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Association between hyperuricemia and outcomes in patients undergoing percutaneous coronary intervention
International Journal of Cardiology 204 (2016) 152–153
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Correspondence
Association between hyperuricemia and outcomes in patients undergoing percutaneous coronary intervention Lei Wu a, Lan-Ju Yang a, Xiao-Yan Meng b, Lan-Hua Wang a, Yan-Hong Zhou a, Tao Liu a, Qian-Feng Han a, De-Yong Zhang a, Heng-Chen Yao a,⁎ a b
Department of Cardiology, Liaocheng People's Hospital and Clinical School of Taishan Medical University, Liaocheng 252000, PR China Department of Echocardiography, Liaocheng People's Hospital and Clinical School of Taishan Medical University, Shandong Province, Liaocheng 252000, PR China
a r t i c l e
i n f o
Article history: Received 23 November 2015 Accepted 27 November 2015 Available online 02 December 2015 Keywords: Hyperuricemia Percutaneous coronary intervention Outcome
Uric acid is the end product of purine catabolism. Lot of previous studies have found that hyperuricemia (HU) as a risk factor for cardiovascular diseases such as atrial fibrillation and coronary artery disease [1,2]. Also, HU is a predictor of adverse prognosis in different cardiocerebral diseases, such as acute ST segment elevation myocardial infarction, congestive heart failure and acute stroke. However, the predictive value of HU in the prognosis in patients undergoing percutaneous coronary intervention (PCI) is less known. Recently, we have read with great interest Dr. Song and colleagues meta-analysis concerning “Association between hyperuricemia and clinical adverse outcomes after percutaneous coronary intervention: a meta-analysis” that published in international journal of cardiology [3]. In this meta-analysis, the authors concluded that hyperuricemia is an independent predictive factor of clinical adverse outcomes after receiving PCI. In this meta-analysis, twelve of 20 studies were selected. The analysis showed that HU is associated with increased risk of adverse clinical outcomes after PCI (RR: 1.46, 95% confidence interval: 1.29–1.65, p b 0.01; I2 = 58.6%). Although some research suggests that HU is related to the increase of adverse effect of PCI, several clinical studies, on the contrary, provided new data on the impact of uric acid on cardiovascular events are controversial. So, there is a need for further clarification or discussion about the conclusions and the potential clinical implications stated by the authors of this well-written meta-analysis. Firstly, recent studies have reported that HU may result in some cardiovascular disease and renal disease such as hypertension, intrarenal vascular disease, atherosclerosis, and renal injury. The reasons might ⁎ Corresponding author. E-mail address: [email protected] (H.-C. Yao).
http://dx.doi.org/10.1016/j.ijcard.2015.11.184 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
be the deposit of uric acid crystalline can trigger the outset of an inflammation response and endothelial dysfunction [4]. Whereas, one recent study including 13,273 patients with coronary artery disease found that HU had a significant association with one year mortality across all subgroups after PCI [5]. Consistently, other previous studies showed that increased serum or plasma levels of uric acid on admission is a strong and independent predictor of poor coronary flow, in hospital MACE, in-hospital mortality, acute kidney injury, and 1-year mortality in patients with ST segment elevation myocardial infarction (STEMI) after primary PCI and can also be used for risk stratification in these patients [6–9]. Moreover, contrast induced nephropathy (CIN), a common complication of PCI, is mediated by oxidative stress and reactive oxygen species generation. HU may inhibit nitric oxide system and increase synthesis of reactive oxygen species. Recent studies suggest that among patients undergoing coronary angiography or PCI increased uric acid levels are independently associated with an increased risk of CIN [10,11]. In brief, as mentioned above, HU can be used as an adverse predictor for patients undergoing PCI. Secondly, although lots of studies suggest that HU might be a poor predictor for patients after receiving PCI, there are still some researches gained promising conclusions. Recently, a clinical study, recruited a total of 1272 patients undergoing PCI (76% men, mean age 67.6 years old. Among them, 43.9% were elective, while the others had acute coronary syndrome at presentation) found that serum uric acid levels do not influence the risk of periprocedural myocardial infarction damage in patients undergoing PCI [12]. Studies also show that coronary distal embolization, coronary dissection, no-reflow, low reflow, or side branches loss may result in periprocedural myocardial infarction damage which occurs in up to 30% of PCI. Also, white blood cells and platelets plugging other than increased uric acid can obstruct microvasculature may increase the occurrence of periprocedural myocardial infarction. Moreover, one previous study including a total of 13,504 healthy middleaged men and women had followed up for up to eight years. The authors found that serum uric acid levels are not an independent risk factor for coronary heart disease [13]. Furthermore, one study on type 2 diabetes patients suggested that HU may not be accounted as an independent risk factor for cardiovascular mortality and increased all cause mortality risk with higher levels of uric acid might be due to increased neoplastic mortality. That is to say that increased serum levels of uric acid are just a coincidence phenomena other than a causal risk factor for cardiovascular events [14].
