However, several studies have shown a biphasic or rapid rise and fall of troponins in response to short term myocardial ischemia, suggesting that some of the circulating troponins may stem from reversible cell damage, probably representing the cytosolic fraction.[15,16] The restricted version of the final model, which includes only patients with a cTnT concentration highly unlikely to represent an acute MI, did not differ appreciably from the full model in effects estimates, but the lower statistical power rendered most covariates marginally significant. This evidence concerns the gene TNNT2 and myocardial ischemia.