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Current Vascular Pharmacology

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ISSN (Print): 1570-1611
ISSN (Online): 1875-6212

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Research Article

Cholesterol Subfraction Analysis in Patients with Acute Coronary Syndrome

Author(s): Michal Kidawa, Anna Gluba-Brzózka*, Marzenna Zielinska, Beata Franczyk, Maciej Banach and Jacek Rysz

Volume 17, Issue 4, 2019

Page: [365 - 375] Pages: 11

DOI: 10.2174/1570161116666180601083225

Price: $65

Abstract

Background: There is a close relationship between lipid metabolism disorders and atherosclerosis. Guidelines focus on lowering Low-Density Lipoprotein Cholesterol (LDL-C) levels. However, it should be kept in mind that LDL and High-Density Lipoprotein (HDL) consist of subfractions which can affect the progression of atherosclerosis.

Objective: We assessed the concentration of LDL and HDL subfractions in patients with Acute Coronary Syndromes (ACS). The influence of the presence of type 2 diabetes mellitus on LDL and HDL subfractions was also analyzed.

Methods: The study group consisted of 127 patients (62 men, 65 women) with ACS. All patients had coronary angiography and coronary angioplasty and stenting when necessary. Medical history was collected during 12 months of follow-up. HDL and LDL subfraction distribution was measured using Lipoprint (Quantimetrix).

Results: No differences in LDL nor HDL subfractions were observed between ST-Segment Elevation Myocardial Infarction (STEMI), Non-ST-Segment Elevation Myocardial Infarction (NSTEMI) and unstable angina (UA) patients. However, those with restenosis and the necessity of repeated revascularization had higher levels of intermediate-density lipoprotein C (IDL-C) (p=0.055) and LDL3 (p=0.048) as compared with the patients without, while the level of IDL A (IDLA) was lower than in the latter group (p=0.036). In diabetic patients, the percentage share of HDL10 and small-dense HDL was significantly higher while the share of HDL1 (small-dense) (p=0.028), HDL4 (intermediate density) (p=0.052) and HDL5 (intermediate density) (p=0.060) were lower than in patients without DM.

Conclusion: Patients with multi-vessel CAD disease had higher levels of LDL3 subfraction and IDL-C and a lower proportion of IDLA.

Keywords: Acute coronary syndrome, HDL subfractions, LDL subfractions, diabetes mellitus, restenosis, atherosclerosis.

