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(Circulation. 1999;99:2239-2242.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Effect of Diabetes Mellitus on Formation of Coronary Collateral Vessels
uzhan, MD
ükrü Ünal, MDFrom the Department of Cardiology, Erciyes University School of Medicine, Kayseri, Turkey.
Correspondence to Adnan Abaci, Selanik Cad, Sinema Onay, Kar
isi, Kiliç Apt 29/15, Kayseri-38010, Turkey. E-mail abacia{at}hotmail.com
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Abstract |
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Background—Although myocardial ischemia is known to be significantly related to the development of coronary collateral vessels (CCVs), there is considerable variation between patients with ischemic heart disease in the presence of collateral development. The nature of this variability is not well known. Likewise, it remains unclear whether diabetes mellitus (DM) has any effect on CCVs. The aim of this study was to evaluate the effect of DM on CCVs.
Methods and Results—Of the patients who underwent
coronary angiography during the interval between March 1, 1993,
and June 20, 1998, in our institution, 306 were diabetic. Those
patients in whom coronary angiography is normal or severity of
coronary artery stenosis is thought not to be
sufficient for the development of CCVs (<75%) were excluded from the
study. A total of 205 patients (mean age, 59±8 years) met the criteria
for the DM group. For case-control matching, 205 consecutive
nondiabetic patients (mean age, 58±9 years) who had 
1 diseased
vessel with >75% stenosis were included in the control group.
The CCVs were graded according to the Rentrop scoring system, and the
collateral score was calculated by summing the Rentrop numbers of every
patient. There was no statistical difference between patients with and
without DM in clinical baseline characteristics. The mean number of
diseased vessels in the DM group (1.58±0.68) was higher than that in
the nondiabetic group (1.42±0.65, P=0.005). The mean
collateral score was 2.41±2.20 in the DM group and 2.60±2.39 in the
control group. After confounding variables were controlled for, the
collateral score in the diabetic group was significantly different from
that in the nondiabetic group (P=0.034).
Conclusions—Our findings suggest that CCV development is poorer in patients with than in patients without DM. Thus, we can speculate that DM is an important factor affecting CCV development.
Key Words: collateral circulation • coronary disease • diabetes mellitus
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Introduction |
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Collaterals develop in the advanced stages of coronary atherosclerosis.1 2 3 Although all aspects of the mechanisms underlying the development of coronary collaterals are not well known, the pivotal role of myocardial ischemia is well established.4 5 However, there is considerable variation between patients with ischemic heart disease in the presence of collateral development. The factors responsible for this variation are not well known.6 Histological studies documented thin-walled capillarylike morphology of "mature" collaterals in the early stages of its development.6 In later stages of development, collaterals actively grow, as demonstrated by mitotic activity in the endothelial and smooth muscle cells.7 Endothelial cells are important in this collateral maturation process.8 9 Coronary artery disease patients with diabetes mellitus (DM) have a less favorable outcome compared with those without diabetes, including a 3- to 4-fold increase in mortality risk.10 11 12 Moreover, diabetic patients whose tests sustain a nonfatal myocardial infarction experience a more complicated course, including more frequent postinfarction angina, infarction extension, and congestive heart failure.13 The precise mechanism underlying this unfavorable effect is not clear.14 However, diffuse endothelial dysfunction is thought to be one of the important elements in this process.15 Endothelial cells are important in the development and maturation of coronary collaterals. Accordingly, we sought to evaluate the relationship between DM and coronary collaterals in patients with advanced coronary artery disease. We have reviewed the coronary angiograms of all diabetic patients that underwent coronary angiogram in our institution in a 5-year period and compared them with those of a control group.
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Methods |
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Patient Population
Between March 1, 1993, and June 20, 1998, 5223 patients underwent coronary angiography in our institution. Of these patients, 306 were diabetic, defined as patients who were treated with insulin or oral hypoglycemic agents. Of the 306 patients, those with <75% diameter stenosis, those who received nitrates or calcium channel blockers immediately before the procedure, and those with technically inadequate studies were excluded from this study. The remaining 205 patients constituted the DM group. The control group consisted of 205 consecutive patients with
1 coronary
stenosis with >75% narrowing. Clinical information, including
age, weight, sex, history of hypertension, serum
cholesterol level, smoking, clinical
presentation, and history of prior myocardial infarction,
was obtained from a review of the patient's chart.
