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Abdi Rasekh

Publications and source records attributed to Abdi Rasekh.

9 recordsLinked to original sources

The effects of pulmonary vein isolation on the dominant frequency and organization of coronary sinus electrical activity during permanent atrial fibrillation.

BACKGROUND: Pulmonary vein isolation (PVI) has been shown to suppress atrial fibrillation (AF). We examined the effects of PVI on disorganization and dominant frequencies (DF) in patients with permanent AF. METHODS AND RESULTS: Twenty-eight patients with permanent AF (>6 months) who failed > or =1 antiarrhythmic drugs (AAD) and > or =2 cardioversions (CV) with AF reversion <30 minutes after CV were included. PVI and isolation of DFs in pulmonary veins (PVs) was performed during AF. Fast Fourier transformations of atrial electrograms were performed. Disorganization index (DI) was defined as the percentage of time spent in type III AF during 1-minute continuous recordings. The temporal stability and reproducibility of DIs from the same sites were verified over time prior to ablation. Highly disorganized AF activity concentrated in the posterior left atrium (PLA) including sites at the left atrial (PV-LA) junction (55.7% of sites in PLA, 32.9% in septum, and 11.4% in other sites). DF and DI from the coronary sinus (CS) before and after PVI were analyzed. PVI reduced the DI (14.3 +/- 25.0% before PVI vs 4.6 +/- 8.6% after PVI; P < 0.02). There was significant reduction of DI in 26 of 28 patients. The DF remained unchanged (5.6 +/- 1.3 Hz before PVI vs 5.9 +/- 0.9 Hz after PVI; P = 0.31). After a follow-up of 30 +/- 11 months, 15 (54%) of patients are free of symptomatic AF, 3 (10%) in sinus rhythm on AAD, 5 (18%) with paroxysmal AF, 4 (14%) in chronic AF, and 1 (4%) with atypical flutter. CONCLUSIONS: In the vast majority of patients with chronic AF, PVI reduces AF disorganization without affecting the DF as measured in the CS.

Action Potentials↗

Slow pathway ablation decreases vulnerability to pacing-induced atrial fibrillation: Possible role of vagal denervation.

BACKGROUND: Studies indicate that success of radiofrequency (RF) ablation of atrial fibrillation (AF) may be in part due to vagal denervation. RFAof supraventricular tachycardia (SVT) has been associated with vagal denervation. The effects of slow pathway (SP) ablation on AF inducibility have not been studied. OBJECTIVE: To test the hypothesis that SP ablation renders AF less inducible. METHODS: Consecutive patients referred for SVT were studied. After atrioventricular nodal reentrant tachycardia (AVNRT) was confirmed they underwent induction of AF. After SP ablation AF induction was reattempted. Vulnerability to AF was reassessed. RESULTS: Twenty-four patients were enrolled; eight were not inducible for AF in the preablative state. Mean CLof the AVNRT was 340 +/- 16 ms. The average RF ablation time was 131 +/- 42 seconds. Presence of junctional rhythm was required. Of the 16 with inducible AF two patients had AF induced during routine invasive electrophysiology study. None of these had inducible AF after SP ablation. Fourteen of 16 patients required specific AF induction. Ten of these were noninducible after SP ablation; two were inducible after SP ablation but with a more aggressive pacing protocol (P < 0.03 compared to preablation) and two had no change in AF vulnerability. Seven of the eight noninducible patients remained noninducible for AF post SP ablation. In the 12 patients who were inducible prior but noninducible after ablation the mean atrial effective refractory period (AERP) increased for both BCL at 400 and 600 ms (400/216 +/- 8 ms preablation vs 400/248 +/- 12 ms postablation, P < 0.03; 600/228 +/- 8 ms preablation vs 600/259 +/- 6 ms postablation, P < 0.04). There were no significant changes in AERP of patients who remained inducible or who were noninducible before ablation. The average ablation time for patients who became noninducible after ablation was significantly higher than those who had no change in inducibility or remained inducible but at a more aggressive pacing threshold (157 +/- 24 seconds vs 35 +/- 5 seconds; P < 0.005). CONCLUSION: SP ablation acutely decreases vulnerability to pacing-induced AF in patients with AVNRT. This may reflect the effect of ablation on atrial vagal tone.

Atrial Fibrillation↗

Postoperative atrial fibrillation and mortality after coronary artery bypass surgery.

OBJECTIVES: We sought to determine if the occurrence of postoperative atrial fibrillation (AF) affects early or late mortality following coronary artery bypass surgery (CABG). BACKGROUND: Atrial fibrillation is the most common arrhythmia seen following CABG. METHODS: The Texas Heart Institute Cardiovascular Research Database was used to identify all patients that developed AF after isolated initial CABG from January 1993 to December 1999 (n = 994). This population was compared with patients who underwent CABG during the same period but did not develop AF (n = 5,481). In-hospital end points were adjusted using logistic regression models to account for baseline differences. Long-term survival was evaluated using a retrospective cohort design, where Cox proportional hazards methods were used to adjust for baseline differences, and with case-matched populations (n = 390, 195 per arm). RESULTS: Atrial fibrillation was diagnosed in 16% of the population. Postoperative AF was associated with greater in-hospital mortality (odds ratio [OR] 1.7, p = 0.0001), more strokes (OR 2.02, p = 0.001), prolonged hospital stays (14 vs. 10 days, p < 0.0001), and a reduced incidence of myocardial infarction (OR 0.62, p = 0.01). At four to five years, survival was worse in patients who developed postoperative AF (74% vs. 87%, p < 0.0001 in the retrospective cohort; 80% vs. 93%, p = 0.003 in the case-matched population). On multivariate analysis, postoperative AF was an independent predictor of long-term mortality (adjusted OR 1.5, p < 0.001 in the retrospective cohort; OR 3.4, p = 0.0018 in the case-matched population). CONCLUSIONS: The occurrence of AF following CABG identifies a subset of patients who have a reduced survival probability following CABG. The impact of various strategies, such as antiarrhythmics and warfarin, aimed at reducing AF and its complications deserves further study.

Aged↗

Inappropriate shock delivery and biventricular pacing cardiac defibrillators.

In the United States, physicians adapt currently available defibrillators to accommodate leads for biventricular pacing in those congestive heart failure patients who might benefit from cardiac resynchronization and who are additionally at risk for sudden cardiac death. The adaptation of the lead system of available defibrillators to also allow them to function as biventricular pacemakers presents occasions in which inappropriate shocks are delivered due to double counting of the right and left ventricular depolarizations by the implantable cardiac defibrillator. We reviewed a series of inappropriate shock deliveries that occurred after the implantation of biventricular pacing cardiac defibrillators at our institution; all of these shocks were related to ventricular double counting. Each had different underlying causes and management strategies. Complications such as these emphasize the importance of attentiveness to ventricular channel electrograms and to device sensing with the use of biventricular pacing cardiac defibrillators. In addition, a thorough working knowledge of pacemaker and defibrillator operation is essential for the prediction and correction of inappropriate therapies.

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Rapid ventricular tachycardias associated with cilostazol use.

A 92-year-old woman with normal systolic function had recently begun using the newly approved phosphodiesterase III inhibitor cilostazol when she was admitted with lower-extremity pain. Cilostazol is indicated for patients with intermittent claudication and contraindicated for patients with congestive heart failure. Two days after admission, the patient developed ventricular tachycardia. Cilostazol was discontinued, and shortly thereafter the ventricular tachycardia subsided. In this case, cilostazol was apparently an important predisposing factor for ventricular tachycardia.

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