pts to allow optimal setting of DDD pacemakers.