Secondary Stroke Prevention - Recent Advances: Inconsistencies

Abstract

The literature cited by Professor Diener needs to be looked at in greater detail. The PROGRESS study – 14% of patients were a priori not evaluated because they did not tolerate the ACE inhibitor perindopril that was used – was based on a definition of hypertension as blood pressure (BP) > 160/90 mm Hg. It is not clear to me how from this, a therapeutic recommendation for hypertension patients is deduced according to the definition of BP > 140/90 mm Hg. The MOSES study compared a sartan with nitrendipine – a substance that has not been shown to lower mortality in hypertension patients. In spite of this, the number of deaths in the study was numerically higher in patients taking eprosartan. Further, nitrendipine was given at too low a dosage in the study. Claiming class effects of the sartans that exceed mere blood pressure lowering is incorrect. Especially the cited LIFE study shows a different extent of blood pressure lowering, which is crucial for the stroke risk. Blood pressure normalized in 49% of patients receiving losartan, but in only 46% receiving atenolol. In the SPARCL study, 1.9% fewer patients had a stroke while being treated with the maximum dosage of atorvastatin. None of my stroke patients would be willing to take atorvastatin as an additional medication if the NNT was 52 over 5 years. The dipyramidole studies ESPS2 and ESPRIT, which the author mentions, are based on a comparison with underdosed acetylsalicylic acid. In the meta-analysis of the Antithrombotic Trialists’ Collaboration, it clearly says that ASA dosages between 75 mg and 150 mg were investigated – the value of lower dosages remained unclear. I fear that these inconsistencies may be a pointer to a conflict of interests in the reporting.