Nitroglycerin Use in Myocardial Infarction Patients - Risks and Benefits

Author(s)

Ferreira, Julio C. B. ; Mochly-Rosen, Daria ^[1]

Affiliation

^[1] Stanford Univ, Sch Med, Dept Chem & Syst Biol, CCSR, Stanford, CA 94305 - USA

• Document type: Review article
• Source: CIRCULATION JOURNAL; v. 76, n. 1, p. 15-21, JAN 2012.
• Web of Science Citations: 32

Abstract

Acute myocardial infarction (MI) and its sequelae are leading causes of morbidity and mortality worldwide. Nitroglycerin (glyceryl trinitrate {[}GIN]) remains a first-line treatment for angina pectoris and acute MI. Nitroglycerin achieves its benefit by giving rise to nitric oxide (NO), which causes vasodilation and increases blood flow to the myocardium. However, continuous delivery of GTN results in tolerance, limiting the use of this drug. Nitroglycerin tolerance is caused, at least in part, by inactivation of aldehyde dehydrogenase 2 (ALDH2), an enzyme that converts GTN to the vasodilator, NO. We recently found that in a MI model in animals, in addition to GTN's effect on the vasculature, sustained treatment negatively affected cardiomyocyte viability following ischemia, thus resulting in increased infarct size. Coadministration of Alda-1, an activator of ALDH2, with GIN improves metabolism of reactive aldehyde adducts and prevents the GIN-induced increase in cardiac dysfunction following MI. In this review, we describe the molecular mechanisms associated with the benefits and risks of GTN administration in MI. (Circ J 2012; 76: 15-21) (AU)

• FAPESP's process: 09/03143-1 - Protein quality control in heart failure: role of different protein kinase C isozymes
• Grantee: Julio Cesar Batista Ferreira
• Support type: Scholarships in Brazil - Post-Doctorate