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Biomedical subjects

Jitendra K Vohra

Publications and source records attributed to Jitendra K Vohra.

9 recordsLinked to original sources

Reversal of atrial mechanical dysfunction after cardioversion of atrial fibrillation: implications for the mechanisms of tachycardia-mediated atrial cardiomyopathy.

BACKGROUND: Atrial mechanical "stunning" develops after cardioversion of atrial fibrillation (AF) and is implicated in the genesis of thromboembolic complications. However, the mechanisms responsible for this phenomenon are poorly understood. Whether atrial mechanical dysfunction caused by AF can be reversed by pacing at increased rates or by pharmacological agents is unknown. METHODS AND RESULTS: Twenty-six patients with AF undergoing cardioversion were dichotomized prospectively on the basis of the duration of arrhythmia as short-duration (1 to 6 months) or long-duration (> or =3 years) AF. Left atrial appendage emptying velocities (LAAEVs) and spontaneous echocardiographic contrast (LASEC) were assessed by transesophageal echocardiography during AF, after reversion to sinus rhythm, during atrial pacing at cycle lengths of 750 to 250 ms, after a postpacing pause, and with isoproterenol. In patients with short-duration AF, LAAEV decreased (42.0+/-2.7 to 18.5+/-2.0 cm/s; P<0.0001) and LASEC increased (0.9+/-0.3 to 2.2+/-0.3; P<0.01) with termination of AF; pacing increased LAAEV (48.3+/-4.1 cm/s; P<0.0001) and decreased LASEC (1.5+/-0.3; P<0.01); isoproterenol increased LAAEV (73.3+/-7.8 cm/s; P<0.0001) and decreased LASEC (0.3+/-0.2; P<0.01); and the postpacing pause increased LAAEV (68.3+/-3.8 cm/s; P<0.0001). In contrast, patients with long-duration AF demonstrated a significantly attenuated response of atrial mechanical function at each time point. With termination of AF, LAAEV decreased (19.1+/-2.6 to 8.2+/-1.0 cm/s; P=0.003) and LASEC increased (2.0+/-0.2 to 3.3+/-0.2; P<0.01); pacing increased LAAEV (18.4+/-2.7 cm/s; P<0.0001) and decreased LASEC (2.3+/-0.2; P<0.01); isoproterenol increased LAAEV (26.1+/-3.9 cm/s; P=NS to equivalent atrial rate) and decreased LASEC (1.0+/-0.3; P<0.01); and the postpacing pause increased LAAEV (27.2+/-2.4 cm/s; P=0.007). CONCLUSIONS: Atrial pacing at increased rates and isoproterenol can reverse atrial mechanical stunning associated with short-duration AF. In contrast, long-duration AF is associated with an attenuated response to these maneuvers. These findings suggest a functional contractile apparatus in the mechanically remodeled atrium caused by AF; however, with longer durations of AF, additional factors may determine atrial mechanical function.

Adrenergic beta-Agonists↗

Electrophysiological and electrocardiographic characteristics of focal atrial tachycardia originating from the pulmonary veins: acute and long-term outcomes of radiofrequency ablation.

BACKGROUND: The objective of this study was to describe the electrophysiological characteristics, anatomic distribution, and long-term outcome after focal ablation (RFA) of pulmonary vein (PV) atrial tachycardia (AT). Both atrial fibrillation (AF) and AT may be due to a rapidly firing focus in the PVs. Whether these represent two aspects of the same process is unknown. METHODS AND RESULTS: Twenty-seven patients with 28 PV(16%) ATs of a consecutive series of 172 undergoing RFA for focal AT are reported. The mean age was 39+/-16 years, with symptoms for 9+/-14 years resistant to 1.7+/-0.8 medications. AT occurred spontaneously or with isoproterenol in all patients and was not inducible with PES in any. The distribution of PV ATs was right superior PV, 11; left superior PV, 11; left inferior PV, 5; and right inferior PV, 1; 26of 28 foci (93%) were ostial. RFA was successful in 28 of 28 PV ATs acutely. RFA was focal in 25 of 28, with PV isolation of a single target vein in 3. There were 4 recurrences at a mean of 3.3 months. Repeat RFA was performed in all 4 and successful in 3 of 4. All but one recurrence occurred from the same site. Long-term success was achieved in 26 of 27 (96%) patients at mean follow-up of 25+/-22 months. No patients have had subsequent development of AF or AT from a different site. CONCLUSIONS: PV AT has a distribution similar to PV AF, with a propensity to upper veins. However, the majority of foci are ostial, and only a small percentage occur from deep in the PV. Focal RFA is associated with high long-term success, with freedom from both AT from other sites and from AF. PV AT is a localized process and therefore may be different from PV AF.

