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Letter by Violi et al Regarding Article, “Molecular Imaging of Inflammation and Platelet Adhesion in Advanced Atherosclerosis Effects of Antioxidant Therapy With NADPH Oxidase Inhibition”

Letter by Violi et al Regarding Article, “Molecular Imaging of Inflammation and Platelet... Correspondence isoprostanes. This result was corroborated by experiments in a flow Letter by Violi et al Regarding Article, “Molecular chamber in which adhesion to collagen was reduced by platelets from Imaging of Inflammation and Platelet Adhesion in CGD patients compared with control subjects; reduced adhesion was Advanced Atherosclerosis Effects of Antioxidant also observed with platelets from control subjects incubated with Therapy With NADPH Oxidase Inhibition” 4 apocynin. To the Editor: Although these data suggest a role of NADPH oxidase in the athero- Liu et al have recently demonstrated that, in an animal model sclerotic process, the potential usefulness of apocynin for the treatment of atherosclerosis, apocynin, an inhibitor of nicotinamide adenine of unstable atherosclerosis should be carefully considered. Thus, the dinucleotide phosphate (NADPH) oxidase, halted atherosclerotic extent to which NADPH oxidase may be reduced without interfering progression with a mechanism involving reduced monocyte infiltra- with the activity of innate immune system is a critical issue that should tion and platelet adhesion; animals prone to atherosclerosis were also be taken into account. In this context, apocynin may be of interest characterized by impaired artery elasticity, which was reversed by because it inhibits the activity of p47 , the hereditary deficiency of phox apocynin treatment. These data show that atherosclerotic progression which is characterized by a milder clinical course and longer survival. is associated with impaired artery elasticity and suggest that inhibi- tion of NADPH oxidase may favorably affect both. We have previ- Disclosures ously addressed this issue in a multicenter study conducted in patients None. with chronic granulomatous disease (CGD), which is a very rare illness characterized by hereditary deficiency of NADPH oxidase. Francesco Violi, MD The study showed that, compared with control subjects, patients with Pasquale Pignatelli, MD CGD had enhanced flow-mediated dilatation, a surrogate marker of Lorenzo Loffredo, MD atherosclerosis, suggesting that NADPH oxidase plays a role in favor- Divisione I Clinica Medica ing artery vasoconstriction. Enhanced flow-mediated dilatation was University Sapienza associated with reduced isoprostane formation, a marker of oxida- Rome, Italy tive stress, and increased generation of nitric oxide, indicating that the enhanced artery elasticity was dependent on NADPH oxidase-- dependent down-generation of reactive oxidant species and enhanced References nitric oxide generation. In parallel with enhanced flow-mediated 1. Liu Y, Davidson BP, Yue Q, Belcik T, Xie A, Inaba Y, McCarty OJ, Tor- dilatation, patients with CGD disclosed reduced intima-media thick- moen GW, Zhao Y, Ruggeri ZM, Kaufmann BA, Lindner JR. Molecular imaging of inflammation and platelet adhesion in advanced atherosclero- ness, another surrogate marker of atherosclerosis, suggesting a role sis: effects of antioxidant therapy with NADPH oxidase inhibition. Circ for NADPH oxidase in promoting functional and structural changes Cardiovasc Imaging. 2013;6:74–82. that are associated with the atherosclerotic process. Consistent with 2. Violi F, Sanguigni V, Carnevale R, Plebani A, Rossi P, Finocchi A, Pig- this hypothesis are the data from another study conducted in patients nata C, De Mattia D, Martire B, Pietrogrande MC, Martino S, Gambineri with peripheral artery disease, which is a marker of systemic athero- E, Soresina AR, Pignatelli P, Martino F, Basili S, Loffredo L. Hereditary sclerosis; in that study, patients with peripheral artery disease were deficiency of gp91(phox) is associated with enhanced arterial dilatation: characterized by upregulation of NADPH oxidase activation, which results of a multicenter study. Circulation. 2009;120:1616–1622. was associated with lowered flow-mediated dilatation and enhanced 3. Loffredo L, Carnevale R, Cangemi R, Angelico F, Augelletti T, Di Santo intima-media thickness. S, Calabrese CM, Della Volpe L, Pignatelli P, Perri L, Basili S, Violi F. The study conducted in CGD patients is also useful in the interpre- Nox2 up-regulation is associated with artery dysfunction in patients with peripheral artery disease. Int J Cardiol. February 13, 2012. tation of another interesting finding by Liu et al, that is, the inhibition 4. Pignatelli P, Carnevale R, Di Santo S, Bartimoccia S, Sanguigni V, of platelet adhesion to the atherosclerotic plaque by apocynin treat- Lenti L, Finocchi A, Mendolicchio L, Soresina AR, Plebani A, Violi ment. Platelets from CGD had an almost complete absence of reac- F. Inherited human gp91phox deficiency is associated with impaired tive oxidant species production and impaired platelet production of isoprostane formation and platelet dysfunction. Arterioscler Thromb isoprostanes, which are proaggregating eicosanoids derived from the Vasc Biol. 2011;31:423–434. interaction of arachidonic acid with reactive oxidant species. Thus, 5. Loffredo L, Carnevale R, Sanguigni V, Plebani A, Rossi P, Pignata C, De compared with control subjects, platelets from CGD patients showed Mattia D, Finocchi A, Martire B, Pietrogrande MC, Martino S, Gambi- reduced platelet recruitment, which is a marker of platelet aggrega- neri E, Giardino G, Soresina AR, Martino F, Pignatelli P, Violi F. Does tion propagation; platelet recruitment was significantly improved NADPH oxidase deficiency cause artery dilatation in humans? Antioxid Redox Signal. [Epub ahead of print] December 7, 2012. in platelets from CGD patients added with scalar concentration of (Circ Cardiovasc Imaging. 2013;6:e3.) © 2013 American Heart Association, Inc. Circ Cardiovasc Imaging is available at http://circimaging.ahajournals.org DOI: 10.1161/CIRCIMAGING.112.000150 e3 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Circulation: Cardiovascular Imaging Wolters Kluwer Health

