Predictor of poor coronary collaterals in chronic kidney disease population with significant coronary artery disease

BMC Nephrology

Tsung-Hsien Lin¹  Sheng-Hsiung Sheu¹  Wen-Ter Lai¹  Wei-chung Tsai²  Szu-Chia Chen⁴  Ho-Ming Su⁴  Suh-Hang Juo³  Po-Chao Hsu⁵ 

[1] Faculty of Medicine, Kaohsiung, Taiwan;Division of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, 100 Tzyou 1st Road, Kaohsiung, 80708, Taiwan, ROC;Center of Excellence for Environmental Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan;Department of Internal Medicine, Kaohsiung Municipal Hsiao-Kang Hospital, Kaohsiung, Taiwan;Graduate Institute of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan

关键词: Coronary collateral circulation, Hypertension, Diabetes;    Coronary artery disease;    Chronic kidney disease;   

Others  :  1083113
DOI  :  10.1186/1471-2369-13-98

 received in 2012-03-14, accepted in 2012-08-22,  发布年份 2012

【 摘 要 】

Background

Coronary collateral circulation plays an important role to protect myocardium from ischemia, preserve myocardial contractility and reduce cardiovascular events. Chronic kidney disease (CKD) is associated with poor coronary collateral development and cardiovascular outcome. However, limited research investigates the predictors for collateral development in the CKD population.

Methods

We evaluated 970 consecutive patients undergoing coronary angiography and 202 patients with CKD, defined as a glomerular filtration rate less than 60 ml/min/1.73 m², were finally analyzed. The collateral scoring system developed by Rentrop was used to classify patients into poor (grades 0 and 1) or good (grades 2 and 3) collateral group.

Results

The patients with poor collateral (n = 122) had a higher incidence of hypertension (82% vs 63.8%, p = 0.005), fewer diseased vessels numbers (2.1 ± 0.9 vs 2.6 ± 0.6, p < 0.001) and a trend to be diabetic (56.6% vs. 43.8%, p = 0.085) or female sex (37.7% vs. 25.0%, p = 0.067). Multivariate analysis showed hypertension (odd ratio (OR) 2.672, p = 0.006), diabetes (OR 1.956, p = 0.039) and diseased vessels numbers (OR 0.402, p < 0.001) were significant predictors of poor coronary collaterals development. Furthermore, hypertension and diabetes have a negative synergistic effect on collateral development (p = 0.004 for interaction).

Conclusions

In the CKD population hypertension and diabetes might negatively influence the coronary collaterals development.

