Hyperlipidemias: Kaczorowska B

Chudzik W, Kaczorowska B, Chmielewski H, Przybyła M, Gałka M. · Klinika Neurologii i Neurorehabilitacji z Oddzialem Udarowym Uniwersyteckiego Szpitala Klinicznego nr 2 w Lodzi. · Pol Merkur Lekarski. · Pubmed #16379334 No free full text.

Abstract: The occurrence of stroke increases with age, particularly affecting the older elderly, a population also at higher risk for coronary heart disease (CHD). Epidemiological and observational studies have not shown a clear association between cholesterol levels and all causes of stroke. Nevertheless, large, long-term statin trials in patients with established CHD or et high risk for CHD (diabetes, hypertension) have shown that statins decrease stroke incidence in these populations even with a normal baseline cholesterol concentration. In patients with previous stroke statins reduce the incidence of coronary events, but whether they actually reduce the incidence of recurrent strokes in secondary prevention is unproved. In this review we discuss the potential reason for the effects of statins on stroke and the mechanisms of action. Statins probably reduce stroke by a variety of mechanisms. Several studies indicate that statins have multiple effects beyond lowering the cholesterol level. There is evidence that statins have neuroprotective properties for the acute ischaemic brain. Statins interfere with platelet aggregation and have anti-inflammatory and antioxidative properties. Also statins promote stabilisation of atherosclerotic plaques and improve blood flow to the ischaemic brain. The protective effects of statins might be due to their direct effect on endothelial cells leading to improved nitric oxide (NO) bioavailability. However further studies are needed to understand the full role of statins in the prevention of stroke in patients without established cardiovascular disease, representative of the typical stroke population.

Pawelczyk M, Baj Z, Chmielewski H, Kaczorowska B, Klimek A. · Departments of Neurology and Epileptology, Medical University of Lodz, Zeromskiego Str. 113, Lodz, Poland. · Cerebrovasc Dis. · Pubmed #19047793 No free full text.

Abstract: BACKGROUND: To investigate the relationship between hyperlipidemia and platelet activation markers--platelet and soluble P-selectin (sP-selectin), and platelet-derived microparticles (PDMPs)--in patients after ischemic stroke. METHODS: 41 patients after ischemic stroke (>3 months) confirmed by CT were divided into 2 groups: with hyperlipidemia (HL, n = 21) and normolipidemia (NL, n = 20). Twenty healthy subjects served as controls. CD62P-positive platelets and PDMPs in whole blood were analyzed by the use of a flow cytometer and anti-CD61 and anti-CD62P monoclonal antibodies. Platelets were activated by thrombin (0.08 units). The level of sP-selectin in serum was measured by ELISA. RESULTS: We observed a significantly higher CD62P expression and percentage of CD62P-positive resting and thrombin-activated platelets in the HL as compared to the NL group. The sP-selectin concentration was also significantly higher in HL than NL subjects (p < 0.05). Moreover, we observed a significantly higher percentage of PDMPs in patients after stroke (NL: p < 0.05; HL: p = 0.005) in comparison with the control group. CONCLUSIONS: Patients after stroke present symptoms of platelet hyperreactivity. HL in the patients may be a risk factor for vascular events due to the increase in platelet activation.