Biomedical subjects
Publications and source records attributed to Jonathan M Kalman.
This study reports that patients with large body mass indexes (BMIs) and long-duration atrial fibrillation (AF) have greater defibrillation thresholds than patients with normal BMIs and AF of short duration. BMI is an independent predictor of defibrillation thresholds in patients with longer duration AF in whom external cardioversion has failed.
OBJECTIVES: The purpose of this study was to characterize the pattern of atrial remodeling seen with human aging. BACKGROUND: Atrial fibrillation (AF) occurs in 3% to 4% of the population over 65 years of age. It is associated with thromboembolic complications, worsening heart failure, and increased mortality, yet the electrical and structural remodeling that occurs with human aging remains unknown. METHODS: Thirteen patients (66.4 +/- 1.7 years) > or =60 years (group A), 13 patients (50 +/- 2.1 years) age 31 to 59 years (group B), and 15 patients (24.7 +/- 1.0 years) < or =30 years (group C) underwent conventional electrophysiologic studies and electroanatomic mapping. We measured atrial refractoriness (ERP) at the distal coronary sinus (CS); low and high lateral right atrium (LRA) and the high septal right atrium at 600, 500, and 400 ms; maximum corrected sinus node recovery time (CSNRT); P-wave duration (PWD); conduction time (CT) along the CS and LRA; and discrete double potentials (DP) along the crista. RESULTS: Aging was associated with an increase in atrial ERP, prolonged CT along the CS, increased PWD and CSNRT. There was no significant change in dispersion of refractoriness or rate adaptation. Electroanatomic mapping revealed diffuse areas of low voltage with regional conduction slowing. Both techniques demonstrated a greater number of DPs and fractionated signals along the crista terminalis with aging. CONCLUSIONS: Aging is associated with regional conduction slowing, anatomically determined conduction delay at the crista, and structural changes that include areas of low voltage. In addition, impairment of sinus node function and an increase in atrial ERP occurred with aging. This electrical and structural remodeling may explain the increased propensity to AF with aging.
BACKGROUND: The normal sinus pacemaker complex is an extensive structure within the right atrium. We hypothesized that patients with sinus node disease (SND) would have evidence of diffuse atrial abnormalities. METHODS AND RESULTS: Sixteen patients with symptomatic SND and 16 age-matched controls were studied. The following were evaluated: effective refractory periods (ERPs) from the high and low lateral right atrium (RA), high septal RA, and distal coronary sinus (CS); conduction time along the CS and lateral RA; P-wave duration; and conduction at the crista terminalis. Electroanatomic mapping was performed to define the sinus node complex and determine regional conduction velocity, double potentials, fractionated electrograms, regional voltage, and areas of electrical silence. Patients with SND demonstrated significant increase in atrial ERP at all right atrial sites, increased atrial conduction time along the lateral RA and CS, prolongation of the P-wave duration, and greater number and duration of double potentials along the crista terminalis. Electroanatomic mapping demonstrated the sinus node complex in SND to be more often unicentric, localized to the low crista terminalis at the site of the largest residual voltage amplitude. There was significant regional conduction slowing with double potentials and fractionation associated with areas of low voltage and electrical silence (or scar). CONCLUSIONS: SND is associated with diffuse atrial remodeling characterized by structural change, conduction abnormalities, and increased right atrial refractoriness. There was a change in the nature of sinus pacemaker activity with loss of the normal multicentric pattern of activation, caudal shift of the pacemaker complex, and abnormal and circuitous conduction around lines of conduction block.
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We report an unusual case of bundle branch reentrant tachycardia, in a patient with normal left ventricular function, cured by radiofrequency catheter ablation. However, the long-term prognosis of these patients is uncertain. We discuss the indications for an implantable defibrillator in this group.
