Grace H. Kim, David K. Hahn, Christopher P. Kellner, Ricardo J. Komotar, Robert Starke, Matthew C. Garrett, Jiang Yao, Justin Cleveland, Stephan A. Mayer and E. Sander Connolly Jr.
Heparin-induced thrombocytopenia Type II (HIT II) is a serious complication that occurs in 0.2–3% of patients treated with heparin and is associated with a high risk of thrombotic events. One center recently reported an incidence of HIT II of 15% in a population of patients with aneurysmal subarachnoid hemorrhage (aSAH). Because these patients are typically exposed to heparin during angiography, controversy exists regarding whether prophylaxis with enoxaparin rather than heparin affords any reduction in the risk of developing HIT II. In this study, the authors investigated the effect of heparin compared with enoxaparin on the incidence of HIT II in patients with aSAH.
The authors reviewed the medical records of 300 patients treated for aSAH who received thromboprophylaxis with either heparin or enoxaparin, and identified patients who developed HIT II. The incidences of HIT II in the 2 treatment groups were then compared.
One hundred sixty-six patients with aSAH were treated with heparin, and 134 patients were treated with enoxaparin. Sixteen (5.3%) of 300 patients met the diagnostic criteria for HIT II. Of those treated with heparin, 8 (4.8%) of 166 developed HIT II, compared with 8 (6%) of 134 treated with enoxaparin (difference not significant).
The authors report a lower incidence of HIT II in patients with aSAH than has previously been reported. The data also suggest that patients with aSAH who receive heparin are at no greater risk of developing HIT II than those who receive enoxaparin. This finding challenges the merit of choosing enoxaparin rather than heparin for thromboprophylaxis in patients with a SAH.
Grace H. Kim, Christopher P. Kellner, David K. Hahn, Brianna M. Desantis, Muhith Musabbir, Robert M. Starke, Michal Rynkowski, Ricardo J. Komotar, Marc L. Otten, Robert Sciacca, J. Michael Schmidt, Stephan A. Mayer and E. Sander Connolly Jr.
Despite efforts to elucidate both the molecular mechanism and the clinical predictors of vasospasm after aneurysmal subarachnoid hemorrhage (ASAH), its pathogenesis remains unclear. Monocyte chemoattractant protein–1 (MCP-1) is a chemokine that has been firmly implicated in the pathophysiology of vasospasm and in neural tissue injury following focal ischemia in both animal models and human studies. The authors hypothesized that MCP-1 would be found in increased concentrations in the blood and cerebrospinal fluid (CSF) of patients with ASAH and would correlate with both outcome and the occurrence of vasospasm.
Seventy-seven patients who presented with ASAH were prospectively enrolled in this study between July 2001 and May 2002. Using an enzyme-linked immunosorbent assay, MCP-1 levels were measured in serum daily and in CSF when available. The mean serum and CSF MCP-1 concentrations were calculated for each patient throughout the entire hospital stay. Neurological outcome was evaluated at discharge or 14 days posthemorrhage using the modified Rankin Scale. Vasospasm was evaluated on angiography.
The serum MCP-1 concentrations correlated with negative outcome such that a 10% increase in concentration predicted a 25% increase in the probability of a poor outcome, whereas the serum MCP-1 levels did not correlate with vasospasm. Concentrations of MCP-1 in the CSF, however, proved to be significantly higher in patients with angiographically demonstrated vasospasm.
These findings suggest a role for MCP-1 in neurological injury and imply that it may act as a biomarker of poor outcome in the serum and of vasospasm in the CSF.