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Charles I. Haffajee

Researcher at Beth Israel Deaconess Medical Center

Publications -  74
Citations -  3734

Charles I. Haffajee is an academic researcher from Beth Israel Deaconess Medical Center. The author has contributed to research in topics: Amiodarone & Ventricular tachycardia. The author has an hindex of 32, co-authored 73 publications receiving 3536 citations. Previous affiliations of Charles I. Haffajee include Tufts Medical Center & University of Massachusetts Amherst.

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Journal ArticleDOI

Treatment of obstructive sleep apnea reduces the risk of atrial fibrillation recurrence after catheter ablation.

TL;DR: CPAP is an important therapy in OSA patients undergoing PVI that improves arrhythmia free survival and PVI offers limited value to OSA Patients not treated with CPAP.
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Environmental iodine intake and thyroid dysfunction during chronic amiodarone therapy

TL;DR: In patients receiving chronic amiodarone therapy, clinically suspected hyperthyroidism is best confirmed by showing elevations in serum T3 or free T3 concentrations; hypothyroidistan is best diagnosed by showing an elevated serum thyrotrophin concentration.
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Amiodarone for refractory atrial fibrillation

TL;DR: Overall, amiodarone therapy was effective long term in 54 of the 68 patients and the presence of chronic AF for longer than 1 year was an adverse factor in maintaining normal sinus rhythm, although the success rate even in this group was relatively high (57%).
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Clinical pharmacokinetics and efficacy of amiodarone for refractory tachyarrhythmias.

TL;DR: The pharmacokinetics of oral amiodarone support the practice of using high loading dosages until arrhythmia suppression or apparent steady state is achieved (usually 2–4 weeks), followed by low-dose maintenance therapy for treatment of symptomatic atrial and ventricular tachyarrhythmias.
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Pulmonary embolism, pulmonary hemorrhage and pulmonary infarction.

TL;DR: It is suggested that obstruction of distal arteries results in pulmonary hemorrhage owing to an influx of bronchial arterial blood at systemic pressure, which causes symptoms and x-ray changes usually attributed to pulmonary infarction in patients without, but progresses to infarctions in those with, heart disease.