Tommasini G, Presta M
Br Heart J. 1979 Sep;42(3):326-32. doi: 10.1136/hrt.42.3.326.
In an attempt to develop improved methods of prediction of infarct size by enzymatic methods, Shell's original algorithm has been critically evaluated in an unselected series of patients. Poor performance of the model is partly the result of a systematic source of error associated with its mathematical formulation. A new model devoid of such limitations has therefore been developed. Residual deviations between predicted and observed CK release seem to be related to frequent and unpredictable extensions of infarction which could be verified by independent clinical, electrocardiographic, and enzymatic criteria. The modified model may possibly be applied to the evaluation of agents aimed at limiting the spread of irreversible injury.
为了尝试通过酶学方法开发改进的梗死面积预测方法,在一组未经挑选的患者中对谢尔最初的算法进行了严格评估。该模型表现不佳部分是由于与其数学公式相关的系统性误差来源。因此,开发了一种没有此类局限性的新模型。预测的和观察到的肌酸激酶(CK)释放之间的残余偏差似乎与梗死的频繁且不可预测的扩展有关,这可以通过独立的临床、心电图和酶学标准得到证实。修改后的模型可能适用于评估旨在限制不可逆损伤扩散的药物。