L. Wu et al. / International Journal of Cardiology 204 (2016) 152–153
Thirdly, the underlying mechanism by which uric acid takes a role of adverse effect in the patients undergoing PCI is not fully clear. Recently, a study indicates that serum uric acid should be considered as an important prothrombotic stimulus and a platelet activator. Because in patients with ischemic heart disease elevated serum uric acid is associated with elevated makers of proinflammatory state. Markers of pro-inflammatory state correlate with prothrombotic markers such as serum fibrinogen and platelet count [15]. Also, uric acid has been found to upregulate expression of C-reactive protein in human endothelial cells and vasculature cells, alters the proliferation/migration and nitric oxide release of human vascular cells, thus result in the pathogenesis of atherosclerosis, pathologic vascular remodeling, and systemic inflammation by endothelial dysfunction. Noncrystalline UA can stimulate rat vascular smooth muscle cell proliferation via the activation of mitogen-activated protein kinase, growth factors, chemokines (monocyte chemoattractant protein-1), and inflammatory enzymes (COX-2) [16]. Furthermore, uric acid can generate aminocarbonyl radicals damaging cells in vasculature [17]. In summary, the association between hyperuricemia and outcomes in patients undergoing percutaneous coronary intervention is still unclear yet totally, further studies should be highlighted in large sample scales and with long enough follow-up. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [18]. Funding This work was supported by the Natural Science Foundation of Shandong Province (ZR2013HL017) and the Natural Science Foundation of Liaocheng City (2012NS13), and the Science and Technology Developing Project of Liaocheng City (2014GJH26). Conflict of interest The authors report no relationships that could be construed as a conflict of interest. References [1] K.P. Letsas, P. Korantzopoulos, G.S. Filippatos, C.C. Mihas, V. Markou, G. Efrmidis, et al., Uric acid elevation in atrial fibrillation, Hell. J. Cardiol. 51 (2010) 209–213.
153
[2] P.F. Hsu, S.Y. Chuang, W.C. Yu, W.L. Chan, C.H. Chen, The impacts of serum uric acid on arterial hemodynamics and cardiovascular risks, Acta Cardiol. Sin. 29 (2013) 142–150. [3] X. Song, Y. Wang, X. Hou, K. Che, R. Wang, Y. Liu, et al., Association between hyperuricemia and clinical adverse outcomes after percutaneous coronary intervention: a meta-analysis, Int. J. Cardiol. 201 (2015) 658–662. [4] K.L. Rock, H. Kataoka, J.J. Lai, Uric acid as a danger signal in gout and its comorbidities, Nat. Rev. Rheumatol. 9 (2013) 13–23. [5] G. Ndrepepa, S. Braun, L. King, M. Fusaro, T. Tada, S. Cassese, et al., Uric acid and prognosis in angiography-proven coronary artery disease, Eur. J. Clin. Investig. 43 (2013) 256–266. [6] M. Akpek, M.G. Kaya, H. Uyarel, M. Yarlioglues, N. Kalay, O. Gunebakmaz, et al., The association of serum uric acid levels on coronary flow in patients with STEMI undergoing primary PCI, Atherosclerosis 219 (2011) 334–341. [7] N. Basar, N. Sen, F. Ozcan, G. Erden, S. Kanat, E. Sokmen, et al., Elevated serum uric acid predicts angiographic impaired reperfusion and 1-year mortality in STsegment elevation myocardial infarction patients undergoing percutaneous coronary intervention, Investig. Med. 59 (2011) 931-927. [8] S.H. Park, W.Y. Shin, E.Y. Lee, H.W. Gil, S.W. Lee, S.J. Lee, et al., The impact of hyperuricemia on in-hospital mortality and incidence of acute kidney injury in patients undergoing percutaneous coronary intervention, Circ. J. 75 (2011) 692–697. [9] C. Lazzeri, S. Valente, M. Chiostri, A. Sori, P. Bernardo, G.F. Gensini, Uric acid in the acute phase of ST elevation myocardial infarction submitted to primary PCI: its prognostic role and relation with inflammatory markers: a single center experience, Int. J. Cardiol. 