Nicorandil: What is Beyond the Anti-Anginal Action?

Abstract

Incidence of Contrast Induced Nephropathy (CIN) among ischemic heart disease patients
subjected to coronary catheterization is highly dependent on the kidney function before
contrast media administration and relevant risk factors, of which diabetes mellitus is the most
important one.1 Incidence of CIN ranges from <2% in the general population up to 50% in patients
with Advanced Kidney Disease (AKD)2 and it is the third most common cause of hospital
acquired renal failure.3 Development of contrast media started by the first ionic, high-osmolar
contrast agent (sodium acetrizoate) brought by Vernon Wallingford in 1953 and continued till
development of the second generation non-ionic media in 1980’s.1 The exact mechanisms underlying
CIN are still unclear. However, it was postulated that in addition to their direct toxic
effects on renal tubular epithelial cells, contrast media trigger acute renal ischemia by inducing
an imbalance between vasodilatory and vasoconstrictive factors.4 Scientific research for
identification of renoprotective agents that can prevent CIN is continuously going on. No pharmacological
approach has yet been shown to provide consistent protection. Furosemide, dopamine,
atrial natriuretic peptide, sodium bicarbonate, sodium chloride, mannitol, endothelin
receptor antagonists, ascorbic acid, fenoldopam, theophylline, N-acetylcysteine, trimetazidine
and statins were all previously evaluated in prospective, randomized trials, showing positive or
controversial results.5-7