Cholesterol Measured Before Stroke Thrombolysis Is Not Associated With Tissue Plasminogen Activator–Related Hemorrhagic Transformation
To the Editor:
A link between cholesterol level and symptomatic hemorrhagic transformation (sHT) after ischemic stroke thrombolysis has been recently described.1 This association might be relevant regarding use of statins in the acute stroke field. Bang et al defined sHT as any clinical worsening associated with HT, either major or minor. In that study any sHT appeared in 17 cases (16.4%). Low LDL cholesterol and previous treatment with statins were related to sHT appearance, and after adjusting for covariates low LDL cholesterol (odds ratio, 0.968 per 1-mg/dL increase; 95% CI, 0.941 to 0.995) was independently associated with sHT risk.
Similar to that study and to evaluate whether stroke patients who receive tissue plasminogen activator (t-PA) have different outcome when statins were taken before stroke, we evaluated 145 patients with a stroke involving the middle cerebral artery who received t-PA treatment.2 In our study, a logistic regression model identified previous treatment with statins (odds ratio 5.26; 95% CI, 1.48 to 18.72; P=0.027) as independent predictor of good functional outcome and no differences for any sHT regarding statin use was found (8.3% sHT among those receiving statins versus 9.3% sHT among those who did not receive statins, P=0.88).
Moreover, we have measured lipids profile in the plasma of 60 stroke patients before (<3 hours from stroke onset) they received t-PA treatment. Among them, 8.3% had any sHT; however, as shown in the the Table none of the measured lipidic parameters was related with that complication (Table). Similarly, any association was found when considering other HT classifications, such as parenchymal hematomas appearance (data not shown).
In Bang et al’s study all patients had fasting lipid panels drawn the day after hospital admission; therefore, in many cases it is possible that the lipid profile was obtained after the hemorrhagic complication. Whether low LDL is a consequence and not the cause of the complication in their patients is a possibility. This was avoided in our study by measuring lipids before t-PA treatment.
Because high rates of sHT in Bang et al’s study (16.4% versus 8.3% in our patients) may be influenced by the use of mechanical devices, it might be interesting to know whether the cholesterol-sHT relationship they found was also true for the subgroups of patients that received only t-PA treatment. In my opinion cholesterol level measured before stroke thrombolysis is not associated with t-PA–related hemorrhagic transformation. In the future, more information coming from acute stroke trials that combine statins with t-PA might show new data on this interesting question.3
Bang OY, Saver JL, Liebeskind DS, Starkman S, Villablanca P, Salamon N, Buck B, Ali L, Restrepo L, Vinuela F, Duckwiler G, Jahan R, Razinia T, Ovbiagele B. Cholesterol level and symptomatic hemorrhagic transformation after ischemic stroke thrombolysis. Neurology. 2007; 68: 737–742.
Alvarez-Sabin J, Huertas R, Quintana M, Rubiera M, Delgado P, Ribo M, Molina CA, Montaner J. Prior statin use may be associated with improved stroke outcome after tissue plasminogen activator. Stroke. 2007; 38: 1076–1078.