Coronary Angiography and Grading of Coronary
Collateral Filling
Selective coronary angiography was performed in multiple
orthogonal projections using the Judkins or Sones technique after
administration of 5000-U intravenous bolus of heparin.
Coronary artery stenosis were estimated visually by 2
independent observers who were blinded to the identities and clinical
information of the patients. Single-vessel disease was defined as
>75% diameter stenosis in only 1 coronary artery.
Two- and 3-vessel diseases were defined according to the same criteria.
Collateral vessels were graded according to the Rentrop classification:
0=no filling of any collateral vessels, 1=filling of side branches of
the artery to be perfused by collateral vessels without visualization
of the epicardial segment, 2=partial filling of the epicardial artery
by collateral vessels, and 3=complete filling of the epicardial artery
by collateral vessels. The reproducibility of this grading system has
previously been validated.16 The collateral score was
based on the injection that best opacified the collateralized vessel.
The collateral score was calculated by summing the Rentrop numbers of
every patient.
Statistical Analysis
Continuous variables were expressed as mean±SD. The
relation between the continuous variables was evaluated by use of
the unpaired Student t test. The 
2
test with Yates' continuity correction was used to assess the
significance of difference between dichotomous variables.
Correlations between collateral score and other variables were
analyzed by linear regression analysis. ANCOVA was used
to assess the confounding effects of variables on comparisons of
the groups according to DM status. Variables analyzed
included age, sex, weight, previous myocardial infarction,
hypertension, serum cholesterol level, number of diseased
vessels, and smoking status. For all tests, P>0.05 was
designated nonsignificant, and a value of P<0.05 was
considered statistically significant. The SPSS statistical software
package (version 5.0) was used to perform all statistical
calculations.
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Results |
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Patient Characteristics
Table 1
describes the
clinical baseline characteristics of the study patients. The 2 groups
were well matched in terms of baseline clinical characteristics. Mean
age and distribution of risk factors for coronary disease did
not differ significantly between groups. The proportion of patients
with a history of myocardial infarction was similar in both groups. A
similar proportion of patients in both groups had stable or unstable
angina. Most patients were male in the 2 groups. The severity of
coronary stenosis was similar in the 2 groups (Table 2), but the mean number of diseased
vessels was significantly higher in the DM patients
(P=0.005). One-vessel disease occurred more frequently in
the nondiabetic group. In contrast, 2- and 3-vessel diseases were more
common in the diabetic group. Therefore, the difference between
diabetic and nondiabetic patients according to the angiographic
variables was only in number of diseased vessels. By linear
regression analysis, the collateral score was not related to
age, smoking habits, hypertension, or total serum, LDL, or HDL
cholesterol. Although sex was not significantly different
between the 2 group, there was a weak relation between collateral score
and sex (r=0.109, P=0.025). As expected, there
was a significant relation between collateral score and number of
diseased vessels (r=0.441, P<0.0001). The mean
collateral score was 2.41±2.20 in the DM group and 2.60±2.39 in the
control group.
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Multivariate Analysis
The effect of these factors on collateral score was evaluated by
performing an ANCOVA with DM as a factor and sex, age, weight, serum
cholesterol level, smoking habits, previous myocardial
infarction, and number of diseased vessels as covariates. Although the
collateral score was related only to sex and the number of diseased
vessels, other variables were also examined by
multivariate analysis to exclude any possible
interactions between these variables. After confounding
variables were controlled for, the collateral score in the DM group
(2.41±2.20) was significantly different from that in the nondiabetic
group (2.60±2.39, P=0.034). The variables of sex and
number of diseased vessels were the only important confounding
variables of the collateral score after ANCOVA (r=0.115,
P=0.015; r=0.467, P<0.001,
respectively).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In the present study, the importance of DM in the development of coronary collateral vessels is documented by the finding that the prevalence of collateral circulation in DM patients is much lower than in those without DM.
