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European Heart Journal Advance Access published online on April 3, 2008
European Heart Journal, doi:10.1093/eurheartj/ehn138
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Prolonged statin-associated reduction in neutrophil reactive oxygen species and angiotensin II type 1 receptor expression: 1 -year follow-up

Luigina Guasti1,*, Franca Marino1, Marco Cosentino1, Ramona C. Maio1, Emanuela Rasini1, Marco Ferrari1, Luana Castiglioni1, Catherine Klersy2, Giovanni Gaudio1, Anna M. Grandi1, Sergio Lecchini1 and Achille Venco1

1 Department of Clinical Medicine, University of Insubria, Viale Borri 57, Varese 21100, Italy
2 Biometry and Clinical Epidemiology, IRCCS Policlinico S. Matteo, Pavia, Italy

Received 29 November 2007; revised 3 February 2008; accepted 10 March 2008.

* Corresponding author. Tel: +39 0332278828, Fax: +39 0332278595, Email: luigina.guasti{at}uninsubria.it

Aims: Our study investigated reactive oxygen species (ROS) generation and angiotensin II type 1 receptor (AT1-R) expression in primed polymorphonuclear leukocytes (PMNs) of dyslipidaemic subjects over prolonged statin treatment.

Methods and results: Sixteen untreated dyslipidaemic subjects with moderately increased cardiovascular risk (National Cholesterol Education Program, Adult Treatment Panel III) were studied before and during long-term (1 year) simvastatin treatment. Neutrophils from dyslipidaemic subjects generated more ROS in comparison with cells from healthy control subjects. After 1 year of simvastatin treatment, ROS production (delta N-formyl-Met-Leu-Phe-induced generation and area under the curve) was significantly reduced. At baseline, AT1-R mRNA expression was also higher in dyslipidaemic subjects than in healthy controls and it was reduced after clinical treatment with simvastatin. In a subgroup of patients, a reduced angiotensin II-induced ROS generation was also observed upon clinical simvastatin treatment. Moreover, a direct effect of statin on the upregulated AT1-R expression was demonstrated in vitro in neutrophils of untreated dyslipidaemic subjects.

Conclusion: A consistent reversion of pro-inflammatory oxidative functional response and reduction of AT1-R expression in primed PMNs was observed in patients during long-term statin treatment. The AT1-R reduction over treatment may contribute to the normalization of dysregulated neutrophil activation which occurs in the pre-clinical phase of atherosclerosis.

Key Words: Neutrophils • Reactive oxygen species • Angiotensin II AT1 receptors • Statins • Dyslipidaemic subjects • Cell function


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