Postprandial Triglyceridemia as a Prediction Factor for Recurrent Cardiac Events of Acute Coronary Syndrome
Abstract
Background. Plasminogen Activator Inhibitor-1 (PAI-1) is an important hemostatic factor of thrombosis that inhibits fibrinolysis mechanism by tissue-Plasminogen Activator (t-PA). PAI-1 is a predictor for recurrentacute coronary syndrome (ACS). PAI-1 is also associated with Insulin Resistance syndrome that manifest as increase level of Triglyceride (Tg), decrease of HDL cholesterol, hypertension and glucose intolerance. Acute or chronic hypertriglyceridemia is often associated with high PAI-1 plasma activity.Objective. To know the relationship between postprandial Tg (ppTg) and increasing PAI-1 plasma levels in patients with ACS that may cause recur-rent cardiac events.
MethodsThis is a case-control study, that included 54 ACS patients (aged 54-63 years), with or without ST segment elevation, without diabetes mel-litus, who were admitted to Emergency Department of National Cardiac Center Harapan Kita, Jakarta. All patients were followed up during hos-pitalization and one month after discharged. Subjects were divided into 2 groups based on ppTg level and compared it to age group, sex, body mass index, smoking habit, systolic blood pressure, pulse, ST segment deviation, CKMB, total cholesterol, low density lipoprotein (LDL), HDL and PAI-1 levels, as haemostatic factor. Patients with ppTg level < 153.5 mg/dL is a control case.
Results.There was an increasing PAI-1 levels (mean 28.9 ± 25.81 ng/dL) as predictor of post ACS events in the study subjects. The level of PAI-1 plasma increased in patients with hypertriglyceridemia (p=0.004). Despite no significant association between pp hipertriglicerydemia and MACE, the overall results showed a significant association between postprandial hipertriglicerydemia and obesity (p=0.037) as well as HDL cholesterol as components of metabolic syndrome.
Conclusions. The postprandial hipertriglicerydemia is a condition that can be found in metabolic disturbances and may influence coagulation status. There are association between pp hipertriglicerydemia and obesity. PAI-1 level is predictor for recurrent cardiac events post ACS.
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References
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Hodis HN. Triglyceride-rich Lipoprotein Remnant Particle and the Risk of Atherosclerosis. Circ.. 1999;99:2852-4.
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Gotto AM. Triglyceride The Forgotten Risk Factor. Circ. 1999;97:1027-8
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Krauss RM. Triglyceride and Atherogenic Lipoproteins: Ra-tionale for Lipid Management. Am J Med 1998;105(1A):58S-62S
Sharrett AR et al. Metabolic and Atherogenic Lifestyle De-teminants of Postprandial Lipemia Differ from Those of Fasting Triglyceride. The Atherosclerosis Risk Communities (ARIC) Study. Arterioscler Throm Vasc. 2001;21:275-81
Farrechi PM, Ozaki CK, CarmelietP, Fay WP. Regulation of Arterial Thrombolysis by Plasminogen Activator Inhibitor-1 in Mice. Circ. 1998;97:1002-8
Moss AJ et al. Thrombogenic Factor and Recurrent Coronary Events. Circ. 1999;99:2517-22
