Acute phase reactants in patients with coronary slow flow phenomenon
In this study, we sought to investigate the serum levels of high sensitivity C-reactive protein (Hs-CRP), N-terminal pro-brain natriuretic peptide (NT proBNP), erythrocyte sedimentation rate, leukocyte, thyroid hormone and fibrinogen levels in patients with coronary slow flow phenomenon (CSFP). A to...
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| Published in | Anadolu kardiyoloji dergisi : AKD Vol. 10; no. 5; pp. 416 - 420 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Turkey
Aves Yayıncılık
01.10.2010
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1302-8723 1308-0032 1308-0032 |
| DOI | 10.5152/akd.2010.139 |
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| Abstract | In this study, we sought to investigate the serum levels of high sensitivity C-reactive protein (Hs-CRP), N-terminal pro-brain natriuretic peptide (NT proBNP), erythrocyte sedimentation rate, leukocyte, thyroid hormone and fibrinogen levels in patients with coronary slow flow phenomenon (CSFP).
A total of 82 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels (45 males and 37 females, mean age 59±11 years) and 34 patients with normal coronary arteries and normal coronary flow (19 males and 15 females, mean age 56±10 years) with similar risk profiles were included in this cross-sectional observational study. Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction (TIMI) frame count, serum level of Hs-CRP, NT proBNP, sedimentation, leukocyte, free triiodothyronine (FT3), free thyroxine (FT4), thyroid stimulating hormone (TSH) and fibrinogen levels were measured. Statistical analysis was performed using t test for independent samples, Chi-square test and Pearson correlation analysis.
Hs-CRP (0.88±0.86 vs 0.36±0.35 mg/L, p=0.001) and NT proBNP (117.83±163.2 vs 47.33±30.6 ng/ml, p=0.01) were found to be significantly higher in patients with coronary slow flow compared with normal control group. There were no significant differences regarding thyroid hormones, fibrinogen, sedimentation rate and leukocyte count between two groups. The mean TIMI frame counts were positively correlated (r=0.454, p=0.001 and r=0.554, p=0.001, respectively) with plasma Hs-CRP levels and NT-proBNP levels.
Hs-CRP and NT proBNP are significantly higher in patients with coronary slow flow compared with normal control group. Their increased levels are positively correlated with TIMI frame count. |
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| AbstractList | In this study, we sought to investigate the serum levels of high sensitivity C-reactive protein (Hs-CRP), N-terminal pro-brain natriuretic peptide (NT proBNP), erythrocyte sedimentation rate, leukocyte, thyroid hormone and fibrinogen levels in patients with coronary slow flow phenomenon (CSFP).
A total of 82 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels (45 males and 37 females, mean age 59±11 years) and 34 patients with normal coronary arteries and normal coronary flow (19 males and 15 females, mean age 56±10 years) with similar risk profiles were included in this cross-sectional observational study. Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction (TIMI) frame count, serum level of Hs-CRP, NT proBNP, sedimentation, leukocyte, free triiodothyronine (FT3), free thyroxine (FT4), thyroid stimulating hormone (TSH) and fibrinogen levels were measured. Statistical analysis was performed using t test for independent samples, Chi-square test and Pearson correlation analysis.
Hs-CRP (0.88±0.86 vs 0.36±0.35 mg/L, p=0.001) and NT proBNP (117.83±163.2 vs 47.33±30.6 ng/ml, p=0.01) were found to be significantly higher in patients with coronary slow flow compared with normal control group. There were no significant differences regarding thyroid hormones, fibrinogen, sedimentation rate and leukocyte count between two groups. The mean TIMI frame counts were positively correlated (r=0.454, p=0.001 and r=0.554, p=0.001, respectively) with plasma Hs-CRP levels and NT-proBNP levels.
