Acute myocardial infarction (AMI) is the major cause of death worldwide. Cardiac troponins (cTns) are structural proteins, unique to the heart, that currently form the cornerstone of the AMI diagnosis. The major limitation of standard cTn assays is a sensitivity deficit at presentation caused by a delayed increase of circulating levels. Recent multicenter studies have demonstrated that novel, more sensitive and precise cTn assays improve the early diagnosis of AMI. cTn has to be interpreted as a quantitative variable. The term 'troponin positive' should, therefore, be avoided. 'Detectable' levels will become the norm and have to be clearly differentiated from 'elevated' levels. The differential diagnosis of a small amount of myocardial injury and, therefore, mild elevation of cTn is broad, and includes acute and chronic disorders. The differential diagnosis of a large amount of myocardial injury and, therefore, substantial elevation of cTn is much smaller and largely restricted to AMI, myocarditis and takotsubo cardiomyopathy. The aim of this article is to guide clinicians in the use of sensitive cTn.