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At least 19 recordsLinked to original sources
PubMed1990

Clinical and electrocardiographic characterization of cattle with atrial premature complexes.

Atrial premature complexes (APC) were identified in 16 cows over a 2-year period. Fourteen cows had concurrent gastrointestinal disease. Variation in the intensity of the first heart sound and an occasionally irregular heart rhythm were evident during thoracic auscultation. Neither cardiac murmurs nor pulse deficits were detected in any cows, and clinical signs of heart failure were lacking. Three cows had APC immediately prior to or after development of atrial fibrillation. The heart rate when APC were diagnosed ranged from 48 to 124 beats/min (mean, 77 +/- 20 beats/min), and the APC frequency ranged from less than 1 to 23/min (mean 9.4 +/- 8.0). The P-wave morphologic characteristics in 4 cows with APC was abnormal. The coupling index of the APC varied between 0.44 and 0.95, with a mean of 0.73. Aberrant ventricular activation was usually associated with a short coupling interval (coupling index less than 0.60) and was observed in 3 cows. Ten cows were determined to be hypocalcemic and 4 cows hypokalemic when APC were identified. Atrial ectopic activity could not be detected in 12 cows after resolution of the concurrent gastrointestinal disorder or electrolyte abnormality. Atrial premature complexes may be a functional cardiac disorder in cattle, unrelated to structural heart disease. The potential for APC to progress to sustained atrial arrhythmias such as atrial fibrillation should be considered.

Animals↗
PubMed1986

Effect of pirmenol on premature atrial complexes.

Suppression of premature atrial complexes by pirmenol, a new Class I antiarrhythmic agent, was examined following oral and intravenous routes of administration. In 4 patients, single intravenous doses of 50 to 150 mg reduced premature atrial beats greater than or equal to 90% for 2 to 4 h. Oral doses of 75 to 200 mg twice daily induced a mean arrhythmia reduction of greater than or equal to 80% in 5 out of 9 patients during a 24-h electrocardiographic recording compared with a baseline period of 48 h. No significant side-effects occurred. The results indicate that pirmenol effectively suppresses premature atrial complexes, which may be of value in the prevention of supraventricular tachyarrhythmias.

Administration, Oral↗
PubMed2004

Prediction of paroxysmal atrial fibrillation by analysis of atrial premature complexes.

Currently, no reliable method exists to predict the onset of paroxysmal atrial fibrillation (PAF). We propose a predictor that includes an analysis of the R-R time series. The predictor uses three criteria: the number of premature atrial complexes (PAC) not followed by a regular R-R interval, runs of atrial bigeminy and trigeminy, and the length of any short run of paroxysmal atrial tachycardia. An increase in activity detected by any of these three criteria is an indication of an imminent episode of PAF. Using the Physionet database of the Computers in Cardiology 2001 Challenge, the predictor achieved a sensitivity of 89% and a specificity of 91%.

Algorithms↗
PubMed2002

Biatrial multisite mapping of atrial premature complexes triggering onset of atrial fibrillation.

Pulmonary veins are considered to be the most common origin of the focal activity that triggers the onset of atrial fibrillation (AF). However, little is known about the importance of ectopic activity located outside the pulmonary veins. This study included 45 patients (8 women and 37 men, mean age 55 +/- 12 years) with paroxysmal (n = 25) and persistent (n = 20) AF in whom multisite mapping of the right and left atria was performed using a 64-electrode basket catheter (n = 21) or a noncontact mapping system (n = 24). Spontaneous or orciprenaline-induced atrial premature complexes (APCs) were mapped. In all, 94 AF onsets from 38 distinct foci in 30 patients were observed and analyzed. Of these foci, 20 (53%) were located in pulmonary veins and 18 (47%) were located outside the pulmonary veins in other parts of the atria. In 22 patients (73%), AF was reproducibly induced by APCs from a single focus (59 episodes). In 8 patients (27%), AF originated from 2 distinct foci (35 episodes). Additionally, 20 of 30 patients (67%) who developed AF had APCs in different locations not inducing AF. APCs inducing AF had shorter coupling intervals than APCs not inducing AF (307 +/- 54 vs 409 +/- 76 ms, p <0.001). This study showed that 47% of ectopic foci triggering the onset of AF were located outside the pulmonary veins in extravenous parts of the left atrium and the right atrium, and 27% of patients had AF onsets of bifocal origin. These data challenge the current opinion that extrapulmonary foci play a minor role in inducing AF.

