Acute and Sustained Release of the Atrial Natriuretic Factor Prohormone N-Terminus with Acute Myocardial Infarction

• Published in: The American journal of the medical sciences 1991-03, Vol.301 (3), p.157-164
• Main Authors: Lam, Ngo, Vesely, David L., Bissett, Joe K., Murphy, Marvin L., Dinh, Ha, Sallman, Alan L., Rico, David M., Winters, Chris J., Wyeth, Richard P.
• Format: Article
• Language: English
• Subjects: Adult; Aged; Angina, Unstable - metabolism; Atrial Natriuretic Factor - metabolism; Biological and medical sciences; Cardiology. Vascular system; Creatine Kinase - blood; Female; Fibrinolytic Agents - therapeutic use; Humans; Infarction; Male; Medical sciences; Middle Aged; Myocardial; Myocardial Infarction - drug therapy; Myocardial Infarction - metabolism; Myocardial Ischemia; Peptide Fragments - metabolism; Prohormone Atrial Natriuretic Peptides; Protein Precursors - metabolism; Thrombolytic Agents
• ISSN: 0002-9629; 1538-2990
• DOI: 10.1097/00000441-199103000-00002

This investigation was designed to determine if acute ischemic cardiac injury causes the release of the 98 amino acid (aa) N-terminus of the 126 aa atrial natriuretic factor prohormone (pro ANF). Seventeen patients with acute myocardial infarction, but without clinical evi- dence of congestive heart failure, had their cir- culating concentrations of the whole N-terminus (ie, pro ANF 1-98), the midportion of the N-terminus of the ANF prohormone (consisting of aa 31–67; pro ANF 31–67) and creatine phospho- kinase (CPK) monitored daily for 14 days. All seventeen patients had elevated plasma pro ANF 1-98 and pro ANF 31–67 concentrations at the time of presentation. Maximal increase on day three post-infarction correlated with the size of infarction estimated by the maximal CPK (r = 0.675; p < 0.05) but did not correlate with the amount of left ventricular dysfunction. Another three patients with acute myocardial infarction were treated with tissue plasminogen activator (tPA). The measured pro ANF 1–98 and pro ANF 31–67 levels in these patients were within our normal range and significantly lower (p < 0.001) than seen in patients with acute myocardial in- farction not given thrombolytic therapy. Six patients with unstable angina, likewise, had normal circulating pro ANFs 1-98 and 31-67 concentrations during prolonged episodes of chest pain. These data suggest that myocardial necrosis but not ischemia triggers the release of the entire 126 aa prohormone.