PY Scarabin et al. Hemostasis in Relation to Dietary Fats Estimated by Erythrocyte Fatty Acid Composition: The Prime Study. Thrombosis Res. 2000;102:285-93
Wiman B et al. Plasma Levels of Tissue Plasminogen Activa-tor/Plasminogen Activator Inhibitor-1 Complex and von Willebrand Factor are Significant Risk Markers for Recurrent Myocardial Infarction in the Stockholm Heart Epidemiol-ogy Program (SHEEP) Study. Arterioscler Thromb Vasc Biol 2000;20:2019-23
Ceriello A. The Post-prandial state and Cardiovascular Dis-ease: Relevance to diabetes mellitus. Diabetes Metab Res Rev 2000;16:125-32
Nong Li X et al. Genotype-Spesific Transcriptional Regulation of PAI-1 Expression by Hypertriglyceridemia VLDL and Lp(a) in Cultural Human Endothelial Cells. Arterioscler Thromb Vasc Biol 1997;17:3215-23
Hong Y, Pederson NL, Egberg N, Ulf de Faire. Moderate Genetic Influence on Plasma Levels of Plasminogen Activator Inhibitor-1 and Evidence of Genetic and Environmental Influences shared by Plasminogen Activator Inhibitor-1, Triglyceride and Body Mass Index. Arterioscler Thromb Vacs Biol 1997;17-2776-82
Ossei-Gerning N et al. Plasminogen Activator Inhibitor-1 Pro-moter Gene 4G/5G Genotype and Plasma Levels in Relation to a Hystory of Myocardial Infarction in Patients Character-ized by Coronary Angiography. Arterioscler Thromb Vasc Biol 1997;17:33-7
Eriksson P, Nilsson L, Karpe F, Hamsten A. A Very-Low-Density Lipoprotein Response Element in the Promoter Region of the Human Plasminogen Activator Inhibitor-1 Gene Implicated in the Impaired Fibrinolysis of Hypertriglyceridemia. Arterioscler Throm Vasc Biol 1998;18:20-6
Nordt TK, Lohrmann, Bode C. Regulation of PA-1 Expression by Gene Polimorphisms Impact on Atherogenesis. Thromb Res 2001;103:S1-S5
Ginsberg et al. Association of Postprandial Triglyceridemia and Retinyl Palmitate Response With Newly Diagnosis Exercise Induce Myocardial Ischemia in Middle-Age Men and Women. Arterioscler Thromb Vasc Biol 1995;15:1829-38
Couillard C et al. Postprandial Triglyceridemia Response in Visceral Obesity in Men. Diabetes 1998;47:953-60
Newby DE. Endothelial Dysfunction, Impaired Endogenous Fibrinolysis, and Cigarette Smoking. Circ. 1999;1411-15
Sasaki A, Kurisu A, Ohno M, Ikeda Y. Overweight/Obesitas, smoking and heavy alcohol consumption are importand deter-minants of plasma PAI-1 levels in healthy men. Am J Med Sci 2001;322:19-23
Pilote L et al. Recurrent Ischemia After Thrombolysis for Acute Myocardial Infarction. Am Heart J 2001;14(4):559-65
Hamsten et el. Plasminogen Activator Inhibitor in Plasma: Risk Factor for Recurrent Myocardial Infarction. Lancet 1987;2:3-9
ECAT Angina pectoris Study Group. ECAT angina pectoris study: baseline associations of haemostatic factors with extent of coronary arteriosclerosis and other coronary risk factor in 3.000 patients with angina pectoris undergoing coronary angiography. Eur Heart J. 1993;14:8-17
Pilote L et al. Recurrent Ischemic After Thrombolysis for Acute Myocardial Infarctio. Am Heart J 2001;141(4):559-65
Hodis HN. Triglyceride-rich Lipoprotein Remnant Particle and the Risk of Atherosclerosis. Circ.. 1999;99:2852-4.
