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      Impact of metabolic syndrome on lipid target achievements in the Arabian Gulf: findings from the CEPHEUS study

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          Abstract

          Background

          The aim of this study was to determine the impact of metabolic syndrome (MetS) on lipid target achievements in the Arabian Gulf.

          Methods

          The centralized pan-middle east survey on the undertreatment of hypercholesterolemia (CEPHEUS) included 4171 high and very high atherosclerotic cardiovascular disease (ASCVD) risk patients from six Arabian Gulf countries. Analyses were performed using univariate statistics.

          Results

          The overall mean age was 57 ± 11 years, 41 % were females and 71 % had MetS. MetS patients were less likely to attain their HDL-C (34 vs. 79 %; P < 0.001), LDL-C (27 vs. 37 %; P < 0.001), non HDL-C (35 vs. 55 %; P < 0.001) and Apo B (35 vs. 54 %; P < 0.001) compared to those without MetS. Within the MetS cohort, those with very high ASCVD risk were less likely to attain their lipid targets compared to those with high ASCVD risk [HDL-C (32 vs. 41 %; P < 0.001), LDL-C (24 vs. 43 %; P < 0.001), non HDL-C (32 vs. 51 %; P < 0.001) and Apo B (33 vs. 40 %; P = 0.001)]. In those with MetS and very high ASCVD risk status, females were less likely to attain their HDL-C (27 vs. 36 %; P < 0.001), LDL-C (19 vs. 27 %; P < 0.001) and Apo B (30 vs. 35 %; P = 0.009) compared to males.

          Conclusions

          MetS was associated with low lipid therapeutic targets. Women and those with very high ASCVD risk were also less likely to attain their lipid targets in the Arabian Gulf.

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          Most cited references32

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          Chronic subclinical inflammation as part of the insulin resistance syndrome: the Insulin Resistance Atherosclerosis Study (IRAS).

          Inflammation has been suggested as a risk factor for the development of atherosclerosis. Recently, some components of the insulin resistance syndrome (IRS) have been related to inflammatory markers. We hypothesized that insulin insensitivity, as directly measured, may be associated with inflammation in nondiabetic subjects. We studied the relation of C-reactive protein (CRP), fibrinogen, and white cell count to components of IRS in the nondiabetic population of the Insulin Resistance Atherosclerosis Study (IRAS) (n=1008; age, 40 to 69 years; 33% with impaired glucose tolerance), a multicenter, population-based study. None of the subjects had clinical coronary artery disease. Insulin sensitivity (S(I)) was measured by a frequently sampled intravenous glucose tolerance test, and CRP was measured by a highly sensitive competitive immunoassay. All 3 inflammatory markers were correlated with several components of the IRS. Strong associations were found between CRP and measures of body fat (body mass index, waist circumference), S(I), and fasting insulin and proinsulin (all correlation coefficients >0.3, P<0.0001). The associations were consistent among the 3 ethnic groups of the IRAS. There was a linear increase in CRP levels with an increase in the number of metabolic disorders. Body mass index, systolic blood pressure, and S(I) were related to CRP levels in a multivariate linear regression model. We suggest that chronic subclinical inflammation is part of IRS. CRP, a predictor of cardiovascular events in previous reports, was independently related to S(I). These findings suggest potential benefits of anti-inflammatory or insulin-sensitizing treatment strategies in healthy individuals with features of IRS.
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            Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels: results of AFCAPS/TexCAPS. Air Force/Texas Coronary Atherosclerosis Prevention Study.

