Bengt Herweg

Association of Atrial Tissue Fibrosis Identified by Delayed Enhancement MRI and Atrial Fibrillation Catheter Ablation: The DECAAF Study

IMPORTANCE Left atrial fibrosis is prominent in patients with atrial fibrillation (AF). Extensive atrial tissue fibrosis identified by delayed enhancement magnetic resonance imaging (MRI) has been associated with poor outcomes of AF catheter ablation. OBJECTIVE To characterize the feasibility of atrial tissue fibrosis estimation by delayed enhancement MRI and its association with subsequent AF ablation outcome. DESIGN, SETTING, AND PARTICIPANTS Multicenter, prospective, observational cohort study of patients diagnosed with paroxysmal and persistent AF (undergoing their first catheter ablation) conducted between August 2010 and August 2011 at 15 centers in the United States, Europe, and Australia. Delayed enhancement MRI images were obtained up to 30 days before ablation. MAIN OUTCOMES AND MEASURES Fibrosis quantification was performed at a core laboratory blinded to the participating center, ablation approach, and procedure outcome. Fibrosis blinded to the treating physicians was categorized as stage 1 (<10% of the atrial wall), 2 (≥10%-<20%), 3 (≥20%-<30%), and 4 (≥30%). Patients were followed up for recurrent arrhythmia per current guidelines using electrocardiography or ambulatory monitor recording and results were analyzed at a core laboratory. Cumulative incidence of recurrence was estimated by stage at days 325 and 475 after a 90-day blanking period (standard time allowed for arrhythmias related to ablation-induced inflammation to subside) and the risk of recurrence was estimated (adjusting for 10 demographic and clinical covariates). RESULTS Atrial tissue fibrosis estimation by delayed enhancement MRI was successfully quantified in 272 of 329 enrolled patients (57 patients [17%] were excluded due to poor MRI quality). There were 260 patients who were followed up after the blanking period (mean [SD] age of 59.1 [10.7] years, 31.5% female, 64.6% with paroxysmal AF). For recurrent arrhythmia, the unadjusted overall hazard ratio per 1% increase in left atrial fibrosis was 1.06 (95% CI, 1.03-1.08; P < .001). Estimated unadjusted cumulative incidence of recurrent arrhythmia by day 325 for stage 1 fibrosis was 15.3% (95% CI, 7.6%-29.6%); stage 2, 32.6% (95% CI, 24.3%-42.9%); stage 3, 45.9% (95% CI, 35.5%-57.5%); and stage 4, 51.1% (95% CI, 32.8%-72.2%) and by day 475 was 15.3% (95% CI, 7.6%-29.6%), 35.8% (95% CI, 26.2%-47.6%), 45.9% (95% CI, 35.6%-57.5%), and 69.4% (95% CI, 48.6%-87.7%), respectively. Similar results were obtained after covariate adjustment. The addition of fibrosis to a recurrence prediction model that includes traditional clinical covariates resulted in an improved predictive accuracy with the C statistic increasing from 0.65 to 0.69 (risk difference of 0.05; 95% CI, 0.01-0.09). CONCLUSIONS AND RELEVANCE Among patients with AF undergoing catheter ablation, atrial tissue fibrosis estimated by delayed enhancement MRI was independently associated with likelihood of recurrent arrhythmia. The clinical implications of this association warrant further investigation.

Power Spectral Analysis of Heart Period Variability of Preceding Sinus Rhythm Before Initiation of Paroxysmal Atrial Fibrillation

Time domain analysis of heart period variability in patients without structural heart disease demonstrated increased parasympathetic modulation before paroxysmal atrial fibrillation (AF) occurring predominantly at night. However, diurnal differences in autonomic activity preceding AF episodes in a diverse patient population have not been assessed. Accordingly, we performed spectral analysis of heart period variability on Holter recordings during sinus rhythm preceding AF in 29 patients, 17 with night and 12 with day episodes. Samples taken 5, 10, and 20 minutes before AF onset were compared. Normalized high-frequency (HF) spectral power change was greater when comparing the interval 10 to 5 minutes with 20 to 10 minutes preceding AF in 26 of 29 patients (0.09 +/- 0.07 vs 0.03 +/- 0.02; p < 0.0001). HF spectral power increased before 3 of 12 AF episodes during the day compared with 15 of 17 AF episodes during the night (p = 0.001). Nocturnal AF episodes were preceded by increased HF spectral power in the 5- versus the 20-minute sample expressed as natural logarithm-transformed values (5.6 +/- 4.8 vs 4.2 +/- 4.0; p < 0.005) and normalized values (0.19 +/- 0.09 vs 0.10 +/- 0.07; p < 0.02), a decrease in low-frequency/HF ratio (1.05 +/- 0.61 vs 2.21 +/- 1.75; p < 0.05) and heart rate (60 +/- 13 vs 71 +/- 13 beats/min; p = 0.06). Structural heart disease was more common with daytime than nocturnal AF episodes (58% vs 18%, p < 0.05). In conclusion, HF spectral power change was increased preceding most AF episodes. However, diurnal differences were demonstrated. Contrary to daytime AF, increased parasympathetic activity preceded predominantly nocturnal AF, mostly in younger patients with structurally normal hearts.

Echocardiographic optimization of the atrioventricular and interventricular intervals during cardiac resynchronization.

