Pentraxin 3 (PTX3) plasma levels and carotid intima media thickness progression in the general population.
OBJECTIVE
Pentraxin 3 (PTX3) is an essential component of the humoral arm of innate immunity and, like C-reactive protein, is independently associated with the risk of developing vascular events. Aim of this study was to investigate, in two large population-based surveys, the Bruneck Study and the PLIC Study, whether PTX3 plasma levels predict the progression of common carotid artery intima-media thickness (CCA-IMT), a surrogate marker of atherosclerosis, in the general population during 5 or 6 years of follow-up.


RESULTS
In the Bruneck Study, PTX3 plasma levels did not predict a faster progression of CCA-IMT either in the carotid artery or in the femoral artery. This finding was confirmed in the PLIC Study where subjects within the highest tertile of PTX3 did not show an increased progression of CCA-IMT. PTX3 plasma levels were also not associated with the fastest maximum IMT progression. In summary, in more than 2400 subjects from the general population, PTX3 plasma level is neither an independent predictor of progression of subclinical atherosclerosis in different arterial territories, including carotid and femoral arteries nor of incident cardiovascular events.


CONCLUSIONS
These findings support the relevance of investigating the predictive value of PTX3 plasma levels only in specific settings, like overt CVD, heart failure or acute myocardial infarction.
Center for the Study of Atherosclerosis, Bassini Hospital, Cinisello Balsamo, Milan, Italy; Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Italy.
A
A
Baragetti
Department of Neurology, Medical University Innsbruck, Austria.
M
M
Knoflach
Department of Inflammation and Immunology, Humanitas Clinical and Research Center, Rozzano, Milan, Italy.
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I
Cuccovillo
Center for the Study of Atherosclerosis, Bassini Hospital, Cinisello Balsamo, Milan, Italy.
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L
Grigore
Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Italy.
M
M
Casula
Center for the Study of Atherosclerosis, Bassini Hospital, Cinisello Balsamo, Milan, Italy.
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K
Garlaschelli
Department of Inflammation and Immunology, Humanitas Clinical and Research Center, Rozzano, Milan, Italy; Department of Translational Medicine, University of Milan, Milan, Italy.
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A
Mantovani
Laboratory of Autoimmunity, Biocenter, Innsbruck, Austria.
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G
Wick
Department of Neurology, Medical University Innsbruck, Austria.
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S
Kiechl
Department of Neurology, Medical University Innsbruck, Austria.
J
J
Willeit
Department of Inflammation and Immunology, Humanitas Clinical and Research Center, Rozzano, Milan, Italy.
B
B
Bottazzi
Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Italy; IRCCS Multimedica, Milan, Italy. Electronic address: alberico.catapano@unimi.it.
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AL
Catapano
Center for the Study of Atherosclerosis, Bassini Hospital, Cinisello Balsamo, Milan, Italy; Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Italy; The Blizard Institute, Centre for Diabetes, Barts and The London School of Medicine & Dentistry, Queen Mary University, London, UK. Electronic address: danilo.norata@unimi.it.
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GD
Norata
D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D015415:Biomarkers / Q000097:blood*; D002097:C-Reactive Protein / Q000378:metabolism*; D002318:Cardiovascular Diseases / Q000097:blood / Q000000981:diagnostic imaging; D017536:Carotid Artery, Common / Q000000981:diagnostic imaging; D059168:Carotid Intima-Media Thickness; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D000683:Serum Amyloid P-Component / Q000378:metabolism*; D000099153:Pentraxins
D015415:Biomarkers; D002097:C-Reactive Protein; D000683:Serum Amyloid P-Component; D000099153:Pentraxins
Bruneck Study; Inflammation; PLIC Study; PTX3