Catheter-tissue contact force determines atrial electrogram characteristics before and lesion efficacy after antral pulmonary vein isolation in humans.

INTRODUCTION: Electrogram (EGM) characteristics are used to infer catheter-tissue contact. We examined if (a) atrial EGM characteristics predicted CF and (b) compared the value of CF versus other surrogates for predicting lesion efficacy. METHODS AND RESULTS: Twelve paroxysmal AF patients underwent pulmonary vein isolation using radiofrequency (RF) ablation facilitated by a novel CF-sensing catheter. Operators were blinded to CF. EGM amplitude, width, and morphology were measured pre- and post-RF. At each RF site, average CF, force-time integral (FTI), impedance fall, time to impedance plateau, maximum power, catheter tip temperature, and total energy delivered were recorded. An effective lesion was defined based on previously validated EGM criteria for transmural lesions. There was a moderate correlation between CF and EGM amplitude (r = 0.19) and EGM width (r = -0.22). Pre-RF, EGM amplitude, and width had modest to poor discriminative capacity for identifying preablation CF (e.g., EGM amplitude identified CF>20 g with sensitivity and specificity of 67% and 60%, respectively). Preablation CF, FTI, and total energy delivered during RF were the only independent predictors of effective lesion formation. Neither pre-RF EGM amplitude/width nor power, temperature, and impedance changes during RF predicted effective lesion formation. An average CF >16 g or FTI >404 g*s had excellent sensitivity and specificity (>80%) for identifying an effective lesion. CONCLUSIONS: EGM characteristics do not reliably predict either CF before the onset of RF, nor do they predict the likelihood of an effective lesion. CF parameters were superior to power, temperature, and impedance changes during RF in predicting lesion efficacy.

Characterization of catheter-tissue contact force during epicardial radiofrequency ablation in an ovine model.

BACKGROUND: Contact force (CF) during radiofrequency ablation (RFA) is an important determinant of endocardial lesion size with limited data on epicardial RFA and CF. We evaluated CF characteristics using irrigated RFA on the epicardium in an ovine model. METHODS AND RESULTS: In 12 sheep, a 7-F irrigated RFA catheter with CF sensor was introduced via a pericardial incision onto/in parallel with ventricular epicardium. RFA (30 W per 30 second duration) was applied at 5g, 10g, 20g, 40g, and 70g: (1) over left and right ventricular myocardium with or without fat, (2) either directly over or adjacent to a coronary artery, or directly over the phrenic nerve. Force-time integral, lesion dimensions, and coronary artery/phrenic nerve injury were recorded. Lesion size, volume, and force-time integral progressively increased with higher CF (P<0.05). Steam pops occurred with high CF. Epicardial fat had an attenuating effect on RF penetration into myocardium (P<0.05); however, myocardial RF lesions could be created at sites with >3.5 mm epicardial fat. At sites with epicardial fat, each 10g increment in CF led to a 0.6 mm increase in lesion depth, whereas each 1 mm of fat reduced lesion depth into underlying myocardium by 0.7 mm. Extent of acute coronary injury with direct and indirect RFA and phrenic nerve palsy occurrence was proportional to CF. CONCLUSIONS: CF is a determinant of epicardial RF lesion size, steam pops, acute coronary artery injury, and phrenic nerve injury. Although epicardial fat limits lesion size, RFA with high CF can produce small myocardial RF lesions at sites of thick epicardial fat.

Predictive value of impedance changes for real-time contact force measurements during catheter ablation of atrial arrhythmias in humans.

