Open AccessBeta‐endorphins in acute myocardial infarction
Author(s) -
Stoupel E.,
Pinchas A.,
Agmon J.,
Gilad I.,
Laron Z.
Publication year - 1986
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.4960090904
Subject(s) - medicine , myocardial infarction , creatine kinase , endorphins , lactate dehydrogenase , endocrinology , hormone , chest pain , gastroenterology , enzyme , biochemistry , chemistry
The endogenous peptide B‐endorphin (B‐EP) is closely connected with different aspects of homeostasis, behavior, and in particular with the perception of pain. The purpose of this study was to investigate the correlation between: (a) the level of plasma B‐EP and the intensity of pain in acute myocardial infarction (AMI); and (b) the B‐EP and specific enzymes for AMI serum glutamic oxolo‐acetic transferase, lactate dehydrogenase, and creatine phosphokinase and some stress hormones (cortisol, growth hormone). Twenty‐six patients hospitalized in the CCU for acute MI were studied during the first 72 hours from the onset of symptoms. Seven normal subjects served as controls. Blood was taken for hormone and B‐EP evaluation before treating the patients by opiates. Plasma B‐EP levels were determined using the protocol of the Immunonuclear Corporation (Stillwater, MN). Statistical analysis of the results showed: (1) Nonsignificant differences between B‐EP levels of all MI patients and control group. (2) Unaltered B‐EP levels in patients with acute MI suffering from moderate pain. (3) Significant differences in drop of B‐EP in the group with most severe pain (p<0.025). (4) A tendency toward decreased B‐EP in patients suffering from more prolonged pain (>6 hours). Significant negative correlation was shown between B‐EP and (a) chest pain intensity (0‐4 graduation) (r=0.8, p<0.01); (b) lactate dehydrogenase (r=0.7, p<0.01); (c) serum glutamic oxolo‐acetic transferase (r=0.6, p<0.01); (d) creatine phosphokinase (r=0.6, p<0.05; (e) plasma cortisol level (r=0.5, p<0.05). (5) A higher level of B‐EP in group of MI with creatine phosphokinase above 1500 units (p<0.05). (6) A significant rise of cortisol level in acute MI patients with low B‐EP and suffering from extreme pain (p<0.0005). (7) A strong tendency to (a) adverse correlation between B‐EP and growth hormone (p‐0.07) and (b) rise of growth hormone in severe pain (p=0.08). in conclusion, our data confirmed an adverse correlation between B‐EP and pain intensity in acute MI. This study shows some prognostic significance of B‐EP levels by confirmed negative correlation with acute MI enzymatic changes reflecting the extent of myocardial damage. in cases with very high creatine phosphokinase level this relationship was absent.