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      Triglyceride to high-density lipoprotein cholesterol and low-density lipoprotein cholestrol to high-density lipoprotein cholesterol ratios are predictors of cardiovascular risk in Iranian adults: Evidence from a population-based cross-sectional study

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          Abstract

          Background:

          The superiority of TG/HDL-C and LDL-C/HDL-C ratios in predicting CVD risk is a matter of debates. Thus, the objective of this study was to compare TG/HDL-C and LDL-C to HDL-C ratios in predicting the risk of CVD events.

          Methods:

          In a population-based cross-sectional study, 567 representative participants aged 40 years or older were entered in the study in Babol, North of Iran. The demographic data, anthropometric measures, and the cardio metabolic risk factors were measured. The individual risk of CVD events was assessed by ACC/AHA risk model. ROC analysis was applied to estimate the diagnostic accuracy and the optimal cut-off points of TG/HDL-C and LDL-C/HDL-C ratios.

          Results:

          The AUC of TG/HDL-C and LDL-C/HDL-C ratios were rather similar and both parameters significantly predicted CVD risk in men comparably, and TG/HDL-C at optimal cutoff point of 3.6 produced 75% sensitivity and 39% specificity. However,in women TG/HDL-C with AUC of 0.65( p=0.091) at optimal cutoff value of 3.4 produced a sensitivity of 82% and specificity of 51%. The LDL-C/HDL-C ratio had no discriminative ability in predicting CVD risk in women.

          The adjusted OR of TG/HDL-C at 2nd quartile was significant (OR=3.22, 95% CI:1.25-8.29) and a greater association was found with 3rd and 4rth quartiles

          Conclusion:

          Both TG/HDL–C and LDL-C/HDL-C ratios comparably predict CVD risk in men, whereas in women only TG/ HDL-C is a significant predictor but not LDL-C/HDL-C.

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          Most cited references32

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          Banting lecture 1988. Role of insulin resistance in human disease.

          G M Reaven (1988)
          Resistance to insulin-stimulated glucose uptake is present in the majority of patients with impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) and in approximately 25% of nonobese individuals with normal oral glucose tolerance. In these conditions, deterioration of glucose tolerance can only be prevented if the beta-cell is able to increase its insulin secretory response and maintain a state of chronic hyperinsulinemia. When this goal cannot be achieved, gross decompensation of glucose homeostasis occurs. The relationship between insulin resistance, plasma insulin level, and glucose intolerance is mediated to a significant degree by changes in ambient plasma free-fatty acid (FFA) concentration. Patients with NIDDM are also resistant to insulin suppression of plasma FFA concentration, but plasma FFA concentrations can be reduced by relatively small increments in insulin concentration. Consequently, elevations of circulating plasma FFA concentration can be prevented if large amounts of insulin can be secreted. If hyperinsulinemia cannot be maintained, plasma FFA concentration will not be suppressed normally, and the resulting increase in plasma FFA concentration will lead to increased hepatic glucose production. Because these events take place in individuals who are quite resistant to insulin-stimulated glucose uptake, it is apparent that even small increases in hepatic glucose production are likely to lead to significant fasting hyperglycemia under these conditions. Although hyperinsulinemia may prevent frank decompensation of glucose homeostasis in insulin-resistant individuals, this compensatory response of the endocrine pancreas is not without its price. Patients with hypertension, treated or untreated, are insulin resistant, hyperglycemic, and hyperinsulinemic. In addition, a direct relationship between plasma insulin concentration and blood pressure has been noted. Hypertension can also be produced in normal rats when they are fed a fructose-enriched diet, an intervention that also leads to the development of insulin resistance and hyperinsulinemia. The development of hypertension in normal rats by an experimental manipulation known to induce insulin resistance and hyperinsulinemia provides further support for the view that the relationship between the three variables may be a causal one.(ABSTRACT TRUNCATED AT 400 WORDS)
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            Prevalence of metabolic syndrome in an urban population: Tehran Lipid and Glucose Study.