BACKGROUND: Catheter-tissue contact force (CF) determines radiofrequency (RF) ablation lesion size. Impedance changes during RF delivery are used as surrogate markers for CF. The relationship between impedance and real-time CF in humans remains unknown. OBJECTIVES: To determine whether impedance changes have predictive value for real-time CF during catheter ablation of atrial arrhythmias. METHODS: Real-time CF, force-time integral, and impedance were measured in 2265 RF lesions for atrial fibrillation or flutter in 34 patients. Operators were blinded to CF measurements. Impedance preablation, at 5-second intervals for 30 seconds after the RF onset, maximal impedance fall and time to impedance plateau during RF were correlated with CF. Average CF was divided into low (≤20 g), intermediate (21-60 g), and high (>60 g) categories. RESULTS: Preablation impedance poorly correlated with preablation CF (R = .07). Maximal impedance fall modestly correlated with average CF and force-time integral (R = .32 and .37, respectively). There was a large degree of overlap in impedance fall between different CF categories. A maximal impedance fall of 10 Ω could predict average CF of >20 g, with a sensitivity and specificity of 71% and 53% and a positive and negative predictive value of 51% and 49%, respectively. Impedance fall was only able to differentiate between different CF categories ≥15 seconds after the RF onset. Higher CFs moderately correlated with delayed plateau in impedance (R = .41). CONCLUSIONS: Impedance measurements (both baseline and impedance fall) are, at best, moderately efficacious as surrogate markers for predicting real-time catheter-tissue CF. These findings highlight the importance of real-time CF measurements, rather than impedance changes to optimize ablation efficacy.

Prospective characterization of catheter-tissue contact force at different anatomic sites during antral pulmonary vein isolation.

BACKGROUND: Catheter-tissue contact is critical for effective lesion creation. We characterized the contact force (CF) at different anatomic sites during antral pulmonary vein (PV) isolation for atrial fibrillation. METHODS AND RESULTS: Two experienced operators performed PV isolation in 22 patients facilitated by a novel CF-sensing ablation catheter in a blinded fashion. Average CF and force-time integral data from 1602 lesions were analyzed. The left and right PV antra were divided into the following: carina, superior, inferior, anterior, and posterior quadrants for analysis. There was significant variability in CF within and between different PV quadrants (P<0.05). Lowest CF of all left PV sites was at the carina and anterior quadrant, whereas highest CF was at the superior and inferior quadrants (P<0.05). Lowest CF of all right PV sites was at the carina, whereas highest CF was at the anterior and inferior quadrants (P<0.05). When comparing similar PV quadrants on the left versus right (eg, left carina versus right carina), CF was always higher in the right PVs (P<0.05), except at the superior quadrant where CF was similar in the left and right PVs (P=0.19). There was no specific pattern of anatomic distribution of excess CF (P=0.39). CONCLUSIONS: Monitoring of catheter-tissue CF during PV isolation demonstrates significant variability in CF within and between different PV antral sites. Sites of lowest CF were the carina and anterior left PVs and the carina of the right PVs. This information may be important for improving ablation efficacy and clinical outcomes during PV isolation.

Esophageal hematoma after atrial fibrillation ablation: incidence, clinical features, and sequelae of esophageal injury of a different sort.

BACKGROUND: Esophageal hematoma recently has been reported as a form of esophageal injury after atrial fibrillation (AF) ablation, attributed to the use of transesophageal echocardiography (TEE). We sought to determine the incidence, clinical features, and sequelae of this form of esophageal injury. METHODS AND RESULTS: This was a prospective series of 1110 AF ablation procedures performed under general anesthesia (GA) over 9 years. TEE was inserted after induction of GA to exclude left atrial appendage thrombus, define cardiac function, and guide transseptal puncture. The procedural incidence of esophageal hematoma was 0.27% (3/1110 procedures, mortality 0%). Odonyphagia, regurgitation, and hoarseness were the predominant symptoms, with an onset within 12 hours. There was absence of fever and neurological symptoms. Chest computed tomography excluded atrio-esophageal fistula and was diagnostic of esophageal hematoma localized to either the upper esophagus or extending the length of the mid and lower esophagus; endoscopy confirmed the diagnosis. Management was conservative in all cases comprising of ceasing oral intake and anticoagulation. Long term sequelae included esophageal stricture formation requiring dilatation, persistent esophageal dysmotility (mid esophageal hematoma), and vocal cord paralysis, resulting in hoarse voice (upper esophageal hematoma). CONCLUSIONS: Esophageal hematoma is a rare but important differential diagnosis for esophageal injury after TEE-guided AF ablation under GA, and can result in significant patient morbidity. Key clinical features differentiate presentation of esophageal hematoma from that of an atrio-esophageal fistula.

Atrial fibrillation inducibility in the absence of structural heart disease or clinical atrial fibrillation: critical dependence on induction protocol, inducibility definition, and number of inductions.

