title: Platelet distribution width and the risk of periprocedural myocardial infarction in patients undergoing percutaneous coronary intervention.
abstract: Periprocedural myocardial infarction (PMI) still occurs in a large amount of percutaneous coronary interventions (PCI), mainly due to increased platelet activation. Platelet size has been suggested as an indicator of enhanced reactivity and platelet distribution width (PDW) could reflect morphologic changes in platelets, therefore affecting their function and potentially increasing the risk of complications after coronary stenting. Aim of the present study was to evaluate the relationship between PDW and PMI. We included 1,300 consecutive patients undergoing PCI. Myonecrosis biomarkers were dosed at intervals from 6 to 48 h after PCI. Periprocedural myonecrosis was defined as troponin I increase by three times the ULN or by 50 % of an elevated baseline value, whereas PMI as CKMB increase by three times the ULN or 50 % of baseline. We grouped patients according to tertiles values of PDW (<12.1; ≥13.9). Higher PDW was associated with age (p = 0.03), diabetes (p < 0.001), previous cerebrovascular accidents (p = 0.04), therapy with statins (p = 0.001) and ARBs (p < 0.001), ASA (p = 0.02), nitrates (p = 0.006), calcium antagonists (p = 0.05) and lower pre-procedural clopidogrel bolus (p = 0.005). PDW related with haemoglobin levels (p < 0.001), while inversely to platelet count (p < 0.001) and glycaemia (p = 0.003). Patients with larger PDW had lower presence of coronary thrombus (p < 0.001), higher rate of coronary calcifications (p = 0.02), higher stenting rate (p = 0.03) and lower rate of distal embolization (p = 0.03). Larger PDW did not increase risk of PMI (p = 0.11; adjusted OR [95 % CI] = 0.94 [0.78-1.1], p = 0.55) or periprocedural myonecrosis (p = 0.73; adjusted OR [95 % CI] = 0.95 [0.82-1.1], p = 0.51). Results were confirmed even in higher-risk subgroups of patients. In patients undergoing coronary stenting, PDW does not increase the risk of periprocedural MI and therefore should not be considered a risk factor for thrombotic periprocedural complications after PCI.
authors.affiliation: Division of Cardiology, Azienda Ospedaliera-Universitaria "Maggiore della Carità", Eastern Piedmont University, C.so Mazzini, 18, 28100, Novara, Italy, ve.monica@libero.it.
authors.forename: Monica
authors.initials: M
authors.lastname: Verdoia
authors.forename: Lucia
authors.initials: L
authors.lastname: Barbieri
authors.forename: Alon
authors.initials: A
authors.lastname: Schaffer
authors.forename: Ettore
authors.initials: E
authors.lastname: Cassetti
authors.forename: Gabriella
authors.initials: G
authors.lastname: Di Giovine
authors.forename: Giorgio
authors.initials: G
authors.lastname: Bellomo
authors.forename: Paolo
authors.initials: P
authors.lastname: Marino
authors.forename: Fabiola
authors.initials: F
authors.lastname: Sinigaglia
authors.forename: Giuseppe
authors.initials: G
authors.lastname: De Luca
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000473:pathology*; D048429:Cell Size; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000209:etiology* / Q000473:pathology*; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects*; D010976:Platelet Count; D011446:Prospective Studies; D019210:Troponin I / Q000378:metabolism
chemical_list: D015415:Biomarkers; D019210:Troponin I