DM and Coronary Collateralization
Development of collateral vessels is triggered by the pressure
gradient between the coronary bed of arteries caused by an
obstruction and myocardial ischemia.4 5 However, a
lack of collateral vessels in some patients despite the presence of
coronary obstruction and evidence of myocardial
ischemia suggests that additional factors may contribute to
collateral development. Limited data are available on the effect of DM
on collateral development. The present study includes the largest
patient population reported thus far. DM has been found to be an
inhibiting factor on coronary collateral development in a small
clinic17 and a postmortem study.18 In an
another study, the effect of carbohydrate intolerance with or without
DM on collateral development was examined.19 Those
investigators have claimed that although DM is known to affect the
vascular tree, these underlying abnormalities do not inhibit the
formation of collateral vessels, and DM affects small arteries, but the
collateral channels usually represent large epicardial vessels
that do not appear to be influenced by DM. However, it must kept in
mind that collaterals are also small vessels at the beginning of their
formation. Therefore, it seems it is not possible to explain their
findings with that assumption. Also, in the study of Heinle et
al,19 data from a large group of patients with collaterals
(80 patients) were compared with the findings of a much smaller group
without such vessels (16 patients). It is conceivable that the
statistical power of such a comparison is low.
The most interesting aspect of coronary anastomosis is their ability to respond with growth when the large epicardial arteries become stenosed or occluded and the tissue becomes potentially ischemic.9 It is now widely accepted that myocardial ischemia somehow triggers collateral growth.20 21 A biochemical signal produced by ischemic myocardium may trigger the events leading to DNA synthesis and to mitosis in collateral vessels.22 During collateral development, the collaterals actively grow, as is evidenced by mitotic activity in both endothelial and smooth muscle cells.7 The endothelium leads the process of growth adaptation; smooth muscle follows.9 Over the past decade, numerous angiogenic factors have been purified, and their amino acid sequences have been determined with subsequent gene cloning.23 In a canine model of myocardial ischemia, intracoronary infusion of vascular endothelial growth factor into the ischemic territory has been shown to accelerate native collateral development.24 Basic fibroblast growth factor has also been shown to enhance collateral development in a canine model of gradual coronary occlusion.25
There has been increasing interest in the literature in the functional impact of DM on coronary vascular function. It has been shown that a high concentration of glucose causes endothelial cell dysfunction.26 27 28 Because the function of the endothelium is important in collateral development and there is dysfunction of endothelium in DM, our finding that the prevalence of collateral circulation in patients with DM is much lower than those without DM may be explained by the effect of DM on endothelial function. It should also be noted that nitric oxide production is impaired in DM,29 and nitric oxide seems to be involved in vascular endothelial growth factor–induced angiogenesis.30
Study Limitations
In the interpretation of our findings, several limitations must be
considered. First, angiographically visible collaterals
represent only a fraction of the total collateral vessels
because collaterals are angiographically demonstrable only when they
reach 100 µm. Moreover, angiography may not detect most
collaterals situated intramurally. Therefore, the collaterals
visualized by angiography may not accurately quantify collateral
circulation. But the effect of this problem on collateral score must be
same in the 2 groups and thus should not change the interpretation of
our results. Second, although the effects of clinical variables on
collateral score were evaluated by multivariate
analysis, because the effects of all potential confounding
patients characteristics cannot be retrospectively controlled, there
may be factors that were not taken into account that may have
influenced our results. The most important of these uncontrolled
variables was the physical activity of study patients. Improvement
in coronary collateral circulation after exercise training has
been shown.31 32 However, exercise is part of DM therapy;
physicians recommend that DM patients perform regular physical
activity. Therefore, there is no reason for the DM patients to be less
physically active than those without DM. Moreover, it is possible that
the DM patients tended to exercise more than the nondiabetics. Finally,
and most importantly, the present study is a retrospective,
observational one. However, the angiographic and clinical data belong
to the same period and come from the same laboratory without
substantial changes in management strategy.
Clinical Implications
This investigation is the first study with a large number of
patients to show the relationship between DM and collateral vessel
development. It demonstrates that collateral vessel development is
poorer in DM than in nondiabetic patients. We can speculate that DM is
an important factor among the factors affecting the development of
coronary collaterals.