Hs-CRP and NT proBNP are significantly higher in patients with coronary slow flow compared with normal control group. Their increased levels are positively correlated with TIMI frame count. Amaç:Çalışmamızda koroner yavaş akımlı hastalarda yüksek-duyarlı C-reaktif protein (Hs-CRP), N-terminal pro-beyin natriüretik peptit (NT-proBNP), eritrosit sedimantasyon hızı, lökosit, tiroid hormonları ve fibrinojen seviyelerini araştırmayı amaçladık. Yöntemler: Bu enine-kesitli gözlemsel çalışmaya koroner arterleri normal olarak değerlendirilen fakat üç koroner damarında da yavaş akımı olan 82 hasta (45 erkek, 37 kadın, ortalama yaş 59±11), normal koroner arter yapısına, normal koroner akıma ve benzer koroner risk faktörlerine sahip 34 olgu (19 erkek, 15 kadın, ortalama yaş:56±10) çalışmaya dahil edildi. Hastaların ve kontrol grubunun koroner akım hızları TIMI kare sayısı yöntemi ile ölçüldü. Kan numunelerinden Hs-CRP, NT ProBNP, sedimantasyon, lökosit sayısı, tiroid hormonları ve fibrinojen seviyeleri ölçüldü. İstatistiksel analiz bağımsız örneklem t testi, Ki-kare testi ve Pearson korelasyon analizi ile yapıldı. Bulgular: Hs-CRP (0.88±0.86'ya karşın 0.36±0.35 mg/L, p<0.001) ve NT proBNP (117.83±163.2'ye karşın 47.33±30.6 ng/ml, p<0.01) seviyeleri koroner yavaş akım grubunda kontrol grubuna göre istatistiksel açıdan anlamlı olarak yüksek bulundu. Tiroid hormonları, fibrinojen, sedimantasyon ve lökosit düzeylerine bakıldığında iki grup arasında anlamlı fark yoktu. TIMI sayısı ve plazma Hs-CRP ve NT-proBNP değerleri arasında pozitif korelasyon mevcuttu (sırası ile r=0.454, p=0.001 ve r=0.554, p=0.001). Sonuç: Hs CRP ve NT ProBNP seviyeleri normal olgulara kıyasla koroner yavaş akımlı olgularda anlamlı düzeyde yüksek bulundu. Hs CRP ve NT ProBNP artmış seviyeleri ve TIMI kare sayısı arasında pozitif korelasyon ilişkisi mevcut. Objective:In this study, we sought to investigate the serum levels of high sensitivity C-reactive protein (Hs-CRP), N-terminal pro-brain natriuretic peptide (NT proBNP), erythrocyte sedimentation rate, leukocyte, thyroid hormone and fibrinogen levels in patients with coronary slow flow phenomenon (CSFP). Methods: A total of 82 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels (45 males and 37 females, mean age 59±11 years) and 34 patients with normal coronary arteries and normal coronary flow (19 males and 15 females, mean age 56±10 years) with similar risk profiles were included in this cross-sectional observational study. Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction (TIMI) frame count, serum level of Hs-CRP, NT proBNP, sedimentation, leukocyte, free triiodothyronine (FT3), free thyroxine (FT4), thyroid stimulating hormone (TSH) and fibrinogen levels were measured. Statistical analysis was performed using t test for independent samples, Chi-square test and Pearson correlation analysis. Results: Hs-CRP (0.88±0.86 vs 0.36±0.35 mg/L, p<0.001) and NT proBNP (117.83±163.2 vs 47.33±30.6 ng/ml, p<0.01) were found to be significantly higher in patients with coronary slow flow compared with normal control group. There were no significant differences regarding thyroid hormones, fibrinogen, sedimentation rate and leukocyte count between two groups. The mean TIMI frame counts were positively correlated (r=0.454, p=0.001 and r=0.554, p=0.001, respectively) with plasma Hs-CRP levels and NT-proBNP levels. Conclusion: Hs-CRP and NT proBNP are significantly higher in patients with