138 (2010) 206–209. [10] L. Barbieri, M. Verdoia, A. Schaffer, E. Cassetti, P. Marino, H. Suryapranata, et al., Novara Atherosclerosis Study Group (NAS), uric acid levels and the risk of contrast induced nephropathy in patients undergoing coronary angiography or PCI, Nutr. Metab. Cardiovasc. Dis. 25 (2015) 181–186. [11] M. Saritemur, M. Turkeli, K. Kalkan, İ.H. Tanboga, E. Aksakal, Relation of uric acid and contrast-induced nephropathy in patients undergoing primary percutaneous coronary intervention in the ED, Am. J. Emerg. Med. 32 (2014) 119–123. [12] M. Verdoia, A. Schaffer, L. Barbieri, G. Di Giovine, P. Marino, G. De Luca, Novara Atherosclerosis Stufy Group, uric acid and risk of procedural myocardial infarction in paitnets undergoing percutaneous coronary intervention, Diabetes Metab. Res. Rev. 30 (2014) 297–304. [13] J.T. Moriarity, A.R. Folsom, C. Iribarren, F.J. Nieto, W.D. Rosamond, Serum uric acid and risk of coronary heart disease: Atherosclerosis Risk in Communities (ARIC) study, Ann. Epidemiol. 10 (2000) 136–143. [14] F. Panero, G. Gruden, M. Perotto, P. Fornengo, F. Barutta, E. Greco, et al., Uric acid is not an independent predictor of cardiovascular mortality in type 2 diabetes: a population-based study, Atherosclerosis 221 (2012) 183–188. [15] T. Zapolski, P. Waciński, B. Kondracki, E. Rychta, M.J. Buraczyńska, A. Wysokiński, Uric acid as a link between renal dysfunction and both pro-inflammatory and prothrombotic state in patients with metabolic syndrome and coronary artery disease, Kardiol. Pol. 69 (2011) 319–326. [16] D.H. Kang, S.K. Park, I.K. Lee, R.J. Johnson, Uric acid-induced C-reactive protein expression: implication on cell proliferation and nitric oxide production of human vascular cells, J. Am. Soc. Nephrol. 16 (2005) 3553–3562. [17] K.R. Maples, R.P. Mason, Free radical metabolite of uric acid, J. Biol. Chem. 263 (1988) 1709–1712. [18] L.G. Shewan, G.M.C. Rosano, M.Y. Henein, A.J.S. Coats, A statement on ethical standards in publishing scientific articles in the International Journal of Cardiology family of journals, Int. J. Cardiol. 170 (2014) 253–254.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Correspondence
Association between hyperuricemia and outcomes in patients undergoing percutaneous coronary intervention Lei Wu a, Lan-Ju Yang a, Xiao-Yan Meng b, Lan-Hua Wang a, Yan-Hong Zhou a, Tao Liu a, Qian-Feng Han a, De-Yong Zhang a, Heng-Chen Yao a,⁎ a b
Department of Cardiology, Liaocheng People's Hospital and Clinical School of Taishan Medical University, Liaocheng 252000, PR China Department of Echocardiography, Liaocheng People's Hospital and Clinical School of Taishan Medical University, Shandong Province, Liaocheng 252000, PR China
a r t i c l e
i n f o
Article history: Received 23 November 2015 Accepted 27 November 2015 Available online 02 December 2015 Keywords: Hyperuricemia Percutaneous coronary intervention Outcome
Uric acid is the end product of purine catabolism. Lot of previous studies have found that hyperuricemia (HU) as a risk factor for cardiovascular diseases such as atrial fibrillation and coronary artery disease [1,2]. Also, HU is a predictor of adverse prognosis in different cardiocerebral diseases, such as acute ST segment elevation myocardial infarction, congestive heart failure and acute stroke. However, the predictive value of HU in the prognosis in patients undergoing percutaneous coronary intervention (PCI) is less known. Recently, we have read with great interest Dr. Song and colleagues meta-analysis concerning “Association between hyperuricemia and clinical adverse outcomes after percutaneous coronary intervention: a meta-analysis” that published in international journal of cardiology [3]. In this meta-analysis, the authors concluded that hyperuricemia is an independent predictive factor of clinical adverse outcomes after receiving PCI. In this meta-analysis, twelve of 20 studies were selected. The analysis showed that HU is associated with increased risk of adverse clinical outcomes after PCI (RR: 1.46, 95% confidence interval: 1.29–1.65, p b 0.01; I2 = 58.6%). Although some research suggests that HU is related to the increase of adverse effect of PCI, several clinical studies, on the contrary, provided new data on the impact of uric acid on cardiovascular events are controversial. So, there is a need for further clarification or discussion about the conclusions and the potential clinical implications stated by the authors of this well-written meta-analysis. Firstly, recent studies have reported that HU may result in some cardiovascular disease and renal disease such as hypertension, intrarenal vascular disease, atherosclerosis, and renal injury. The reasons might ⁎ Corresponding author. E-mail address: [email protected] (H.-C. Yao).
