The association of circulating monocyte count with coronary collateral growth in patients with diabetes mellitus
Tóm tắt
The status of inflammation may affect the collateral development in patients with diabetes mellitus (DM). Monocytes were found to have an important role in collateral growth in animal studies. We aimed to investigate the possible association of circulating monocyte count with collateral development in patients with DM and severe coronary artery disease (CAD). We enrolled 134 consecutive patients with DM who had ≥95 stenosis in at least one major coronary artery and investigated the relationship between circulating monocyte count and collateral growth. When we analyzed the coronary angiograms of eligible patients, we found that 64 of them had good collateral growth and 70 had poor collateral growth according to the Cohen–Rentrop method. The monocyte count was significantly different between good and poor collateral growth groups (643 ± 184 vs. 479 ± 143 per mm3, P < 0.001). In the analysis comparing the Rentrop score with the Gensini score and circulating monocyte count, we found significant correlations (r = 0.293, P = 0.001 and r = 0.455, P < 0.001, respectively). The duration of ischemic symptoms tended to be longer in the good collateral group (1.9 ± 4.1 vs. 0.8 ± 1.3 years, P = 0.079). The Gensini score was also correlated with the duration of myocardial ischemic symptoms (r = 0.299, P = 0.004). Multivariate analysis revealed an increased monocyte count in the good collateral group [odds ratio (OR), 5.726; 95% confidence interval (CI), 1.817–18.040, P = 0.003, the cut-off value for monocyte was defined as 550 cell/mm3]. The increased circulating monocyte count in diabetic patients was evidently related to good coronary collateral growth. This finding may be potentially important in clinical and basic cardiovascular medicine.
Tài liệu tham khảo
Billinger M, Kloos P, Eberli FR, Windecker S, Meier B, Seiler C (2002) Physiologically assessed coronary collateral flow and adverse cardiac ischemic events: a follow up study in 403 patients with coronary artery disease. J Am Coll Cardiol 40:1545–1550
Habib GB, Heibig J, Forman SA, Brown BG, Roberts R, Terrin ML, Bolli R (1991) Influence of coronary collateral vessels on myocardial infarct size in humans: results of phase I thrombolysis in myocardial infarction (TIMI) trial. The TIMI investigators. Circulation 83:739–746
Hansen JF (1989) Coronary collateral circulation: clinical significance and influence on survival in patients with coronary artery occlusion. Am Heart J 117:290–295
Maseri A, Araujo L, Finocchiaro ML (1993) Collateral development and function in man. In: Schaper W, Schaper J (eds) Collateral circulation: heart, brain, kidney, limbs. Kluwer, Boston, pp 381–402
Tayebjee MH, Lip GY, MacFadyen RJ (2004) Collateralization and the response to obstruction of epicardial coronary arteries. QJM 97:259–272
Kornowsky R (2003) Collateral formation and clinical variables in obstructive coronary artery disease: the influence of hypercholesterolemia and diabetes mellitus. Coron Artery Dis 14:61–64
Kilian JG, Keech A, Adams MR, Celermajer DS (2002) Coronary collateralisation: determinants of adequate distal vessel filling after arterial occlusion. Coron Artery Dis 13:155–159
Pohl T, Seiler C, Billinger M, Herren E, Wustmann K, Mehta H, Windecker S, Eberli FR, Meier B (2001) Frequency distribution of collateral flow and factors influencing collateral channel development. J Am Coll Cardiol 38:1872–1878
Abaci A, Oguzhan A, Kahraman S, Eryol NK, Unal S, Arinc H, Ergin A (1999) Effect of diabetes mellitus on formation of coronary collateral vessels. Circulation 99:2239–2242
Rentrop KP, Cohen M, Blanke H, Phillips RA (1985) Changes in collateral channel filling immediately after controlled coronary artery occlusion by an angioplasty balloon in human subjects. J Am Coll Cardiol 5:587–592
Gensini GG (1983) A more meaningful scoring system for determining the severity of coronary heart disease. Am J Cardiol 51:606
Sherman JA, Hall A, Malenka DJ, De Muinck ED, Simons M (2006) Humoral and cellular factors responsible for coronary collateral formation. Am J Cardiol. 98(9):1194–1197 (Epub 2006 Aug 31)
Chittenden TW, Sherman JA, Xiong F, Hall AE, Lanahan AA, Taylor JM, Duan H, Pearlman JD, Moore JH, Schwartz SM, Simons M (2006) Transcriptional profiling in coronary artery disease: indications for novel markers of coronary collateralization. Circulation 114(17):1811–1820 (Epub 2006 Oct 16)
Arras M, Ito WD, Scholz D, Winkler B, Schaper J, Schaper W (1998) Monocyte activation in angiogenesis and collateral growth in the rabbit hindlimb. J Clin Invest 101:40–50
Herold J, Pipp F, Fernandez B, Xing Z, Heil M, Tillmanns H, Braun-Dullaeus RC (2004) Transplantation of monocytes: a novel strategy for in vivo augmentation of collateral vessel growth. Hum Gene Ther 15:1–12
Helisch A, Schaper W (2003) Arteriogenesis: the development and growth of collateral arteries. Microcirculation 10:83–97
Schaper J, Konig R, Franz D, Schaper W (1976) The endothelial surface of growing coronary collateral arteries. Intimal margination and diapedesis of monocytes. A combined SEM and TEM study. Virchows Arch A Pathol Anat Histol 370:193–205
Heil M, Ziegelhoeffer T, Pipp F, Kostin S, Martin S, Clauss M, Schaper W (2002) Blood monocyte concentration is critical for the enhancement of collateral artery growth (arteriogenesis). Am J Physiol Heart Circ Physiol 3:3
Hoefer IE, van Royen N, Rectenwald JE, Deindl E, Hua J, Jost M, Grundmann S, Voskuil M, Ozaki CK, Piek JJ, Buschmann IR (2004) Arteriogenesis proceeds via ICAM-1/Mac-1- mediated mechanisms. Circ Res 94:1179–1185
Kocaman SA, Arslan U, Tavil Y, Okuyan H, Abaci A, Cengel A (2007) Increased circulating monocyte count is related to good collateral development in coronary artery disease. Atherosclerosis. doi: 10.1016/j.atherosclerosis.2007.07.010 [Epub ahead of print]
Waltenberger J, Lange J, Kranz A (2000) 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 102:185–190
Czepluch FS, Bergler A, Waltenberger J (2007) Hypercholesterolaemia impairs monocyte function in CAD patients. J Intern Med 261:201–204
Stadler N, Eggermann J, Voo S, Kranz A, Waltenberger J (2007) Smoking-induced monocyte dysfunction is reversed by vitamin C supplementation in vivo. Arterioscler Thromb Vasc Biol 27:120–126
Lambiase PD, Edwards RJ, Anthopoulos P, Rahman S, Meng YG, Bucknall CA, Redwood SR, Pearson JD, Marber MS (2004) Circulating humoral factors and endothelial progenitor cells in patients with differing coronary collateral support. Circulation 109:2986–2992
Shintani S, Murohara T, Ikeda H, Ueno T, Sasaki K, Duan J, Imaizumi T (2001) Augmentation of postnatal neovascularization with autologous bone marrow transplantation. Circulation 103:897–903
Shantsila E, Watson T, Lip GY (2007) Endothelial progenitor cells in cardiovascular disorders. J Am Coll Cardiol 49(7):741–752