We believe that in the future, a complete understanding of the exact mechanisms of collateral growth and regression will help to establish a new therapeutic strategy for patients with coronary artery disease. Although this is not a biochemical study investigating the relation between DM and growth factors, it may stimulate such a study in this interesting field.
Received September 25, 1998; revision received February 1, 1999; accepted February 4, 1999.
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artery occlusion pigs. Circulation. 1990;82:1778–1789.To evaluate the effect of diabetes mellitus on
coronary collateral vessels, 205 diabetic patients (mean age,
59±8 years) were compared with 205 nondiabetic patients (mean age,
58±10 years). Collateral vessels were graded according to the Rentrop
scoring system, and the collateral score was calculated by summing the
Rentrop numbers of every patient. The collateral score was
significantly lower in diabetic patients (2.41±2.20) than in those
without diabetes mellitus (2.60±2.39, P=0.034). Our
findings suggest that coronary collateral development is poorer
in patients with DM than in patients without DM.
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M. Boodhwani, Y. Nakai, P. Voisine, J. Feng, J. Li, S. Mieno, B. Ramlawi, C. Bianchi, R. Laham, and F. W. Sellke High-Dose Atorvastatin Improves Hypercholesterolemic Coronary Endothelial Dysfunction Without Improving the Angiogenic Response Circulation, July 4, 2006; 114(1_suppl): I-402 - I-408. [Abstract] [Full Text] [PDF]
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V. van Weel, M. de Vries, P. J. Voshol, R. E. Verloop, P. H.C. Eilers, V. W.M. van Hinsbergh, J. H. van Bockel, and P. H.A. Quax Hypercholesterolemia Reduces Collateral Artery Growth More Dominantly Than Hyperglycemia or Insulin Resistance in Mice Arterioscler Thromb Vasc Biol, June 1, 2006; 26(6): 1383 - 1390. [Abstract] [Full Text] [PDF]
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J.-S. Silvestre and B. I. Levy Molecular Basis of Angiopathy in Diabetes Mellitus Circ. Res., January 6, 2006; 98(1): 4 - 6. [Full Text] [PDF]
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S. Varma, B. K. Lal, R. Zheng, J. W. Breslin, S. Saito, P. J. Pappas, R. W. Hobson II, and W. N. Duran Hyperglycemia alters PI3k and Akt signaling and leads to endothelial cell proliferative dysfunction Am J Physiol Heart Circ Physiol, October 1, 2005; 289(4): H1744 - H1751. [Abstract] [Full Text] [PDF]
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N. P. Kadoglou, S. S. Daskalopoulou, D. Perrea, and C. D. Liapis Matrix Metalloproteinases and Diabetic Vascular Complications Angiology, March 1, 2005; 56(2): 173 - 189. [Abstract] [PDF]
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J. K. Olijhoek, J. Koerselman, P. P.Th. de Jaegere, M. C. Verhaar, D. E. Grobbee, Y. van der Graaf, F. L.J. Visseren, and for the SMART Study Group Presence of the Metabolic Syndrome Does Not Impair Coronary Collateral Vessel Formation in Patients With Documented Coronary Artery Disease Diabetes Care, March 1, 2005; 28(3): 683 - 689. [Abstract] [Full Text] [PDF]
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A. W. Stitt, C. McGoldrick, A. Rice-McCaldin, D. R. McCance, J. V. Glenn, D. K. Hsu, F.-T. Liu, S. R. Thorpe, and T. A. Gardiner Impaired Retinal Angiogenesis in Diabetes: Role of Advanced Glycation End Products and Galectin-3 Diabetes, March 1, 2005; 54(3): 785 - 794. [Abstract] [Full Text] [PDF]
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K P Morgan, A Kapur, and K J Beatt Anatomy of coronary disease in diabetic patients: an explanation for poorer outcomes after percutaneous coronary intervention and potential target for intervention Heart, July 1, 2004; 90(7): 732 - 738. [Abstract] [Full Text] [PDF]
