Intérêt des marqueurs biologiques de la souffrance myocardique en périopératoire

Auricular myocytes stretching is the main stimulus of Brain Natriuretic Peptide (BNP) synthesis and excretion. BNP is synthetized as an inactive precursor, PreProBNP, splitted into ProBNP and a peptide signal. High volume and pressure induce ProBNP splitting into BNP, an active peptide and another inactive peptide. BNP inhibits sympathetic tone, rennin-angiotensin system and many vasoconstrictors synthesis. BNP is a vasodilator, a natriuretic and a diuretic agent. Normal plasma values range between 37 and 80 ng/ml. BNP and ProBNP plasma concentrations allow to support the diagnosis of cardiac insufficiency and to evaluate its severity; changes in these values may be used as a guide for treatment optimization. High BNP values are predictive for the risk of cardiac complications after non cardiac surgery, but the postoperative increase in plasma concentration is less specific after cardiac surgery. Tropinine TnT is bind to tropomyosin and Tnl is linked at rest to actin, inhibitin binding to myosin. Both have myocardium specific isomers. Plasma circulating troponins are detectable two to three hours after myocardial infarction, peak concentration is achieved at the 20th hour and plasma concentration remains elevated up to seven days. Any increase in plasma troponin is indicative of myocardial injury. The value of troponin plasma concentration is correlated to the risk of cardiac complication after surgery. Troponin plasma concentration could be increased after pulmonary embolism and septic shock in case of myocardial damnage. TnTC is a better marker of myocardial injury in case of renal failure.