Thomas M. Munger

A population study of the natural history of Wolff-Parkinson-White syndrome in Olmsted County, Minnesota, 1953-1989.

BackgroundVirtually all natural history studies of Wolff-Parkinson-White (WPW) syndrome have been case series and, as such, have been constrained by referral biases, skewed age and sex distributions, or brief follow-up periods. The purpose of our study was to examine the natural history, the development of arrhythmias, and the incidence of sudden death in an entire cohort of pediatric and adult WPW patients from a community-based local population. Methods and ResultsWe identified 113 residents of Olmsted County, Minnesota, during the period 1953-1989 using the centralized records-linkage system provided by the Mayo Clinic and the Rochester Epidemiology Program Project. Medical records and ECGs were reviewed to confirm the diagnosis and to establish pathway location by ECG criteria. Follow-up, via record review and telephone interview, was complete in 95% of subjects through 1990. The incidence of newly diagnosed cases was approximately four per 100,000 per year. Preexcitation was not present on the initial ECG of22% of the cohort. Approximately 50%o of the population was asymptomatic at diagnosis, with 30%, o subsequently having symptoms related to arrhythmia at follow-up. Two sudden cardiac deaths (SCD) occurred over 1,338 patient-years of follow-up, yielding an overall SCD rate of 0.0015 (95% confidence interval, 0.0002-0.0054) per patient-year. No SCD occurred in patients asymptomatic at diagnosis. ConclusionsThe incidence of sudden death in a local community-based population is low and suggests that electrophysiological testing should not be performed routinely in asymptomatic patients with WPW syndrome. Nevertheless, young, asymptomatic patients, particularly those <40 years old, should return for medical follow-up should symptoms develop.

Clinical Presentation, Investigation, and Management of Pulmonary Vein Stenosis Complicating Ablation for Atrial Fibrillation

Background—Although segmental or circumferential ablation is effective in eliminating pulmonary vein (PV)–mediated atrial fibrillation (AF), this procedure may be complicated by the occurrence of PV stenosis. Methods and Results—To establish the clinical presentation, diagnostic manifestations, and interventional management of PV stenosis, 23 patients with stenosis of 34 veins complicating ablation of AF were evaluated. Each patient became symptomatic 103±100 days after undergoing ablation. In 8 veins, the ablation producing the PV stenosis was a repeated procedure for continued AF. Nineteen patients presented with dyspnea on exertion, 7 with dyspnea at rest, 9 with cough, and 6 with chest pain. On multirow spiral computed tomography examination, the narrowest lumen of the affected PVs measured 3±2 mm compared with 13±3 mm at baseline (P≤0.001). The relative perfusion of affected lung segments on isotope scans was reduced to 4±3% of total perfusion compared with 22±10% in unaffected segments. At percutaneous intervention, these veins showed 80±13% stenosis, with a mean gradient of 12±5 mm Hg. This was significantly reduced to a residual stenosis of 9±8% (P≤0.001) and a residual gradient of 3±4 mm Hg (P≤0.001). Twenty veins were treated with balloon dilatation alone, whereas 14 veins were stented with standard 10-mm-diameter bare-metal stents. Although the symptomatic response was nearly immediate and impressive, 14 patients developed in-stent or in-segment restenosis, requiring repeated interventions in 13. Conclusions—Percutaneous intervention produces rapid and dramatic symptom relief in patients with highly symptomatic PV stenosis after radiofrequency ablation for AF. Nevertheless, alternative treatment methods will be required to decrease recurrent in-stent or in-segment restenosis.

Dual-Chamber Versus Single-Chamber Detection Enhancements for Implantable Defibrillator Rhythm Diagnosis The Detect Supraventricular Tachycardia Study

Background— Delivery of inappropriate shocks caused by misdetection of supraventricular tachycardia (SVT) remains a substantial complication of implanted cardioverter/defibrillator (ICD) therapy. Whether use of optimally programmed dual-chamber ICDs lowers this risk compared with that in single-chamber ICDs is not clear. Methods and Results— Subjects with a clinical indication for ICD (n=400) at 27 participating centers received dual-chamber ICDs and were randomly assigned to strictly defined optimal single- or dual-chamber detection in a single-blind manner. Programming minimized ventricular pacing. The primary end point was the proportion of SVT episodes inappropriately detected from the time of programming until crossover or end of study. On a per-episode basis, 42% of the episodes in the single-chamber arm and 69% of the episodes in the dual-chamber arm were due to SVT. Mortality (3.5% in both groups) and early study withdrawal (14% single-chamber, 11% dual-chamber) were similar in both groups. The rate of inappropriate detection of SVT was 39.5% in the single-chamber detection arm compared with 30.9% in the dual-chamber arm. The odds of inappropriate detection were decreased by almost half with the use of the dual-chamber detection enhancements (odds ratio, 0.53; 95% confidence interval, 0.30 to 0.94; P=0.03). Conclusions— Dual-chamber ICDs, programmed to optimize detection enhancements and to minimize ventricular pacing, significantly decrease inappropriate detection.