Adolescent↗

Electrical remodeling of the atria in congestive heart failure: electrophysiological and electroanatomic mapping in humans.

BACKGROUND: Atrial fibrillation (AF) frequently complicates congestive heart failure (CHF). However, the electrophysiological substrate for AF in humans with CHF remains unknown. We evaluated the electrophysiological and electroanatomic characteristics of the atria in patients with CHF. METHODS AND RESULTS: Twenty-one patients (aged 53.7+/-13.6 years) with symptomatic CHF (left ventricular ejection fraction 25.5+/-6.0%) and 21 age-matched controls were studied. The following were evaluated: effective refractory periods (ERPs) from the high and low lateral right atrium (LRA), high septal right atrium, and distal coronary sinus (CS); conduction time along the CS and LRA; corrected sinus node recovery times; P-wave duration; and conduction at the crista terminalis. In a subset, electroanatomic mapping was performed to determine atrial activation, regional conduction velocity, double potentials, fractionated electrograms, regional voltage, and areas of electrical silence. Patients with CHF demonstrated an increase in atrial ERP with no change in the heterogeneity of refractoriness, an increase of atrial conduction time along the LRA and the CS, prolongation of the P-wave duration and corrected sinus node recovery times, and greater number and duration of double potentials along the crista terminalis. Electroanatomic mapping demonstrated regional conduction slowing with a greater number of electrograms with fractionation or double potentials, associated with areas of low voltage and electrical silence (scar). Patients with CHF demonstrated an increased propensity for AF with single extrastimuli, and induced AF was more often sustained. CONCLUSIONS: Atrial remodeling due to CHF is characterized by structural changes, abnormalities of conduction, sinus node dysfunction, and increased refractoriness. These abnormalities may be responsible in part for the increased propensity for AF in CHF.

Atrial Function↗

Focal atrial tachycardia arising from the mitral annulus: electrocardiographic and electrophysiologic characterization.

OBJECTIVES: The study was done to characterize the electrocardiographic and electrophysiologic features of focal atrial tachycardia originating at the mitral annulus (MA). BACKGROUND: Though the majority of left atrial tachycardias originate around the ostia of the pulmonary veins, only isolated reports have described focal tachycardia originating from the MA. METHODS: Seven patients of a consecutive series of 172 patients undergoing radiofrequency ablation for focal atrial tachycardia are reported. Electrophysiologic study involved catheters positioned along the coronary sinus (CS), crista terminalis (CT), His bundle, and a mapping/ablation catheter. RESULTS: All seven patients had tachycardia foci originating from the superior region of the MA in close proximity to the left fibrous trigone and mitral-aortic continuity. These foci demonstrated a characteristic P-wave morphology and endocardial activation pattern. The P-wave morphology in the precordial leads typically showed a biphasic pattern, with an inverted component followed by an upright component. The P-wave was consistently of low amplitude in the limb leads. Earliest endocardial activity occurred at the His bundle region in all seven patients. In general, CS activation was proximal to distal, and mid-CT activation was earlier than high or low CT. Ablation was successful at the superior aspect of the MA in all patients. CONCLUSIONS: The MA is an unusual but important site of origin for focal atrial tachycardia, with a propensity to be localized to the superior aspect. It can be suspected as a potential anatomic site of tachycardia origin from analysis of P-wave morphology and the atrial endocardial activation sequence map. Using mapping targeted to anatomic structures achieved a high success rate for ablation.

Adult↗

Effect of chronic right atrial stretch on atrial electrical remodeling in patients with an atrial septal defect.