BACKGROUND: Inducibility of atrial fibrillation (AF) after pulmonary vein isolation has been used to guide additional left atrial ablation in paroxysmal AF. The sensitivity and specificity of AF induction in this setting remains uncertain. We examined the incidence and characteristics of inducible AF in patients without structural heart disease or clinical AF and the effect of different induction protocols on AF inducibility. METHODS AND RESULTS: In 44 patients with supraventricular tachycardia with no history of AF or risk factors for AF, atrial refractoriness and conduction were measured, followed by AF induction attempts (10/patient). Each induction was performed after a waiting time that exceeded twice the duration of induced AF from the preceding induction. AF≥1 minute was considered inducible, and ≥5 minutes as sustained. Burst pacing (at 200 ms for 10 seconds) was compared to decremental pacing (from 200 ms to shortest cycle length, resulting in 1:1 atrial capture for 10 seconds). After 10 inductions, AF was inducible in 49.5%, and sustained in 29.5% of patients. The incidence of both inducible and sustained AF increased with each induction. Apart from male gender, no clinical or electrophysiological features were associated with sustained AF. Decremental pacing was associated with a higher incidence of sustained AF (41.2% versus 14.8%, P=0.049), longer duration of AF (P=0.006), and shorter mean AF cycle length (P<0.001) compared with burst pacing. CONCLUSIONS: Inducible and sustained AF is common in patients in the absence of structural heart disease or clinical AF, and its incidence varies according to gender, method of induction, and number of inductions. There is a direct relationship between AF persistence and number of inductions, which has not reached a plateau after 10 inductions.

Effect of respiration on catheter-tissue contact force during ablation of atrial arrhythmias.

BACKGROUND: Catheter-tissue contact is important for effective lesion creation. OBJECTIVE: To assess the effect of respiration on contact force (CF) during atrial fibrillation and cavotricuspid isthmus (CTI)-dependent atrial flutter ablation. METHODS: Patients undergoing CTI ablation alone (n = 15) and pulmonary vein (PV) isolation alone (n = 12) under general anesthesia were recruited. Lesions were delivered under ventilation (30 seconds) alternating with lesions delivered under apnea (30 seconds) at an adjacent anatomical site at CTI or PV antra. The average force (F(av)), force-time integral (FTI), and force variability were measured in a region-specific manner by using a novel CF-sensing ablation catheter. Operators were blinded to CF data. RESULTS: F(av) and FTI were higher with apnea than with ventilation in all CTI and PV segments (P <.05), an effect attributed to drop in CF with each respiratory swing, resulting in greater force variability during ventilation (P <.05). Low FTI lesions (<500 g) were strongly associated with longer ablation time to achieve bidirectional CTI block (r(2) = .81; P <.001), left PVI (r(2) = .65; P = .009), and right PVI (r(2) = .41; P = .05). Sites with transient CTI block were associated with lower F(av) and FTI than were sites with persistent CTI block (P <.05). Sites of acute PV reconnection were associated with lower F(av) and FTI compared with non-reconnected sites (P <.001). CONCLUSIONS: Catheter-tissue CF is critically influenced by respiration; greater CF is observed with ablation during apnea. Poor CF is implicated in longer ablation time to achieve CTI block or PV isolation and in acute reconnection.

Atrial electrical and structural remodeling associated with longstanding pulmonary hypertension and right ventricular hypertrophy in humans.