Letter by Violi et al Regarding Article, “Molecular Imaging of Inflammation and Platelet Adhesion in Advanced Atherosclerosis Effects of Antioxidant Therapy With NADPH Oxidase Inhibition”

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Copyright
© 2013 American Heart Association, Inc.
ISSN
1941-9651
eISSN
1942-0080
DOI
10.1161/CIRCIMAGING.112.000150
pmid
23512785
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Abstract

Correspondence isoprostanes. This result was corroborated by experiments in a flow Letter by Violi et al Regarding Article, “Molecular chamber in which adhesion to collagen was reduced by platelets from Imaging of Inflammation and Platelet Adhesion in CGD patients compared with control subjects; reduced adhesion was Advanced Atherosclerosis Effects of Antioxidant also observed with platelets from control subjects incubated with Therapy With NADPH Oxidase Inhibition” 4 apocynin. To the Editor: Although these data suggest a role of NADPH oxidase in the athero- Liu et al have recently demonstrated that, in an animal model sclerotic process, the potential usefulness of apocynin for the treatment of atherosclerosis, apocynin, an inhibitor of nicotinamide adenine of unstable atherosclerosis should be carefully considered. Thus, the dinucleotide phosphate (NADPH) oxidase, halted atherosclerotic extent to which NADPH oxidase may be reduced without interfering progression with a mechanism involving reduced monocyte infiltra- with the activity of innate immune system is a critical issue that should tion and platelet adhesion; animals prone to atherosclerosis were also be taken into account. In this context, apocynin may be of interest characterized by impaired artery elasticity, which was reversed by because it inhibits the activity of p47 , the hereditary deficiency of phox apocynin treatment. These data show that atherosclerotic progression which is characterized by a milder clinical course and longer survival. is associated with impaired artery elasticity and suggest that inhibi- tion of NADPH oxidase may favorably affect both. We have previ- Disclosures ously addressed this issue in a multicenter study conducted in patients None. with chronic granulomatous disease (CGD), which is a very rare illness characterized by hereditary deficiency of NADPH oxidase. Francesco Violi, MD The study showed that, compared with control subjects, patients with Pasquale Pignatelli, MD CGD had enhanced flow-mediated dilatation, a surrogate marker of Lorenzo Loffredo, MD atherosclerosis, suggesting that NADPH oxidase plays a role in favor- Divisione I Clinica Medica ing artery vasoconstriction. Enhanced flow-mediated dilatation was University Sapienza associated with reduced isoprostane formation, a marker of oxida- Rome, Italy tive stress, and increased generation of nitric oxide, indicating that the enhanced artery elasticity was dependent on NADPH oxidase-- dependent down-generation of reactive oxidant species and enhanced References nitric oxide generation. In parallel with enhanced flow-mediated 1. Liu Y, Davidson BP, Yue Q, Belcik T, Xie A, Inaba Y, McCarty OJ, Tor- dilatation, patients with CGD disclosed reduced intima-media thick- moen GW, Zhao Y, Ruggeri ZM, Kaufmann BA, Lindner JR. Molecular imaging of inflammation and platelet adhesion in advanced atherosclero- ness, another surrogate marker of atherosclerosis, suggesting a role sis: effects of antioxidant therapy with NADPH oxidase inhibition. Circ for NADPH oxidase in promoting functional and structural changes Cardiovasc Imaging. 