Hyperviscoucity In Cyanotic Congenital Heart Disease
Abstract
Increased whole blood viscosity in adults with cyanotic congenital heart disease (CCHD) is an unavoidable result of secondary erythropoiesis and it showed a significant bleeding tendency. The most frequently disturbance of hemostasis are thrombocytopenia and defective platelet aggregation. Acute phlebotomy without volume replacement in patients with hypoxic polycythemia may result in vascular collapse, cyanotic spells, cerebral vascular accidents (CVA), or seizures and repeated phlebotomies may also increase the risk of a CVA by causing chronic iron deficiency.Downloads
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References
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Broberg CS, Bax BE, Okonko DO, Blood Viscosity and its Re-lationship to Iron Deficiency, Symptoms, and Exercise Capacity in Adults With Cyanotic Congenital Heart Disease. J Am Coll Cardiol 2006; 48: 356–65.
Park, Myung K. Mosby, Elsevier. Pathophysiology of Cyanotic Congenital Heart Defects. 5th ed.2008: chapter 11.
Modi P, Suleiman MS, Reeves DO, Basal Metabolic State of Hearts of Patients With Congenital Heart Disease: The Effects of Cyanosis, Age, and Pathology. Ann Thorac Surg. 2004;78:1710–6.
Rose SS, Shah AA, Hoover DR, Saidi P. Cyanotic Congenital Heart Disease (CCHD) with Symptomatic Erythrocytosis. J Gen Intern Med. 2007;22: 1775-7.
Rosenthal A, Nathan DG, Marty AT, dkk. Acute hemodynamic effects of red cell volume reduction in polycythemia of cyanotic congenital heart disease. Circulation 1990;42:297–307.
Perloff JK, Marelli AJ, Miner PD. Risk of stroke in adults with cyanotic congenital heart disease. Circulation 1993; 87: 1954–9.
Shibata J, Hasegawa J, Siemens HJ. Hemostasis and coagula-tion at a hematocrit level of 0.85: functional consequences of erythrocytosis. Blood. 2003;101: 4416-22.
Replogle RL, Meiselman HJ, Merrill EW: Clinical implications of blood rheology studies. Circulation. 1997; 36: 148.
Craig S. Broberg, Bridget E. Bax, Darlington O. Okonko Blood Viscosity and its Relationship to Iron Deficiency, Symptoms, and Exercise Capacity in Adults With Cyanotic Congenital Heart Disease.J Am Coll Cardiol. 2006; 48: 356–65.
Rim SJ, Leong-Poi H, Lindner JR, Wei K, Fisher NG, Kaul S. Decrease in coronary blood flow reserve during hyperlipidemia is secondary to an increase in blood viscosity. Circulation. 2001;104: 2704–9.
Territo MC, Rosove MH. Cyanotic congenital heart disease: hematologic management. J Am Coll Cardiol. 1991;18:320–2.
Miyazaki Y, Nomura S, Miyake T, dkk. High shear stress can initiate both platelet aggregation and shedding of procoagulant containing microparticles. Blood. 1996; 88: 3456–64.
Adatia I, Barrow SE, Stratton P, Ritter JM, Haworth SG. Abnor-malities in the biosynthesis of thromboxane A2 and prostacyclin in children with cyanotic congenital heart disease. Br Heart J. 1993; 69: 179–82.
Olgun N, Uysal KM, Irken G, dkk. Platelet activation in con-genital heart diseases. Acta Paediatr Jpn. 1997; 39: 566–9.
Michelson AD, Barnard MR, Hechtman HB, dkk. In vivo tracking of platelets: circulating degranulated platelets rapidly lose surface P-selectin but continue to circulate and function. Proc Natl Acad Sci. 1996; 93:1877–82.
Holme PA, Orvim U, Hamers MJAG, dkk. Shear-induced platelet activation and platelet microparticle formation at blood flow conditions as in arteries with a severe stenosis. Arterioscler Thromb Vasc Biol 1997;17:646–531.
Lill MC, Perloff JC, Child JS. Pathogenesis of Thrombocy-topenia in Cyanotic Congenital Heart Disease. Am J Cardiol. 2006; 98: 254–8.
Ueber AL. Capillare embolie von riesenkernhaltigen zellen. Arch. Pathol Anat Physiol. 1983;134:11–4.
Michelson AD, ed. Platelets. New York: Academic Press, Clin Appl Thrombosis/Hemostasis. 2002; 21–32.
Behnke O, Forer A. From megakaryocytes to platelets: platelet morphogenesis takes place in the blood stream. Eur J Hematol. 1998; 60: 3–24.
