Open AccessTransient increase in plasma brain (b‐type) natriuretic peptide after percutaneous transluminal coronary angioplasty
Author(s) -
Tateishi Jun,
Masutani Motomaru,
Ohyanagi Mitsumasa,
Iwasaki Tadaaki
Publication year - 2000
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960231016
Subject(s) - medicine , cardiology , myocardial infarction , natriuretic peptide , brain natriuretic peptide , ischemia , angioplasty , percutaneous transluminal coronary angioplasty , heart failure
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.