BACKGROUND: Adults with an atrial septal defect (ASD) frequently develop late atrial arrhythmias. We sought to characterize the pattern and persistence of atrial electrical remodeling caused by chronic right atrial (RA) stretch in this group. METHODS AND RESULTS: Thirteen ASD patients without atrial arrhythmia (42+/-10 years old; RA volume, 65+/-16 mL) and 17 normal control subjects (44+/-11 years old; RA volume, 38+/-8 mL) had electrophysiological study to measure (1) atrial effective refractory period (AERP) from the low lateral/high lateral/high septal RA and distal coronary sinus (CS), (2) dispersion of AERP, (3) lateral-RA and CS conduction time during constant pacing, (4) conduction delay across the crista terminalis measuring the number of crista catheter bipoles (0-10) recording discrete double potentials during pacing, (5) corrected sinus node recovery time, and (6) P-wave duration. After ASD closure (8.3+/-5.6 months), follow-up echo studies (n=12) and electrophysiological study (n=4) were performed. The low-lateral AERP, P-wave duration, sinus node recovery time, and extent of conduction delay across the crista terminalis were significantly greater in ASD patients. No differences were found for other measured electrophysiological study parameters. At follow-up, there was incomplete resolution of RA volume (47+/-12 mL; P<0.01 versus before surgery), a trend toward shortening of the AERP at the lateral RA and an increase at the distal CS and high septal RA, but persisting extensive, widely split crista double potentials. CONCLUSIONS: Chronic RA stretch because of ASD causes electrical remodeling with modest increases in RA ERP, conduction delay at the crista terminalis, and sinus node dysfunction. Conduction delay at the crista terminalis persists beyond ASD closure and may contribute to the long-term atrial arrhythmia substrate in this condition.

Adult↗

Pacemaker ventricular block.

Pacemaker ventricular block is a rare and poorly recognized electrocardiographic abnormality usually identified in terminally ill pacemaker patients. Because the patient is frequently moribund and the phenomenon transient, it is probably overlooked and not well documented. It is characterized by an altered temporal relationship between the pacemaker stimulus artifact and the subsequent paced QRS. The most common presentation is a delay or latency between the stimulus artifact and the QRS called first-degree pacemaker ventricular block. This can then deteriorate to periodic episodes of failure to capture the myocardium referred to as second-degree pacemaker ventricular block that may manifest as a classical Wenckebach or higher levels of block. Any further deterioration results in a third-degree pacemaker ventricular block, which is failure to capture the ventricle and asystole. This article describes electrocardiographic examples of this phenomenon.

Aged↗

Phased-array intracardiac echocardiography for defining cavotricuspid isthmus anatomy during radiofrequency ablation of typical atrial flutter.

INTRODUCTION: Cavotricuspid isthmus (CTI) topography includes ridges, pouches, recesses, and trabeculations. These features may limit the success of radiofrequency ablation (RFA) of typical atrial flutter (AFL). The aim of this study was to assess the utility of phased-array intracardiac echocardiography (ICE) for imaging the CTI and monitoring RFA of AFL. METHODS AND RESULTS: Fifteen patients (mean age 64 +/- 9 years) underwent ICE assessment (imaging frequency 7.5-10 MHz) before and after RFA of AFL. The ICE catheter was positioned at the inferior vena cava-right atrial junction and the following parameters were measured: (1) CTI length from the tricuspid valve to the eustachian ridge; (2) extent of CTI pouching; and (3) thickness pre/post RFA of the anterior, mid, and posterior CTI. CTI length was 35 +/- 6 mm at end-ventricular systole but shorter (30 +/- 6 mm) and more pouched at end-ventricular diastole (P = 0.02). A pouch or recess was seen in 11 of 15 patients (mean depth 6 +/- 2 mm). The septal CTI was more pouched than the lateral CTI, but the latter had more prominent trabeculations. Trabeculations were seen in 10 of 15 patients, and at these locations the CTI was 4.6 +/- 1 mm thick. Anterior, mid, and posterior CTI thickness pre-RFA was 4.1 +/- 0.8, 3.3 +/- 0.5, and 2.7 +/- 0.9 mm, respectively (P < 0.001 by analysis of variance). ICE guided RFA away from unfavorable CTI features (recesses/thick trabeculations). RFA applications created discrete CTI lesions that coalesced, forming diffuse CTI swelling. Post-RFA thickness was as follows: anterior 4.8 +/- 0.8 mm (P = NS vs pre); mid 3.8 +/- 0.8 mm (P = 0.05 vs pre); and posterior 3.8 +/- 0.8 mm (P = 0.02 vs pre). CONCLUSION: Phased-array ICE permits novel real-time CTI imaging with excellent endocardial resolution and may facilitate RFA of AFL.