coronary slow flow compared with normal control group. Their increased levels are positively correlated with TIMI frame count. In this study, we sought to investigate the serum levels of high sensitivity C-reactive protein (Hs-CRP), N-terminal pro-brain natriuretic peptide (NT proBNP), erythrocyte sedimentation rate, leukocyte, thyroid hormone and fibrinogen levels in patients with coronary slow flow phenomenon (CSFP).OBJECTIVEIn this study, we sought to investigate the serum levels of high sensitivity C-reactive protein (Hs-CRP), N-terminal pro-brain natriuretic peptide (NT proBNP), erythrocyte sedimentation rate, leukocyte, thyroid hormone and fibrinogen levels in patients with coronary slow flow phenomenon (CSFP).A total of 82 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels (45 males and 37 females, mean age 59±11 years) and 34 patients with normal coronary arteries and normal coronary flow (19 males and 15 females, mean age 56±10 years) with similar risk profiles were included in this cross-sectional observational study. Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction (TIMI) frame count, serum level of Hs-CRP, NT proBNP, sedimentation, leukocyte, free triiodothyronine (FT3), free thyroxine (FT4), thyroid stimulating hormone (TSH) and fibrinogen levels were measured. Statistical analysis was performed using t test for independent samples, Chi-square test and Pearson correlation analysis.METHODSA total of 82 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels (45 males and 37 females, mean age 59±11 years) and 34 patients with normal coronary arteries and normal coronary flow (19 males and 15 females, mean age 56±10 years) with similar risk profiles were included in this cross-sectional observational study. Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction (TIMI) frame count, serum level of Hs-CRP, NT proBNP, sedimentation, leukocyte, free triiodothyronine (FT3), free thyroxine (FT4), thyroid stimulating hormone (TSH) and fibrinogen levels were measured. Statistical analysis was performed using t test for independent samples, Chi-square test and Pearson correlation analysis.Hs-CRP (0.88±0.86 vs 0.36±0.35 mg/L, p=0.001) and NT proBNP (117.83±163.2 vs 47.33±30.6 ng/ml, p=0.01) were found to be significantly higher in patients with coronary slow flow compared with normal control group. There were no significant differences regarding thyroid hormones, fibrinogen, sedimentation rate and leukocyte count between two groups. The mean TIMI frame counts were positively correlated (r=0.454, p=0.001 and r=0.554, p=0.001, respectively) with plasma Hs-CRP levels and NT-proBNP levels.RESULTSHs-CRP (0.88±0.86 vs 0.36±0.35 mg/L, p=0.001) and NT proBNP (117.83±163.2 vs 47.33±30.6 ng/ml, p=0.01) were found to be significantly higher in patients with coronary slow flow compared with normal control group. There were no significant differences regarding thyroid hormones, fibrinogen, sedimentation rate and leukocyte count between two groups. The mean TIMI frame counts were positively correlated (r=0.454, p=0.001 and r=0.554, p=0.001, respectively) with plasma Hs-CRP levels and NT-proBNP levels.Hs-CRP and NT proBNP are significantly higher in patients with coronary slow flow compared with normal control group. Their increased levels are positively correlated with TIMI frame count.CONCLUSIONHs-CRP and NT proBNP are significantly higher in patients with coronary slow flow compared with normal control group. Their increased levels are positively correlated with TIMI frame count. |