Sniderman AD. Postprandial hypertriglyceridemia(s): time to enlarge our physiology perspective. Eur J Clin Invest 2000;30:935-7
Gotto AM. Triglyceride The Forgotten Risk Factor. Circ. 1999;97:1027-8
Krauss RM. Atherogenicity of Triglyceride-Rich Lipoproteins. Am J Cardiol 1998;81(4A):13B-17B
Krauss RM. Triglyceride and Atherogenic Lipoproteins: Ra-tionale for Lipid Management. Am J Med 1998;105(1A):58S-62S
Sharrett AR et al. Metabolic and Atherogenic Lifestyle De-teminants of Postprandial Lipemia Differ from Those of Fasting Triglyceride. The Atherosclerosis Risk Communities (ARIC) Study. Arterioscler Throm Vasc. 2001;21:275-81
Farrechi PM, Ozaki CK, CarmelietP, Fay WP. Regulation of Arterial Thrombolysis by Plasminogen Activator Inhibitor-1 in Mice. Circ. 1998;97:1002-8
Moss AJ et al. Thrombogenic Factor and Recurrent Coronary Events. Circ. 1999;99:2517-22
PY Scarabin et al. Hemostasis in Relation to Dietary Fats Estimated by Erythrocyte Fatty Acid Composition: The Prime Study. Thrombosis Res. 2000;102:285-93
Wiman B et al. Plasma Levels of Tissue Plasminogen Activa-tor/Plasminogen Activator Inhibitor-1 Complex and von Willebrand Factor are Significant Risk Markers for Recurrent Myocardial Infarction in the Stockholm Heart Epidemiol-ogy Program (SHEEP) Study. Arterioscler Thromb Vasc Biol 2000;20:2019-23
Ceriello A. The Post-prandial state and Cardiovascular Dis-ease: Relevance to diabetes mellitus. Diabetes Metab Res Rev 2000;16:125-32
Nong Li X et al. Genotype-Spesific Transcriptional Regulation of PAI-1 Expression by Hypertriglyceridemia VLDL and Lp(a) in Cultural Human Endothelial Cells. Arterioscler Thromb Vasc Biol 1997;17:3215-23
Hong Y, Pederson NL, Egberg N, Ulf de Faire. Moderate Genetic Influence on Plasma Levels of Plasminogen Activator Inhibitor-1 and Evidence of Genetic and Environmental Influences shared by Plasminogen Activator Inhibitor-1, Triglyceride and Body Mass Index. Arterioscler Thromb Vacs Biol 1997;17-2776-82
Ossei-Gerning N et al. Plasminogen Activator Inhibitor-1 Pro-moter Gene 4G/5G Genotype and Plasma Levels in Relation to a Hystory of Myocardial Infarction in Patients Character-ized by Coronary Angiography. Arterioscler Thromb Vasc Biol 1997;17:33-7
Eriksson P, Nilsson L, Karpe F, Hamsten A. A Very-Low-Density Lipoprotein Response Element in the Promoter Region of the Human Plasminogen Activator Inhibitor-1 Gene Implicated in the Impaired Fibrinolysis of Hypertriglyceridemia. Arterioscler Throm Vasc Biol 1998;18:20-6
Nordt TK, Lohrmann, Bode C. Regulation of PA-1 Expression by Gene Polimorphisms Impact on Atherogenesis. Thromb Res 2001;103:S1-S5
Ginsberg et al. Association of Postprandial Triglyceridemia and Retinyl Palmitate Response With Newly Diagnosis Exercise Induce Myocardial Ischemia in Middle-Age Men and Women. Arterioscler Thromb Vasc Biol 1995;15:1829-38
Couillard C et al. Postprandial Triglyceridemia Response in Visceral Obesity in Men. Diabetes 1998;47:953-60
Newby DE. Endothelial Dysfunction, Impaired Endogenous Fibrinolysis, and Cigarette Smoking. Circ. 1999;1411-15
Sasaki A, Kurisu A, Ohno M, Ikeda Y. Overweight/Obesitas, smoking and heavy alcohol consumption are importand deter-minants of plasma PAI-1 levels in healthy men. Am J Med Sci 2001;322:19-23
Pilote L et al. Recurrent Ischemia After Thrombolysis for Acute Myocardial Infarction. Am Heart J 2001;14(4):559-65
Hamsten et el. Plasminogen Activator Inhibitor in Plasma: Risk Factor for Recurrent Myocardial Infarction. Lancet 1987;2:3-9
ECAT Angina pectoris Study Group. ECAT angina pectoris study: baseline associations of haemostatic factors with extent of coronary arteriosclerosis and other coronary risk factor in 3.000 patients with angina pectoris undergoing coronary angiography. Eur Heart J. 1993;14:8-17
Pilote L et al. Recurrent Ischemic After Thrombolysis for Acute Myocardial Infarctio. Am Heart J 2001;141(4):559-65
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How to Cite
Sungkar, M., Kalim, H., & Karim, S. (1). Postprandial Triglyceridemia as a Prediction Factor for Recurrent Cardiac Events of Acute Coronary Syndrome. Indonesian Journal of Cardiology, 29(1), 5-11. https://doi.org/10.30701/ijc.v29i1.196
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Clinical Research
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