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R. D. Galiano, O. M. Tepper, C. R. Pelo, K. A. Bhatt, M. Callaghan, N. Bastidas, S. Bunting, H. G. Steinmetz, and G. C. Gurtner Topical Vascular Endothelial Growth Factor Accelerates Diabetic Wound Healing through Increased Angiogenesis and by Mobilizing and Recruiting Bone Marrow-Derived Cells Am. J. Pathol., June 1, 2004; 164(6): 1935 - 1947. [Abstract] [Full Text] [PDF]
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S. Verma, M. A. Kuliszewski, S.-H. Li, P. E. Szmitko, L. Zucco, C.-H. Wang, M. V. Badiwala, D. A.G. Mickle, R. D. Weisel, P. W.M. Fedak, et al. C-Reactive Protein Attenuates Endothelial Progenitor Cell Survival, Differentiation, and Function: Further Evidence of a Mechanistic Link Between C-Reactive Protein and Cardiovascular Disease Circulation, May 4, 2004; 109(17): 2058 - 2067. [Abstract] [Full Text] [PDF]
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C. Emanueli, G. Graiani, M. B. Salis, S. Gadau, E. Desortes, and P. Madeddu Prophylactic Gene Therapy With Human Tissue Kallikrein Ameliorates Limb Ischemia Recovery in Type 1 Diabetic Mice Diabetes, April 1, 2004; 53(4): 1096 - 1103. [Abstract] [Full Text] [PDF]
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C. S. Fox, L. Sullivan, R. B. D'Agostino Sr, and P. W.F. Wilson The Significant Effect of Diabetes Duration on Coronary Heart Disease Mortality: The Framingham Heart Study Diabetes Care, March 1, 2004; 27(3): 704 - 708. [Abstract] [Full Text] [PDF]
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E. Larger, M. Marre, P. Corvol, and J.-M. Gasc Hyperglycemia-Induced Defects in Angiogenesis in the Chicken Chorioallantoic Membrane Model Diabetes, March 1, 2004; 53(3): 752 - 761. [Abstract] [Full Text] [PDF]
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M Fujita and K Tambara Recent insights into human coronary collateral development Heart, March 1, 2004; 90(3): 246 - 250. [Abstract] [Full Text] [PDF]
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C. Calvi, P. Dentelli, M. Pagano, A. Rosso, M. Pegoraro, S. Giunti, G. Garbarino, G. Camussi, L. Pegoraro, and M. F. Brizzi Angiopoietin 2 Induces Cell Cycle Arrest in Endothelial Cells: A Possible Mechanism Involved in Advanced Plaque Neovascularization Arterioscler Thromb Vasc Biol, March 1, 2004; 24(3): 511 - 518. [Abstract] [Full Text]
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N. E.J. West, P. N. Ruygrok, C. M.C. Disco, M. W.I. Webster, W. K. Lindeboom, W. W. O'Neill, N. F. Mercado, and P. W. Serruys Clinical and Angiographic Predictors of Restenosis After Stent Deployment in Diabetic Patients Circulation, February 24, 2004; 109(7): 867 - 873. [Abstract] [Full Text] [PDF]
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C. J.M. Loomans, E. J.P. de Koning, F. J.T. Staal, M. B. Rookmaaker, C. Verseyden, H. C. de Boer, M. C. Verhaar, B. Braam, T. J. Rabelink, and A.-J. van Zonneveld Endothelial Progenitor Cell Dysfunction: A Novel Concept in the Pathogenesis of Vascular Complications of Type 1 Diabetes Diabetes, January 1, 2004; 53(1): 195 - 199. [Abstract] [Full Text] [PDF]
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M. M. Graham, W. A. Ghali, P. D. Faris, P. D. Galbraith, C. M. Norris, and M. L. Knudtson Sex Differences in the Prognostic Importance of Diabetes in Patients With Ischemic Heart Disease Undergoing Coronary Angiography Diabetes Care, November 1, 2003; 26(11): 3142 - 3147. [Abstract] [Full Text] [PDF]
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R. Tamarat, J.-S. Silvestre, M. Huijberts, J. Benessiano, T. G. Ebrahimian, M. Duriez, M.-P. Wautier, J. L. Wautier, and B. I. Levy Blockade of advanced glycation end-product formation restores ischemia-induced angiogenesis in diabetic mice PNAS, July 8, 2003; 100(14): 8555 - 8560. [Abstract] [Full Text] [PDF]
