20: IMPACT OF MYOCARDIAL INJURY AFTER SUBARACHNOID HEMORRHAGE (SAHMI) UPON PERFUSION

Abstract

Patients with aneurysmal subarachnoid hemorrhage (aSAH) are known to experience myocardial injury (SAHMI) manifested by elevated cardiac troponin I (cTnI) and myocardial wall motion abnormality (WMA). Although SAHMI usually resolves during hospitalization, these patients experience poorer outcomes for reasons not understood. We suspect that SAHMI patients exhibit early perfusion impairment as a potential mechanism for poorer outcomes.

SAHMI impairs dynamic systemic perfusion in the immediate post injury period (days 0-3), which in turn, impairs cerebral perfusion.

Convenience sample of 30 patients diagnosed with aSAH. Fifteen patients with cTnI>=0.3ng/ml and WMA by echocardiographic determination were matched to 15 patients with cTnI=0 and no WMA, matched on age±5 yrs, gender, race, Fisher grade and Hunt/Hess score (HH). Systemic perfusion (HR, systolic [SBP], diastolic [SBP] mean arterial [MAP], and central venous pressures [CVP]) and intracranial (ICP) and cerebral perfusion pressure (CPP) were measured every 2 hours from admission to day 3 post-aSAH. SAHMI patients (cases) and no-SAHMI (controls) perfusion parameters across days 0-3 were compared with generalized estimating equations (GEE) to fit a repeated measure linear regression.

The sample was primarily female (83%) and white race (87%) with mean age 57 ± 9 yrs. SAHMI case patients peak mean cTnI was 8.2 ± 11ng/ml. SAHMI cases exhibited significantly lower SBP (b= -14.4, p<0.001) and MAP (b= -6.3, p=0.032), and higher HR (b= 7.7, p=0.010) and trended to higher CVP (b= 2.4, p=0.62) across days 0-3 days post injury than controls. SAHMI cases also trended toward lower CPP (b= -6.1, p=0.079).

SAHMI is not an innocuous aSAH complication. In the acute post-injury phase, afflicted patients exhibited lower early perfusion compared to patients with similar aSAH severity but no SAHMI. Further study in a larger sample is needed to determine if the perfusion parameters chosen translate into peripheral and cerebral tissue hypoxia as an explanatory mechanism, and correlate to poorer outcomes. Funding NHLBI R01HL074316