JACC
HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK
QUICK SEARCH:   [advanced]


     

J Am Coll Cardiol, 2003; 41:1071-1077, doi:10.1016/S0735-1097(03)00088-3
© 2003 by the American College of Cardiology Foundation
This Article
Right arrow Abstract Freely available
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Biondi-Zoccai, G. G. L.
Right arrow Articles by Biasucci, L. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Biondi-Zoccai, G. G. L.
Right arrow Articles by Biasucci, L. M.

Atherothrombosis, inflammation, and diabetes

Giuseppe G. L. Biondi-Zoccai, MD*, Antonio Abbate, MD*, Giovanna Liuzzo, MD* and Luigi M. Biasucci, MD, FACC*,*

* Institute of Cardiology, Catholic University, Rome, Italy



View larger version (33K):

[in a new window]
  		Figure 1 The pathogenetic mechanisms involved in the initiation of subclinical atherosclerosis and progression to atherosclerotic clinical events in diabetic patients include infection, inflammation, hyperglycemia, insulin resistance, dyslipidemia, and thrombosis. AGE = advanced glycation end products; CRP = C-reactive protein; HDL = high-density lipoprotein; HTN = hypertension; IL-6 = interleukin-6; LDL = low-density lipoprotein; PAI-1 = plasminogen activator inhibitor-1; SAA = serum amyloid A protein; TF = tissue factor; TG = triglycerides; tPA = tissue-type plasminogen activator.

 


View larger version (13K):

[in a new window]
  		Figure 2 Reciprocal interplay between inflammation and diabetes mellitus in the pathogenesis of atherothrombosis, with emphasis on both the role of inflammation in the development of overt diabetes mellitus and the proinflammatory action of hyperglycemia and insulin resistance. Potential or established modulating agents are shown by dashed arrows. ACEi = angiotensin-converting enzyme inhibitors; ARB = angiotensin receptor blockers; PPAR = peroxisome proliferator-activated receptor.

 




HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK
Copyright © 2003 by the American College of Cardiology Foundation.