Thorne SA. Management of polycythaemia in adults with cyanotic congenital heart disease. Heart. 1998; 79: 315-6.
Broberg CS, Bax BE, Okonko DO, Blood Viscosity and its Re-lationship to Iron Deficiency, Symptoms, and Exercise Capacity in Adults With Cyanotic Congenital Heart Disease. J Am Coll Cardiol 2006; 48: 356–65.
Park, Myung K. Mosby, Elsevier. Pathophysiology of Cyanotic Congenital Heart Defects. 5th ed.2008: chapter 11.
Modi P, Suleiman MS, Reeves DO, Basal Metabolic State of Hearts of Patients With Congenital Heart Disease: The Effects of Cyanosis, Age, and Pathology. Ann Thorac Surg. 2004;78:1710–6.
Rose SS, Shah AA, Hoover DR, Saidi P. Cyanotic Congenital Heart Disease (CCHD) with Symptomatic Erythrocytosis. J Gen Intern Med. 2007;22: 1775-7.
Rosenthal A, Nathan DG, Marty AT, dkk. Acute hemodynamic effects of red cell volume reduction in polycythemia of cyanotic congenital heart disease. Circulation 1990;42:297–307.
Perloff JK, Marelli AJ, Miner PD. Risk of stroke in adults with cyanotic congenital heart disease. Circulation 1993; 87: 1954–9.
Shibata J, Hasegawa J, Siemens HJ. Hemostasis and coagula-tion at a hematocrit level of 0.85: functional consequences of erythrocytosis. Blood. 2003;101: 4416-22.
Replogle RL, Meiselman HJ, Merrill EW: Clinical implications of blood rheology studies. Circulation. 1997; 36: 148.
Craig S. Broberg, Bridget E. Bax, Darlington O. Okonko Blood Viscosity and its Relationship to Iron Deficiency, Symptoms, and Exercise Capacity in Adults With Cyanotic Congenital Heart Disease.J Am Coll Cardiol. 2006; 48: 356–65.
Rim SJ, Leong-Poi H, Lindner JR, Wei K, Fisher NG, Kaul S. Decrease in coronary blood flow reserve during hyperlipidemia is secondary to an increase in blood viscosity. Circulation. 2001;104: 2704–9.
Territo MC, Rosove MH. Cyanotic congenital heart disease: hematologic management. J Am Coll Cardiol. 1991;18:320–2.
Miyazaki Y, Nomura S, Miyake T, dkk. High shear stress can initiate both platelet aggregation and shedding of procoagulant containing microparticles. Blood. 1996; 88: 3456–64.
Adatia I, Barrow SE, Stratton P, Ritter JM, Haworth SG. Abnor-malities in the biosynthesis of thromboxane A2 and prostacyclin in children with cyanotic congenital heart disease. Br Heart J. 1993; 69: 179–82.
Olgun N, Uysal KM, Irken G, dkk. Platelet activation in con-genital heart diseases. Acta Paediatr Jpn. 1997; 39: 566–9.
Michelson AD, Barnard MR, Hechtman HB, dkk. In vivo tracking of platelets: circulating degranulated platelets rapidly lose surface P-selectin but continue to circulate and function. Proc Natl Acad Sci. 1996; 93:1877–82.
Holme PA, Orvim U, Hamers MJAG, dkk. Shear-induced platelet activation and platelet microparticle formation at blood flow conditions as in arteries with a severe stenosis. Arterioscler Thromb Vasc Biol 1997;17:646–531.
Lill MC, Perloff JC, Child JS. Pathogenesis of Thrombocy-topenia in Cyanotic Congenital Heart Disease. Am J Cardiol. 2006; 98: 254–8.
Ueber AL. Capillare embolie von riesenkernhaltigen zellen. Arch. Pathol Anat Physiol. 1983;134:11–4.
Michelson AD, ed. Platelets. New York: Academic Press, Clin Appl Thrombosis/Hemostasis. 2002; 21–32.
Behnke O, Forer A. From megakaryocytes to platelets: platelet morphogenesis takes place in the blood stream. Eur J Hematol. 1998; 60: 3–24.
Thorne SA. Management of polycythaemia in adults with cyanotic congenital heart disease. Heart. 1998; 79: 315-6.
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How to Cite
Puspitasari, F., & Harimurti, G. (1). Hyperviscoucity In Cyanotic Congenital Heart Disease. Indonesian Journal of Cardiology, 31(1), 41-47. https://doi.org/10.30701/ijc.v31i1.157
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