            Although cholesterol-reducing treatment has been shown to reduce fatal and nonfatal coronary disease in patients with coronary heart disease (CHD), it is unknown whether benefit from the reduction of low-density lipoprotein cholesterol (LDL-C) in patients without CHD extends to individuals with average serum cholesterol levels, women, and older persons. To compare lovastatin with placebo for prevention of the first acute major coronary event in men and women without clinically evident atherosclerotic cardiovascular disease with average total cholesterol (TC) and LDL-C levels and below-average high-density lipoprotein cholesterol (HDL-C) levels. A randomized, double-blind, placebo-controlled trial. Outpatient clinics in Texas. A total of 5608 men and 997 women with average TC and LDL-C and below-average HDL-C (as characterized by lipid percentiles for an age- and sex-matched cohort without cardiovascular disease from the National Health and Nutrition Examination Survey [NHANES] III). Mean (SD) TC level was 5.71 (0.54) mmol/L (221 [21] mg/dL) (51 st percentile), mean (SD) LDL-C level was 3.89 (0.43) mmol/L (150 [17] mg/dL) (60th percentile), mean (SD) HDL-C level was 0.94 (0.14) mmol/L (36 [5] mg/dL) for men and 1.03 (0.14) mmol/L (40 [5] mg/dL) for women (25th and 16th percentiles, respectively), and median (SD) triglyceride levels were 1.78 (0.86) mmol/L (158 [76] mg/dL) (63rd percentile). Lovastatin (20-40 mg daily) or placebo in addition to a low-saturated fat, low-cholesterol diet. First acute major coronary event defined as fatal or nonfatal myocardial infarction, unstable angina, or sudden cardiac death. After an average follow-up of 5.2 years, lovastatin reduced the incidence of first acute major coronary events (1 83 vs 116 first events; relative risk [RR], 0.63; 95% confidence interval [CI], 0.50-0.79; P<.001), myocardial infarction (95 vs 57 myocardial infarctions; RR, 0.60; 95% CI, 0.43-0.83; P=.002), unstable angina (87 vs 60 first unstable angina events; RR, 0.68; 95% CI, 0.49-0.95; P=.02), coronary revascularization procedures (157 vs 106 procedures; RR, 0.67; 95% CI, 0.52-0.85; P=.001), coronary events (215 vs 163 coronary events; RR, 0.75; 95% CI, 0.61-0.92; P =.006), and cardiovascular events (255 vs 194 cardiovascular events; RR, 0.75; 95% CI, 0.62-0.91; P = .003). Lovastatin (20-40 mg daily) reduced LDL-C by 25% to 2.96 mmol/L (115 mg/dL) and increased HDL-C by 6% to 1.02 mmol/L (39 mg/dL). There were no clinically relevant differences in safety parameters between treatment groups. Lovastatin reduces the risk for the first acute major coronary event in men and women with average TC and LDL-C levels and below-average HDL-C levels. These findings support the inclusion of HDL-C in risk-factor assessment, confirm the benefit of LDL-C reduction to a target goal, and suggest the need for reassessment of the National Cholesterol Education Program guidelines regarding pharmacological intervention.
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              High-density lipoprotein cholesterol and cardiovascular disease. Four prospective American studies.

              The British Regional Heart Study (BRHS) reported in 1986 that much of the inverse relation of high-density lipoprotein cholesterol (HDLC) and incidence of coronary heart disease was eliminated by covariance adjustment. Using the proportional hazards model and adjusting for age, blood pressure, smoking, body mass index, and low-density lipoprotein cholesterol, we analyzed this relation separately in the Framingham Heart Study (FHS), Lipid Research Clinics Prevalence Mortality Follow-up Study (LRCF) and Coronary Primary Prevention Trial (CPPT), and Multiple Risk Factor Intervention Trial (MRFIT). In CPPT and MRFIT (both randomized trials in middle-age high-risk men), only the control groups were analyzed. A 1-mg/dl (0.026 mM) increment in HDLC was associated with a significant coronary heart disease risk decrement of 2% in men (FHS, CPPT, and MRFIT) and 3% in women (FHS). In LRCF, where only fatal outcomes were documented, a 1-mg/dl increment in HDLC was associated with significant 3.7% (men) and 4.7% (women) decrements in cardiovascular disease mortality rates. The 95% confidence intervals for these decrements in coronary heart and cardiovascular disease risk in the four studies overlapped considerably, and all contained the range 1.9-2.9%. HDLC levels were essentially unrelated to non-cardiovascular disease mortality. When differences in analytic methodology were eliminated, a consistent inverse relation of HDLC levels and coronary heart disease event rates was apparent in BRHS as well as in the four American studies.
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                Author and article information