2013;6:74–82. that are associated with the atherosclerotic process. Consistent with 2. Violi F, Sanguigni V, Carnevale R, Plebani A, Rossi P, Finocchi A, Pig- this hypothesis are the data from another study conducted in patients nata C, De Mattia D, Martire B, Pietrogrande MC, Martino S, Gambineri with peripheral artery disease, which is a marker of systemic athero- E, Soresina AR, Pignatelli P, Martino F, Basili S, Loffredo L. Hereditary sclerosis; in that study, patients with peripheral artery disease were deficiency of gp91(phox) is associated with enhanced arterial dilatation: characterized by upregulation of NADPH oxidase activation, which results of a multicenter study. Circulation. 2009;120:1616–1622. was associated with lowered flow-mediated dilatation and enhanced 3. Loffredo L, Carnevale R, Cangemi R, Angelico F, Augelletti T, Di Santo intima-media thickness. S, Calabrese CM, Della Volpe L, Pignatelli P, Perri L, Basili S, Violi F. The study conducted in CGD patients is also useful in the interpre- Nox2 up-regulation is associated with artery dysfunction in patients with peripheral artery disease. Int J Cardiol. February 13, 2012. tation of another interesting finding by Liu et al, that is, the inhibition 4. Pignatelli P, Carnevale R, Di Santo S, Bartimoccia S, Sanguigni V, of platelet adhesion to the atherosclerotic plaque by apocynin treat- Lenti L, Finocchi A, Mendolicchio L, Soresina AR, Plebani A, Violi ment. Platelets from CGD had an almost complete absence of reac- F. Inherited human gp91phox deficiency is associated with impaired tive oxidant species production and impaired platelet production of isoprostane formation and platelet dysfunction. Arterioscler Thromb isoprostanes, which are proaggregating eicosanoids derived from the Vasc Biol. 2011;31:423–434. interaction of arachidonic acid with reactive oxidant species. Thus, 5. Loffredo L, Carnevale R, Sanguigni V, Plebani A, Rossi P, Pignata C, De compared with control subjects, platelets from CGD patients showed Mattia D, Finocchi A, Martire B, Pietrogrande MC, Martino S, Gambi- reduced platelet recruitment, which is a marker of platelet aggrega- neri E, Giardino G, Soresina AR, Martino F, Pignatelli P, Violi F. Does tion propagation; platelet recruitment was significantly improved NADPH oxidase deficiency cause artery dilatation in humans? Antioxid Redox Signal. [Epub ahead of print] December 7, 2012. in platelets from CGD patients added with scalar concentration of (Circ Cardiovasc Imaging. 2013;6:e3.) © 2013 American Heart Association, Inc. Circ Cardiovasc Imaging is available at http://circimaging.ahajournals.org DOI: 10.1161/CIRCIMAGING.112.000150 e3

Journal

Circulation: Cardiovascular Imaging – Wolters Kluwer Health

Published: Mar 1, 2013

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