title: [Periprocedural myocardial damage: chronicle of a (cellular) death foretold].
abstract: Cardiac marker monitoring after percutaneous coronary intervention (PCI) is now widespread; thus, the recognition of just how frequently myocardial enzyme elevations result from even successful PCI has become increasingly important, despite some physician's interest in minimizing the significance of isolated asymptomatic creatine phosphokinase elevations without an angiographically apparent cause. The meaningfulness of elevated cardiac enzymes after revascularization procedures is one of the most controversial issues in interventional cardiology. The rate of periprocedural damage detection is highly dependent on the intensity of enzyme and ECG measurement. With the use of more sensitive and specific cardiac markers of myocardial necrosis, the traditional definition of "acute myocardial infarction" has been expanded to include even small and asymptomatic biomarker elevations. On the other hand, most debate has focused on the clinical relevance of an elevation in CK-MB levels to 1 to 3 times the upper limit of normal, and many cardiologists argue that the appropriate cut-off point after PCI is even higher. Doubts whether "small" cardiac marker elevations have per se any impact on survival after uncomplicated procedures, as well as the excess of fideism on the effectiveness of contemporary coronary stenting couple with the mistaken equation "excellent angiographic result = excellent clinical outcome". Pre and postprocedural ECG recording and serial cardiac marker measurement should be incorporated into clinical pathways, and routine CK-MB levels tracking is now mandatory even in asymptomatic subjects having successful PCI. A consensus about how to check myocardial damage after PCI (i.e. which and how serum markers should be measured and reported) is eagerly awaited. A broader agreement will contribute to a better understanding of pathophysiology and long-term prognostic implications of "minor" periprocedural myocardial damage, allowing to improve our strategies to prevent and treat it.
authors.affiliation: U.O. di Cardiologia Ospedali Riuniti Azienda USL 6 Area Livornese Viale Alfieri, 36 57100 Livorno. m.galli@nord.usl6.toscana.it
authors.forename: Michele
authors.initials: M
authors.lastname: Galli
authors.forename: Alberto Genovesi
authors.initials: AG
authors.lastname: Ebert
mesh_terms: D001291:Attitude of Health Personnel; D015415:Biomarkers / Q000097:blood; D006348:Cardiac Surgical Procedures / Q000009:adverse effects*; D002309:Cardiology; D016923:Cell Death; D003402:Creatine Kinase / Q000097:blood*; D052279:Creatine Kinase, MB Form; D006801:Humans; D007527:Isoenzymes / Q000097:blood*; D009203:Myocardial Infarction / Q000097:blood* / Q000209:etiology; D009204:Myocardial Revascularization / Q000009:adverse effects; D012016:Reference Values; D012680:Sensitivity and Specificity; D015607:Stents; D019210:Troponin I / Q000097:blood
chemical_list: D015415:Biomarkers; D007527:Isoenzymes; D019210:Troponin I; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form