http://dx.doi.org/10.1016/j.ijcard.2015.11.184 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
be the deposit of uric acid crystalline can trigger the outset of an inflammation response and endothelial dysfunction [4]. Whereas, one recent study including 13,273 patients with coronary artery disease found that HU had a significant association with one year mortality across all subgroups after PCI [5]. Consistently, other previous studies showed that increased serum or plasma levels of uric acid on admission is a strong and independent predictor of poor coronary flow, in hospital MACE, in-hospital mortality, acute kidney injury, and 1-year mortality in patients with ST segment elevation myocardial infarction (STEMI) after primary PCI and can also be used for risk stratification in these patients [6–9]. Moreover, contrast induced nephropathy (CIN), a common complication of PCI, is mediated by oxidative stress and reactive oxygen species generation. HU may inhibit nitric oxide system and increase synthesis of reactive oxygen species. Recent studies suggest that among patients undergoing coronary angiography or PCI increased uric acid levels are independently associated with an increased risk of CIN [10,11]. In brief, as mentioned above, HU can be used as an adverse predictor for patients undergoing PCI. Secondly, although lots of studies suggest that HU might be a poor predictor for patients after receiving PCI, there are still some researches gained promising conclusions. Recently, a clinical study, recruited a total of 1272 patients undergoing PCI (76% men, mean age 67.6 years old. Among them, 43.9% were elective, while the others had acute coronary syndrome at presentation) found that serum uric acid levels do not influence the risk of periprocedural myocardial infarction damage in patients undergoing PCI [12]. Studies also show that coronary distal embolization, coronary dissection, no-reflow, low reflow, or side branches loss may result in periprocedural myocardial infarction damage which occurs in up to 30% of PCI. Also, white blood cells and platelets plugging other than increased uric acid can obstruct microvasculature may increase the occurrence of periprocedural myocardial infarction. Moreover, one previous study including a total of 13,504 healthy middleaged men and women had followed up for up to eight years. The authors found that serum uric acid levels are not an independent risk factor for coronary heart disease [13]. Furthermore, one study on type 2 diabetes patients suggested that HU may not be accounted as an independent risk factor for cardiovascular mortality and increased all cause mortality risk with higher levels of uric acid might be due to increased neoplastic mortality. That is to say that increased serum levels of uric acid are just a coincidence phenomena other than a causal risk factor for cardiovascular events [14].
L. Wu et al. / International Journal of Cardiology 204 (2016) 152–153
Thirdly, the underlying mechanism by which uric acid takes a role of adverse effect in the patients undergoing PCI is not fully clear. Recently, a study indicates that serum uric acid should be considered as an important prothrombotic stimulus and a platelet activator. Because in patients with ischemic heart disease elevated serum uric acid is associated with elevated makers of proinflammatory state. Markers of pro-inflammatory state correlate with prothrombotic markers such as serum fibrinogen and platelet count [15]. Also, uric acid has been found to upregulate expression of C-reactive protein in human endothelial cells and vasculature cells, alters the proliferation/migration and nitric oxide release of human vascular cells, thus result in the pathogenesis of atherosclerosis, pathologic vascular remodeling, and systemic inflammation by endothelial dysfunction. Noncrystalline UA can stimulate rat vascular smooth muscle cell proliferation via the activation of mitogen-activated protein kinase, growth factors, chemokines (monocyte chemoattractant protein-1), and inflammatory enzymes (COX-2) [16]. Furthermore, uric acid can generate aminocarbonyl radicals damaging cells in vasculature [17]. In summary, the association between hyperuricemia and outcomes in patients undergoing percutaneous coronary intervention is still unclear yet totally, further studies should be highlighted in large sample scales and with long enough follow-up. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [18]. Funding This work was supported by the Natural Science Foundation of Shandong Province (ZR2013HL017) and the Natural Science Foundation of Liaocheng City (2012NS13), and the Science and Technology Developing Project of Liaocheng City (2014GJH26). Conflict of interest The authors report no relationships that could be construed as a conflict of interest. References [1] K.P. Letsas, P. Korantzopoulos, G.S. Filippatos, C.C. Mihas, V. Markou, G. Efrmidis, et al., Uric acid elevation in atrial fibrillation, Hell. J. Cardiol. 51 (2010) 209–213.