Syncope Evaluation in the Emergency Department Study (SEEDS) A Multidisciplinary Approach to Syncope Management

Background—The primary aim and central hypothesis of the study are that a designated syncope unit in the emergency department improves diagnostic yield and reduces hospital admission for patients with syncope who are at intermediate risk for an adverse cardiovascular outcome. Methods and Results—In this prospective, randomized, single-center study, patients were randomly allocated to 2 treatment arms: syncope unit evaluation and standard care. The 2 groups were compared with &khgr;2 test for independence of categorical variables. Wilcoxon rank sum test was used for continuous variables. Survival was estimated with the Kaplan-Meier method. One hundred three consecutive patients (53 women; mean age 64±17 years) entered the study. Fifty-one patients were randomized to the syncope unit. For the syncope unit and standard care patients, the presumptive diagnosis was established in 34 (67%) and 5 (10%) patients (P<0.001), respectively, hospital admission was required for 22 (43%) and 51 (98%) patients (P<0.001), and total patient-hospital days were reduced from 140 to 64. Actuarial survival was 97% and 90% (P=0.30), and survival free from recurrent syncope was 88% and 89% (P=0.72) at 2 years for the syncope unit and standard care groups, respectively. Conclusions—The novel syncope unit designed for this study significantly improved diagnostic yield in the emergency department and reduced hospital admission and total length of hospital stay without affecting recurrent syncope and all-cause mortality among intermediate-risk patients. Observations from the present study provide benchmark data for improving patient care and effectively utilizing healthcare resources.

Long-term survival after ablation of the atrioventricular node and implantation of a permanent pacemaker in patients with atrial fibrillation

Background In patients with atrial fibrillation that is refractory to drug therapy, radio-frequency ablation of the atrioventricular node and implantation of a permanent pacemaker are an alternative therapeutic approach. The effect of this procedure on long-term survival is unknown. Methods We studied all patients who underwent ablation of the atrioventricular node and implantation of a permanent pacemaker at the Mayo Clinic between 1990 and 1998. Observed survival was compared with the survival rates in two control populations: age- and sex-matched members of the Minnesota population between 1970 and 1990 and consecutive patients with atrial fibrillation who received drug therapy in 1993. Results A total of 350 patients (mean [±SD] age, 68±11 years) were studied. During a mean of 36±26 months of follow-up, 78 patients died. The observed survival rate was significantly lower than the expected survival rate based on the general Minnesota population (P<0.001). Previous myocardial infarction (P< 0.001), a hi...

Long-Term Quality of Life After Ablation of Atrial Fibrillation The Impact of Recurrence, Symptom Relief, and Placebo Effect

OBJECTIVES We sought to determine the relationship between atrial fibrillation (AF) ablation efficacy, quality of life (QoL), and AF-specific symptoms at 2 years. BACKGROUND Although the primary goal of AF ablation is QoL improvement, this effect has yet to be demonstrated in the long term. METHODS A total of 502 symptomatic AF ablation recipients were prospectively followed for recurrence, QoL, and AF symptoms. RESULTS In 323 patients with 2 years of follow-up, 72% achieved AF elimination off antiarrhythmic drugs (AADs), 15% achieved AF control with AADs, and 13% had recurrent AF. The physical component summary scores of the Medical Outcomes Study Short Form 36 increased from 58.8 +/- 20.1 to 76.2 +/- 19.2 (p < 0.001) and the mental component summary scores of the Short Form 36 increased from 65.3 +/- 18.6 to 79.8 +/- 15.8 (p < 0.001). Post-ablation QoL improvements were noted across ablation outcomes, including recurrent AF (change in physical component summary: 12.1 +/- 19.7 and change in mental component summary: 9.7 +/- 17.9), with no significant differences in QoL improvement across 3 ablative efficacy outcomes. However, in 103 patients who completed additional assessment with Mayo AF Symptom Inventories (on a scale of 0 to 48), those with AF elimination off AADs had a change in AF symptom frequency score of -9.5 +/- 6.3, which was significantly higher than those with AF controlled with AADs (-5.6 +/- 3.8, p = 0.03) or those with recurrent AF (-3.4 +/- 8.4, p = 0.02). Independent predictors of limited QoL improvement included higher baseline QoL, obesity, and warfarin use at follow-up. CONCLUSIONS AF ablation produces sustained QoL improvement at 2 years in patients with and without recurrence. AF-specific symptom assessment more accurately reflects ablative efficacy.