INTRODUCTION: Focal atrial fibrillation (AF) may initiate with an irregular rapid burst of atrial ectopic (AE) activity from a pulmonary vein (PV) focus, but how AF is maintained it is not known. The crista terminalis (CT) is an important line of block in atrial flutter (AFL), but its role in AF has not been determined. The aim of this study was to examine the conduction properties of the CT during onset of AF. METHODS AND RESULTS: In 10 patients (mean age 38 +/- 8 years), we analyzed conduction across the CT during onset of focal AF from an arrhythmogenic PV and during pacing from the same PV at cycle lengths of 700 and 300 ms. A 20-pole catheter was positioned on the CT using intracardiac echocardiography. In 10 control patients with no history of AF, we analyzed conduction across the CT during pacing from the distal coronary sinus at 700 and 300 ms. In all 10 AF patients, AF was initiated with 1 to 9 AE beats (median 5) from a PV. During sinus rhythm, there were no split components (SC) recorded on the CT. During PV AE activity, discrete SC were recorded on the CT in all patients over 6.3 +/- 0.9 bipoles (3.7 +/- 0.3 cm). Maximal splitting of SC was 66 +/- 31 ms (37-139). There was an inverse relationship between AE coupling intervals and the degree of splitting between SC in all patients. Degeneration to AF was preceded by progressive decrement across the CT. SC were recorded during PV pacing at 700 and 300 ms (maximal distance between SC of 24 +/- 3 ms and 43 +/- 5 ms, respectively, P < 0.001). Maximum SC at CT in controls was 13 +/- 8 ms at 700 ms (P = 0.06 vs AF patients) and 16 +/- 9 ms at 300 ms (P < 0.01 vs AF patients). CONCLUSION: (1) These observations provide evidence of anisotropic, decremental conduction across the CT during onset of focal AF and during pacing from the same PV. A line of functional conduction block develops along this anatomic structure (CT). Whether this line of block acts as an initiator of AF or simply contributes passively to nonuniform fibrillatory conduction is unknown. (2) In some patients with focal AF, development of conduction block along the CT may provide a substrate for typical AFL.
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Recent years have seen an enormous amount of experimental and clinical research into role of the pulmonary veins (PVs) in atrial fibrillation (AF). Advanced imaging techniques have confirmed the findings of earlier postmortem studies and added further dimension to our knowledge of PV anatomy. Such work is vital for an effective approach to successful ablation of AF. Detailed mapping studies suggest that reentry within the PVs is most likely responsible for their arrhythmogenicity, although focal or triggered activity cannot be excluded. Further work also implicates the posterior left atrium in the genesis of AF. Investigation into the interplay between the PVs and left atrium has led to a reevaluation of the mechanisms underlying AF and suggests that the PVs may play a role in both the initiation and maintenance of this arrhythmia. In order for electrophysiologists to further develop the technical approach to ablation of AF and improve the clinical outcomes, these crucial issues must be resolved.
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.
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.
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.
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.
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.
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.
We report the case of an accessory pathway in a left inferoposterior diverticulum. The pathway masqueraded as a true left lateral pathway due to the direction of activation over a coronary sinus to left atrium connection. The patient had undergone four prior failed ablation attempts at other institutions using both a transseptal and retrograde approach.
We compared transesophageal and phased-array intracardiac echocardiography (TEE/ICE) for the 2-dimensional and spectral Doppler assessment of left atrial (LA) mechanical function. TEE is commonly used to assess LA body and LA appendage mechanical function in patients who are undergoing radiofrequency ablation of typical atrial flutter. Fifteen patients underwent TEE and ICE imaging before and after ablation of typical atrial flutter. The following parameters were measured: (1) LA appendage emptying velocity and fractional area change, (2) severity of LA spontaneous echo contrast (graded 0 to 4), (3) maximal inflow velocity of the left and right upper pulmonary veins, and (5) maximal mitral valve E- and A-wave inflow velocities in sinus rhythm. Diagnostic quality imaging was achieved in all patients with TEE and ICE. Comparing TEE and ICE, the following absolute values and linear correlation coefficient (R) were obtained: preablation LA appendage emptying velocity: 0.45 +/- 0.21 versus 0.44 +/- 0.21 m/s (r = 0.95, p = <0.001); postablation LA appendage velocity: 0.33 +/- 0.24 versus 0.34 +/- 0.24 m/s (r = 0.97, p <0.001); LA appendage fractional area change: 35.3 +/- 13.7 versus 35.9 +/- 17.1% (r = 0.81, p <0.001); left upper/right upper pulmonary vein inflow velocity: 0.50 +/- 0.17/0.49 +/- 0.18 versus 0.51 +/- 0.17/0.47 +/- 0.20 m/s (r = 0.93/0.90, p <0.001); mitral valve E/A wave: 0.66 +/- 0.14/0.31 +/- 0.14 versus 0.69 +/- 0.17/0.35 +/- 0.23 (r = 0.84/0.97, p <0.002); LA spontaneous echo contrast (pre- and postablation): 1.1 +/- 1.2/1.3 +/- 1.2 versus 1.2 +/- 1.3/1.4 +/- 1.3 (r = 0.92/0.90, p <0.001). No patients were identified with LA appendage thrombus. Thus, TEE and phased-array ICE provided equivalent imaging data with high statistical correlation. ICE may be an imaging alternative to TEE in the evaluation of a "stunned" left atrium.
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.