de Beer F C, Hind C R, Fox K M, Allan R M, Maseri A, Pepys M B
Br Heart J. 1982 Mar;47(3):239-43. doi: 10.1136/hrt.47.3.239.
Serum C-reactive protein (CRP) and creatine kinase (CK) MB levels were measured prospectively in patients with definite myocardial infarction, patients with spontaneous or exercise-induced angina, subjects undergoing coronary arteriography, and patients with non-cardiac chest pain. All individuals with infarction developed raised CRP levels and there was a significant correlation between the peak CRP and CK MB values. The CRP, however, peaked around 50 hours after the onset of pain at a time when the CK MB, which peaked after about 15 hours, had already returned to normal. In 20 patients who recovered uneventfully, CRP levels fell, returning to normal about seven days after infarction in four cases who were followed to this point. In eight complicated cases, including four who died within the first 10 days, the CRP level remained high. Angina alone or coronary arteriography did not cause a rise in the CRP or CK MB concentrations. Increased CRP production is a non-specific response to tissue injury and raised CRP levels in cases of chest pain with a normal CK MB indicated a pathological process other than myocardial infarction. Regular monitoring of CRP levels may also assist in early recognition of intercurrent complications occurring after myocardial infarction.
前瞻性地测定了确诊心肌梗死患者、自发性或运动诱发型心绞痛患者、接受冠状动脉造影的受试者以及非心源性胸痛患者的血清C反应蛋白(CRP)和肌酸激酶(CK)MB水平。所有梗死患者的CRP水平均升高,且CRP峰值与CK MB值之间存在显著相关性。然而,CRP在疼痛发作后约50小时达到峰值,此时CK MB在约15小时后达到峰值且已恢复正常。在20例顺利康复的患者中,CRP水平下降,在随访至该阶段的4例患者中,梗死约7天后恢复正常。在8例复杂病例中,包括4例在最初10天内死亡的患者,CRP水平持续升高。单纯心绞痛或冠状动脉造影并未导致CRP或CK MB浓度升高。CRP产生增加是对组织损伤的非特异性反应,在CK MB正常的胸痛病例中CRP水平升高表明存在心肌梗死以外的病理过程。定期监测CRP水平也可能有助于早期识别心肌梗死后发生的并发并发症。