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Propranolol for neurocardiogenic syncope with sympathoadrenal imbalance
Author(s) -
Eldadah B.,
Pechnik S.,
Holmes C.,
Goldstein D. S.
Publication year - 2005
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1016/j.clpt.2004.12.100
Subject(s) - propranolol , medicine , placebo , epinephrine , anesthesia , vasodilation , volunteer , clinical pharmacology , sympathoadrenal system , tilt table test , crossover study , syncope (phonology) , heart rate , cardiology , blood pressure , pharmacology , alternative medicine , pathology , agronomy , biology
Background Neurocardiogenic syncope with sympathoadrenal imbalance (SAI) is characterized by loss of consciousness preceded by a disproportionately greater increase in plasma epinephrine than norepinephrine. In SAI, forearm vascular resistance decreases, probably because of skeletal muscle vasodilation from beta‐2 adrenoceptor activation by epinephrine. We hypothesized that a non‐selective beta blocker, propranolol, would prevent syncope associated with SAI, by attenuating beta‐2‐receptor‐mediated vasodilation. Methods Volunteer patients with recurrent neurocardiogenic syncope with SAI are participating in an ongoing randomized, double‐blind, placebo‐controlled, crossover trial at the NIH Clinical Center. Propranolol or placebo is administered orally every 6–8 hours for 3 days prior to tilt table testing at a dosage sufficient to reduce resting heart rate by 10%. Results Of 7 patients studied to date, all have had positive tilt tests while on placebo, and 6 have also had positive tests on propranolol. The one patient with a negative tilt test on propranolol did not develop SAI during upright tilt. Conclusions So far propranolol has not prevented tilt‐induced neurocardiogenic syncope in most patients with SAI. When successful, propranolol may work through mechanisms other than blocking beta‐adrenoceptors in skeletal muscle. Clinical Pharmacology & Therapeutics (2005) 77 , P55–P55; doi: 10.1016/j.clpt.2004.12.100