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Articles by R. D Berger
Total Records ( 2 ) for R. D Berger
  A Kolandaivelu , M. M Zviman , V Castro , A. C Lardo , R. D Berger and H. R. Halperin
  Background—

Failure to achieve properly localized, permanent tissue destruction is a common cause of arrhythmia recurrence after cardiac ablation. Current methods of assessing lesion size and location during cardiac radiofrequency ablation are unreliable or not suited for repeated assessment during the procedure. MRI thermography could be used to delineate permanent ablation lesions because tissue heating above 50°C is the cause of permanent tissue destruction during radiofrequency ablation. However, image artifacts caused by cardiac motion, the ablation electrode, and radiofrequency ablation currently pose a challenge to MRI thermography in the heart. In the current study, we sought to demonstrate the feasibility of MRI thermography during cardiac ablation.

Methods and Results—

An MRI-compatible electrophysiology catheter and filtered radiofrequency ablation system was used to perform ablation in the left ventricle of 6 mongrel dogs in a 1.5-T MRI system. Fast gradient-echo imaging was performed before and during radiofrequency ablation, and thermography images were derived from the preheating and postheating images. Lesion extent by thermography was within 20% of the gross pathology lesion.

Conclusions—

MR thermography appears to be a promising technique for monitoring lesion formation and may allow for more accurate placement and titration of ablation, possibly reducing arrhythmia recurrences.

  E. S Chung , D Dan , S. D Solomon , A. J Bank , J Pastore , A Iyer , R. D Berger , J. O Franklin , G Jones , C Machado and C. M. Stolen
  Background—

Left ventricular (LV) remodeling has been attributed to the segmental loss of viable myocardium due to myocardial infarction (MI), which results in redistribution of cardiac workload, with increased regional wall stress in and around the infarct zone. Because ventricular pacing has been shown to reduce regional wall stress and workload in regions near the pacing site, this trial was designed to test whether chronic pacing near the infarct attenuates LV remodeling.

Methods and Results—

Eighty patients with an anterior MI, peak creatine kinase >2000 mU/mL, ejection fraction ≤35%, wall motion abnormality (WMA) in >5 of 16 segments, and QRS <120 ms, were randomized to either control (implantable cardioverter-defribillator [ICD]) or biventricular pacing with peri-infarct LV lead placement (cardiac resynchronization therapy [CRT]-D) arms between 2 and 14 days after the MI. The primary end point—change in LV end-diastolic volume (LVEDV) from baseline to 12 months—was not significantly different between the 2 groups (CRT, 10.6±27.7 mL; ICD, 11.2±31.2 mL; 2-sample t test P>0.05). In a hypothesis-generating secondary analysis, there was a sustained reduction in the WMA score at 12 months in paced patients (CRT, –0.16±0.28; ICD, –0.01±0.24, 2-sample t test P=0.03). No differences were found in the therapy-related event rate, hospitalizations, or mortality (all P>0.05).

Conclusions—

Chronic pacing in the infarct region did not alter the primary end point of LV remodeling over 1 year.

Clinical Trial Registration—

URL: http://www.clinicaltrials.gov. Unique identifier: NCT00605631.

 
 
 
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