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G. S. Werner, B. M. Richartz, S. Heinke, M. Ferrari, and H. R. Figulla Impaired acute collateral recruitment as a possible mechanism for increased cardiac adverse events in patients with diabetes mellitus Eur. Heart J., June 2, 2003; 24(12): 1134 - 1142. [Abstract] [Full Text] [PDF]
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N. van Royen, I. Hoefer, M. Bottinger, J. Hua, S. Grundmann, M. Voskuil, C. Bode, W. Schaper, I. Buschmann, and J.J. Piek Local Monocyte Chemoattractant Protein-1 Therapy Increases Collateral Artery Formation in Apolipoprotein E-Deficient Mice but Induces Systemic Monocytic CD11b Expression, Neointimal Formation, and Plaque Progression Circ. Res., February 7, 2003; 92(2): 218 - 225. [Abstract] [Full Text] [PDF]
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K. Hirata, T.-S. Li, M. Nishida, H. Ito, M. Matsuzaki, S. Kasaoka, and K. Hamano Autologous bone marrow cell implantation as therapeutic angiogenesis for ischemic hindlimb in diabetic rat model Am J Physiol Heart Circ Physiol, January 1, 2003; 284(1): H66 - H70. [Abstract] [Full Text] [PDF]
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O. M. Tepper, R. D. Galiano, J. M. Capla, C. Kalka, P. J. Gagne, G. R. Jacobowitz, J. P. Levine, and G. C. Gurtner Human Endothelial Progenitor Cells From Type II Diabetics Exhibit Impaired Proliferation, Adhesion, and Incorporation Into Vascular Structures Circulation, November 26, 2002; 106(22): 2781 - 2786. [Abstract] [Full Text] [PDF]
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F. Facchiano, A. Lentini, V. Fogliano, S. Mancarella, C. Rossi, A. Facchiano, and M. C. Capogrossi Sugar-Induced Modification of Fibroblast Growth Factor 2 Reduces Its Angiogenic Activity in Vivo Am. J. Pathol., August 1, 2002; 161(2): 531 - 541. [Abstract] [Full Text] [PDF]
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E. Chou, I. Suzuma, K. J. Way, D. Opland, A. C. Clermont, K. Naruse, K. Suzuma, N. L. Bowling, C. J. Vlahos, L. P. Aiello, et al. Decreased Cardiac Expression of Vascular Endothelial Growth Factor and Its Receptors in Insulin-Resistant and Diabetic States: A Possible Explanation for Impaired Collateral Formation in Cardiac Tissue Circulation, January 22, 2002; 105(3): 373 - 379. [Abstract] [Full Text] [PDF]
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Z S Kyriakides, S Psychari, N Chrysomallis, M Georgiadis, E Sbarouni, and D T Kremastinos Type II diabetes does not prevent the recruitment of collateral vessels and the normal reduction of myocardial ischaemia on repeated balloon inflations during angioplasty Heart, January 1, 2002; 87(1): 61 - 66. [Abstract] [Full Text] [PDF]
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J. L. Tuttle, R. D. Nachreiner, A. S. Bhuller, K. W. Condict, B. A. Connors, B. P. Herring, M. C. Dalsing, and J. L. Unthank Shear level influences resistance artery remodeling: wall dimensions, cell density, and eNOS expression Am J Physiol Heart Circ Physiol, September 1, 2001; 281(3): H1380 - H1389. [Abstract] [Full Text] [PDF]
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S. Dimmeler and A. M. Zeiher Endothelial Cell Apoptosis in Angiogenesis and Vessel Regression Circ. Res., September 15, 2000; 87(6): 434 - 439. [Abstract] [Full Text] [PDF]
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T. Hammoud, J.-F. Tanguay, and M. G. Bourassa Management of coronary artery disease: therapeutic options in patients with diabetes J. Am. Coll. Cardiol., August 1, 2000; 36(2): 355 - 365. [Abstract] [Full Text] [PDF]
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J. Waltenberger, J. Lange, and A. Kranz Vascular Endothelial Growth Factor-A-Induced Chemotaxis of Monocytes Is Attenuated in Patients With Diabetes Mellitus : A Potential Predictor for the Individual Capacity to Develop Collaterals Circulation, July 11, 2000; 102(2): 185 - 190. [Abstract] [Full Text] [PDF]
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