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“We are constantly misled by the ease with which our minds fall into the ruts of the one or two experiences.”
Sir William Osler.
Clinical trials are essential in our drive to continuously improve the understanding on how to reduce the burden of heart disease. Yet they are not enough. Clinical trials have to be implementable and finally effectuated. One critical component to do so is the credibility versus the scientific vulnerability of the major endpoints, upon which the trial is built. Procedural myocardial infarction (MI) is and has historically always been among the major endpoints upon which the effect of coronary devices and/or drugs has been evaluated. The rationale for this lies in the solid evidence linking procedural MI to long-term mortality. This topic has been debated for at least a decade. Meanwhile, we have witnessed an evolution of the definition of procedural MI based on troponin, which is more specific, but also more sensitive for the detection of myocardial injury. While the prognostic implications of troponin elevations have been validated extensively in the setting of spontaneous MI,1 ,2 the transition from Creatine kinase/ Creatine kinase- Myocardial band (CK/CK-MB) to troponin for defining procedural MI has been more consensus than evidence-driven. In other terms, the availability of a more specific and sensitive marker of myocardial injury, troponin, has dictated its adoption into the clinical definition of myocardial infarction, including periprocedural events, without the evidence that this change in practice was justified. Availability does not always go hand in hand with appropriateness, and the time has come to scientifically challenge this consensus-driven practice.
In this issue of the journal, Vranckx and colleagues explored …
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