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Articles by U. B Tedrow
Total Records ( 2 ) for U. B Tedrow
  D Conen , U. B Tedrow , N. R Cook , J. E Buring and C. M. Albert

Background— Few if any studies have assessed the relationship between birth weight and incident atrial fibrillation (AF).

Methods and Results— From 1993 to 2009, we prospectively followed 27 982 women who were >45 years of age and free of cardiovascular disease and AF at baseline. Information on birth weight was categorized into 5 different categories: <2.5, 2.5 to 3.2, 3.2 to 3.9, 3.9 to 4.5, and >4.5 kg. The primary outcome was time to incident AF. During 14.5 years of follow-up, 735 AF events occurred. Age-adjusted incidence rates for incident AF from the lowest to the highest birth weight category were 1.45, 1.82, 1.88, 2.57, and 2.55 events per 1000 person-years of follow-up. After multivariable adjustment, hazard ratios for incident AF across increasing birth weight categories were 1.0, 1.30 (95% confidence interval [CI], 0.96 to 1.75), 1.28 (95% CI, 0.96 to 1.69), 1.70 (95% CI, 1.23 to 2.37), and 1.71 (95% CI, 1.12 to 2.61) (P for linear trend=0.002). Adding body mass index, blood pressure, and diabetes mellitus at study entry did not have a large effect on these estimates (P for linear trend=0.004). In contrast, including height in the multivariable model substantially attenuated the relationship between birth weight and AF (P for linear trend=0.17), and additional adjustment for maximum weight in young adulthood further attenuated this association (multivariable-adjusted hazard ratio across birth weight categories, 1.0, 1.27 [95% CI, 0.94 to 1.71], 1.10 [95% CI, 0.83 to 1.46], 1.41 [95% CI, 1.01 to 1.96], and 1.29 [95% CI, 0.84 to 1.98]; P for linear trend=0.23).

Conclusions— Birth weight is significantly associated with incident AF among women, suggesting that early life determinants may play an important role in the pathogenesis of AF.

Clinical Trial Registration— URL: Unique identifier: NCT00000479.

  D Steven , K. C Roberts Thomson , J Seiler , K Inada , U. B Tedrow , R. N Mitchell , P. S Sobieszczyk , A. C Eisenhauer , G. S Couper and W. G. Stevenson

Background— The aortomitral continuity (AMC) has been described as a site of origin for ventricular tachycardias (VT) in structurally normal hearts. There is a paucity of data on the contribution of this region to VTs in patients with structural heart disease.

Methods and Results— Data from 550 consecutive patients undergoing catheter ablation for VT associated with structural heart disease were reviewed. Twenty-one (3.8%) had a VT involving the peri-AMC region (age, 62.7±11 years; median left ventricular ejection fraction, 43.6±17%). Structural heart disease was ischemic in 7 (33%), dilated cardiomyopathy in 10 (47.6%), and valvular cardiomyopathy in 4 (19%) patients, respectively. After 1.9±0.8 catheter ablation procedures (including 3 transcoronary ethanol ablations) the peri-AMC VT was not inducible in 19 patients. The remaining 2 patients underwent cryosurgical ablation. Our first catheter ablation procedure was less often successful (66.7%) for peri-AMC VTs compared with that for 246 VTs originating from the LV free wall (81.4%, P=0.03). During a mean follow-up of 1.9±2.1 years, 12 (57.1%) patients remained free of VT, peri-AMC VT recurred in 7 patients, and 1 patient had recurrent VT from a remote location. Three patients died. Analysis of 50 normal coronary angiograms demonstrated an early septal branch supplying the peri-AMC area in 58% of cases that is a potential target for ethanol ablation.

Conclusions— VTs involving the peri-AMC region occur in patients with structural heart disease and appear to be more difficult to ablate compared with VTs originating from the free LV wall. This region provides unique challenges for radiofrequency ablation, but cryosurgery and transcoronary alcohol ablation appear feasible in some cases.

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