Coronary artery diseaseEndothelial Nitric Oxide Synthase T-786C Mutation, A Reversible Etiology of Prinzmetal's Angina Pectoris
Section snippets
Methods
The present study was conducted according to the principles of the Declaration of Helsinki, and all patients provided written informed consent, following a protocol approved by the Jewish Hospital of Cincinnati institutional review board.
The polymerase chain reaction analyses were done at the Molecular Diagnostic Laboratory (Cincinnati, Ohio).
The patients were studied in the consecutive order of their referral by their cardiologists and physicians. The diagnosis of PVA was confirmed by
Results
The 43 patients with PVA included 31 women and 12 men (42 white and 1 black American, median age 50 years, age range 35 to 74). Of these patients, 3 were current smokers, 6 were previous smokers, 27 had never smoked, and 7 had failed to provide a detailed smoking history. Of the 31 women, 18 were premenopausal and 13 were postmenopausal; 3 were taking exogenous estrogen at diagnosis. All 43 patients were taking calcium channel blockers at study entry and throughout the follow-up period.
Discussion
Despite conventional calcium channel binding drug therapy,11 the median perception of overall quality of life was only 33 of 100 for our 41 patients with PVA who completed the Seattle questionnaire at study entry, consistent with reports by Bory et al,11 Keller and Lemberg,12 and Ogawa et al.20 A better understanding of the pathophysiology of PVA might facilitate the development of more effective drug therapy.21 Our finding of a significant enrichment of the eNOS T-786C mutation in 43
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2016, International Journal of CardiologyThe eNOS T786C mutation, Prinzmetal's Variant Angina, and amelioration of angina by l-arginine in 59 patients with intractable angina despite calcium channel blocker-nitrate therapy
2015, IJC Metabolic and EndocrineCitation Excerpt :Our previous studies [10,11], current report, and Blum et al. [30] suggest that l-arginine, an amino-acid precursor for NO [20], effectively reduces intractable angina in PVA patients. Dose ranging studies were not performed in the current report, nor in the two previous studies [10,11] and should be done in the future. In the current study, in 28 patients, after 1 and 5 months of therapy with 9 g l-arginine/day, all 5 components of the Seattle Anginal Questionnaire improved, p ≤ .03 for all.
Some observations on and controversies about coronary arterial spasm
2015, International Journal of CardiologyCitation Excerpt :A clue to possible genetic predisposition is given by some recent studies showing increased incidences of certain variants of genes controlling expression of angiotensin converting enzyme, endothelial nitric oxide synthase (e-NOS) and endothelin-1, and greater Rho-kinase activity in CAS cases [6,49–52]. Some gene variants seem to be actually protective against coronary spasm [49,51,52]. However, if genetic predisposition plays a major role in CAS, why are reports of familial occurrence of coronary spasm so rare [53]?
The endothelial nitric oxide synthase T-786c mutation, a treatable etiology of Prinzmetal's angina
2013, Translational Research
This study was supported by grants from the Medical Research Council, London, United Kingdom, and the Lipoprotein Research Fund of the Jewish Hospital, Cincinnati, Ohio.