Elevated cardiac troponin I and relationship to persistence of electrocardiographic and echocardiographic abnormalities after aneurysmal subarachnoid hemorrhage.
Elevated cardiac troponin I and relationship to persistence of electrocardiographic and echocardiographic abnormalities after aneurysmal subarachnoid hemorrhage.
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DOI：
10.1161/strokeaha.109.556753
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发表时间：
2009-11
期刊：
影响因子：
8.3
通讯作者：
Horowitz MB
中科院分区：
文献类型：
--
作者：
Hravnak M;Frangiskakis JM;Crago EA;Chang Y;Tanabe M;Gorcsan J 3rd;Horowitz MB
蛛网膜下腔出血（aSAH）后心脏损伤的持续性还没有很好的描述。我们假设aSAH后心脏损伤（通过心肌肌钙蛋白I（cTnI）升高检测）与aSAH严重程度相关，并与持续的心电图和结构性超声心动图异常相关。对Fisher分级≥2和/或Hunt/Hess分级≥3的aSAH患者进行了前瞻性纵向研究。在第1 - 5天采集血清cTnI;队列分为cTnI峰值≥0.3 ng/mL（升高）或cTnI ≥0.3 ng/mL。评价cTnI与aSAH严重程度、早期（≤4天）和晚期（≥7天）12导联心电图、第1 - 5天霍尔特监测以及早期（0 - 5天）和晚期（5 - 12天）经胸超声心动图（左心室射血分数和局部室壁运动异常）之间的关系。在204例受试者中，31%的受试者cTnI ≥0.3 ng/mL。cTnI ≥0.3 ng/mL与入院症状（Hunt/Hess P=0.001）和血负荷（Fisher P=0.028）的aSAH严重程度递增相关。cTnI ≥0.3 ng/mL的患者中，早期（63% vs. 30%，P<0.0001）和晚期（24% vs. 7%，P=0.024）心电图QTc延长者较多。在霍尔特动态心电图监测中，cTnI ≥0.3 ng/mL的患者中，室性心动过速/室颤的发生率较高（22% vs 9%，P=0.018），而房颤/房扑的发生率较低（P=0.241）。心肌肌钙蛋白I ≥0.3 ng/mL与早期射血分数<50%（44%对5%，P<0.0001）和局部室壁运动异常（44%对4%，P<0.0001）相关。局部室壁运动异常主要发生在基底段和心室中段，73%的受累患者在一定程度上持续存在，而射血分数<50%的受累患者持续存在59%。心脏损伤随着aSAH严重程度的增加而逐渐加重，并与持续性QTc延长和室性心律失常相关。局部室壁运动异常和射血分数降低在大多数受影响的患者中持续存在一定程度。
Cardiac injury persistence after aneurysmal subarachnoid hemorrhage (aSAH) is not well described. We hypothesized that post-aSAH cardiac injury, detected by elevated cardiac troponin I (cTnI), is related to aSAH severity and associated with electrocardiographic and structural echocardiographic abnormalities that are persistent. Prospective longitudinal study was conducted of patients with aSAH with Fisher grade ≥2 and/or Hunt/Hess grade ≥3. Serum cTnI was collected on Days 1 to 5; cohort dichotomized into peak cTnI ≥0.3 ng/mL (elevated) or cTnI ≥0.3 ng/mL. Relationships among cTnI and aSAH severity, 12-lead electrocardiography early (≤4 days) and late (≥7 days), Holter monitoring on Days 1 to 5, and transthoracic echocardiogram (left ventricular ejection fraction and regional wall motion abnormalities) early (Days 0 to 5) and late (Days 5 to 12) were evaluated. Of 204 subjects, 31% had cTnI ≥0.3 ng/mL. cTnI ≥0.3 ng/mL was incrementally related to aSAH severity by admission symptoms (Hunt/Hess P=0.001) and blood load (Fisher P=0.028). More patients with cTnI ≥0.3 ng/mL had prolonged QTc on early (63% versus 30%, P<0.0001) and late electrocardiography (24% versus 7%, P=0.024). On Holter monitoring, more patients with cTnI ≥0.3 ng/mL had ventricular tachycardia/fibrillation (22% versus 9%, P=0.018) but not atrial fibrillation/flutter (P=0.241). Cardiac troponin I ≥0.3 ng/mL was associated with both early ejection fraction <50% (44% versus 5%, P<0.0001) and regional wall motion abnormalities (44% versus 4%, P<0.0001). Regional wall motion abnormalities predominated in basal and midventricular segments and persisted to some degree in 73% of patients affected, whereas ejection fraction <50% persisted in 59% of patients affected. Cardiac injury is incrementally worse with increasing aSAH severity and associated with persistent QTc prolongation and ventricular arrhythmias. Regional wall motion abnormalities and depressed ejection fraction persist to some degree in the majority of those affected.