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. 2018 Jun 19;17:142. doi: 10.1186/s12944-018-0732-6

Table 2.

Correlation between total HDL-P concentration and CVD events

Author Baseline of subjects Adjusted for Events Follow-up time HR(95%CI) or OR for 1-SD increment HR(95%CI) or OR for Q4 vs Q1
Mackey MESA articipants without self-reported CVD,pregnancy, cancer, cognitive impairment, or weight > 136 kg,lipid-lowering medication use,TG > 400 mg/dl model1:age,sex,ethnicity,hypertension,smoking; model2: model1 + HDL-C,LDL-P,LDL-C,TG myocardial infarction, CHD death, resuscitated cardiac arrest, or definite or probable angina (followed by revascularization) mean of 6.0 years model1:0.70(0.59–0.82); model2: 0.68(0.54–0.85) model 1: 0.46(0.30–0.71);model2: 0.49(0.27–0.86)
Hsia(group1) postmenopausal women with intact uterus in Estrogen Plus Progestin Trial age, treatment arm, smoking, alcohol use, diabetes, hypertension CHD MI/coronary death 4 years 0.87 (0.67–1.13)
Hsia(group2) postmenopausal women with prior hysterectomy in Estrogen Alone Trial age, treatment arm, smoking, alcohol use, diabetes, hypertension CHD MI/coronary death 4 years 0.64 (0.44–0.93)
Akinkuolie subjects in the WHS free of self-reported CVD or cancer or lipid-lowering medications model 1:age, race,blood pressure, smoking, menopausal status,hormone replacement therapy,and treatment assignment.model 2: model 1 + BMI,diabetes,LDL-C, LDL-P,TG and other HDL subclasses. nonfatal MI, percutaneous coronary,intervention, coronary artery bypass grafting, and CHD death median of 17 years model1: 0.91(0.86–0.97); model2: 0.88(0.83–0.93) model 1:0.77(0.64–0.92); model2:0.70(0.58–0.85)
Berger postmenopausal women from the WHI-OS with no prior history of MI or stroke smoking status,BMI,systolic blood pressure,use of anti-hypertensive medication,diabetes and physical activity Ischemic stroke mean follow-up of 7.9 years 0.90(0.63–1.30)
Duprez HIV-infected patients model1:age, race, HIV-RNA and ART status, smoking, prior CVD, diabetes, use of BP-lowering drugs, use of lipid-lowering drugs, hepatitis co-infection, CD4+, BMI and major baseline ECG abnormalities;model2:model1 + LDL and triglycerides+D-dimer, IL-6 and hsCRP non-fatal CHD events (defined as clinical and silent myocardial infarction, coronary revascularization and coronary artery disease requiring drug treatment), non-fatal atherosclerotic non-CHD (defined as stroke and peripheral arterial disease), congestive heart failure and fatal CVD (defines as CVD death and unwitnessed death) model1: 0.41(0.2–0.7); model2: 0.57(0.3–1.1)
Kuller men with metabolic syndrome within the MRFIT white blood cell count,smoking status CHD death 18 years 0.50(0.26–0.96)
Otvos men with an established diagnosis of CHD in the VA-HIT treatment,age, hypertension,smoking,BMI, diabetes a nonfatal MI or CHD death median of 5.1 years 0.78(0.69–0.90)
Chandra participants from the Dallas Heart Study not taking any lipid lowering medication or hormone replacement therapy,free from malignancy, connective tissue disease, or HIV model1:age, sex, ethnicity, hypertension, diabetes, smoking, BMI, non-HDL-C, logTG, any lipid-lowering therapy, hormone replacement therapy, menopause, alcohol intake, and history of CHD at baseline; model2:model1 + HDL-C non-fatal myocardial infarction, stroke,coronary artery bypass graft (CABG), percutaneous coronary intervention, or cardiovascular death median of 9.3 years model1: 0.75(0.65–0.86); model2: 0.73(0.62–0.86)
Parish high-risk individuals in the MRC/BHF HPS.A nonfasting blood total cholesterol concentration of at least 3.5 mmol/L (135 mg/dL) and either had a previous diagnosis of CHD, cerebrovascular disease, other occlusive disease of noncoronary arteries, or diabetes mellitus (type I or II) or men 65 years of age undergoing treatment for hypertension model1:age, sex, simvastatin and vitamin allocation, smoking, prior disease, systolic blood pressure, estimated glomerular filtration rate, medication, and N-terminal pro-B-type natriuretic peptide;model2 = model1 + LDL-P nonfatal MI or coronary death other than death from heart failure or sudden death mean of 5.3 years model1: 0.88(0.83–0.92); model2: 0.89(0.85–0.93)
Musunuru healthy people in the MDC-CC. Subjects with prior MI/stroke or on baseline lipid-lowering therapy were excluded age, gender, systolic blood pressure, use of antihypertensivemedications,diabetes status, and current smoking status myocardial infarction, stroke, and death from coronary heart disease, a secondary coronary endpoint of myocardial infarction and death from coronary heart disease mean of 12.2 years 0.78(0.68–0.90)
Harchaoui participants in EPIC-Norfolk cohort.All individuals who reported a history of heart attack or stroke or use of lipid-lowering drugs at the baseline clinic visit were excluded model1:smoking,myeloperoxidase, paraoxonase 1, and C-reactive protein levels; model2 = smoking+apol poprotein B and logTG fatal or nonfatal CAD which was defined as codes 410 to 414 according to the International Classification of Diseases, Ninth Revision average of 6 years model1: 0.78(0.59–1.03); model2: 0.53(0.40–0.72)

TG triglyeride, CHD coronary heart disease, NMR nuclear magnetic resonance, LDL-P low density lipoprotein particles, LDL-C low density lipoprotein cholesterol, MI myocardial infarction, BMI body mass index, CAD coronary artery disease, HIV Human immunoddficiency virus, ART antiretroviral therapy, ECG electrocardiography, hsCRP high sensitivity C-Reactive Protein, MESA ulti-ethnic study of atherosclerosis, WHS omen’s Health Study, WHI-OS Women’s Health Initiative Observational Study, MRFIT Multiplle Risk Factor Intervention Trial, VA-HIT Veterans Affairs High-Density Lipoprotein Intervantion Trial, HPS Heart Protection Study, MDC-CC Malmö Diet and Cancer Study, EPIC European Prospective Investigation into Cancer and Nutrition