Aged↗

Reversal of atrial mechanical stunning after cardioversion of atrial arrhythmias: implications for the mechanisms of tachycardia-mediated atrial cardiomyopathy.

BACKGROUND: Atrial mechanical stunning develops on termination of chronic atrial arrhythmias and is implicated in the genesis of thromboembolic complications after cardioversion. The mechanisms responsible for atrial mechanical stunning are unknown. The effects of atrial rate, isoproterenol, and calcium on atrial mechanical function in patients with atrial stunning have not been evaluated, and it is not known if atrial stunning can be reversed. METHODS AND RESULTS: Thirty-five patients with chronic atrial flutter (AFL) undergoing radiofrequency ablation were studied. Fifteen patients in sinus rhythm undergoing ablation for paroxysmal AFL were studied as control for effects of the procedure. Left atrial appendage emptying velocities (LAAEVs) and spontaneous echocardiographic contrast (LASEC) were assessed by transesophageal echocardiography during AFL, after reversion to sinus rhythm, during atrial pacing at cycle lengths of 750 to 250 ms, after a postpacing pause, and with isoproterenol or calcium. With termination of AFL, LAAEV decreased from 59.0+/-3.7 cm/s to 18.8+/-1.4 cm/s (P<0.0001) and LASEC grade increased from 0.9+/-0.1 to 2.2+/-0.2 (P<0.0001). Pacing increased LAAEV to a maximum of 38.4+/-3.2 cm/s (P<0.0001) and reduced LASEC grade to 1.9+/-0.2 (P=0.005). Isoproterenol and calcium reversed atrial mechanical stunning with LAAEV increasing to 89.3+/-12.6 cm/s (P=0.0007) and 50.2+/-10.5 cm/s (P=0.005), respectively, and LASEC grade decreasing to 0.2+/-0.1 (P=0.001) and 1.4+/-0.2 (P=0.01), respectively. The postpacing pause increased LAAEV to 69.3+/-3.7 cm/s (P<0.0001). No change in LAAEV was observed in the paroxysmal AFL group. CONCLUSION: Atrial mechanical stunning can be reversed by pacing at increased rates and through the administration of isoproterenol or calcium. These findings suggest a functional contractile apparatus in the mechanically remodeled atrium as a result of chronic atrial flutter.

Atrial Flutter↗

Pulmonary vein paced activation sequence mapping: comparison with activation sequences during onset of focal atrial fibrillation.

INTRODUCTION: Atrial fibrillation (AF) may originate from a single focus, with the vast majority observed within the pulmonary veins. To facilitate mapping, we hypothesized that there would be a characteristic right atrial endocardial activation sequence pattern associated with pacing and spontaneous focal activity from each of the four pulmonary veins. METHODS AND RESULTS: In 10 patients with focal AF, a standardized set of catheters was positioned in the right atrium. These included a 20-pole catheter along the crista terminalis, a decapolar catheter in the coronary sinus (CS), and a His-bundle electrode. Pacing (700 and 300 msec) was performed with a mapping catheter from each of the four pulmonary veins. Activation sequence maps were created by measurement of activation times to each of the recording bipoles with the proximal CS bipole as the arbitrary reference point. Similar maps were constructed for the activation sequence of the pulmonary vein ectopic that initiated AF. There was a characteristic right atrial activation map created by pacing each pulmonary vein that corresponded closely with the map from the same pulmonary vein during initiation of focal AF. The pulmonary vein of origin could be distinguished on the basis of this characteristic pattern and some stereotypic observations. CS activation occurred proximal to distal for right pulmonary veins and distal to proximal for left pulmonary veins. Significant differences in activation timing between the CS and crista terminalis differentiated upper from lower pulmonary veins. CONCLUSION: There is a characteristic right atrial activation map for activity arising from each of the four pulmonary veins that corresponded closely with the map from the same pulmonary vein during initiation of focal AF. These findings may facilitate mapping and ablation of focal AF.

Adult↗