【 授权许可】

   
2012 Hsu et al.; licensee BioMed Central Ltd.

【 参考文献 】

• [1]Levey AS, Atkins R, Coresh J, Cohen EP, Collins AJ, Eckardt KU, Nahas ME, Jaber BL, Jadoul M, Levin A, Powe NR, Rossert J, Wheeler DC, Lameire N, Eknoyan G: Chronic kidney disease as a global public health problem: Approaches and initiatives - a position statement from Kidney Disease Improving Global outcomes. Kidney Int 2007, 72:247-259.
• [2]Johnson CA, Levey AS, Coresh J, Levin A, Lau J, Eknoyan G: Clinical practice guidelines for chronic kidney disease in adults: Part I. Definition, disease stages, evaluation, treatment, and risk factors. Am Fam Physician 2004, 70(5):869-76. Review
• [3]Go AS, Chertow GM, Fan D, McCulloch CE, Hsu CY: Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization. N Engl J Med 2004, 351:1296-1305.
• [4]Ford ML, Tomlinson LA, Chapman TP, Rajkumar C, Holt SG: Aortic stiffness is independently associated with rate of renal function decline in chronic kidney disease stages 3 and 4. Hypertension 2010, 55:1110-5.
• [5]Tonelli M, Wiebe N, Culleton B, House A, Rabbat C, Fok M, McAlister F, Garg AX: Chronic kidney disease and mortality risk: a systematic review. J Am Soc Nephrol 2006, 17:2034-47.
• [6]Rodriguez-Iturbe B, Correa-Rotter R: Cardiovascular risk factors and prevention of cardiovascular disease in patients with chronic renal disease. Expert Opin Pharmacother 2010, 11:2687-2698.
• [7]Zoccali C, Benedetto FA, Tripepi G, Mallamaci F, Rapisarda F, Seminara G, Bonanno G, Malatino LS: Left ventricular systolic function monitoring in asymptomatic dialysis patients: a prospective cohort study. J Am Soc Nephrol 2006, 17:1460-1465.
• [8]Fujita M, Sasayama S, Ohno A, Nakajima H, Asanoi H: Importance of angina for development of collateral circulation. Br Heart J 1987, 57:139.
• [9]Tayebjee MH, Lip GY, MacFadyen RJ: Collateralization and the response to obstruction of epicardial coronary arteries. QJM 2004, 97:259.
• [10]Cohen M, Rentrop KP: Limitation of myocardial ischemia by collateral circulation during sudden controlled coronary artery occlusion in human subjects: a prospective study. Circulation 1986, 74(3):469-76.
• [11]Meier P, Gloekler S, Zbinden R, Beckh S, de Marchi SF, Zbinden S, Wustmann K, Billinger M, Vogel R, Cook S, Wenaweser P, Togni M, Windecker S, Meier B, Seiler C: Beneficial effect of recruitable collaterals: a 10-year follow-up study in patients with stable coronary artery disease undergoing quantitative collateral measurements. Circulation 2007, 116(9):975-83.
• [12]Regieli JJ, Jukema JW, Nathoe HM, Zwinderman AH, Ng S, Grobbee DE, van der Graaf Y, Doevendans PA: Coronary collaterals improve prognosis in patients with ischemic heart disease. Int J Cardiol 2009, 132(2):257-62.
• [13]Sezer M, Ozcan M, Okcular I, Elitok A, Umman S, Umman B, Tayyareci Y, Olcay A, Nisanci Y, Bilge AK, Meric M: A potential evidence to explain the reason behind the devastating prognosis of coronary artery disease in uraemic patients: renal insufficiency is associated with poor coronary collateral vessel development. Int J Cardiol 2007, 115(3):366-72.
• [14]Xie SL, Li HY, Deng BQ, Luo NS, Geng DF, Wang JF, Nie RQ: Poor coronary collateral vessel development in patients with mild to moderate renal insufficiency. Clin Res Cardiol 2011, 100(3):227-33.
• [15]Levey AS, Bosch JP, Lewis JB, Greene T, Rogers N, Roth D: A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in Renal Disease Study Group. Ann Intern Med 1999, 130:461-470.
• [16]Rentrop KP, Cohen M, Blanke H, Phillips RA: Changes in collateral channel filling immediately after controlled coronary artery occlusion by an angioplasty balloon in human subjects. J Am Coll Cardiol 1985, 5(3):587-92.
• [17]Werner GS, Ferrari M, Heinke S, Kuethe F, Surber R, Richartz BM, Figulla HR: Angiographic assessment of collateral connections in comparison with invasively determined collateral function in chronic coronary occlusions. Circulation 2003, 107:1972-7.
• [18]Levin DC: Pathways and functional significance of the coronary collateral circulation. Circulation 1974, 50:831-7.
• [19]Brown G, Rockstroh J: Coronary collateral size, flow capacity, and growth estimates from the angiogram in patients with obstructive coronary disease. Circulation 2002, 105:168-73.
