Author + information
- Purushothaman K–Raman,
- Prakash Krishnan,
- Meerarani Purushothaman,
- Usman Baber,
- Arthur Tarricone,
- Jose Wiley,
- Annapoorna Kini,
- Samin Sharma,
- Valentin Fuster and
- Pedro Moreno
Medial artery calcification (MAC) is increased in diabetic mellitus (DM) patients with peripheral vascular disease (PVD), and Chronic Kidney Disease (CKD). These patients may have altered homeostasis of calcification mediators. Bone Morphogenetic Protein–2 (BMP–2), a calcification inducer, and Fetuin–A, a calcification inhibitor were quantified in in patients with symptomatic PVD with/without DM and CKD, and correlated with the degree of MAC.
Fifty symptomatic patients with PVD undergoing directional atherectomy were evaluated. Plaque specimens were grouped by no DM/no CKD (n=14), DM alone (n=12), CKD alone (n= 10), and DM+CKD (n=14). BMP–2 and Fetuin–A protein density were quantified by immunohistochemistry. MAC was quantified by Alizarin Red stain.
The BMP–2 protein density was progressively increased, and Fetuin–A protein density was progressively decreased in DM–CKD group when compared to other groups (p=0.0001 for both comparisons). lncremental increase in medial artery calcification was observed in DM+CKD group. (p<0.02) (See Figureand Table).
Altered calcification mediators of bone morphogenetic protein–2 and Fetuin–A protein expression are associated with progressive increments of medial artery calcification in DM patients with PVD and CKD. Careful screening, early detection, and aggressive therapy may reduce progression of MAC and PVD in DM patients with CKD.
Moderated Poster Contributions
Poster Sessions, Expo North
Monday, March 11, 2013, 9:45 a.m.–10:30 a.m.
Session Title: Vascular Medicine: Endovascular Therapy IV
Abstract Category: 34. Vascular Medicine: Endovascular Therapy
Presentation Number: 1298M–168
- 2013 American College of Cardiology Foundation