Global right atrial mapping of human atrial flutter : The presence of posteromedial (sinus venosa region) functional block and double potentials : A study in biplane fluoroscopy and intracardiac echocardiography

BACKGROUND Previous studies of atrial flutter have found linear block at the crista terminalis; this was thought to predispose the patient to the arrhythmia. More recent observations, however, have demonstrated crista conduction. We sought to characterize the posterior boundary of atrial flutter. METHODS AND RESULTS Patients with counterclockwise flutter (n=20), clockwise flutter (n=3), or both (n=5) were studied using two 20-pole catheters. Biplane fluoroscopy determined catheter positions. During counterclockwise flutter, craniocaudal activation occurred along the entire lateral and posterior right atrial walls. Septal activation proceeded caudocranially. In all patients, a line of block was seen in the posteromedial (sinus venosa) right atrium; this was manifested by the presence of double potentials where the upward and downward activations collided. Anatomic location was confirmed by intracardiac echocardiography in 9 patients. In patients with clockwise flutter, the line of block and double potentials were seen in the same location during counterclockwise flutter, but the activation sequence around the line of block was reversed. Pacing near the site of double potentials during sinus rhythm excluded a fixed line of block, and premature atrial complexes demonstrated functional block with manifest double potentials. In 2 patients, posterior ectopy organized to subsequently initiate isthmus-dependent atrial flutter. CONCLUSIONS (1) A functional line of block is seen at the posteromedial (sinus venosa region) right atrium during counterclockwise and clockwise atrial flutter. (2) All lateral wall right atrial activation can be uniform during flutter, without linear block or double potentials in the region of the crista terminalis. (3) Activation at the site of posteromedial right atrial functional block can organize to subsequently initiate isthmus-dependent atrial flutter.