| Author | Kandaz, Muhammet Nazli, Yunus Aysel, Süleyman Tavli, Talat Mergen, Haluk Yanik, Ekrem Cekdemir, Demet Madak, Nihat |
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| References | 17. Yazıcı M, Aksakal E, Demircan S, Şahin M, Sağkan O. Is slow coronary flow related with inflammation and procoagulant state? Anadolu Kardiyol Derg 2005; 5: 3-7. 24. Baykan M, Baykan EC, Turan S, Gedikli O, Kaplan S, Kiriş A, et al. Assessment of left ventricular function and Tei index by tissue Doppler imaging in patients with slow coronary flow. Echocardiography 2009: 26; 1167-72. 19. Slevin M, Krupinski J. A role of C-reactive protein in the regulation of angiogenesis, endothelial cell inflammation and thrombus formation in cardiovascular disease. Histol Histopathol 2009; 24: 1473-8. 10. Sezgin AT, Sığırcı A, Barutçu I, Topal E, Sezgin N, Özdemir R, et al. Vascular endothelial function in patients with slow coronary flow. Coron Artery Dis 2003;14: 155-61. 13. Vila G, Resl M, Stelzeneder D, Strucks J, Maier C, Riedl M, et al. Plasma NT-proBNP increases in response to LPS administration in healthy men. J Appl Physiol 2008;105: 1741-5. 3. Folkman J, Shing Y. Angiogenesis. J Biol Chem 1992; 267: 10931-4. 5. Shah PK, Falk E, Badimon JJ, Fernandez-Ortiz A, Mailhac A, Villareal-Levy G, et al. Human monocyte-derived macrophages induce collagen breakdown in fibrous caps of atherosclerotic plaques. Potential role of matrix-degrading metalloproteinases and implications for plaque rupture. Circulation 1995; 92: 1565-9. 9. Mosseri M, Yarom R, Gotsman MS, Hasin Y. Histologic evidence for small vessel coronary artery disease in patients with angina pectoris and patent large coronary arteries. Circulation 1986; 74: 964-72. 25. Hak AE, Pols HA, Visser TJ, Drexhage HA, Hofman A, Witteman JC. Subclinical hypothyroidism is an independent risk factor for atherosclerosis and myocardial infarction in elderly women: The Rotterdam Study. Ann Intern Med 2000; 132: 270-8. 23. Turhan H, Saydam GS, Erbay AR, Ayaz S, Yaşar AS, Aksoy Y, et al. Increased plasma soluble adhesion molecules: ICAM-1, VCAM-1, and E-selectin concentrations in patients with slow coronary flow. Int J Cardiol 2006; 108: 224-30. 2. Tambe AA, Demany MA, Zimmerman HA, Mascarenhas E. Angina pectoris and slow flow velocity of dye in coronary arteries. A new angiographic finding. Am Heart J 1972; 84: 66-71. 22. De Meyer GR, Herman AG. Vascular endothelial dysfunction. Prog Cardiovasc Dis 1997; 39: 325-42. 11. Evrengül H, Tanrıverdi H, Enli Y, Kuru O, Seleci D, Baştemir M, et al. Interaction of plasma homocysteine and thyroid hormone concentrations in the pathogenesis of the slow coronary flow phenomenon. Cardiology 2007; 108: 186-92. 6. Ross R. The pathogenesis of atherosclerosis-an update. N Engl J Med 1986; 314: 488-500. 8. Miwa K, Igawa A, Inoue H. Soluble E-selectin, ICAM-1 and VCAM-1 levels in systemic and coronary circulation in patients with variant angina. Cardiovasc Res 1997; 36: 37-44. 4. Jang IK, Lassila R, Fuster V. Atherogenesis and inflammation. Eur Heart J 1993; 14 Suppl, K: 2-6. 16. Li JJ, Qin XW, Li ZC, Zeng HS, Gao Z, Xu B, et al. Increased plasma C-reactive protein and interleukin-6 concentrations in patients with slow coronary flow. Clin Chim Acta 2007; 385: 43-7. 