Atrial Fibrillation↗
PubMed2004

Turbulence slope after atrial premature complexes is an independent predictor of mortality in survivors of acute myocardial infarction.

INTRODUCTION: Heart rate turbulence is a potent postinfarction risk predictor that originally was investigated when it was triggered by ventricular premature complexes. Similar heart rate response is present after atrial premature complexes. "Atrial" turbulence slope (TSA) moderately correlates with "ventricular" turbulence slope (TSV). This study investigated the value of TSA assessed in 24-hour Holter recordings for postinfarction risk stratification. METHODS AND RESULTS: Predictive power of TSA was investigated in the placebo arm of the European Myocardial Infarction Amiodarone Trial, which enrolled patients surviving acute myocardial infarction with left ventricular ejection fraction (LVEF) < or =40%. Of 633 patients with available 24-hour Holter recordings, 87 died during the follow-up period of 662 +/- 105 days. The same methodology was used to calculate TSA and TSV. TSA was significantly lower in nonsurvivors compared to survivors (2.0 +/- 2.7 vs 3.0 +/- 3.3 msec/RR, P = 0.014). TSA< or =0.8 msec/RR was associated with relative risk all-cause mortality of 2.5 (95% confidence interval 1.6-3.9, P = 0.000046). In a multivariate Cox regression model including age, LVEF, QRS duration, mean RR interval, heart rate variability index, presence of nonsustained ventricular tachycardia, and TSV, TSA remained a significant predictor of total mortality with relative risk of 2.0 (95% confidence interval 1.2-3.4, P = 0.014). CONCLUSION: TSA is a significant and independent predictor of all-cause mortality in postinfarction patients with left ventricular dysfunction.

Aged↗
PubMed2005

Premature atrial complex with P'R prolongation indicates multiple atrioventricular nodal pathways.

BACKGROUND: The goal of the present study was to test if ambulatory Holter recordings can predict the electrophysiologic study (EPS) findings in patients with supraventricular tachycardia (SVT). METHODS AND RESULTS: The study involved 110 patients with SVT who underwent Holter recording, and then EPS. The hypotheses were that (1) a P'R interval of premature atrial complexes (PACs) between 280 and 400 ms in the Holter recordings predicted dual atrioventricular nodal (AVN) pathways, (2) P'R interval >400 ms predicted triple or more AVN pathways, and (3) SVT initiated by a single PAC suggested easy SVT induction during the EPS. The EPS revealed dual AVN pathways in 14 (93%) of 15 patients with P'R intervals between 280 and 400 ms on the Holter recordings, and triple or more AVN pathways in 18 (90%) of 20 patients with P'R intervals >400 ms. In addition, a single extrastimulus easily induced SVT during the EPS in 11 (85%) of 13 patients in whom SVT was initiated by a single PAC during Holter recording. CONCLUSION: The ambulatory Holter recording criteria specifically predicted the EPS findings, thereby providing useful advance information.

Aged↗
PubMed2004

ECG criteria for localizing the pulmonary vein origin of spontaneous atrial premature complexes: validation using intracardiac recordings.

We have shown that pacemapping from each of the pulmonary veins reveals unique surface ECG characteristics. However, application of these criteria to spontaneous atrial premature complexes is often difficult because of obscuration by the prior T wave. We hypothesized that the pulmonary vein of origin of spontaneous atrial premature complexes can be determined by measuring characteristics of the P wave whether or not the P wave was superimposed on the prior T wave. We analyzed 58 spontaneous atrial premature complexes of known pulmonary vein origin in 30 patients referred for atrial fibrillation ablation. The origin of all the atrial premature complexes was documented by detailed, intracardiac multipolar catheter mapping. Based on previous work, the criteria for distinguishing right-sided from left-sided pulmonary vein origin of atrial premature complex includes: (1) P wave duration < 120 ms; (2) P wave amplitude in lead I > 0.05 mV; and (3) P wave amplitude in leads II/III > 1.25. The criteria to separate superior from inferior pulmonary veins included the sum of the P wave amplitude in all the inferior leads greater than 0.3 mV. The combination of the P wave duration < 120 ms and the ratio of the P wave amplitude in leads II/III > 1.25, distinguished right-sided from left-sided pulmonary vein origin of spontaneous atrial premature complexes with a sensitivity of 82% and specificity of 100%. The sum of the P wave amplitude in leads II, III, and aVF > 0.3 mV distinguished superior from inferior pulmonary vein of origin with a sensitivity of 39% and specificity of 73%. The pulmonary vein origin of spontaneous atrial premature complexes can often be localized using careful quantitative analysis of the surface ECG despite superimposition of the P wave upon the T wave. Separation of right-sided from left-sided pulmonary vein origin of spontaneous atrial premature complexes can be determined with good specificity and sensitivity, while the ability to distinguish inferior from superior pulmonary vein origin is limited.