The Natural History of Lone Atrial Flutter

Context While the adverse consequences of atrial fibrillation have received much attention, we know little about the outcomes of people with lone atrial flutter. Contribution Among 59 patients with lone atrial flutter cared for at the Mayo Clinic between 1965 and 1995, 33 developed atrial fibrillation and 19 sustained a cerebrovascular event over an average follow-up of 10 years. The rate of thromboembolic events observed in this sample of patients with lone atrial flutter was at least as high as that observed in patients with atrial fibrillation. Cautions This observational study cannot tell us whether treatment for atrial flutter and anticoagulation would improve outcomes for people with lone atrial flutter. The Editors The objective of this study was to determine the long-term rate of thromboembolism and the risk for subsequent development of atrial fibrillation in patients who initially presented with lone atrial flutter. Methods Between 1965 and 1995, 567 patients from Olmsted County, Minnesota, were seen with atrial flutter. We excluded patients with any of the following conditions at the time of initial presentation: coronary artery disease, hyperthyroidism, valvular heart disease, congestive heart failure, cardiomyopathy, congenital heart disease, obstructive pulmonary disease, uncontrolled hypertension, or antecedent atrial fibrillation. We included patients with a history of controlled hypertension. We also excluded patients who were missing electrocardiographic documentation of atrial flutter, who had life-shortening disease, or whose atrial flutter occurred only as a consequence of an acute illness. Two physicians reviewed electrocardiograms to confirm the diagnosis. Atrial flutter was defined as a regular monomorphic rhythm with atrial rate greater than 240 beats/min and less than 350 beats/min. The Mayo Institutional Review Board, Rochester, Minnesota, approved the study. Control Groups The first control group was a previously defined sample in Rochester, Minnesota, in which age- and sex-specific ischemic cerebrovascular event rates were determined for the period of 1965 to 1994 (referred to as the incident cohort). The second control group consisted of Olmsted County patients who had no history of hypertension and received a diagnosis of lone atrial fibrillation from 1950 to 1980 (1, 2). Statistical Analysis Continuous variables were summarized as means 1 SD, and categorical variables were summarized as percentages. Survival without atrial fibrillation or stroke or transient ischemic attack was estimated by using the KaplanMeier method, and comparisons between patient groups were based on the log-rank test. The standardized stroke or transient ischemic attack rates were defined as the ratio of observed strokes or transient ischemic attacks in the patient cohorts divided by the expected number of strokes or transient ischemic attacks when applying the age- and sex-specific rates obtained from the incident cohort. The estimated rate of survival without stroke is expressed as the ratio of observed rates to the age- and sex-adjusted expected rates. Cox proportional hazards techniques were used to identify variables associated with rates of survival without atrial fibrillation and survival without stroke or transient ischemic attack. Because of the small numbers of events, the multivariate models consisted of only 3 variables: age; sex; and 1 of the following: body mass index, ejection fraction, duration of first atrial flutter episode (dichotomized as <24 hours or 24 hours), diabetes, history of cerebrovascular event, history of hypertension, and symptoms. All tests were 2-tailed, and a P value of 0.05 was the level of significance. Follow-up continued until January 2001 or death. A neurologist adjudicated all cerebrovascular events. Role of the Funding Source This study was funded through a grant from Mayo Foundation, which had no role in the collection, analysis, or interpretation of the data or in the decision to publish the manuscript. Results Fifty-nine patients developed lone atrial flutter during the 30-year period (Table); 75% developed recurrent episodes or chronic flutter. The average age at diagnosis was 70 years (range, 40 to 97 years). No patient with atrial flutter had clinically evident heart disease at the time of initial diagnosis. However, 20 patients had controlled hypertension, 11 had diabetes mellitus, 3 had had a transient ischemic attack (2 years, 6 years, and 10 years before diagnosis of atrial flutter, respectively), and 1 had had an ischemic stroke (9 years before diagnosis of atrial flutter). The clinical characteristics of the patients with controlled hypertension and atrial flutter did not statistically significantly differ from those of the nonhypertensive patients with atrial flutter. Table. Characteristics of Patients with Lone Atrial Flutter Medical therapy was started in 88% of patients: digitalis (61%), -blockers (17%), calcium-channel blockers (31%), and antiarrhythmic drugs (24%). Four patients underwent atrial flutter ablation. At the time of diagnosis, 31 patients received antithrombotic or antiplatelet therapy (25 patients received aspirin, and 6 patients received warfarin) to prevent embolic events. The other patients did not receive any antithrombotic or antiplatelet therapy. At latest follow-up, 41 patients were being treated with antithrombotic or antiplatelet agents (28 patients received aspirin, and 13 patients received warfarin) to prevent embolic events. Subsequent Development of Atrial Fibrillation Atrial fibrillation developed in 33 patients (paroxysmal in 25 patients and chronic in 8 patients). The average (SD) time from atrial flutter diagnosis to atrial fibrillation was 5 6 years (range, 0 to 25 years) (Figure). Unadjusted associations for the risk for atrial fibrillation were female sex (hazard ratio, 2.0 [95% CI, 0.95 to 4.2]; P = 0.07), diabetes (hazard ratio, 2.6 [CI, 1.1 to 6.0]; P = 0.028), hypertension (hazard ratio, 2.9 [CI, 1.4 to 6.1]; P = 0.005), recurrent atrial flutter (hazard ratio, 2.6 [CI, 0.91 to 7.6]; P = 0.074), and older age at the time of diagnosis of atrial flutter (hazard ratio, 1.05 [CI, 1.01 to 1.08]; P = 0.007). Significant age- and sex-adjusted predictors for developing atrial fibrillation were diabetes (hazard ratio, 2.7 [CI, 1.1 to 6.4]; P = 0.029), hypertension (hazard ratio, 2.4 [CI, 1.2 to 5.1]; P = 0.02), and recurrent atrial flutter (hazard ratio, 3.1 [CI, 1.03 to 9.1]; P = 0.044). Figure. KaplanMeier curves depict the time without conversion to atrial fibrillation from the initial lone atrial flutter diagnosis. Cerebrovascular Events Nineteen patients, with a mean (SD) age of 80 10 years, experienced at least 1 cerebrovascular ischemic event during follow-up. The mean (SD) time from atrial flutter diagnosis to cerebrovascular event was 4.3 3.9 years. Of the 19 patients, 6 developed atrial fibrillation after the atrial flutter diagnosis but before the event. Of the 4 patients with a history of stroke or transient ischemic attack before the atrial flutter diagnosis, only 1 patient had a cerebrovascular event during follow-up. Among patients with atrial flutter, 77% were free of ischemic stroke or transient ischemic attack, whichever occurred first, at 5 years and 65% were free of one of these events at 10 years. Among the incident cohort, 94% at 5 years and 89% at 10 years were free of one of these events (standardized stroke or transient ischemic attack rate, 3.3 [CI, 2.1 to 5.2]; P < 0.001). Patients with controlled hypertension and atrial flutter had an estimated 5- and 10-year survival rate without cerebrovascular events of 70% and 52%, respectively, as compared with 80% and 75% for nonhypertensive patients, respectively (log-rank P = 0.099), with an age- and sex-adjusted hazard ratio of 2.3 (CI, 0.87 to 6.0; P = 0.094). However, both the patients with controlled hypertension and atrial flutter and nonhypertensive patients with atrial flutter had statistically significant higher rates of stroke or transient ischemic attack than the incident cohort (standardized stroke or transient ischemic attack rate, 5.2 [CI, 2.7 to 9.9; P < 0.001] and 2.5 [CI, 1.3 to 4.6; P = 0.002], respectively). Comparison with Patients with Lone Atrial Fibrillation Data from the 59 patients with atrial flutter were compared with those from 145 patients with atrial fibrillation. The atrial flutter group had a larger percentage of women (44% vs. 28%; P = 0.04), was older on average (70 12 years of age vs. 55 17 years of age; P < 0.001), and had less follow-up time on average (10 6 years vs. 13 8 years; P = 0.002) than the atrial fibrillation group. Also, the atrial fibrillation group excluded patients with a history of hypertension before their diagnosis. After adjustment for age and sex, patients with atrial flutter had a higher incidence of ischemic stroke or transient ischemic attack than patients with atrial fibrillation (hazard ratio, 2.6 [CI, 1.2 to 5.3]; P = 0.011). Moreover, when nonhypertensive patients with atrial flutter were compared with patients with atrial fibrillation, the rate of stroke or transient ischemic attack did not differ (hazard ratio, 1.9 [CI, 0.85 to 4.4]; P = 0.119). Discussion In our study, 32% of patients with atrial flutter had a cerebrovascular event at 10-year follow-up. Compared with the age- and sex-adjusted expected thromboembolic rates, patients with atrial flutter experienced a statistically higher risk. Also, the rate of thromboembolism was higher in the patients with atrial flutter than in patients with atrial fibrillation. This observation, in part, is probably due to inclusion of patients with controlled hypertension in the atrial flutter group. However, when nonhypertensive patients with atrial flutter were compared with the incident cohort, there was a higher incidence of thromboembolic events in patients with atrial flutter. This suggests that atrial flutter, even without hypertension, carries

