Search for: [Abstract = "Introduction Arginine is a substrate for nitric oxide \(NO\) synthesis and depends on the competition of nitric oxide synthase \(NOS\) and arginase. Experimental models provide arguments that during acute phase of myocardial infarction \(MI\) arginase activity increases simultaneously with decreased NO synthesis. There is no sufficient data about alterations in arginine metabolism during MI in human and its association with myocardial injury, incidence of vulnerable coronary plaques and burden of stable coronary intima\-media lesions. I hypothesize that i\) during acute MI phase in human arginine metabolism is shifted from NOS towards arginase, ii\) enhanced arginase activity expressed as an altered balance of arginine metabolites is associated with myocardial damage and with unfavorable morphology of a culprit lesion in the infarct\-related artery \(IRA\), iii\) persistent enhanced arginase activity during follow\-up is associated with increased intima\-media burden adjacent to culprit region and that iv\) enhanced arginase activity potentially might be useful for prediction of adverse clinical events. Aims\: 1. To measure arginine metabolites in acute phase of MI and during stable 6\-month follow up and to estimate shifts in arginine metabolism in human. 2. To compare alterations in arginine metabolites balance with myocardial injury. 3. To compare alterations in a"]

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