• [20]Negri M, Sheiban I, Arigliano PL, Tonni S, Montresor G, Carlini S, Manzato F: Interrelation between angiographic severity of coronary artery disease and plasma levels of insulin, C-peptide and plasminogen activator inhibitor-1. Am J Cardiol 1993, 72:397-401.
• [21]Birnie DH, Holme ER, McKay IC, Hood S, McColl KE, Hillis WS: Association between antibodies to heat shock protein 65 and coronary atherosclerosis. Possible mechanism of action of Helicobacter pylori and other bacterial infections in increasing cardiovascular risk. Eur Heart J 1998, 19:387-94.
• [22]Song YR, You SJ, Lee YM, Chin HJ, Chae DW, Oh YK, Joo KW, Han JS, Na KY: Activation of hypoxia-inducible factor attenuates renal injury in rat remnant kidney. Nephrol Dial Transplant 2010, 25(1):77-85.
• [23]Nangaku M: Chronic hypoxia and tubulointerstitial injury: a final common pathway to end-stage renal failure. J Am Soc Nephrol 2006, 17(1):17-25.
• [24]Nangaku M, Eckardt KU: Hypoxia and the HIF system in kidney disease. J Mol Med (Berl) 2007, 85(12):1325-30.
• [25]Deng A, Arndt MA, Satriano J, Singh P, Rieg T, Thomson S, Tang T, Blantz RC: Renal protection in chronic kidney disease: hypoxia-inducible factor activation vs. angiotensin II blockade. Am J Physiol Renal Physiol 2010, 299(6):F1365-73.
• [26]Chen SM, Li YG, Zhang HX, Zhang GH, Long JR, Tan CJ, Wang DM, Fang XY, Mai RQ: Hypoxia-inducible factor-1alpha induces the coronary collaterals for coronary artery disease. Coron Artery Dis. 2008, 19(3):173-9.
• [27]Resar JR, Roguin A, Voner J, Nasir K, Hennebry TA, Miller JM, Ingersoll R, Kasch LM, Semenza GL: Hypoxia-inducible factor 1alpha polymorphism and coronary collaterals in patients with ischemic heart disease. Chest 2005, 128(2):787-91.
• [28]Lin TH, Wang CL, Su HM, Hsu PC, Juo SH, Voon WC, Shin SJ, Lai WT, Sheu SH: Functional vascular endothelial growth factor gene polymorphisms and diabetes: effect on coronary collaterals in patients with significant coronary artery disease. Clin Chim Acta. 2010, 411(21–22):1688-93.
• [29]Struijker Boudier HA, le Noble JL, Messing MW, Huijberts MS, le Noble FA, van Essen H: The microcirculation and hypertension. J Hypertens 1992, 10(Suppl):S147-S156.
• [30]Levy BI, Ambrosio G, Pries AR, Struijker-Boudier HA: Microcirculation in hypertension: a new target for treatment? Circulation 2001, 104:735-740.
• [31]Koerselman J, de Jaegere PP, Verhaar MC, van der Graaf Y, Grobbee DE: SMART Study Group: High blood pressure is inversely related with the presence and extent of coronary collaterals. J Hum Hypertens 2005, 19(10):809-17.
• [32]Stamler J, Vaccaro O, Neaton JD, Wentworth D: Diabetes, other risk factors and 12-yr cardiovascular mortality for men screened in the Multiple Risk Factor Interventional Trial. Diabetes Care 1993, 16:434-444.
• [33]Abbott RD, Donahue RP, Kannel WB, Wilson PF: The impact of diabetes on survival following myocardial infarction in men vs women: the Framingham study. JAMA 1988, 260:3456-3460.
• [34]Tesfamariam B, Brown ML, Deykin D, Cohen RA: Elevated glucose promotes generation of endothelium-derived vasoconstrictor prostanoids in rabbit aorta. J Clin Invest 1990, 85:929-932.
• [35]Pieper GM, Peltier BA: Amelioration by L-arginine of a dysfunctional arginine/nitric oxide pathway in diabetic endothelium. J Cardiovasc Pharmacol 1995, 25:397-403.
• [36]Marfella R, Esposito K, Nappo F, Siniscalchi M, Sasso FC, Portoghese M, Di Marino MP, Baldi A, Cuzzocrea S, Di Filippo C, Barboso G, Baldi F, Rossi F, D'Amico M, Giugliano D: Expression of angiogenic factors during acute coronary syndromes in human type 2 diabetes. Diabetes 2004, 53(9):2383-91.
• [37]Kersten JR, Toller WG, Tessmer JP, Pagel PS, Warltier DC: Hyperglycemia reduces coronary collateral blood flow through a nitric oxide-mediated mechanism. Am J Physiol Heart Circ Physiol 2001, 281(5):H2097-104.
• [38]Abaci A, Oğuzhan A, Kahraman S, Eryol NK, Unal S, Arinç H, Ergin A: Effect of diabetes mellitus on formation of coronary collateral vessels. Circulation 1999, 99(17):2239-42.
• [39]Kobayashi S, Maesato K, Moriya H, Ohtake T, Ikeda T: Insulin resistance in patients with chronic kidney disease. Am J Kidney Dis 2005, 45(2):275-80.
• [40]Ruan X, Guan Y: Metabolic syndrome and chronic kidney disease. J Diabetes 2009, 1(4):236-45.
• [41]Fortes PC, de Moraes TP, Mendes JG, Stinghen AE, Ribeiro SC, Pecoits-Filho R: Insulin resistance and glucose homeostasis in peritoneal dialysis. Perit Dial Int 2009, 29(Suppl 2):S145-8.