Atrial Fibrillation↗
PubMed2001

Correlation of spontaneous and induced premature atrial complexes initiating atrial fibrillation in humans: electrophysiologic parameters for guiding therapy.

INTRODUCTION: The low frequency of spontaneous premature atrial contractions (PACs) may be an impediment to mapping and ablation of atrial fibrillation (AF). It has been shown that PACs following external or internal cardioversion of AF can initiate AF. If this method could reproducibly induce PACs from the same location as spontaneous PACs, it would be clinically significant. High-resolution noncontact mapping can map a single beat, should help identify the sites of spontaneously occurring PACs and PACs induced following cardioversion of spontaneous or induced AF, and could help correlate the trigger sites for AF induction. METHODS AND RESULTS: Twelve patients (8 men and 4 women; mean age 49+/-10 years) with spontaneous PACs were included in the study. In all patients, AF was induced and subsequently cardioverted to assess and map isolated PACs or PACs that induced AF. Using the EnSite 3000 noncontact mapping system, mapping was performed of spontaneously occurring isolated PACs and PACs that induced AF and PACs (both with and without AF) that occurred on at least two different occasions following cardioversion. The locations of the spontaneous and the induced PACs were similar; 97% of induced PACs came from the same locations as those of spontaneous PACs (P = 0.5). Radiofrequency lesions guided by this mapping technique were delivered at 14 pulmonary vein sites. Following a single ablation attempt during a mean follow-up of 19+/-4 weeks, 42% of the patients were in sinus rhythm and drug-free, whereas an additional 24% of patients could be maintained in sinus rhythm on drugs that had failed before. CONCLUSION: There is a high degree of correlation between spontaneous and induced PACs as the trigger sites for AF initiation. Cardioversion of spontaneous or induced AF could be used as an electrophysiologic parameter for guiding therapy.

Adult↗
PubMed2005

Arrhythmias after orthotopic heart transplantation.

BACKGROUND: Arrhythmias frequently occur after orthotopic heart transplantation (OHT). METHODS AND RESULTS: The most common are ventricular premature complexes, atrial premature complexes, sinus or junctional bradycardia, atrial fibrillation, and atrial flutter, all of which have varying clinical significance depending on associated or causative conditions. Unique etiologic factors such as allograft rejection, transplant coronary artery disease, and altered anatomy and autonomic nervous system changes require that arrhythmias be treated differently after OHT compared with the general population. CONCLUSION: The potentially severe ramifications of allograft rejection and coronary artery disease make treatment of these disorders in the setting of arrhythmias as important as treating the arrhythmias themselves. At the same time, autonomic denervation and altered anatomy after transplantation complicate drug and device therapies.

Arrhythmias, Cardiac↗
PubMed2001

Computer-assisted ECG interpretation for confirmation of premature atrial complexes.

UNLABELLED: Current programs for computerized ECG analysis are not interactive. We developed custom software for computer-assisted ECG interpretation that functioned interactively with an observer directing the computerized process. The software was first used for recognition of PACs superimposed on ST-T waveforms. The interactive process included 6 steps. 1) The computer displayed the 12-lead ECG and the user selected the most frequent QRS-T waveforms for averaging. 2) The computer generated and displayed the averaged QRS-T waveform. 3) The user selected waveforms suspected to have PACs superimposed on the ST-T segments. 4) The computer generated and displayed the difference waveform by subtracting the average waveform from the suspect waveforms. 5) The user recognized and p-waves in the difference waveform and marked the onset and offset by positioning the cursor and clicking. 6) The computer then measured p-wave amplitudes, durations, and areas and displayed the recognized p-wave. The program was developed using digital data from 2 ECGs and tested on 39 ECGs with suspected PACs and 26 control ECGs. RESULTS: The software and user interaction recognized 79 PACs in the suspect group. Control ECGs were analyzed using 3 complexes with the same leads and onsets as the test group. Of the 79 PACs found in the suspect group, mean values included an area under the curve of 4.0 +/- 3.2 microV-s for the test group versus 0.4 +/- 0.4 microV-s for the control (P < 0.001) and peak-to-trough voltage amplitudes of 104 +/- 66 microV versus 15 +/- 7 microV for the control (P < 0.001). The average time of onset of the premature complexes was 282 +/- 120 msec, and their duration was 100 +/- 28 msec. CONCLUSION: Custom software combined the superior human pattern recognition with the digital signal processing of the computer. This enhanced recognition of ectopic atrial activity.

