BACKGROUND: Brain (B-type) natriuretic peptide (BNP) is known to be secreted predominantly from the myocardium. Brain natriuretic peptide plasma concentrations have been shown to be markedly increased in patients with acute myocardial infarction; however, plasma BNP response during episodes of myocardial ischemia has not been established. HYPOTHESIS: This study was designed to examine plasma BNP in patients with transient myocardial ischemia induced by inflation of a percutaneous transluminal coronary angioplasty (PTCA) balloon. METHODS: Thirty consecutive patients (26 men and 4 women; mean age 61 years) who underwent PTCA, and another 49 patients (39 men and 10 women; mean age 63 years) who underwent diagnostic coronary angiography were enrolled in this study. Serum BNP concentrations were assayed in all patients. RESULTS: Plasma BNP was increased significantly with a peak concentration of 66.1 +/- 65.2 pg/ml 24 h after PTCA. Coronary angiography did not cause plasma BNP increase (immediately before 30.4 +/- 29.0 pg/ml, 24 h after 33.7 +/- 30.6 pg/ml). No significant differences were present in hemodynamic parameters measured immediately before and 24 h after PTCA. CONCLUSION: Plasma BNP is increased by transient myocardial ischemia induced by PTCA.
BACKGROUND: Brain (B-type) natriuretic peptide (BNP) is known to be secreted predominantly from the myocardium. Brain natriuretic peptide plasma concentrations have been shown to be markedly increased in patients with acute myocardial infarction; however, plasma BNP response during episodes of myocardial ischemia has not been established. HYPOTHESIS: This study was designed to examine plasma BNP in patients with transient myocardial ischemia induced by inflation of a percutaneous transluminal coronary angioplasty (PTCA) balloon. METHODS: Thirty consecutive patients (26 men and 4 women; mean age 61 years) who underwent PTCA, and another 49 patients (39 men and 10 women; mean age 63 years) who underwent diagnostic coronary angiography were enrolled in this study. Serum BNP concentrations were assayed in all patients. RESULTS: Plasma BNP was increased significantly with a peak concentration of 66.1 +/- 65.2 pg/ml 24 h after PTCA. Coronary angiography did not cause plasma BNP increase (immediately before 30.4 +/- 29.0 pg/ml, 24 h after 33.7 +/- 30.6 pg/ml). No significant differences were present in hemodynamic parameters measured immediately before and 24 h after PTCA. CONCLUSION: Plasma BNP is increased by transient myocardial ischemia induced by PTCA.
Authors: Sean van Diepen; Matthew T Roe; Renato D Lopes; Amanda Stebbins; Stefan James; L Kristin Newby; David J Moliterno; Franz-Josef Neumann; Justin A Ezekowitz; Kenneth W Mahaffey; Judith S Hochman; Christian W Hamm; Paul W Armstrong; Pierre Theroux; Christopher B Granger Journal: J Thromb Thrombolysis Date: 2012-07 Impact factor: 2.300
Authors: Nora E Zois; Emil D Bartels; Ingrid Hunter; Birgitte S Kousholt; Lisbeth H Olsen; Jens P Goetze Journal: Nat Rev Cardiol Date: 2014-05-13 Impact factor: 32.419