PMID- 16337037
OWN - NLM
STAT- MEDLINE
DCOM- 20060321
LR  - 20070822
IS  - 0167-5273 (Print)
IS  - 0167-5273 (Linking)
VI  - 106
IP  - 3
DP  - 2006 Jan 26
TI  - New insights into molecular mechanisms of diffuse coronary ectasiae: a possible 
      role for VEGF.
PG  - 307-12
AB  - BACKGROUND: Diffuse coronary artery ectasiae (DCE) are occasionally found at 
      necropsy or at angiography. Pathogenetic mechanisms of DCE are still poorly 
      known. Matrix metalloproteinases (MMPs), tissue inhibitors of MMPs (TIMPs) and 
      vascular endothelial growth factor (VEGF) are involved in vascular remodeling and 
      may play a role in DCE. METHODS: A total of 1280 consecutive coronary angiograms 
      performed in a single institution in 1 year were screened. DCE were found in 15 
      patients. Diagnosis at hospital admission was acute coronary syndromes in all of 
      them. Two patients died during initial admission and 1 refused blood sampling; 
      the remaining 12 patients were enrolled in the study. No patient with DCE 
      exhibited coronary stenoses. Plasma levels of VEGF, MMP-2, TIMP-1, TIMP-2 and 
      C-reactive protein (CRP) were measured in these 12 patients 12 months after 
      discharge during a silent clinical phase, in 12 age- and sex-matched patients 
      with stable angina (SA) and coronary artery disease, and in 12 age- and 
      sex-matched patients with normal coronary arteries (NCA). RESULTS: VEGF levels 
      were higher in patients with DCE than in SA or NCA (151.6 pg/ml [36.2-252.9] vs. 
      66.6 pg/ml [36.4-93.3] and 54.8 pg/ml [14.5-87.1], respectively, p = 0.012]. 
      TIMP-2 levels were lower in DCE and SA than in NCA (5.9 ng/ml [0-33.6] and 5.0 
      [0-17.4] vs. 139.3 ng/ml [114.4-237.4], respectively, p < 0.001). TIMP-1 and 
      MMP-2 plasma levels were similar in all groups (p = NS), and CRP levels were 
      within normal limits (< 3 mg/L) in most patients, irrespective of their coronary 
      anatomy (75% for DCE, 66% for SA, and 84% for NCA [p = NS]). CONCLUSIONS: 
      Symptomatic patients with DCE typically present with an acute coronary syndrome 
      and exhibit lack of obstructive stenosis at angiography, decreased plasma levels 
      of TIMP-2 and raised plasma levels of VEGF. The simultaneous occurrence of 
      reduced MMPs inhibition and increased angiogenetic activity suggests an 
      accelerated and persistent extracellular matrix remodeling process favouring 
      arterial remodeling and aneurysms formation which is likely to enhance the risk 
      of thrombosis because of low shear stress.
FAU - Savino, Marinica
AU  - Savino M
AD  - Institute of Cardiology, Catholic University of the Sacred Heart, Largo A. 
      Gemelli 8, 00168 Rome, Italy.
FAU - Parisi, Quintino
AU  - Parisi Q
FAU - Biondi-Zoccai, Giuseppe G L
AU  - Biondi-Zoccai GG
FAU - Pristipino, Christian
AU  - Pristipino C
FAU - Cianflone, Domenico
AU  - Cianflone D
FAU - Crea, Filippo
AU  - Crea F
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - Netherlands
TA  - Int J Cardiol
JT  - International journal of cardiology
JID - 8200291
RN  - 0 (Tissue Inhibitor of Metalloproteinase-1)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 127497-59-0 (Tissue Inhibitor of Metalloproteinase-2)
RN  - EC 3.4.24.24 (Matrix Metalloproteinase 2)
SB  - IM
CIN - Int J Cardiol. 2007 May 31;118(2):241. PMID: 16959337
MH  - Adult
MH  - Aged
MH  - Coronary Aneurysm/blood/diagnosis
MH  - Coronary Angiography
MH  - Coronary Disease/*blood/diagnosis/physiopathology
MH  - Dilatation, Pathologic/blood
MH  - Female
MH  - Humans
MH  - Male
MH  - Matrix Metalloproteinase 2/blood
MH  - Middle Aged
MH  - Retrospective Studies
MH  - Tissue Inhibitor of Metalloproteinase-1/blood
MH  - Tissue Inhibitor of Metalloproteinase-2/*blood
MH  - Vascular Endothelial Growth Factor A/*blood
EDAT- 2005/12/13 09:00
MHDA- 2006/03/22 09:00
CRDT- 2005/12/13 09:00
PHST- 2004/11/26 00:00 [received]
PHST- 2005/01/01 00:00 [accepted]
PHST- 2005/12/13 09:00 [pubmed]
PHST- 2006/03/22 09:00 [medline]
PHST- 2005/12/13 09:00 [entrez]
AID - S0167-5273(05)00372-4 [pii]
AID - 10.1016/j.ijcard.2005.01.025 [doi]
PST - ppublish
SO  - Int J Cardiol. 2006 Jan 26;106(3):307-12. doi: 10.1016/j.ijcard.2005.01.025.