                Contributors
                ial_zakwani@yahoo.com
                wmahmeed@gmail.com
                a.shehab@uaeu.ac.ae
                arafah1157@hotmail.com
                alihinai1@gmail.com
                oaltamimi@hmc.org.qa
                mahmoudalawadhi@yahoo.ca
                herzs@ngha.med.sa
                ksainjury@hotmail.com
                alnemerk@hotmail.com
                o.mutwalli@hotmail.com
                alkhadraakram@gmail.com
                mfibrahim@uod.edu.sa
                hossam_elghetany@yahoo.com
                ahyusufali@dha.gov.ae
                aaamadani@gmail.com
                obaidtx@yahoo.com
                ohallak@ahdubai.com
                fahadbaslaib@yahoo.ca
                haitham_amin@yahoo.com
                khalidalwaili@hotmail.com
                kalhashmi1@gmail.com
                rauldsf@gmail.com
                +968-96780908 , k.alrasadi@gmail.com
                Journal
                Diabetol Metab Syndr
                Diabetol Metab Syndr
                Diabetology & Metabolic Syndrome
                BioMed Central (London )
                1758-5996
                26 July 2016
                26 July 2016
                2016
                : 8
                : 49
                Affiliations
                [1 ]Department of Pharmacology & Clinical Pharmacy, College of Medicine & Health Sciences, Sultan Qaboos University, Muscat, Oman
                [2 ]Gulf Health Research, Muscat, Oman
                [3 ]Heart and Vascular Institute-Cleveland Clinic, Abu Dhabi, United Arab Emirates
                [4 ]UAE University, Alain, United Arab Emirates
                [5 ]King Saud University Hospital, Riyadh, Kingdom of Saudi Arabia
                [6 ]Ministry of Health, Muscat, Oman
                [7 ]Hamad Medical Corporation, Doha, Qatar
                [8 ]Al Amiri Hospital, Kuwait City, Kuwait
                [9 ]King Fahad National Guard Hospital, Riyadh, Kingdom of Saudi Arabia
                [10 ]Ministry of Health, Riyadh, Kingdom of Saudi Arabia
                [11 ]School of Medicine, Al-Imam Mohammad Ibn Saud Islamic University (IMSIU), Riyadh, Kingdom of Saudi Arabia
                [12 ]King Fahad General Hospital, Jeddah, Kingdom of Saudi Arabia
                [13 ]King Fahad Hospital of the University, Khobar, Kingdom of Saudi Arabia
                [14 ]Soliman Fakieh Hospital, Jeddah, Kingdom of Saudi Arabia
                [15 ]Dubai Hospital, Dubai, United Arab Emirates
                [16 ]American Hospital, Dubai, United Arab Emirates
                [17 ]Rashid Hospital, Dubai, United Arab Emirates
                [18 ]Bahrain Defense Force Hospital, Manama, Bahrain
                [19 ]Department of Biochemistry, Sultan Qaboos University Hospital, P.O. Box 38, Al-Khod, 123 Muscat, Oman
                [20 ]Department of Physiology, College of Medicine & Health Sciences, Sultan Qaboos University, Muscat, Oman
                [21 ]Lipid Clinic Heart Institute (InCor), University of Sao Paulo Medical School Hospital, Sao Paulo, Brazil
                Article
                160
                10.1186/s13098-016-0160-6
                4962507
                27468314
                045fdb2e-a0a5-4ead-ba8c-18416d7687ae
                © The Author(s) 2016

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 18 November 2015
                : 10 July 2016
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/100004325, AstraZeneca;
                Award ID: CEPHEUS; Study Code: SRP-CB-CRE-2006/01
                Categories
                Research
                Custom metadata
                © The Author(s) 2016

                Nutrition & Dietetics
                metabolic syndrome,cardiovascular diseases,triglycerides,obesity,blood pressure,hdl cholesterol,ldl cholesterol,arabian gulf

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