Characteristics of premature ventricular complexes as correlates of reduced left ventricular systolic function: study of the burden, duration, coupling interval, morphology and site of origin of PVCs.

PVCs and Left Ventricular Dysfunction. Background: Frequent premature ventricular complexes (PVCs) can cause a decline in left ventricular ejection fraction (LVEF). We investigated whether the site of origin and other PVC characteristics are associated with LVEF.

Noncontact mapping to guide ablation of right ventricular outflow tract arrhythmias

BACKGROUND There is limited data on outcomes after noncontact mapping (NCM)-guided right ventricular outflow tract (RVOT) ventricular arrhythmia (VA) ablation. OBJECTIVES To assess outcomes of NCM-guided RVOT VA ablation in a large cohort with extended follow-up, to determine optimal ablation site, and to analyze limitations of conventional mapping techniques. METHODS In consecutive patients undergoing RVOT VA ablation, 2 sites of early activation--earliest activation (EA) and breakout (BO) sites--were identified on NCM maps. Pace mapping and activation mapping were performed at both sites. The area of depolarized myocardium during the first 10 ms of spontaneous VA and pacing was measured. The initial site of ablation was randomized to either EA or BO sites, with crossover to the alternate site if ablation was not successful. RESULTS In 136 patients, prematurity of local activation and pace maps were similar at EA and BO sites. More myocardium was depolarized 10 ms after pacing than during spontaneous VA (12.9 ± 7.8 cm(2) vs 5.3 ± 3.9 cm(2); P < .01). Clinical success was more likely achieved when initial ablation was directed toward the EA site (P < .05). A wider EA-BO separation was associated with acute procedural failure (P < .01). With a follow-up of 36.2 ± 17.5 months, the success rate after a single procedure without antiarrhythmic agents was 86.8%. CONCLUSIONS NCM-guided RVOT VA ablation is highly effective, and clinical success is best achieved by ablating the EA site. Broad regions of early activation are associated with worsened clinical outcomes. Spatial resolution of activation and pace mapping is limited by rapid electrical propagation in the RVOT.