            Fereidoun Azizi, Payam Salehi, Arash Etemadi … (2003)
            The aim of the present investigation was to determine the prevalence of the metabolic syndrome among 103,68 of the adults (4,397 men and 5,971 women) aged 20 years and over, participating in the Tehran Lipid and Glucose Study. The metabolic syndrome was defined by the presence of three or more of the following components: abdominal obesity, hypertriglyceridemia, low HDL-C, high blood pressure, and high fasting glucose. The unadjusted prevalence of metabolic syndrome in the study population was 30.1% (CI 95%: 29.2-31.0) and age-standardized prevalence was 33.7% (CI 95%: 32.8-34.6). The prevalence increased with age in both sexes. The metabolic syndrome was more commonly seen in women than in men (42% vs. 24%, P<0.001). Low HDL-C was the most common metabolic abnormality in both sexes. Except for high FPG, all abnormalities were more common in women than in men (P<0.001). Most of those with metabolic syndrome had three components of the syndrome (58%), 33% had four, and 9% had five components. This report on the metabolic syndrome from Iran shows a high prevalence of this disorder. Efforts on promoting healthy diets, physical activity, and blood pressure control must be undertaken.
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              Statins, high-density lipoprotein cholesterol, and regression of coronary atherosclerosis.

              Stephen Nicholls, E. Murat Tuzcu, Ilke Sipahi … (2007)
              Statins reduce low-density lipoprotein cholesterol (LDL-C) levels and slow progression of coronary atherosclerosis. However, no data exist describing the relationship between statin-induced changes in high-density lipoprotein cholesterol (HDL-C) and disease progression. To investigate the relationship between changes in LDL-C and HDL-C levels and atheroma burden. Post-hoc analysis combining raw data from 4 prospective randomized trials (performed in the United States, North America, Europe, and Australia between 1999 and 2005), in which 1455 patients with angiographic coronary disease underwent serial intravascular ultrasonography while receiving statin treatment for 18 months or for 24 months. Ultrasound analysis was performed in the same core laboratory for all of the studies. Relationship between changes in lipoprotein levels and coronary artery atheroma volume. During statin therapy, mean (SD) LDL-C levels were reduced from 124.0 (38.3) mg/dL (3.2 [0.99] mmol/L) to 87.5 (28.8) mg/dL (2.3 [0.75] mmol/L) (a 23.5% decrease; P or =5% reduction in atheroma volume) was observed in patients with levels of LDL-C less than the mean (87.5 mg/dL) during treatment and percentage increases of HDL-C greater than the mean (7.5%; P<.001). No significant differences were found with regard to clinical events. Statin therapy is associated with regression of coronary atherosclerosis when LDL-C is substantially reduced and HDL-C is increased by more than 7.5%. These findings suggest that statin benefits are derived from both reductions in atherogenic lipoprotein levels and increases in HDL-C, although it remains to be determined whether the atherosclerotic regression associated with these changes in lipid levels will translate to meaningful reductions in clinical events and improved clinical outcomes.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Caspian J Intern Med
                Journal ID (iso-abbrev): Caspian J Intern Med
                Journal ID (publisher-id): CJIM
                Title: Caspian Journal of Internal Medicine
                Publisher: Babol University of Medical Sciences (Babol, Iran )
                ISSN (Print): 2008-6164
                ISSN (Electronic): 2008-6172
                Publication date (Print): Winter 2020
                Volume: 11
                Issue: 1
                Pages: 53-61
                Affiliations
                [1 ]Social Determinants of Health Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran
                [2 ]Mobility Impairment Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran
                [3 ]Department of Midwifery, Babol University of Medical Sciences, Babol, Iran
                Author notes
                [* ]Correspondence: Karimollah Hajian-Tilaki, Social Determinants of Health Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran. E-mail: drhajian@yahoo.com , Tel: 0098 1132190560, Fax: 0098 1132190560
                Article
                DOI: 10.22088/cjim.11.1.53
                PMC ID: 6992727
                PubMed ID: 32042387
                SO-VID: afb6fd17-976f-44df-8fc5-00fac48c6747
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License, ( http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 12 May 2019
                Date revision received : 8 August 2019
                Date accepted : 21 September 2019
                Categories
                Subject: Original Article

                Keywords: triglyceride,hdl- cholesterol,triglyceride/hdl-cholesterol ratio,ldl-cholesterol,ldl-cholesterol/hdl-cholesterol ratio,cardiovascular risk
                Data availability:
                Keywords: triglyceride, hdl- cholesterol, triglyceride/hdl-cholesterol ratio, ldl-cholesterol, ldl-cholesterol/hdl-cholesterol ratio, cardiovascular risk

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