Obesity and dysrhythmias.

In the United States, obesity has reached epidemic proportions. Results from the 2003-2004 National Health and Nutrition Examination Survey estimated that 66% of US adults are either overweight (body mass index [BMI] 25-30 kg/m(2)) or obese (BMI>30 kg/m(2)) as defined by the BMI cutoffs established by the World Health Organization. In the 1970s, only 15% of the US population between the ages of 20 and 74 years was categorized as obese. In 2003, approximately 32% of the adult population was obese. Obesity plays an important role in the evolution of cardiovascular disease. This article reviews the histopathophysiologic changes that occur in cardiac structure and function in response to obesity, explores the relationship between obesity and arrhythmias such as atrial fibrillation and sudden cardiac death, and analyzes electrocardiographic changes in an obese patient.

Long-term mortality in patients with pauses in ventricular electrical activity.

BACKGROUND: The long-term significance of ventricular pauses of > or =3.0 seconds observed on Holter monitor is unclear, as previously conducted retrospective studies have been poorly controlled. We compared the prognosis of patients with pauses > or =3.0 seconds on Holter monitor with a well-matched control group without such pauses. METHODS: Scanning the Holter database at Ochsner Clinic (n = 11,730; January 1998 to June 2003) for pauses > or =3.0 seconds identified 70 patients (pause group). Of those, 29 (37.1%) received a permanent pacemaker (PPM group) and 41 (62.9%) did not (No-PPM group). For each No-PPM patient, two patients without pauses (<2.0 seconds) exactly matched for age, sex, ejection fraction (EF), rhythm, and duration of follow-up were randomly chosen from the Holter database (control group, n = 82) and survival of the two groups was compared. RESULTS: Mean age was 72.5 +/- 15.0 years, mean EF was 52.2 +/- 12.7%, and 68.3% were men. Mean follow-up was 2.2 years (0.5-4.5 years). There was no difference in survival between the No-PPM and the control groups (82.9% vs 84.1%, P = NS). Compared with the PPM group, pauses in the No-PPM group were more commonly asymptomatic, nocturnal, and due to sinus pauses or atrial fibrillation (AF) with slow ventricular response. CONCLUSIONS: Pauses in ventricular electrical activity > or =3 seconds on Holter monitor due to sinus pauses or AF with slow ventricular response are not predictive of heightened mortality.

Left atrial tachycardia originating from the mitral annulus-aorta junction.

BACKGROUND: At the mitral annulus-aorta (MA-Ao) junction, the left atrium is continuous through the subaortic curtain with the musculature of the anterior mitral leaflet. Under experimental conditions, this region can generate abnormal electrical activity. In patients with left atrial tachycardia, we investigated whether this region could be the source of this arrhythmia. METHODS AND RESULTS: In 10 (28%) of 35 consecutive patients with left atrial tachycardia, the arrhythmia originated from the MA-Ao junction. Sustained, self-limited episodes of atrial tachycardia (cycle length, 340+/-56 ms; duration, 125+/-69 seconds) were repeatedly induced. Prematurity of the extrastimulus and time to first atrial tachycardia complex were directly correlated (R=0.66; P<0.001). During tachycardia, bipolar electrograms at the earliest site preceded onset of the P wave by 44+/-14 ms and were of longer duration and lower amplitude than those recorded from nearby left atrial sites (52+/-8 versus 24+/-4 ms, P<0.001; and 0.53+/-0.08 versus 3.45+/-0.96 mV, respectively; P<0.001). Ablation eliminated the tachycardia with no recurrence after a mean follow-up of 24+/-19 months. A comparative study in mouse embryos demonstrated the presence of the developing specialized conduction system in the MA-Ao region starting at embryonic age 11.5. CONCLUSIONS: The MA-Ao junction can be a frequent source of left atrial tachycardia. This previously unrecognized site of origin may explain why catheter ablation has been less successful in eliminating left versus right atrial tachycardias. Remnants of the developing specialized conduction system could be the underlying substrate of this arrhythmia.