title: Hemodynamic significance of periprocedural myocardial injury assessed with N-terminal pro-B-type natriuretic peptide after percutaneous coronary intervention in patients with stable and unstable coronary artery disease (from the JUMBO-TIMI 26 trial).
abstract: The clinical relevance of periprocedural myocardial injury related to percutaneous coronary intervention (PCI) remains controversial. N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) is a sensitive indicator of hemodynamic stress and when increased is associated with higher mortality in patients with acute and chronic ischemic heart disease. We measured the serum level of NT-pro-BNP using the Elecsys 2010 proBNP assay at baseline, 4 to 6 hours, and 12 to 24 hours in 747 patients undergoing elective or urgent PCI and enrolled in the JUMBO-TIMI 26 trial. Periprocedural myocardial infarction (MI) was independently adjudicated and required a new increase in creatine kinase-MB >3 times the upper limit of normal distinct from MI as the indication for PCI. Patients with procedural MI had significantly higher levels of NT-pro-BNP at 12 to 24 hours (405 vs 146 pg/ml, p <0.001). Moreover, the greater increase in NT-pro-BNP in patients with periprocedural MI was independent of each clinical and other procedural correlates of NT-pro-BNP after PCI (p <0.001). In addition, the magnitude of increase in NT-pro-BNP correlated strongly with extent of myocardial injury, including in patients with evidence of injury (creatine kinase-MB 1 to 3 times upper limit of normal) not meeting criteria for MI (p = 0.001) or low-level increase in troponin T (p = 0.001). In conclusion, periprocedural myocardial injury, even at low levels, during PCI is associated with increased hemodynamic stress as measured by increasing NT-pro-BNP. This finding supports the physiologic relevance of procedural MI and the continued effort to define therapies that decrease the risk of this complication.
authors.affiliation: TIMI Study Group, Cardiovascular Division, Brigham and Women's Hospital, Boston, Massachusetts, USA. mbonaca@partners.org
authors.forename: Marc P
authors.initials: MP
authors.lastname: Bonaca
authors.forename: Stephen D
authors.initials: SD
authors.lastname: Wiviott
authors.forename: Marc S
authors.initials: MS
authors.lastname: Sabatine
authors.forename: Jacqueline
authors.initials: J
authors.lastname: Buros
authors.forename: Sabina A
authors.initials: SA
authors.lastname: Murphy
authors.forename: Benjamin M
authors.initials: BM
authors.lastname: Scirica
authors.forename: Nader
authors.initials: N
authors.lastname: Rifai
authors.forename: Elliott M
authors.initials: EM
authors.lastname: Antman
authors.forename: David A
authors.initials: DA
authors.lastname: Morrow
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000787:Angina Pectoris / Q000097:blood / Q000503:physiopathology* / Q000628:therapy; D015906:Angioplasty, Balloon, Coronary; D015415:Biomarkers / Q000097:blood; D005260:Female; D006801:Humans; D015994:Incidence; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000453:epidemiology / Q000503:physiopathology*; D020097:Natriuretic Peptide, Brain / Q000097:blood*; D010446:Peptide Fragments / Q000097:blood*; D011379:Prognosis; D011498:Protein Precursors / Q000097:blood; D012307:Risk Factors; D015996:Survival Rate; D016276:Ventricular Function / Q000502:physiology*
chemical_list: D015415:Biomarkers; D010446:Peptide Fragments; D011498:Protein Precursors; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain