Neurological Intensive Care Unit, Columbia University College of Physicians and Surgeons, New York, NY, USA.
Neurocrit Care. 2010 Dec;13(3):359-65. doi: 10.1007/s12028-010-9447-x.
Although neurogenic stunned myocardium (NSM) after aneurysmal subarachnoid hemorrhage (SAH) is well described, its clinical significance remains poorly defined. We investigated the influence of left ventricular (LV) dysfunction and cerebral vasospasm on cerebral infarction, serious cardiovascular events, and functional outcome after SAH.
Of the 481 patients enrolled in the University Columbia SAH Outcomes Project between 10/96 and 05/02, we analyzed a subset of 119 patients with at least one echocardiogram, serial transcranial Doppler (TCD) data, and with no prior history of cardiac disease. LV dysfunction was defined as an ejection fraction <40% on echocardiography. Infarction from vasospasm was adjudicated by the study team after comprehensive review of all clinical and imaging data. Functional outcome was assessed at 15 and 90 days with the modified Rankin Scale (mRS).
Eleven percent of patients had LV dysfunction (N = 13). Younger age, hydrocephalus, and complete filling of the quadrigeminal and fourth ventricles were associated with LV dysfunction (all P < 0.05). Despite a similar frequency of pre-existing hypertension, 0% of patients with LV dysfunction reported taking antihypertensive medication, compared to 35% of those without (P = 0.009). There was a significant association between LV dysfunction and infarction from vasospasm after adjusting for clinical grade, age, and peak TCD flow velocity (P = 0.03). Patients with LV dysfunction also had higher rates of hypotension requiring vasopressors (P = 0.001) and pulmonary edema (P = 0.002). However, there was no association between LV dysfunction and outcome at 14 days after adjustment for established prognostic variables.
LV dysfunction after SAH increases the risk of cerebral infarction from vasospasm, hypotension, and pulmonary edema, but with aggressive ICU support does not affect short-term survival or functional outcome. Antihypertensive medication may confer cardioprotection and reduce the risk of catecholamine-mediated injury after SAH.
尽管神经源性顿抑心肌(NSM)在蛛网膜下腔出血(SAH)后已得到充分描述,但它的临床意义仍未得到明确界定。我们研究了左心室(LV)功能障碍和脑血管痉挛对 SAH 后脑梗死、严重心血管事件和功能结局的影响。
在 1996 年 10 月至 2002 年 5 月期间,哥伦比亚大学 SAH 结局项目共纳入 481 例患者,我们分析了其中一个子集 119 例患者,这些患者至少进行了一次超声心动图检查、连续经颅多普勒(TCD)检查,且无先前心脏病病史。LV 功能障碍定义为超声心动图上射血分数<40%。通过综合审查所有临床和影像学数据,由研究小组判定由血管痉挛引起的梗死。功能结局在 15 天和 90 天用改良 Rankin 量表(mRS)评估。
11%的患者有 LV 功能障碍(N=13)。年轻、脑积水和四脑室和第四脑室完全充盈与 LV 功能障碍相关(均 P<0.05)。尽管高血压的发生率相似,但 LV 功能障碍患者中,0%的人报告服用降压药,而无 LV 功能障碍患者中,35%的人报告服用降压药(P=0.009)。在校正临床分级、年龄和 TCD 峰值流速后,LV 功能障碍与血管痉挛引起的梗死之间存在显著关联(P=0.03)。LV 功能障碍患者低血压需要升压药的发生率更高(P=0.001),肺水肿的发生率更高(P=0.002)。然而,在校正既定预后变量后,LV 功能障碍与 14 天后的结局之间没有关联。
SAH 后 LV 功能障碍增加了血管痉挛性脑梗死、低血压和肺水肿的风险,但在 ICU 积极支持下,并不影响短期生存或功能结局。降压药可能提供心脏保护作用,并降低 SAH 后儿茶酚胺介导损伤的风险。