Association of Low-Density Lipoprotein-Cholesterol and Its Small, Dense Phenotype with Six-Month Cardiovascular Morbidity

  • سال انتشار: 1401
  • محل انتشار: مجله گزارش های بیوشیمی و زیست شناسی مولکولی، دوره: 11، شماره: 2
  • کد COI اختصاصی: JR_RBMB-11-2_019
  • زبان مقاله: انگلیسی
  • تعداد مشاهده: 120
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نویسندگان

Sufyan Ibrahim

Kasturba Medical College, Manipal, Manipal Academy of Higher Education, Manipal, Karnataka, India.

Anurupa Udupi

Kasturba Medical College, Manipal, Manipal Academy of Higher Education, Manipal, Karnataka, India.

Cleeta Rebeiro

Department of Biochemistry, Kasturba Medical College, Manipal, Manipal Academy of Higher Education, Manipal, Karnataka, India.

Varashree Bolar Suryakanth

Department of Biochemistry, Kasturba Medical College, Manipal, Manipal Academy of Higher Education, Manipal, Karnataka, India.

Asha Kamath

Department of Data Science, Prasanna School of Public Health, Manipal Academy of Higher Education, Manipal, Karnataka, India.

Revathi Panduranga Shenoy

Department of Biochemistry, Kasturba Medical College, Manipal, Manipal Academy of Higher Education, Manipal, Karnataka, India.

چکیده

Background: Globally, cardiovascular diseases (CVDs) are the leading cause of death and disability. Elevated low-density lipoprotein-cholesterol (LDL-C) and more specifically, elevation of its small, dense phenotype (sdLDL-C) has been regarded as the key modifiable risk factors associated with atherogenesis. This study aimed to determine the association of LDL-C and sdLDL-C with the development of CVDs in the next six months to establish their predictive efficacy.   Methods: A batch of ۱۶۲ anonymized serum samples sent for analysis of lipid profile parameters, were classified into tests and controls based on the calculated LDL-C values obtained by Fried Ewald formula. Direct LDL-C was also estimated automatically using assay kits. Using the formula provided by Srisawasdi et al., sdLDL-C was then computed for all samples. Six months later, samples were deanonymized, and the lipid profiles were compared with cardiovascular outcomes of these patients, to determine which parameter had the greatest correlation.   Results: Four control group patients and three test group patients developed the outcome (any cardiovascular event) during the ۶-month follow-up period. Binary logistic regression analysis showed that none of the lipid profile parameters: calculated LDL-C (OR= ۰.۹۹; ۹۵% CI= ۰.۹۷-۱.۰۱; p= ۰.۸۲۶), direct LDL-C (OR= ۰.۹۹; ۹۵% CI= ۰.۹۷-۱.۰۱; p= ۰.۸۱۸) or sdLDL-C (OR= ۰.۹۹; ۹۵% CI= ۰.۹۳-۱.۰۴; p= ۰.۷۳۴), were significantly associated with the occurrence of outcome. The median % sdLDL-C both with respect to direct and calculated LDL-C was slightly higher in patients with the outcome.   Conclusions: The levels of LDL-C or its individual phenotypes may not be used singly as indicator of cardiovascular morbidity in the next six months.

کلیدواژه ها

Biomarkers, Cardiovascular diseases, Cholesterol, LDL, Lipoprotein, Myocardial infarction.

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