心肌肌钙蛋白-I和危重病患者心肌坏死

目的 :明确非心源性疾病的危重病患者在低血压事件后是否会发生心肌坏死 ,并寻找心肌坏死指标。方法 :脓毒症及脓毒性休克患者按预后分为 2组。每 2 4h检测心肌肌钙蛋白 -Ⅰ (cTnI)、肌酸激酶 (CK)、肌酸激酶同功酶 (CKMB) ,并动态观察ECG。结果 :5 0例患者死亡 2 8例 ,存活 2 2例 ,死亡组cTnI阳性率 (10 0 % )显著高于存活组 (36 4 % ) ,P <0 .0 1;5 0例患者cTnI阳性率 (72 % )显著高于ECG阳性率 (36 % ) ,P <0 .0 1。低血压持续时间越长 ,cTnI阳性率越高 (重度低血压组 10 0 % ,轻中度低血压组 5 3.3% ,P <0 .0 1)。结论 :急性非心源性疾病的危重患者低血压后可以引起心肌损害 ,表现出cTnI阳性 ,且心电图可能大多并未表现出心肌坏死特征

Cardiac troponin I and myocardial necrosis in critical ILL patiants

Objective: To ascertain if, after an episode of hypotension, myocardial necrosis could occur in critical ill patients with acute non-cardiac illness and to search for signs of cardiac necrosis. Methods: Fifty patients of general ICU with severe sepsis/septic shock in two groups by outcome. Cardiac troponin I (cTnl), creatine kinase (CK),creatine kinase MB mass(CKMB) were measured per 24h after enrollment. And the ECG were observed continuously. Results: The sensitivity of cTnl of Death group were 100%, which were significantly higher than that of Survival group(36.4%, respectively, P<0.01 ).The sensitivity of cTnl of 50 patients was significantly higher than that of ECG(72% VS 36% ,respectively, P<0.01 ).Moreover, the longer the hypotension episode was, the greater was the sensitivity of cTnl (moderate hypotension:53.3%; severe hypotension :100%, P<0.01). Conclusion: Hypotension may cause cardiac damage in critical ill patients with acute non-cardiac diseases as shown by positive of cTnl. It is likely that a high number of these myocardial necroses may go unnoticed on the ECG.