Collagen scar formation after acute myocardial infarction : Relationships to infarct size, left ventricular function, and coronary artery patency

Left ventricular function after acute myocardial infarction (AMI) is determined by the expansion of the infarct zone and remodeling of the noninfarcted myocardium. An occluded infarct-related artery (IRA) is an independent risk factor for remodeling. Changes in myocardial collagen metabolism were ev...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 1997-10, Vol.96 (8), p.2565-2572
Main Authors: UUSIMAA, P, RISTELI, J, NIEMELÄ, M, LUMME, J, IKÄHEIMO, M, JOUNELA, A, PEUHKURINEN, K
Format: Article
Language:English
Subjects:
Adult
Aged
Aldosterone - urine
Biological and medical sciences
Cardiology. Vascular system
Cicatrix - pathology
Cicatrix - physiopathology
Cineangiography
Collagen
Coronary Angiography
Coronary heart disease
Coronary Vessels - physiopathology
Creatine Kinase - blood
Heart
Humans
Hydrocortisone - urine
Isoenzymes
Medical sciences
Middle Aged
Myocardial Infarction - pathology
Myocardial Infarction - physiopathology
Myocardial Reperfusion
Peptide Fragments - blood
Procollagen - blood
Renin - blood
Renin-Angiotensin System
Vascular Patency
Ventricular Function, Left
Wound Healing
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Summary:Left ventricular function after acute myocardial infarction (AMI) is determined by the expansion of the infarct zone and remodeling of the noninfarcted myocardium. An occluded infarct-related artery (IRA) is an independent risk factor for remodeling. Changes in myocardial collagen metabolism were evaluated in 36 patients with suspected AMI. The plasma creatine kinase MB fraction and myoglobin release curves were analyzed for assessment of early reperfusion and infarct size. Collagen scar formation was evaluated by measurement of serum concentrations of the aminoterminal propeptide of type III procollagen (PIIINP), the aminoterminal propeptide of type I procollagen (intact PINP), and the carboxyterminal propeptide of type I procollagen (PICP). Plasma renin activity and urine excretion of cortisol and aldosterone were also measured. Coronary angiography and left ventricular cineangiography were performed during early hospitalization. The serum concentration of PIIINP increased from 3.50+/-0.20 to a maximum of 5.08+/-0.36 microg/L (n=32) in the patients with AMI, whereas the concentrations of intact PINP and PICP tended to decrease. The area under the curve (AUC) of PIIINP during the first 10 postinfarction days was larger in patients with severe heart failure or ejection fractions < or = 40% than in those with no heart failure or with an ejection fraction > 40% (P
ISSN:0009-7322
1524-4539
DOI:10.1161/01.CIR.96.8.2565