Uusimaa P, Risteli J, Niemelä M, Lumme J, Ikäheimo M, Jounela A, Peuhkurinen K
Department of Internal Medicine, Oulu University, Finland.
Circulation. 1997 Oct 21;96(8):2565-72. doi: 10.1161/01.cir.96.8.2565.
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<.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.
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.
急性心肌梗死（AMI）后的左心室功能由梗死区域的扩展和未梗死心肌的重塑决定。梗死相关动脉（IRA）闭塞是重塑的独立危险因素。
对36例疑似AMI患者的心肌胶原代谢变化进行评估。分析血浆肌酸激酶同工酶MB分数和肌红蛋白释放曲线，以评估早期再灌注和梗死面积。通过测量血清III型前胶原氨基端前肽（PIIINP）、I型前胶原完整氨基端前肽（完整PINP）和I型前胶原羧基端前肽（PICP）的浓度来评估胶原瘢痕形成。还测量了血浆肾素活性以及皮质醇和醛固酮的尿排泄量。在早期住院期间进行冠状动脉造影和左心室电影造影。AMI患者血清PIIINP浓度从3.50±0.20μg/L升至最高5.08±0.36μg/L（n = 32），而完整PINP和PICP浓度则趋于下降。与无心力衰竭或射血分数>40%的患者相比，严重心力衰竭或射血分数≤40%的患者在心肌梗死后最初10天内PIIINP的曲线下面积（AUC）更大（分别为P<0.05和P<0.01），并且与TIMI血流0至2级的患者相比，TIMI血流3级的患者的AUC也更大（P<0.05），尽管酶学测定的梗死面积相似。未观察到PIIINP与神经体液参数之间存在显著相关性。PIIINP的AUC以及最初4天内PIIINP的变化与心功能指标显著相关。
AMI后胶原瘢痕形成可通过测量血清PIIINP浓度进行量化。在导致左心室功能障碍的大面积梗死以及IRA闭塞的患者中，瘢痕形成更为明显。
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