Delay to Tissue Plasminogen Activator in Hypertensive Stroke Patients: An Analysis of Delay Duration Across Agents.

BACKGROUND AND PURPOSE: A subset of ischemic stroke patients present with blood pressures above that considered safe for thrombolytic administration, requiring antihypertensive therapy. Guideline statements are ambivalent regarding which antihypertensive agent should be used to obtain a satisfactory blood pressure < 185/110 mm Hg prior to alteplase. METHODS: We reviewed data from consecutive patients at a single institution treated with alteplase from January 2014 to January 2019, collecting door-to-needle times, antihypertensive agent (if used), and antihypertensive-to-needle times. Patients were grouped by initial agent administered. We assessed for differences in door-to-needle times between those needing antihypertensive(s) and those who did not. Antihypertensive-to-needle times were compared across 3 antihypertensive groups (labetalol, nicardipine, and hydralazine). RESULTS: Analysis included 239 patients: 177 receiving no antihypertensive, 44 labetalol, 13 nicardipine, and 5 hydralazine. Those not administered an antihypertensive prior to alteplase had shorter door-to-needle times (52.6 minutes versus 62.1 minutes, P = .016). We found no statistical differences when comparing door-to-needle times across all groups (no med 52.6 minutes, labetalol 64.3 minutes, nicardipine 53.0 minutes, hydralazine 67.4 minutes, P = .052). No differences were found in antihypertensive-to-needle amongst the 3 antihypertensive groups (labetalol 18.75 minutes, nicardipine 12.15 minutes, hydralazine 25.40 minutes, P = .239). CONCLUSIONS: Patients requiring antihypertensives experienced slower door-to-needle times. No statistically significant changes were observed in door-to-needle times by antihypertensive used, however these results may have clinical importance. This study is limited by relatively small sample size. Pooling data from multiple institutions could provide more robust assessment and inform clinical practice.

Tyrosine kinase inhibitor induced rapidly progressive vasculopathy after intracranial stent placement.

Tyrosine kinase inhibitor (TKI) therapy for chronic myeloid leukemia (CML) has been associated with progressive peripheral arterial disease and, more recently, rare cases of intracranial vascular stenosis have been reported. We report the fourth case of TKI treatment associated intracranial vasculopathy and rapid progression of intracranial vascular stenosis following intracranial stent placement. This was a 49-year-old woman who developed right-sided weakness, paresthesias, numbness, and speech difficulties 7 years following TKI treatment for CML. Cerebral catheter angiography demonstrated 90% stenosis of the left supraclinoid internal carotid artery, for which the patient underwent intracranial stent placement with no residual stenosis and improved distal blood flow. Approximately 1 month following the procedure, the patient returned with similar symptoms. Catheter angiography demonstrated 70% and 50% stenosis just distal and proximal to the stent construct, respectively. Rapid disease progression and non-atherosclerotic vasculopathy may argue against endovascular therapy.

Tyrosine kinase inhibitor induced rapidly progressive vasculopathy after intracranial stent placement.

Tyrosine kinase inhibitor (TKI) therapy for chronic myeloid leukemia (CML) has been associated with progressive peripheral arterial disease and, more recently, rare cases of intracranial vascular stenosis have been reported. We report the fourth case of TKI treatment associated intracranial vasculopathy and rapid progression of intracranial vascular stenosis following intracranial stent placement. This was a 49-year-old woman who developed right-sided weakness, paresthesias, numbness, and speech difficulties 7 years following TKI treatment for CML. Cerebral catheter angiography demonstrated 90% stenosis of the left supraclinoid internal carotid artery, for which the patient underwent intracranial stent placement with no residual stenosis and improved distal blood flow. Approximately 1 month following the procedure, the patient returned with similar symptoms. Catheter angiography demonstrated 70% and 50% stenosis just distal and proximal to the stent construct, respectively. Rapid disease progression and non-atherosclerotic vasculopathy may argue against endovascular therapy.