INTRODUCTION: Pulmonary hypertension (PH) is common to a range of cardiopulmonary conditions and is associated with atrial arrhythmias. However, little is known of the isolated atrial effects of PH and right atrial dilatation (RA) in humans. To avoid the confounding effects of PH-associated disease states, we performed detailed electrophysiological (EP) and electroanatomic (EA) mapping of the RA in patients with idiopathic PH. METHODS AND RESULTS: Eight PH patients (mean pulmonary arterial [PA] pressure 39.0 ± 15.8 mmHg) and 16 age-matched controls (mean PA pressure 11.5 ± 4.1 mmHg, P < 0.0001) were studied. Corrected sinus node recovery times (cSNRT), atrial effective refractory periods (ERPs), conduction delay at the crista terminalis (CT), and inducibility of atrial fibrillation (AF) were evaluated. EA mapping (pacing cycle length 600 and 300 milliseconds) was performed to determine RA global and regional voltage, conduction velocities, atrial activation times, fractionated electrograms and double potentials. Patients with PH demonstrated a prolongation in cSNRT without significant change in atrial ERP and an increase in AF inducibility. PH was associated with lower tissue voltage (1.8 ± 0.4 mV in PH vs 2.2 ± 0.4 mV in controls, P = 0.02), increased low voltage areas (13.7 ± 8.2% in PH vs 6.2 ± 3.7% in controls, P < 0.01) and the presence of electrically silent areas. Conduction velocities were slower (global 67.3 ± 5.6 cm/s vs 92.8 ± 4.0 cm/s, P < 0.001) and fractionated electrograms and double potentials were more prevalent (14.7 ± 4.4% vs 6.3 ± 4.1, P < 0.01) in PH compared with controls, respectively. CONCLUSION: Idiopathic PH is associated with RA remodeling characterized by: generalized conduction slowing with marked regional abnormalities; reduced tissue voltage; and regions of electrical silence. These changes provide important insights into the isolated effects of PH fundamental to a range of clinical conditions associated with AF.

Electroanatomic remodeling of the left atrium in paroxysmal and persistent atrial fibrillation patients without structural heart disease.

INTRODUCTION: The nature of the atrial substrate thought to contribute toward maintaining atrial fibrillation (AF) outside the pulmonary veins remains poorly defined. Therefore, our objective was to determine whether patients with paroxysmal and persistent AF have an abnormal electroanatomic substrate within the left atrium (LA). METHODS AND RESULTS: Thirty-one patients with AF (17 paroxysmal AF and 14 persistent AF) were compared with 15 age-matched controls with left-sided supraventricular tachycardia (SVT). High-density 3-dimensional electroanatomic maps were created and the LA was divided into 8 segments for regional analysis. Bipolar voltage, conduction, and effective refractory periods (ERPs) of the posterior LA, left atrial appendage (LAA), and distal coronary sinus (CSd) and percentage complex signals were assessed. In the majority of LA regions, compared with controls, AF patients had: (1) lower mean voltage and a higher percentage low voltage; (2) slower conduction; and (3) more prevalent complex signals. Many of these changes were more marked in the persistent than the paroxysmal AF group. CONCLUSIONS: Patients with AF have lower regional voltage, increased proportion of low voltage, slowed conduction, and increased proportion of complex signals compared to controls. Many of these changes are more pronounced in persistent AF patients, suggesting there may be a progressive nature to the changes. Differences occurred in the absence of structural heart disease. These substrate abnormalities provide further insight into the progressive nature of atrial remodeling and the mechanisms involved in maintenance of AF.

Long-term effects of catheter ablation for lone atrial fibrillation: progressive atrial electroanatomic substrate remodeling despite successful ablation.

BACKGROUND: Whether curative ablation can prevent progression of the atrial electroanatomic remodeling associated with atrial fibrillation (AF) is not known. OBJECTIVE: The purpose of this study was to determine whether successful radiofrequency ablation (RFA) of AF can prevent progression of the atrial substrate associated with AF. METHODS: Detailed right atrial electroanatomic maps from 11 patients without apparent structural heart disease undergoing RFA of AF at baseline and ≥6 months following successful RFA were compared to 11 control patients undergoing electrophysiologic evaluation of supraventricular tachycardia. Bipolar voltage, conduction, effective refractory periods (ERPs), and signal complexity were assessed. RESULTS: At baseline compared with the control group, the AF group demonstrated (1) lower voltage (P <.001); (2) slowed conduction (P = .005); (3) more prevalent complex signals (P <.001); (4) prolonged regional refractoriness (P <.05), and (5) left atrial dilation (P = .01). At 10 ± 13 month follow-up, the AF group demonstrated the following compared to baseline: (1) lower voltage (P <.05); (2) either no improvement or further slowing of conduction; (3) further prolongation of regional refractoriness (P <.05); and (4) reversal of left atrial dilation (P <.05). CONCLUSION: Patients with lone AF demonstrate evidence of an abnormal atrial substrate at baseline compared to control patients without AF. This substrate does not appear to reverse even after successful catheter ablation. These findings may have implications for long-term outcomes of ablation and for timing of ablative intervention.

Electroanatomic remodelling of the pulmonary veins associated with age.