15. Dodge JT, Brown BG, Bolson EL, Dodge HT. Intrathoracic spatial location of specified coronary segments on the normal human heart: application in quantitative arteriography, assessment of regional risk and contraction, and anatomic display. Circulation 1988; 78: 1167-80. 14. Gibson CM, Cannon CP, Daley WL, Dodge JT, Alexander B, Marble SJ, et al. TIMI frame count: a quantitative method of assessing coronary artery flow. Circulation 1996; 93: 879-88. 21. Vane JR, Anggard EE, Botting RM. Regulatory functions of the vascular endothelium. N Engl J Med 1990; 323: 27-36. 7. Girardi LN, Coselli JS. Inflammatory aneurysm of the ascending aorta and aortic arch. Ann Thorac Surg 1997; 64: 251-3. 20. Sullivan GW, Sarembock IJ, Linden J. The role of inflammation in vascular disease. J Leukoc Biol 2000; 67: 591-602. 1. Goel PK, Gupta SK, Agarwal A, Kapoor A. Slow coronary flow: a distinct angiographic subgroup in syndrome X. Angiology 2001; 52: 507-14. 12. Li JJ, Fang CH. C-reactive protein is not only an inflammatory marker but also a direct cause of cardiovascular disease. Med Hypotheses 2004; 62: 499-506. 18. Pekdemir H, Cin VG, Çiçek D, Çamsarı A, Akkuş N, Döven O, et al. Slow coronary flow may be a sign of diffuse atherosclerosis: contribution of FFR and IVUS. Acta Cardiol 2004; 59: 127-33. |
| References_xml | – reference: 18. Pekdemir H, Cin VG, Çiçek D, Çamsarı A, Akkuş N, Döven O, et al. Slow coronary flow may be a sign of diffuse atherosclerosis: contribution of FFR and IVUS. Acta Cardiol 2004; 59: 127-33. – reference: 12. Li JJ, Fang CH. C-reactive protein is not only an inflammatory marker but also a direct cause of cardiovascular disease. Med Hypotheses 2004; 62: 499-506. – reference: 19. Slevin M, Krupinski J. A role of C-reactive protein in the regulation of angiogenesis, endothelial cell inflammation and thrombus formation in cardiovascular disease. Histol Histopathol 2009; 24: 1473-8. – reference: 11. Evrengül H, Tanrıverdi H, Enli Y, Kuru O, Seleci D, Baştemir M, et al. Interaction of plasma homocysteine and thyroid hormone concentrations in the pathogenesis of the slow coronary flow phenomenon. Cardiology 2007; 108: 186-92. – reference: 1. Goel PK, Gupta SK, Agarwal A, Kapoor A. Slow coronary flow: a distinct angiographic subgroup in syndrome X. Angiology 2001; 52: 507-14. – reference: 5. Shah PK, Falk E, Badimon JJ, Fernandez-Ortiz A, Mailhac A, Villareal-Levy G, et al. Human monocyte-derived macrophages induce collagen breakdown in fibrous caps of atherosclerotic plaques. Potential role of matrix-degrading metalloproteinases and implications for plaque rupture. Circulation 1995; 92: 1565-9. – reference: 15. Dodge JT, Brown BG, Bolson EL, Dodge HT. Intrathoracic spatial location of specified coronary segments on the normal human heart: application in quantitative arteriography, assessment of regional risk and contraction, and anatomic display. Circulation 1988; 78: 1167-80. – reference: 8. Miwa K, Igawa A, Inoue H. Soluble E-selectin, ICAM-1 and VCAM-1 levels in systemic and coronary circulation in patients with variant angina. Cardiovasc Res 1997; 36: 37-44. – reference: 20. Sullivan GW, Sarembock IJ, Linden J. The role of inflammation in vascular disease. J Leukoc Biol 2000; 67: 591-602. – reference: 13. Vila G, Resl M, Stelzeneder D, Strucks J, Maier C, Riedl M, et al. Plasma NT-proBNP increases in response to LPS administration in healthy men. J Appl Physiol 2008;105: 1741-5. – reference: 9. Mosseri M, Yarom R, Gotsman MS, Hasin Y. Histologic evidence for small vessel