Short-term effects of atorvastatin on haemorheologic parameters, platelet aggregation and endothelium dysfunction in patients with hypercholesterolaemia

Beata Horvatha, Laszlo Szaparyb, Zsolt Martona, Tamas Alexya, Gabor Kesmarkya and Kalman Totha,*

a 1st Department of Medicine, Division of Cardiology, University of Pecs, School of Medicine, Ifjusag u. 13 H-7624, Pecs, Hungary
b Department of Neurology, University of Pecs, School of Medicine, Ifjusag u. 13 H-7624, Pecs, Hungary

* Corresponding author: Prof. Kalman Toth M.D., D.Sc., FESC, 1st Department of Medicine, Division of Cardiology, University of Pecs School of Medicine, Ifjusag u. 13; H-7624, Pecs, Hungary. Tel.: +36-72-536-001/5383; Fax: +36-72-536-472
E-mail address: kalman.toth{at}aok.pte.hu

Received 10 March 2003; accepted 7 May 2003

We read the paper by Riesen et al.1with great interest. It provides important information on a new beneficial effect of the administration of atorvastatin. Their study concentrated on parameters of inflammation (C-reactive protein) as well as lipid profile in patients with hypercholesterolemia and with or at risk for coronary heart disease. Besides studying anti-inflammatory effect, another important aspect could be the measurement of haemorheological parameters, platelet aggregation and endotheliumdysfunction.2

We investigated the effect of atorvastatin therapy on haemorheological parameters, platelet aggregation and von Willebrand factor activity (vWf) as a marker of endothelium dysfunction in patients with hyperlipidaemia and chronic cerebrovascular diseases. 27 patients (mean age: 51±8 years) were examined and treated with 10mg atorvastatin daily for 3 months. Besides routine laboratory parameters, haemorheological measurements (plasma fibrinogen, plasma and whole blood viscosity, red blood cell (RBC) aggregation and filterability), collagen induced platelet aggregation and vWf activity were determined at baseline and after 3 months of treatment.

The median reduction of plasma total cholesterol level was 28% (P<0.001), LDL-cholesterol was lowered by 42% (P<0.001), plasma triglycerides by 10% (P<0.01), while HDL-cholesterol level did not change significantly. Whole blood viscosity (P<0.05) and RBC deformability (P<0.05) showed a significant improvement after the three-month treatment. Collagen induced platelet aggregation also decreased significantly (P<0.001) beside unaltered antiplatelet therapy. vWf activity provided a significant (P<0.05) reduction compared to that of the baseline values. Both plasma fibrinogen and CRP showed a decreasing tendency (in our study ‘high sensitivity-CRP’ method was not applied), which did not reach the level of significance.

Our findings indicate that besides lipid and inflammation marker reduction atorvastatin improves also haemorheological parameters, another group of risk factors of cardiovascular diseases. The reduction in vWf activity implies that this drug can improve endothelium dysfunction and decrease high shear induced plateletaggregation. The possible direct antiplatelet property of atorvastatin and the decrease of high shear induced platelet aggregation may contribute to the effectiveness in the prevention of cardio- and cerebrovascular events. These improvements in blood flow properties give further explanation of the beneficial effects of atorvastatin on cardiovascular risk in patients with hypercholesterolaemia and atherosclerotic vascular disease.3

References

  1. Riesen WF, Engler H, Risch M et al. Short-term effects of atorvastatin on C-reactive protein. Eur Heart J. 2002;23:794–799.[Abstract/Free Full Text]
  2. Yarnell JW, Baker IA, Sweetnam PM et al. Fibrinogen, viscosity, and white blood cell count are major risk factors for ischaemic heart disease. The Caerphilly and Speedwell collaborative heart disease studies. Circulation. 1991;83:836–844.[Abstract]
  3. Szapary L, Horvath B, Marton ZS et al. Short term effect of low dose atorvastatin on hemorheological parameters, platelet aggregation and endothelial function in cerebrovascular patients with dyslipidemia. CNS drugs, under publication..