(Circulation. 1997;96:2565-2572.)
© 1997 American Heart Association, Inc.
Articles |
Collagen Scar Formation After Acute Myocardial Infarction
Relationships to Infarct Size, Left Ventricular Function, and Coronary Artery Patency
From the Departments of Internal Medicine and Clinical Chemistry (J.R.), Oulu University, Oulu, Finland.
Correspondence to Dr Keijo Peuhkurinen, Department of Internal Medicine, Division of Cardiology, Oulu University Hospital, Kajaanintie 50, 90220 Oulu, Finland.
Background 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.
Methods and Results 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 µg/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
40% than in those with no heart failure or with an ejection fraction
>40% (P<.05 and P<.01, respectively), and it
was also larger in the patients with TIMI grade 0 to 2 flows than in
those with TIMI 3 flows (P<.05), despite similar
enzymatically determined infarct sizes. No significant correlations
between PIIINP and neurohumoral parameters were observed.
The AUC of PIIINP and the change in PIIINP during the first 4 days were
significantly correlated with indices of cardiac function.
Conclusions Collagen scar formation after AMI can be quantified by measurement of serum PIIINP concentrations. Scar formation is more prominent in large infarctions causing left ventricular dysfunction and in patients with occluded IRAs.
Key Words: collagen • remodeling • myocardial infarction
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