The prognosis of periprocedural myocardial infarction after percutaneous coronary interventions

Abstract

An increase of biomarkers of myocardial necrosis is observed frequently after percutaneous coronary interventions (PCI) even when the procedure seems angiographically successful and otherwise uncomplicated. The recently updated Universal Definition of Myocardial infarction (MI) arbitrarily defined periprocedural MI (type 4a) by elevation of cardiac troponin (cTn) values >5 × the upper reference limit (URL) in patients with normal baseline values or a rise of cTn values >20% if the baseline values are elevated, together with either angina or new ECG changes or angiographic loss of patency of a coronary artery or a side branch or persistent slow or no-flow or embolization, or imaging demonstration of new loss of viable myocardium. Most frequent causes of such event are side-branch closure and/or plaque microembolization. The present review is focused on the prognostic implication of periprocedural necrosis. The risk related to a PCI-induced MI is significantly lower as compared to a spontaneous event where a similar increase of biomarkers is detected. Moreover, although an association between CK-MB elevations and adverse prognosis after PCI has been documented, existing data do not support the statement that an isolated elevation of troponins after PCI is associated with an adverse prognosis after PCI; increased troponin levels before PCI seem far more predictive of future events than a peri-procedural itself. Caution should be paid in the interpretation of clinical trials using type 4a MI as a primary endpoint. Nevertheless, patients with periprocedural myocardial damage should be treated as a higher-risk cohort, carefully monitored and receive an intensified secondary prevention program.