Mechanism of action of ranolazine [8]

Archives of Internal Medicine

Volumn 166, Issue 12, 2006, Pages 1325-1326

  Marx, Celeste ^a   Sweeney, Michael ^b  

^a CV THERAPEUTICS INC   (United States)

^b NONE

Author keywords

[No Author keywords available]

Indexed keywords

CALCIUM ION; RANOLAZINE; SODIUM CHANNEL; SODIUM ION;

ANGINA PECTORIS; CLINICAL EFFECTIVENESS; CLINICAL TRIAL; CORONARY ARTERY BLOOD FLOW; DIASTOLE; DRUG EFFECT; DRUG EFFICACY; DRUG INHIBITION; DRUG MECHANISM; HEART MUSCLE ISCHEMIA; HUMAN; LETTER; PRIORITY JOURNAL; SODIUM CURRENT; TREATMENT RESPONSE;

ANGINA PECTORIS; CALCIUM; CORONARY CIRCULATION; HUMANS; PIPERAZINES; SODIUM CHANNELS; TREATMENT OUTCOME;

EID: 33745661885     PISSN: 00039926     EISSN: 15383679     Source Type: Journal    
DOI: 10.1001/archinte.166.12.1325-b     Document Type: Letter

References (7)

1. Nash DT. The case for medical treatment in chronic stable coronary artery disease. Arch Intern Med. 2005;165:2587-2589.
2. McCormack JG, Barr RL, Wolff AA, Lopaschuk GD. Ranolazine stimulates glucose oxidation in normoxic, ischemic, and reperfused ischemic rat hearts. Circulation. 1996;93:135-142.
3. Clarke B, Wyatt KM, McCormack JG. Ranolazine increases active pyruvate dehydrogenase in perfused normoxic rat hearts: evidence for an indirect mechanism. J Mol Cell Cardiol. 1996;28:341-350.
4. Antzelevitch C, Belardinelli L, Zygmunt AC, et al. Electrophysiological effects of ranolazine, a novel antianginal agent with antiarrhythmic properties. Circulation. 2004;110:904-910.
5. Chaitman BR, Pepine CJ, Parker JO, et al. Effects of ranolazine with atenolol, amlodipine, or diltiazem on exercise tolerance and angina frequency in patients with severe chronic angina: a randomized controlled trial. JAMA. 2004;291:309-316.
6. Chaitman BR, Skettino SL, Parker JO, et al. Anti-ischemic effects and long-term survival during ranolazine monotherapy in patients with chronic severe angina. J Am Coll Cardiol. 2004;43:1375-1382.
7. Belardinelli L, Antzelevitch C, Fraser H. Inhibition of late (sustained persistent) sodium current: a potential drug target to reduce intracellular sodium-dependent calcium overload and its detrimental effects on cardiomyocyte function. Eur Heart J Suppl. 2004;6(suppl I):i3-i7.