Intra-arterial nicardipine infusion improves CT perfusion-measured cerebral blood flow in patients with subarachnoid hemorrhage-induced vasospasm.

BACKGROUND AND PURPOSE: Our aim was to determine the effects of intra-arterial (IA) nicardipine infusion on the cerebral hemodynamics of patients with aneurysmal subarachnoid hemorrhage (aSAH)-induced vasospasm by using first-pass quantitative cine CT perfusion (CTP). MATERIALS AND METHODS: Six patients post-aSAH with clinical and transcranial Doppler findings suggestive of vasospasm were evaluated by CT angiography and CTP immediately before angiography for possible vasospasm treatment. CTP was repeated immediately following IA nicardipine infusion. Maps of mean transit time (MTT), cerebral blood volume (CBV), and cerebral blood flow (CBF) were constructed and analyzed in a blinded manner. Corresponding regions of interest on these maps from the bilateral middle cerebral artery territories and, when appropriate, the bilateral anterior or posterior cerebral artery territories, were selected from the pre- and posttreatment scans. Normalized values were compared by repeated measures analysis of variance. RESULTS: Angiographic vasospasm was confirmed in all patients. In 5 of the 6 patients, both CBF and MTT improved significantly in affected regions in response to nicardipine therapy (mean increase in CBF, 41 +/- 43%; range, -9%-162%, P = .0004; mean decrease in MTT, 26 +/- 24%; range, 0%-70%, P = .0002). In 1 patient, we were unable to quantify improvement in flow parameters due to section-selection differences between the pre- and posttreatment examinations. CONCLUSIONS: IA nicardipine improves CBF and MTT in ischemic regions in patients with aSAH-induced vasospasm. Our data provide a tissue-level complement to the favorable effects of IA nicardipine reported on prior angiographic studies. CTP may provide a surrogate marker for monitoring the success of treatment strategies in patients with aSAH-induced vasospasm.

Rapid infusion of cold saline (4 degrees C) as adjunctive treatment of fever in patients with brain injury.

The use of rapid infusion of large-volume cold saline (CS) as an adjunctive therapy for treating refractory fever in nine patients is reported. A decline in temperature (39.2 +/- 0.3 vs 37.1 +/- 1.2 degrees C, p = 0.006) at 2 hours and fever burden (97.3 +/- 343.8 vs 734.3 +/- 422.3 degrees C*min, p = 0.02) at 12 hours was noted after CS bolus. Rapid infusion of large-volume CS may be used as an adjunct for inducing normothermia in refractory febrile patients.

CT angiography in the rapid triage of patients with hyperacute stroke to intraarterial thrombolysis: accuracy in the detection of large vessel thrombus.

PURPOSE: The purpose of this work was to evaluate the accuracy of CT angiography (CTA) for the detection of large vessel intracranial thrombus in clinically suspected hyperacute (<6 h) stroke patients. METHOD: Forty-four consecutive intraarterial thrombolysis candidates underwent noncontrast CT followed immediately by CTA. Axial source and two-dimensional collapsed maximum intensity projection reformatted CTA images were rated for the presence or absence of large vessel occlusion. Five hundred seventy-two circle-of-Willis vessels were reviewed; arteriographic correlation was available for 224 of these. RESULTS: Sensitivity and specificity for the detection of large vessel occlusion were 98.4 and 98.1%; accuracy, calculated using receiver operating characteristic analysis, was 99%. Mean time for acquisition, reconstruction, and analysis of CTA images was approximately 15 min. CONCLUSION: CTA is highly accurate for the detection and exclusion of large vessel intracranial occlusion and may therefore be valuable in the rapid triage of hyperacute stroke patients to intraarterial thrombolytic treatment.

Regional patterns of left ventricular systolic dysfunction after subarachnoid hemorrhage: evidence for neurally mediated cardiac injury.

Although left ventricular (LV) dysfunction has been described after subarachnoid hemorrhage (SAH), its pathophysiology, regional distribution, and reversibility remain uncertain. To test the hypothesis that regional wall motion patterns in SAH patients do not match the typical patterns observed in coronary artery disease, a segmental wall motion analysis was performed in 30 SAH patients with LV dysfunction. Both regional (n = 21) and global (n = 9) wall motion patterns were observed. Preservation of apical function relative to the base was observed in 17 (57%) of the 30 patients. Many of the wall motion patterns were atypical of coronary artery disease but correlated with the distribution of the myocardial sympathetic nerve terminals. Five subjects had follow-up echocardiograms with resolution of LV dysfunction in all cases. In conclusion, a previously unreported, apex-sparing pattern of LV dysfunction is described, providing indirect evidence for a neurally mediated mechanism of cardiac injury. Limited data indicate that LV dysfunction in SAH patients is potentially reversible.

Regional myocardial perfusion after experimental subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: The pathophysiology of cardiac injury after subarachnoid hemorrhage (SAH) remains controversial. Data from animal models suggest that catecholamine-mediated injury is the most likely cause of cardiac injury after SAH. However, researchers also have proposed myocardial ischemia to be the underlying cause, as a result of coronary artery disease, coronary artery spasm, or hypertension and tachycardia. To test the hypothesis that SAH-induced cardiac injury occurs in the absence of myocardial hypoperfusion, we developed an experimental canine model that reproduces the clinical and pathological cardiac lesions of SAH and defines the epicardial and microvascular coronary circulation. METHODS: Serial ECG, hemodynamic measurements, coronary angiography, regional myocardial blood flow measurements by radiolabeled microspheres, 2D echocardiography, and myocardial contrast echocardiography were performed in 9 dogs with experimental SAH and 5 controls. RESULTS: Regional wall motion abnormalities were identified in 8 of 9 SAH dogs and 1 of 5 controls (Fisher's Exact Test, P=0.02) but no evidence was seen of coronary artery disease or spasm by coronary angiography and of significant myocardial hypoperfusion by either regional myocardial blood flow or myocardial contrast echocardiography. CONCLUSIONS: In this experimental model of SAH, a unique form of regional left ventricular dysfunction occurs in the absence of myocardial hypoperfusion. Future studies are justified to determine the cause of cardiac injury after SAH.

Cardiac outcome in patients with subarachnoid hemorrhage and electrocardiographic abnormalities.

OBJECTIVE: Approximately 25% of patients with subarachnoid hemorrhage (SAH) have electrocardiographic (ECG) abnormalities consistent with myocardial ischemia or myocardial infarction (MI), and their cardiac prognosis remains unclear. The objective of this study was to determine the cardiac and all-cause mortality rate of a series of patients with SAH with ECG changes consistent with ischemia or MI. METHODS: Using an existing database of patients with SAH and predetermined ECG criteria for ischemia or MI, a study group of patients with abnormal ECG results within 3 days of presentation and before aneurysm surgery was identified. Database patients without abnormal ECG results served as a control group. Cardiac mortality, defined as death resulting from arrhythmia, congestive heart failure, or cardiogenic shock, was assessed by chart review. RESULTS: Of 439 patients with SAH in the database, 58 met the criteria for the study group. Forty-one of these patients were treated neurosurgically. No deaths resulting from cardiac causes occurred, and 20 patients died as a result of noncardiac causes. In a multivariable analysis, age older than 65 years and Hunt and Hess grade of at least 3 were predictive of all-cause mortality. ECG abnormalities, however, were not a statistically significant predictor. CONCLUSION: In patients with SAH and ECG readings consistent with ischemia or MI, the risk of death resulting from cardiac causes is low, with or without aneurysm surgery. The ECG abnormalities are associated with more severe neurological injury but are not independently predictive of all-cause mortality.