AIMS: Increasing age is a significant risk factor for developing atrial fibrillation (AF). Pulmonary vein (PV) triggers are critical in the mechanism of AF, but little is known of the substrate changes that occur within the PVs with ageing. Therefore, we sought to identify whether ageing is associated with electroanatomic changes within the pulmonary veins. METHODS AND RESULTS: Twenty-five patients undergoing ablation for left-sided supraventricular tachycardia had high-density 3D electroanatomic maps of all four PVs created. Patients were divided into two groups: group 1 aged <50 years and group 2 aged >50 years. Mean-voltage (MV), % low-voltage (LV < 0.5 mV), conduction, signal complexity, and PV muscle sleeve length and diameter were assessed. Age was 33 ± 8 vs. 66 ± 8 years for groups 1 and 2, respectively (P < 0.001). Group 2 demonstrated: (i) lower MV within the PVs (1.66 ± 1.1 vs. 1.88 ± 1.1 mV, P < 0.001); (ii) increased % LV (5.0 vs. 1.1%, P < 0.001), and increased voltage heterogeneity within the PVs (65 ± 14 vs. 55 ± 8%, P < 0.05); (iii) regional and global conduction slowing in the PVs; and (iv) increased % complex signals within the PVs (1.4 vs. 0.4%, P = 0.009). There was no difference in PV sleeve length or diameter. CONCLUSION: Increasing age is associated with PV electroanatomic changes characterized by a significant reduction in PV voltage, conduction slowing, and increasing signal complexity. These observations provide new insights into the potential mechanisms behind the increased prevalence of AF with advancing age.

Atrial electrical and structural changes associated with longstanding hypertension in humans: implications for the substrate for atrial fibrillation.

UNLABELLED: INTRODUCTION: Hypertension (HT) is the most common modifiable risk factor for atrial fibrillation (AF), yet little is known of the atrial effects of chronic HT in humans. We aimed to characterize the electrophysiologic (EP) and electroanatomic (EA) remodeling of the right atrium (RA) in patients with chronically treated systemic HT and left ventricular hypertrophy (LVH) without a history of AF. METHODS AND RESULTS: Twenty patients with (systolic BP 145 ± 10 mmHg) and without (BP 119 ± 11 mmHg, P < 0.01) systemic HT underwent detailed conventional EP and EA voltage and activation mapping. We measured RA refractoriness at the coronary sinus and high septum at cycle lengths (CLs) 600 and 450 ms, and RA conduction velocities, activation times, and voltages at a global and regional level at CLs 600 ms and 300 ms. HT was associated with slowing of global (73 ± 17 cm/s vs 96 ± 12 cm/s in controls, P < 0.01) and regional conduction velocity particularly in the posterior RA (70 ± 17 cm/s vs 96 ± 12 cm/s in controls, P < 0.01) at the crista terminalis (fractionation and double potentials in HT 72%± 4 vs 43%± 23 in controls, P = 0.04). Mean RA voltage was similar between the 2 groups, however HT was associated with an increase in areas of low voltage (<0.5 mV; HT 13% vs controls 9%, P = 0.04). Sustained AF was induced in 30% HT patients and no controls. CONCLUSION: Chronically treated systemic HT with LVH is accompanied by atrial remodeling characterized by: (i) global conduction slowing, (ii) regional conduction delay particularly at the crista terminalis, and (iii) increased AF inducibility. These changes may in part be responsible for the increased propensity to AF associated with systemic HT.

The relationship between complex fractionated electrograms and atrial low-voltage zones during atrial fibrillation and paced rhythm.