coronary artery disease in patients with angina pectoris and patent large coronary arteries. Circulation 1986; 74: 964-72. – reference: 16. Li JJ, Qin XW, Li ZC, Zeng HS, Gao Z, Xu B, et al. Increased plasma C-reactive protein and interleukin-6 concentrations in patients with slow coronary flow. Clin Chim Acta 2007; 385: 43-7. – reference: 7. Girardi LN, Coselli JS. Inflammatory aneurysm of the ascending aorta and aortic arch. Ann Thorac Surg 1997; 64: 251-3. – reference: 23. Turhan H, Saydam GS, Erbay AR, Ayaz S, Yaşar AS, Aksoy Y, et al. Increased plasma soluble adhesion molecules: ICAM-1, VCAM-1, and E-selectin concentrations in patients with slow coronary flow. Int J Cardiol 2006; 108: 224-30. – reference: 3. Folkman J, Shing Y. Angiogenesis. J Biol Chem 1992; 267: 10931-4. – reference: 17. Yazıcı M, Aksakal E, Demircan S, Şahin M, Sağkan O. Is slow coronary flow related with inflammation and procoagulant state? Anadolu Kardiyol Derg 2005; 5: 3-7. – reference: 21. Vane JR, Anggard EE, Botting RM. Regulatory functions of the vascular endothelium. N Engl J Med 1990; 323: 27-36. – reference: 4. Jang IK, Lassila R, Fuster V. Atherogenesis and inflammation. Eur Heart J 1993; 14 Suppl, K: 2-6. – reference: 14. Gibson CM, Cannon CP, Daley WL, Dodge JT, Alexander B, Marble SJ, et al. TIMI frame count: a quantitative method of assessing coronary artery flow. Circulation 1996; 93: 879-88. – reference: 25. Hak AE, Pols HA, Visser TJ, Drexhage HA, Hofman A, Witteman JC. Subclinical hypothyroidism is an independent risk factor for atherosclerosis and myocardial infarction in elderly women: The Rotterdam Study. Ann Intern Med 2000; 132: 270-8. – reference: 24. Baykan M, Baykan EC, Turan S, Gedikli O, Kaplan S, Kiriş A, et al. Assessment of left ventricular function and Tei index by tissue Doppler imaging in patients with slow coronary flow. Echocardiography 2009: 26; 1167-72. – reference: 6. Ross R. The pathogenesis of atherosclerosis-an update. N Engl J Med 1986; 314: 488-500. – reference: 22. De Meyer GR, Herman AG. Vascular endothelial dysfunction. Prog Cardiovasc Dis 1997; 39: 325-42. – reference: 2. Tambe AA, Demany MA, Zimmerman HA, Mascarenhas E. Angina pectoris and slow flow velocity of dye in coronary arteries. A new angiographic finding. Am Heart J 1972; 84: 66-71. – reference: 10. Sezgin AT, Sığırcı A, Barutçu I, Topal E, Sezgin N, Özdemir R, et al. Vascular endothelial function in patients with slow coronary flow. Coron Artery Dis 2003;14: 155-61. |
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| Snippet | In this study, we sought to investigate the serum levels of high sensitivity C-reactive protein (Hs-CRP), N-terminal pro-brain natriuretic peptide (NT proBNP),... Amaç:Çalışmamızda koroner yavaş akımlı hastalarda yüksek-duyarlı C-reaktif protein (Hs-CRP), N-terminal pro-beyin natriüretik peptit (NT-proBNP), eritrosit... |
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| SubjectTerms | Aged C-Reactive Protein - metabolism Coronary Angiography - methods Coronary Circulation - physiology Cross-Sectional Studies Female Humans Interleukin-6 - blood Male Middle Aged Natriuretic Peptide, Brain - blood No-Reflow Phenomenon - blood No-Reflow Phenomenon - diagnostic imaging Reference Values Thyrotropin - blood Thyroxine - blood Triiodothyronine - blood |
| Title | Acute phase reactants in patients with coronary slow flow phenomenon |
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