An optimized atrioventricular (AV) interval can maximize the benefits of cardiac resynchronization therapy (CRT). If programmed poorly, it may curtail beneficial effects of CRT. AV optimization will not convert non-responder to responder, but may convert under-responder to improved status. There are many echocardiographic techniques for AV optimization but there is no universally accepted gold standard. The optimal AV delay varies with time, necessitating periodic re-evaluation. As the optimal AV delay may lengthen on exercise, a rate-adaptive AV delay should not be routinely programmed. Intra- and interatrial conduction delays may require AV junctional ablation when AV optimization is impossible in patients with a poor clinical response. Fusion with the spontaneous QRS complex may be acceptable on a trial basis to seek a better clinical response or with a short PR interval. Routine VV optimization is presently controversial but programming may prove beneficial in some patients with a suboptimal CRT response where no cause is found. It may partially compensate for less than optimal left ventricular (LV) lead position and may correct for heterogeneous ventricular activation including a prolonged LV latency interval and slow conduction (scarring) near the LV pacing site. VV timing is generally programmed using the aortic velocity-time integral, and long-term variations of the optimal value necessitate periodic re-evaluation.

Usefulness of the 12-lead electrocardiogram in the follow-up of patients with cardiac resynchronization devices. Part II

Cardiac resynchronization therapy (CRT) has added a new dimension to the electrocardiographic evaluation of pacemaker function. During left ventricular (LV) pacing from the posterior or posterolateral coronary vein, a correctly positioned lead V1 registers a tall R wave and there is right axis deviation in the frontal plane with few exceptions. During simultaneous biventricular stimulation from the right ventricular (RV) apex and LV site in the coronary venous system, the QRS complex is often positive (dominant) in lead V1 and the frontal plane QRS axis usually points to the right superior quadrant and occasionally the left superior quadrant. The reported incidence of a dominant R wave in lead V1 during simultaneous biventricular pacing (RV apex) varies from 50% to almost 100% for reasons that are not clear. During simultaneous biventricular pacing from the posterior or posterolateral coronary vein with the RV lead in the outflow tract, the paced QRS in lead V1 is often negative and the frontal plane paced QRS axis is often directed to the right inferior quadrant (right axis deviation). A negative paced QRS complex in lead V1 during simultaneous biventricular pacing with the RV lead at the apex can be caused by incorrect placement of the lead V1 electrode (too high on the chest), lack of LV capture, LV lead displacement, pronounced latency (true exit block), conduction delay around the LV stimulation site, ventricular fusion with the intrinsic QRS complex, coronary venous LV pacing via the middle or anterior cardiac vein, unintended placement of two leads in the RV and severe conduction abnormalities within the LV myocardium. Most of these situations can cause a QS complex in lead V1 which should be interpreted (excluding fusion) as reflecting RV preponderance in the depolarization process. Barring the above causes, a negative complex in lead V1 is unusual and it probably reflects a different activation of a heterogeneous biventricular substrate (ischemia, scar, His-Purkinje participation). The latter is basically a diagnosis of exclusion. With a non-dominant R wave in lead V1, programming the V-V interval with LV preceding RV may bring out a diagnostic dominant R wave in lead V1 representing the contribution of LV stimulation to the overall depolarization process. In this situation the emergence of a dominant R wave confirms the diagnosis of prolonged LV latency (exit delay) or an LV intramyocardial conduction abnormality near the LV pacing site but it rules out the various causes of LV lead malfunction or misplacement.

MRI Assessment of Ablation-Induced Scarring in Atrial Fibrillation: Analysis from the DECAAF Study.

There is limited knowledge on the extent and location of scarring that results from catheter ablation and its role in suppressing atrial fibrillation (AF). We examined the effect of atrial fibrosis and ablation‐induced scarring on catheter ablation outcomes in AF.

Hypertension and Hypertensive Heart Disease Are Associated with Increased Ostial Pulmonary Vein Diameter

Introduction: Atrial fibrillation (AF) is associated with increased ostial pulmonary vein (PV) diameter and commonly with hypertension. We sought to investigate ostial PV anatomy in patients with and without AF with the goal of characterizing the relationship to hypertension and cardiovascular disease.

Latency During Left Ventricular Pacing From the Lateral Cardiac Veins: A Cause of Ineffectual Biventricular Pacing

We report three patients with cardiomyopathy and pronounced stimulus to QRS latency during left ventricular (LV) pacing from an epicardial cardiac vein. Delayed LV activation during simultaneous biventricular pacing produced an electrocardiographic pattern dominated by right ventricular stimulation. Hemodynamic parameters improved immediately after advancing LV stimulation (in one patient) or pacing the LV only (in two patients) coupled with dramatic improvement of heart failure symptoms.

Site-Specific Differences in Latency Intervals during Biventricular Pacing: Impact on Paced QRS Morphology and Echo-Optimized V-V Interval

Objective:  To investigate differences in latency intervals during right ventricular (RV) pacing and left ventricular (LV) pacing from the (postero‐)lateral cardiac vein in cardiac resynchronization therapy (CRT) patients and their relationship to echo‐optimized interventricular (V‐V) intervals and paced QRS morphology.

Termination of persistent atrial fibrillation resistant to cardioversion by a single radiofrequency application.

This report describes the termination of persistent AF refractory to multiple cardioversions and antiarrhythmic therapy in a patient without structural heart disease, with a single radiofrequency application delivered in the left upper pulmonary vein. The observations and failure of repeated internal and external cardioversion suggest a rapidly firing arrhythmia focus sustaining atrial fibrillation amenable to curative pulmonary vein ablation. (PACE 2003; 26:1420–1423)

Double Counting of the Ventricular Electrogram in Biventricular Pacemakers and ICDs

Dual site or multisite ventricular pacing (resynchronization) has emerged as promising therapy for patients with dilated cardiomyopathy and congestive heart failure associated with major left intraand interventricular conduction disorders. Implantable cardioverter defibrillators (ICDs) have also been combined with biventricular pacemakers into single devices. Biventricular devices have introduced new problems related to their complex timing mechanism.1 In this regard, double counting of the ventricular electrogram has surfaced as an important clinical problem.2−7