AIMS: Mapping of atrial fibrillation (AF) involves identification of low-voltage regions associated with complex fractionated electrograms (CFE) which theoretically represent abnormal substrate and targets for ablation. Whether low-voltage CFE areas also identify abnormal substrate during paced rhythm is unknown. METHODS AND RESULTS: Twelve patients with persistent AF undergoing ablation of AF had high-density three-dimensional electroanatomic maps created during AF and paced rhythm (24 maps) and the mean voltage during AF and paced rhythm was compared for eight segments of the left atrium (LA). The following were correlated during AF and paced rhythm: regional mean voltage; %low voltage (defined as <0.5 mV); and extent of CFE. In addition, the relationship between the extent of CFE in AF: (i) %low voltage and (ii) conduction during paced rhythm were determined. Mean voltage was lower during AF than paced rhythm for all regions and globally (0.7 ± 0.2 mV vs. 2.1 ± 0.6 mV, P < 0.001). The regional and overall %low voltage of the LA was greater during AF than paced rhythm (53 ± 19% vs. 9 ± 2%, P < 0.001). There was no correlation between mean voltage or %low voltage during AF and paced rhythm. Complex fractionated electrograms were prevalent throughout all regions during AF, but did not correlate with %low voltage, fractionation, or slowed conduction during paced rhythm. CONCLUSION: Areas of CFE and low voltage recorded during AF frequently demonstrate normal atrial myocardial characteristics (normal conduction, electrograms, and voltage) during sinus rhythm. Therefore, AF CFE sites do not necessarily identify regions of an abnormal atrial substrate. However, this does not exclude the possibility that CFE might identify a focal driver or source occurring in a region of normal atrial myocardium.

The role of chronic atrial stretch and atrial fibrillation on posterior left atrial wall conduction.

BACKGROUND: The posterior left atrium (LA) is involved in the initiation and maintenance of atrial fibrillation (AF). OBJECTIVE: The purpose of this study was to compare conduction patterns on the posterior LA in patients with mitral regurgitation (MR), with and without AF. METHODS: Epicardial mapping of the posterior LA was performed in 23 patients undergoing cardiac surgery. Patients were included in one of three groups: Group A-patients in sinus rhythm with normal left ventricular function undergoing coronary artery bypass grafting, Group B-patients in sinus rhythm with MR undergoing mitral valve surgery, or Group C-patients in persistent AF with MR undergoing mitral valve surgery. Conduction patterns, regional conduction velocity, conduction heterogeneity, conduction anisotropy, and complex fractionated atrial electrograms (CFAEs) were assessed. RESULTS: LA diameter was greater in patients in Groups C (57 +/- 4mm) and B (54 +/- 6mm) than in Group A (39 +/- 7 mm, P <0.01). Patients in Group C had a greater number of lines of conduction delay than Groups A and B (2.0 +/- 0.8 vs 1 +/- 0 and 1 +/- 0, P <0.05). The extent of conduction delay and conduction heterogeneity was greater in Group C than in Group B, which was greater than in Group A (P <0.05). The percentage of CFAEs that remained stable during AF was 61% +/- 17%. There was a significant correlation between CFAEs during AF and regions of slow conduction during pacing (R = 0.36, P <0.001). CONCLUSION: Patients with MR, LA enlargement, and AF have more extensive regions of conduction slowing in the posterior LA. Anatomically constant lines of conduction delay in this region lead to circuitous wavefront propagation. During persistent AF, fractionated electrograms in the posterior LA are distributed to regions demonstrating slow conduction, and the majority remain stable over time.

Atrial electrical and structural abnormalities in an ovine model of chronic blood pressure elevation after prenatal corticosteroid exposure: implications for development of atrial fibrillation.

AIMS: Elevated blood pressure (EBP) is the most prevalent and potentially modifiable risk factor for AF, yet little is known of its atrial effects. We aimed to characterize the atrial electrical and structural changes in a chronic ovine model of EBP after prenatal corticosteroid exposure. METHODS AND RESULTS: Twelve sheep with chronically EBP (mean arterial pressure 94+/-3 mmHg) and six controls (71+/-4 mmHg, P<0.01) underwent acute open chest electrophysiologic and pathologic studies. We measured refractoriness at the atrial appendages at 3 cycle lengths (CL); conduction velocities at Bachmann's bundle, both atrial appendages and free walls at 4 CLs; conduction heterogeneity; atrial wavelength and AF duration. We performed light microscopy (LM) and electron microscopy (EM) and collagen and apoptosis studies. EBP was associated with widespread conduction abnormalities, shortening of atrial wavelength, and increased AF. There was no significant change in refractoriness. LM demonstrated atrial myocyte hypertrophy and myolysis in all EBP sheep and focal scarring in six. EM demonstrated mitochondrial and nuclear enlargement and increased collagen fibrils in EBP sheep, findings not present in any controls. Atrial collagen and apoptosis were increased in EBP animals. CONCLUSION: This study demonstrates that chronically, EBP is associated with significant atrial electrical and structural remodelling. These changes may explain the increased propensity to atrial arrhythmias observed with long-standing EBP.