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[1]
Ramirez A, Hu PP. Low high-density lipoprotein and risk of myocardial infarction. Clin Med Insights Cardiol 2015; 9: 113-7.
[2]
Ueda Y. Mechanisms and prevention of acute myocardial infarction stop mi campaign. J Jpn Coron Assoc 2016; 22: 228-30.
[3]
Mikhailidis DP, Elisaf M, Rizzo M, et al. European panel on low density lipoprotein (LDL) subclasses: A statement on the pathophysiology, atherogenicity and clinical significance of LDL subclasses: executive summary. Curr Vasc Pharmacol 2011; 9: 531-2.
[4]
Mikhailidis DP, Elisaf M, Rizzo M, et al. European panel on low density lipoprotein (LDL) subclasses: A statement on the pathophysiology, atherogenicity and clinical significance of LDL subclasses. Curr Vasc Pharmacol 2011; 9: 533-71.
[5]
Pérez-Méndez Ó, Pacheco HG, Martínez-Sánchez C, Franco M. HDL-cholesterol in coronary artery disease risk: Function or structure? Clin Chim Acta 2014; 429: 111-22.
[6]
Pedersen T, Kjekshus J, Faergerman O, et al. Scandinavian simvastatin survival study group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: The Scandinavian simvastatin survival study (4S). Lancet 1994; 344: 1383-9.
[7]
Burke AP, Farb A, Malcom GT. Coronary risk factors and plaque morphology in men with coronary disease who died suddenly. N Engl J Med 1997; 336: 1276-82.
[8]
Virmani R, Burke AP, Farb A, Kolodgie FD. Pathology of the vulnerable plaque. J Am Coll Cardiol 2006; 47: C13-8.
[9]
Jafri H, Alsheikh-Ali AA, Karas RH. Meta-analysis: Statin therapy does not alter the association between low levels of high-density lipoprotein cholesterol and increased cardiovascular risk. Ann Intern Med 2010; 153: 800-8.
[10]
Schwartz GG, Olsson AG, Abt M, et al. Effects of dalcetrapib in patients with a recent acute coronary syndrome. N Engl J Med 2012; 367: 2089-99.
[11]
Femlak M, Gluba-Brzózka A, Ciałkowska-Rysz A, et al. The role and function of HDL in patients with diabetes mellitus and the related cardiovascular risk. Lipids Health Dis 2017; 16: 207.
[12]
American Diabetes Association.Standards of medical care in diabetes-2016. Diabetes Care 2016; 39(Suppl. 1): 1-106.
[13]
National Kidney Foundation KDOQI clinical practice guidelines for chronic kidney disease: Evaluation, classification, and stratification. Am J Kidney Dis 2002; 39(Suppl. 1): 1-266.
[14]
Lang RM, Bierig M, Devereux RB, et al. Recommendations for chamber quantification: A report from the American society of echocardiography’s guidelines and standards committee and the chamber quantification writing group, developed in conjunction with the European association of echocardiography, a branch of the European society of cardiology. J Am Soc Echocardiogr 2005; 18: 1440-63.
[15]
Franczyk B, Gluba-Brzózka A, Bartnicki P, Banach M, Rysz J. Are markers of cardiac dysfunction useful in the assessment of cardiovascular risk in dialysis patients? Curr Pharm Des 2017; 23: 3024-33.
[16]
Gluba-Brzózka A, Franczyk B, Banach M, Rysz-Górzyńska M. Do HDL and LDL subfractions play a role in atherosclerosis in end-stage renal disease (ESRD) patients? Int Urol Nephrol 2017; 49: 155-64.
[17]
Gluba-Brzozka A, Franczyk B, Bartnicki P, Rysz-Gorzynska M, Rysz J. Lipoprotein subfractions, uric acid and cardiovascular risk in end-stage renal disease (ESRD) patients. Curr Vasc Pharmacol 2017; 15: 123-4.
[18]
Krauss RM, Lindgren FT, Williams PT, et al. Intermediate-density lipoproteins and progression of coronary artery disease in hypercholesterolaemic men. Lancet 1987; 2: 62-6.
[19]
Kugiyama K, Doi H, Takazoe K, et al. Remnant lipoprotein levels in fasting serum predict coronary events in patients with coronary artery disease. Circulation 1999; 99: 2858-60.
[20]
Fukushima H, Kugiyama K, Sugiyama S, et al. Comparison of remnant-like lipoprotein particles in postmenopausal women with and without coronary artery disease and in men with coronary artery disease. Am J Cardiol 2001; 88: 1370-3.
[21]
Mistríková L, Sabaka P, Oravec S, Dukát A. Intermediate and very low density lipid particle sizes are important in the clinical manifestation of younger patients with acute coronary syndromes. JSM Atheroscler 2016; 1: 1006.
[22]
van Wijk DF, Stroes ESG, Kastelein JJP. Lipid measures and cardiovascular disease prediction. Dis Markers 2009; 26: 209-16.
[23]
Cobble M, Mize PD, Brinton EA. Lipoprotein subclasses and cardiovascular disease risk in insulin-resistant diabetes. In: Lipoproteins in diabetes mellitus, contemporary diabetes, Jenkins AJ (ed),. Springer Science Business Media New York 2014.
[24]
Maas AHEM, Appelman YEA. Gender differences in coronary heart disease. Neth Heart J 2010; 18: 598-602.
[25]
Gong B, Li Z. Total mortality, major adverse cardiac events, and echocardiographic-derived cardiac parameters with fragmented QRS Complex. Ann Noninvasive Electrocardiol 2006; 21: 404-12.
[26]
Heusch G, Libby P, Gersh B, et al. Cardiovascular remodelling in coronary artery disease and heart failure. Lancet 2014; 383: 1933-43.
[27]
Parikh SV, de Lemos JA. Biomarkers in cardiovascular disease: Integrating pathophysiology into clinical practice. Am J Med Sci 2006; 332: 186-97.
[28]
Kumar A, Cannon CP. Acute coronary syndromes: Diagnosis and management, Part I. Mayo Clin Proc 2009; 84: 917-38.