Atrial Premature Complexes↗
PubMed1985

Endless loop tachycardia started by an atrial premature complex in a patient with a dual chamber pacemaker.

In a patient with a dual chamber pacemaker that senses in both the atrium and ventricle (VDD, DDD), a ventricular depolarization temporally displaced from a P wave can cause retrograde atrial activation and initiate an endless loop pacemaker-mediated tachycardia. A case in which an endless loop tachycardia was initiated by an end-diastolic atrial premature complex is reviewed. Retrograde conduction occurred because of the change in the temporal relation of atrial sensing and atrioventricular (AV) node depolarization. The implanted pacemaker did not have the capability of atrial refractory programmability. Atrial refractory interval extension, which occurs in this model after a ventricular premature complex to protect against a retrograde P wave, was not invoked since the tachycardia was begun by an atrial rather than a ventricular premature complex. The tachycardia was controlled by shortening the programmable AV delay. The mechanism of tachycardia induction and its management are outlined. Atrial refractory programmability is required in all VDD or DDD pacemakers.

Aged↗
PubMed2001

Impact of consistent atrial pacing algorithm on premature atrial complexe number and paroxysmal atrial fibrillation recurrences in brady-tachy syndrome: a randomized prospective cross over study.

AIM OF THE STUDY: The Consistent Atrial Pacing (CAP) algorithm has been designed to achieve a high percentage of atrial pacing to suppress paroxysmal atrial fibrillation. The aim of our study was to compare the impact of DDDR+CAP versus DDDR pacing on paroxysmal atrial fibrillation recurrences and triggers in patients with Brady-Tachy Syndrome. METHODS: 61 patients, 23 M and 38 F, mean age 75+/-9 y, affected by Brady-Tachy Syndrome, implanted with a DDDR pacemaker, were randomized to DDDR or DDDR+CAP pacing with cross over of pacing modality after 1 month. RESULTS: 78 % of patients in DDDR pacing and 73 % in DDDR + CAP pacing (p=n.s.) were free from symptomatic paroxysmal atrial fibrillation recurrences. During DDDR+CAP pacing, the atrial pacing percentage increased from 77+/-29 % to 96+/-7 % (p<0.0001). Automatic mode switch episodes/day were 0.73+/-1.09 in DDDR and 0.79+/-1.14 (p=n.s.) in DDDR+CAP. In patients with less than 50 % of atrial pacing during DDDR, automaticmode switch episodes/day decreased during DDDR+CAP from 1.13+/-1.59 to 0.23+/-0.32 (p<0.05) and in patients with less than 90 % from 1.23+/-1.27 to 0.75+/-1.10 (p<0.001). The number of premature atrial complexes per day decreased during DDDR + CAP from 2665+/-4468 to 556+/-704 (p<0.02). CONCLUSION: CAP algorithm allowed continuous overdrive atrial pacing without major side effects. Triggers of paroxysmal atrial fibrillation induction, such as premature atrial complexes, were critically decreased. Paroxysmal atrial fibrillation episodes were reduced in patients with atrial pacing percentage lower than 90 % during DDDR pacing.

Aged↗
PubMed1984

Interpreting an ECG. Atrial premature complex.

When APCs are symptomatic or are a potential trigger for supraventricular tachycardia or atrial fibrillation, suppressive therapy with beta-blocking drugs or type I antiarrhythmic agents is indicated. If APCs are infrequent and produce no symptoms, attention to possible provocative factors--excess tobacco or caffeine, or drugs (eg, sympathomimetic amines, monoamine oxidase inhibitors, tricyclic antidepressants)--is all that is required.

Adrenergic beta-Antagonists↗