Cholesterol level and symptomatic hemorrhagic transformation after ischemic stroke thrombolysis.

BACKGROUND: Prestroke statin use may improve ischemic stroke outcomes, yet there is also evidence that statins and extremely low cholesterol levels may increase the risk of intracranial hemorrhage. We evaluated the independent effect of statin use and admission cholesterol level on risk of symptomatic hemorrhagic transformation (sHT) after recanalization therapy for acute ischemic stroke. METHODS: We analyzed ischemic stroke patients recorded in a prospectively maintained registry that received recanalization therapies (IV or intra-arterial fibrinolysis or endovascular embolectomy) at a university medical center from September 2002 to May 2006. The independent effect of premorbid statin use on sHT post intervention was evaluated by logistic regression, adjusting for prognostic and treatment variables known to predict increased HT risk after ischemic stroke. RESULTS: Among 104 patients, mean age was 70 years, and 49% were men. Male sex, hypertension, statin use, low total cholesterol and low-density lipoprotein (LDL) cholesterol, current smoking, elevated glucose levels, and higher admission NIH Stroke Scale (NIHSS) score were all associated with a greater risk of sHT in univariate analysis. After adjusting for covariates, low LDL cholesterol (odds ratio [OR], 0.968 per 1-mg/dL increase; 95% CI, 0.941 to 0.995), current smoking (OR, 14.568; 95% CI, 1.590 to 133.493), and higher NIHSS score (OR, 1.265 per 1-point increase; 95% CI, 1.047 to 1.529) were independently associated with sHT risk. CONCLUSIONS: Lower admission low-density lipoprotein cholesterol level with or without statin use, current smoking, and greater stroke severity are associated with greater risk for symptomatic hemorrhagic transformation after recanalization therapy for ischemic stroke.

Are elevated admission calcium levels associated with better outcomes after ischemic stroke?

Calcium (Ca(2+)) and magnesium (Mg(2+)) influence the molecular pathways of ischemic neuronal death. The authors evaluated the impact of admission serum Ca(2+) and Mg(2+) levels, on incident stroke severity and discharge functional outcome. After adjusting for covariates, higher admission Ca(2+) was significantly associated with lesser stroke severity and better discharge functional outcome. Admission Mg(2+) was not an independent clinical outcome prognosticator.

Premorbid antiplatelet use and ischemic stroke outcomes.

OBJECTIVE: To evaluate the independent effect of premorbid antiplatelet use on incident ischemic stroke severity and outcome at discharge. METHODS: The authors studied consecutive patients presenting within 24 hours of ischemic stroke over a 1-year period. National Institutes of Health Stroke Scale (NIHSS) score at presentation was used as index of stroke severity and a modified Rankin scale of 0 to 1 at discharge as index of good functional outcome. Patients were categorized according to their premorbid antiplatelet use as antiplatelet-inclusive (AI) and no antiplatelet (NA). Demographic data, risk factors, pertinent laboratory tests, other medications, and stroke mechanisms were controlled for across the two groups using multivariate logistic regression. RESULTS: A total of 260 individuals met study criteria: 92 patients were on antiplatelet agents prior to admission, 168 were on no antiplatelets. Pretreatment with antiplatelet was associated with lower presenting median NIHSS (4.5 vs 7, p = 0.005). Antiplatelet use was associated with less severe stroke at presentation in those having no history of stroke or TIA (4.8 vs 8.0, p = 0.03) but not in those with a prior history of stroke or TIA (4.9 vs 4.9, p = 0.987). The likelihood of a good outcome was increased in those on antiplatelets after adjusting for other variables (OR 2.105, p = 0.0073). CONCLUSIONS: Prestroke use of antiplatelet may be associated with reduced severity of incident ischemic strokes in those with no prior history of stroke or TIA, and with an increased likelihood of a good discharge outcome regardless of prior cerebrovascular event history.

Angiotensin 2 type 2 receptor activity and ischemic stroke severity.

BACKGROUND: Drugs that increase angiotensin 2 formation, including thiazides, calcium channel blockers, and angiotensin 2 type 1 (AT1) receptor blockers, may be more effective in stroke prevention than angiotensin 2 suppressive drugs such as angiotensin-converting enzyme inhibitors and beta-blockers. OBJECTIVE: To assess whether angiotensin 2 formation increasing drugs reduce incident stroke severity compared with angiotensin 2 formation suppressive drugs. METHODS: Consecutive patients presenting within 24 hours of first-ever ischemic stroke over an 18-month period were studied. Subjects were only included if they were on only angiotensin 2 formation increasers, only angiotensin 2 formation suppressors, or no antihypertensive agents. NIH Stroke Scale (NIHSS) score at presentation was used as the index of stroke severity. Demographic data, risk factors, admission blood pressures, other medications, and stroke mechanisms were controlled for across the three groups using least absolute deviation linear regression. RESULTS: One hundred seventy-five individuals met study criteria. Mean age was 67.4 years; 45% were women. Forty-nine patients were on angiotensin 2 formation suppressors and 16 on angiotensin 2 formation increasers. Age at admission, atrial fibrillation, previous antithrombotic use, cardioembolic and large-vessel atherosclerotic mechanisms, and mean systolic and diastolic blood pressure were significant univariate predictors of presenting median NIHSS score. On multivariate analysis, the adjusted median NIHSS score was lower in the angiotensin 2 increasers (median = 2.2; p = 0.005) and trended lower for angiotensin 2 suppressors (median = 4.4; p = 0.054) compared with the no-antihypertensive group (median = 6.0). There was no difference in stroke severity between angiotensin 2 increasers compared with angiotensin 2 suppressors (p = 0.123). CONCLUSIONS: Angiotensin 2 formation increasing agents did not reduce ischemic stroke severity more than angiotensin 2 formation suppressing agents. However, the prestroke use of antihypertensives was associated with reduced severity of incident ischemic strokes.

PROTECT: a coordinated stroke treatment program to prevent recurrent thromboembolic events.

OBJECTIVE: To assess the impact of the Preventing Recurrence of Thromboembolic Events through Coordinated Treatment (PROTECT) Program on achievement of its eight secondary prevention goals at the time of discharge. METHODS: Achievement rates for the eight program goals at time of discharge were compared in all patients discharged from a university hospital-based stroke service with a diagnosis of ischemic stroke or TIA during a 1-year period after implementation of the PROTECT Program vs rates obtained from a comparable group of patients admitted to the same service during the preceding year. RESULTS: Demographic and medical features were comparable in the baseline and intervention cohorts for all patients with cerebral ischemia presumed due to large-vessel atherosclerosis or small-vessel disease (baseline year n = 117, intervention n = 130). Implementation rates in patients without specific contraindications increased for all four medication goals: 97 to 100% for antithrombotic agents, 68 to 97% for statins, 42 to 90% for angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, and 14 to 70% for diuretics. Although data were not collected on baseline lifestyle instruction rates, instruction in the program's four lifestyle interventions was achieved by discharge in 100% of the intervention cohort. CONCLUSION: Implementation of this single-center, systems-based, in-hospital program to initiate secondary stroke prevention therapies was associated with a substantial increase in treatment utilization at the time of hospital discharge.