[29]
Bassand JP, Hamm CW, Ardissino D, et al. Guidelines for the diagnosis and treatment of non-ST-segment elevation acute coronary syndromes. Eur Heart J 2007; 28: 1598-660.
[30]
Carillo S, Zhang Y, Fay R, et al. Heart failure with systolic dysfunction complicating acute myocardial infarction - differential outcomes but similar eplerenone efficacy by ST-segment or non-ST-segment elevation: A post hoc substudy of the EPHESUS trial. Arch Cardiovasc Dis 2014; 107: 149-57.
[31]
Van de Werf F, Bax J, Betriu A, et al. Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation: The task force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology. Eur Heart J 2008; 29: 2909-45.
[32]
Uchida Y, Uchida Y, Sakurai T, Kanai M, Shirai S, Morita T. Characterization of coronary fibrin thrombus in patients with acute coronary syndrome using dye-staining angioscopy. Arterioscler Thromb Vasc Biol 2011; 31: 1452-60.
[33]
Goto K, Lansky AJ, Nikolsky E, et al. Prognostic significance of coronary thrombus in patients undergoing percutaneous coronary intervention for acute coronary syndromes: A subanalysis of the ACUITY (acute catheterization and urgent intervention triage strategy) trial. JACC Cardiovasc Interv 2011; 4: 769-77.
[34]
Svilaas T, Vlaar PJ, van der Horst IC, et al. Thrombus aspiration during primary percutaneous coronary intervention. N Engl J Med 2008; 358: 557-67.
[35]
Stemmer EA. Diabetes mellitus and vascular disease. In: Aronow WS, Stemmer EA, Wilson SE, Eds Vascular disease in the elderly. Armon, NY 1997; pp. 199-220.
[36]
Gregoratos G. Diabetes mellitus and cardiovascular disease in the older patient. Am J Geriatr Cardiol 2000; 9: 49-60.
[37]
Kesani M, Aronow WS, Weiss MB. Prevalence of multivessel coronary artery disease in patients with diabetes mellitus plus hypothyroidism, in patients with diabetes mellitus without hypothyroidism, and in patients with no diabetes mellitus or hypothyroidism. J Gerontol Biol Sci Med Sci 2003; 58: 857-8.
[38]
Ledru F, Ducimetiere P, Battaglia S, et al. New diagnostic criteria for diabetes and coronary artery disease: Insights from an angiographic study. J Am Coll Cardiol 2001; 37: 1543-50.
[39]
Moreno PR, Murcia AM, Palacios IF, et al. Coronary composition and macrophage infiltration in atherectomy specimens from patients with diabetes mellitus. Circulation 2000; 102: 2180-4.
[40]
Marso SP, Mercado N, Maehara A, et al. Plaque composition and clinical outcomes in acute coronary syndrome patients with metabolic syndrome or diabetes. JACC Cardiovasc Imaging 2012; 5: 42-52.
[41]
Kim TN, Kim S, Yang SJ, et al. Vascular inflammation in patients with impaired glucose tolerance and type 2 diabetes: Analysis with 18F-fluorodeoxyglucose positron emission tomography. Circ Cardiovasc Imaging 2010; 3: 142-8.
[42]
Abaci A, Oguzhan A, Kahraman S, et al. Effect of diabetes mellitus on formation of coronary collateral vessels. Circulation 1999; 99: 2239-42.
[43]
Vavuranakis M, Stefanadis C, Toutouzas K, Pitsavos V, Spanos V, Toutouzas P. Impaired compensatory coronary artery enlargement in atherosclerosis contributes to the development of coronary artery stenosis in diabetic patients: An in vivo intravascular ultrasound study. Eur Heart J 1997; 18: 1090-4.
[44]
Zhao X, Zhang HW, Zhang Y, et al. Analysis of lipoprotein subfractions in 920 patients with and without type 2 diabetes. Heart Lung Circ 2017; 26: 211-8.
[45]
Fonseca MIH, da Silva IT, Ferreira SRG. Impact of menopause and diabetes on atherogenic lipid profile: Is it worth to analyse lipoprotein subfractions to assess cardiovascular risk in women? Diabetol Metab Syndr 2017; 9: 22.
[46]
Vergès B. New insight into the pathophysiology of lipid abnormalities in type 2 diabetes. Diabetes Metab 2005; 31: 429-39.
[47]
Otocka-Kmiecik A, Mikhailidis DP, Nicholls SJ, Davidson M, Rysz J, Banach M. Dysfunctional HDL: A novel important diagnostic and therapeutic target in cardiovascular disease? Prog Lipid Res 2012; 51: 314-24.
[48]
Cartolano FC, Dias GD, de Freitas MCP, Figueiredo Neto AM, Damasceno NRT. Insulin resistance predicts atherogenic lipoprotein profile in nondiabetic subjects. J Diabetes Res 2017; 2017: 1018796.
[49]
DeFronzo RA, Ferrannini E. Insulin resistance. A multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia and atherosclerotic cardiovascular disease. Diabetes Care 1991; 14: 173-94.
[50]
Hindieh W, Pilote L, Cheema A, et al. Association between family history, a genetic risk score, and severity of coronary artery disease in patients with premature acute coronary syndromes. Arterioscler Thromb Vasc Biol 2016; 36: 1286-92.
[51]
Kathiresan S, Voight BF, Purcell S, et al. Genome-wide association of early-onset myocardial infarction with single nucleotide polymorphisms and copy number variants. Nat Genet 2009; 41: 334-41.
[52]
Tregouet DA, König IR, Erdmann J, et al. Genome-wide haplotype association study identifies the SLC22A3-LPAL2-LPA gene cluster as a risk locus for coronary artery disease. Nat Genet 2009; 41: 283-5.
[53]
Erdmann J, Linsel-Nitschke P, Schunkert H. Genetic causes of myocardial infarction new insights from genome-wide association studies. Dtsch Arztebl Int 2010; 107: 694-9.

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