153
[2] P.F. Hsu, S.Y. Chuang, W.C. Yu, W.L. Chan, C.H. Chen, The impacts of serum uric acid on arterial hemodynamics and cardiovascular risks, Acta Cardiol. Sin. 29 (2013) 142–150. [3] X. Song, Y. Wang, X. Hou, K. Che, R. Wang, Y. Liu, et al., Association between hyperuricemia and clinical adverse outcomes after percutaneous coronary intervention: a meta-analysis, Int. J. Cardiol. 201 (2015) 658–662. [4] K.L. Rock, H. Kataoka, J.J. Lai, Uric acid as a danger signal in gout and its comorbidities, Nat. Rev. Rheumatol. 9 (2013) 13–23. [5] G. Ndrepepa, S. Braun, L. King, M. Fusaro, T. Tada, S. Cassese, et al., Uric acid and prognosis in angiography-proven coronary artery disease, Eur. J. Clin. Investig. 43 (2013) 256–266. [6] M. Akpek, M.G. Kaya, H. Uyarel, M. Yarlioglues, N. Kalay, O. Gunebakmaz, et al., The association of serum uric acid levels on coronary flow in patients with STEMI undergoing primary PCI, Atherosclerosis 219 (2011) 334–341. [7] N. Basar, N. Sen, F. Ozcan, G. Erden, S. Kanat, E. Sokmen, et al., Elevated serum uric acid predicts angiographic impaired reperfusion and 1-year mortality in STsegment elevation myocardial infarction patients undergoing percutaneous coronary intervention, Investig. Med. 59 (2011) 931-927. [8] S.H. Park, W.Y. Shin, E.Y. Lee, H.W. Gil, S.W. Lee, S.J. Lee, et al., The impact of hyperuricemia on in-hospital mortality and incidence of acute kidney injury in patients undergoing percutaneous coronary intervention, Circ. J. 75 (2011) 692–697. [9] C. Lazzeri, S. Valente, M. Chiostri, A. Sori, P. Bernardo, G.F. Gensini, Uric acid in the acute phase of ST elevation myocardial infarction submitted to primary PCI: its prognostic role and relation with inflammatory markers: a single center experience, Int. J. Cardiol. 138 (2010) 206–209. [10] L. Barbieri, M. Verdoia, A. Schaffer, E. Cassetti, P. Marino, H. Suryapranata, et al., Novara Atherosclerosis Study Group (NAS), uric acid levels and the risk of contrast induced nephropathy in patients undergoing coronary angiography or PCI, Nutr. Metab. Cardiovasc. Dis. 25 (2015) 181–186. [11] M. Saritemur, M. Turkeli, K. Kalkan, İ.H. Tanboga, E. Aksakal, Relation of uric acid and contrast-induced nephropathy in patients undergoing primary percutaneous coronary intervention in the ED, Am. J. Emerg. Med. 32 (2014) 119–123. [12] M. Verdoia, A. Schaffer, L. Barbieri, G. Di Giovine, P. Marino, G. De Luca, Novara Atherosclerosis Stufy Group, uric acid and risk of procedural myocardial infarction in paitnets undergoing percutaneous coronary intervention, Diabetes Metab. Res. Rev. 30 (2014) 297–304. [13] J.T. Moriarity, A.R. Folsom, C. Iribarren, F.J. Nieto, W.D. Rosamond, Serum uric acid and risk of coronary heart disease: Atherosclerosis Risk in Communities (ARIC) study, Ann. Epidemiol. 10 (2000) 136–143. [14] F. Panero, G. Gruden, M. Perotto, P. Fornengo, F. Barutta, E. Greco, et al., Uric acid is not an independent predictor of cardiovascular mortality in type 2 diabetes: a population-based study, Atherosclerosis 221 (2012) 183–188. [15] T. Zapolski, P. Waciński, B. Kondracki, E. Rychta, M.J. Buraczyńska, A. Wysokiński, Uric acid as a link between renal dysfunction and both pro-inflammatory and prothrombotic state in patients with metabolic syndrome and coronary artery disease, Kardiol. Pol. 69 (2011) 319–326. [16] D.H. Kang, S.K. Park, I.K. Lee, R.J. Johnson, Uric acid-induced C-reactive protein expression: implication on cell proliferation and nitric oxide production of human vascular cells, J. Am. Soc. Nephrol. 16 (2005) 3553–3562. [17] K.R. Maples, R.P. Mason, Free radical metabolite of uric acid, J. Biol. Chem. 263 (1988) 1709–1712. [18] L.G. Shewan, G.M.C. Rosano, M.Y. Henein, A.J.S. Coats, A statement on ethical standards in publishing scientific articles in the International Journal of Cardiology family of journals, Int. J. Cardiol. 170 (2014) 253–254.