Scar-related right atrial macroreentrant tachycardia in patients without prior atrial surgery: electroanatomic characterization and ablation outcome.

BACKGROUND: Few descriptions of right atrial macroreentrant atrial tachycardia involving regions of spontaneous "scar" have been reported. OBJECTIVES: We describe the electrocardiographic, electrophysiologic, and electroanatomic characteristics of an unusual RA macroreentrant atrial tachycardia in eight patients with spontaneous RA scarring. METHODS: Eight of 286 patients with macroreentrant atrial tachycardia treated with radiofrequency ablation had RA spontaneous scarring and underwent conventional electrophysiologic studies and electroanatomic mapping. RESULTS: Eight patients (age 53 +/- 12 years) had symptoms for 58 +/- 62 months and had not responded to 2.5 +/- 0.8 antiarrhythmic drugs and 1.0 +/- 0.9 DC cardioversions. All patients had overall normal systolic function, and five had mild atrial enlargement. Scarring was present in the posterolateral wall extending from the crista terminalis toward the tricuspid annulus. The proportion of RA classified as scar was 31% +/- 14% (range 11%-46%). Stable circuits were around scar in seven patients, through a "channel" within the scar in four, and typical cavotricuspid isthmus-dependent flutter in five. Radiofrequency ablation sites included the cavotricuspid isthmus; between the inferior vena cava, superior vena cava, or crista terminalis and scar; or a channel in the scar. ECG morphology of the RA free wall tachycardias varied, depending upon whether cavotricuspid isthmus block was present. Radiofrequency ablation of all inducible circuits was successful in six patients and of all clinical circuits in seven. At follow-up of 20 +/- 13 months, six patients are free from macroreentrant atrial tachycardia, one has infrequent nonsustained macroreentrant atrial tachycardia, and one is controlled with previously ineffective medication. Five had sinus node dysfunction requiring permanent pacemaker implant. CONCLUSIONS: Extensive spontaneous scarring of the RA is an unusual cause of macroreentrant atrial tachycardias, both cavotricuspid isthmus dependent and independent in the same patient. Radiofrequency ablation is an effective treatment. Sinus node dysfunction requiring permanent pacemaker is common. The cause is unknown.

Remodeling of sinus node function in patients with congestive heart failure: reduction in sinus node reserve.

BACKGROUND: Experimental and clinical studies have demonstrated diffuse atrial remodeling in congestive heart failure (CHF). We hypothesized that patients with CHF would demonstrate derangement of sinus node function. METHODS AND RESULTS: Eighteen patients with symptomatic CHF (left ventricular ejection fraction, 26+/-5%) and 18 age-matched control subjects were studied. Under autonomic blockade, the following were evaluated: intrinsic sinus cycle length, corrected sinus node recovery time (CSNRT), sinoatrial conduction time, number and duration of fractionated electograms or double potentials along the crista terminalis, and location of the earliest sinus activity. Electroanatomic mapping was performed to evaluate the location and nature of the sinus node complex, to characterize sinoatrial propagation, and to evaluate conduction abnormalities and voltage amplitude along the crista terminalis. Patients with CHF demonstrated the following findings compared with age-matched control subjects: prolongation of the intrinsic sinus cycle length (P=0.005), prolongation of CSNRT (P<0.0001), caudal localization of sinus activity both during sinus rhythm (P=0.03) and after pacing (P=0.002), prolongation of sinoatrial conduction time (P=0.02), greater number (P<0.0001) and duration (P<0.0001) of fractionated electrograms or double potentials along the crista terminalis, loss of voltage amplitude along the crista terminalis (P=0.02), and abnormal and circuitous propagation of the sinus impulse. CONCLUSIONS: This study demonstrates that patients with CHF have significant sinus node remodeling characterized by anatomic and structural changes along the crista terminalis with a reduction in functional sinus node reserve. This finding may have implications for the development of clinical bradycardia in CHF and for the use of negatively chronotropic agents and pacing in this condition.

Electrophysiologic and electroanatomic changes in the human atrium associated with age.

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.

Electrophysiological and electroanatomic characterization of the atria in sinus node disease: evidence of diffuse atrial remodeling.

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.