(i) In the ROC curve analysis, serum ApoA-I was shown to be inferior as a marker of cardiovascular morbidity, with a likelihood ratio of 2.8 (ii) On logistic regression analysis, the age- and sex-adjusted OR for the presence of CVD was 2.0 (95% CI: 1.6 to 2.4), when ApoB/ApoA-I ratio values above 1.13 were compared with values below this cut-off point (iii) For ApoB/ApoA-I ratio values above 1.13, the OR did not change essentially after controlling for various confounders: nonlipid risk factors (; 95% CI: 1.7-2.3), Lp(a) (; 95% CI: 1.7-2.2), or markers of inflammation (; 95% CI: 1.5-2.3)
(i) In multivariate logistic regression analysis, the ApoB/ApoA-I ratio was significantly associated with an increased risk of coronary artery calcification in participants with normal kidney function (, 95% CI: 1.224-4.748, ), while in the participants with mild renal insufficiency, the ApoB/ApoA-I ratio was not associated with coronary artery calcification (, 95% CI: 0.395-2.925, )
(i) Univariate analysis revealed that ApoA-I was associated with CHD (ii) Multivariate logistic regression analysis showed that ApoA-I was associated with CHD (, 95% CI: 1.96–5.43, )
(i) In the ROC curve analyses, the ApoA-I concentrations were negatively associated with mortality, but with a lower level of significance (;) (ii) The only parameter that was significantly associated with the development of new CV episodes was the concentration of ApoA-I (;) (iii) In a multivariate Cox model adjusted by confounders, the risk ratio (RR) for each 10 mg/dl of ApoA-I was 0.915, with 95% confidence intervals (CI) of 0.844 and 0.992 ()
(i) CKD was associated with significantly higher concentrations of ApoB/ApoA-I ratios and significantly lower concentrations of ApoA-I (ii) ApoB/ApoA-I was associated with CHD risk (, 95% CI: 1.02-1.46)
(i) In patients with CKD (G2-G3), the univariate analysis indicated that PWV was inversely related to ApoA-I () (ii) In the stepwise multiple regression model that included all subjects (with normal function and CKD G2-G3), PWV was not associated with ApoA-I
(i) ApoA-I was correlated with all-cause mortality in model 2 (, 95% CI: 0.25-0.89, ) and model 3 (, 95% CI: 0.24-0.94, ) and with cardiovascular events in model 1 (, 95% CI: 0.25-0.90, ) and model 2 (, 95% CI: 0.18-0.83, ) (ii) In Cox regression analysis, after the adjustment in models, the ApoB/ApoA-I ratio was still associated with all-cause mortality (in model 3 , 95% CI: 1.02-2.49, ) and with cardiovascular events (in model 2: , 95% CI: 1.05-2.81, and in model 3: , 95% CI: 1.21-3.44, )
(i) In the survival analyses, ApoA-I and the ApoB/ApoA-1 ratio were significantly related to all-cause and CVD-related mortality. Estimated survival curves by ApoA-I quartiles for all-cause and CVD-related mortality were significant ( and , respectively) (ii) In a multivariate Cox analysis, the ApoA-I (per 1-SD increase) was associated with all-cause mortality and CVD-related mortality (in model 2: , 95% CI: 0.63–0.89, ;, 95% CI: 0.59–0.99, , respectively) (iii) In a multivariate Cox analysis, the ApoA-I (quartile IV versus quartile I) was associated with all-cause mortality and CVD-related mortality (in model 2: , 95% CI: 0.32–0.81, ;, 95% CI: 0.24–0.98, , respectively) (iv) Survival curves by ApoB/ApoA-I ratio quartiles for all-cause and CVD-related mortality were significant ( and ) (v) In a multivariate Cox analysis, the ApoB/ApoA-I ratio (per 1-SD increase) was associated with all-cause mortality and CVD-related mortality, even after adjustment in models (in model 3: , 95% CI: 1.00–1.35, ;, 95% CI: 1.11–1.71, , respectively) (vi) In a multivariate Cox analysis, the ApoB/ApoA-I ratio (quartile IV versus quartile I) was associated with all-cause mortality and CVD-related mortality, even after adjustment in models (in model 3: , 95% CI: 1.05–2.57, ;, 95% CI: 1.21–5.40, , respectively)
(i) Quartiles of apolipoproteins were not associated with all-cause mortality () (ii) Quartiles of ApoA-I were not associated with composite CVD events in models adjusted for age, sex, dialysis vintage, DM, history of CVD, and malnutrition () (iii) ApoA-I was an independent risk factor in models adjusted for confounders including hs-CRP (, 95% CI: 0.43-0.90, ) (iv) Quartiles of ApoB/ApoA-I ratio was independently associated with CVD events in models adjusted with and without hs-CRP (, 95% CI: 1.13-4.56, ) and IL-6 (, 95% CI: 1.09-4.33, ) (v) Associations of apolipoproteins and ApoB/ApoA-I ratio with composite CVD events were also estimated in Cox hazards models of a 1-SD increase of variables (, 95% CI: 1.04-1.85, ) (vi) Each variable of ApoB/ApoA-I ratio was an independent biomarker of composite CVD events in this model adjusted for the time-varying covariates of HDL-C (, 95% CI: 1.62-20.86, ) and hs-CRP (, 95% CI: 1.50-20.29, ) (vii) The association of ApoB/ApoA-I ratio with composite CVD events disappeared when adjusted for IL-6 ()
Asymptomatic atherosclerosis (IMT, plaque occurrence, and number of plaques)
91
91
G5D
HD
(i) Multiple linear regression analysis of nontraditional risk factors showed no relationship between ApoA-I values and IMTc (), plaque occurrence (), and the number of plaques ()
(i) In the logistic regression analysis, ApoA-IV emerged as a significant and independent predictor for the presence of atherosclerotic events (, 95% CI: 0.86–0.98, )
(i) In a multivariable logistic regression analysis, after adjusting for confounders, high ApoA-IV concentration was associated with CVD and with maximum cIMT (, 95% CI: 0.09–0.60, ;, 95% CI: 0.12–0.86, , respectively) (ii) In a stepwise multivariate regression analysis, A-IV concentrations were associated with maximum cIMT () (iii) The serum ApoA-IV concentration was independently associated with maximum cIMT (adjusted )
Post hoc analysis of prospective, randomized, controlled trial 4D
ApoA-IV
Death from all causes Death from cardiac causes Combined cardiac events Combined cerebrovascular events Combined cardiovascular events
1224
1224
G5D
HD
(i) At baseline, ApoA-IV was inversely associated with the prevalence of congestive heart failure ( per 10 mg dl-1 increment in ApoA-IV, ) (ii) At baseline, ApoA-IV was correlated with ECG abnormalities such as arrhythmia, atrial fibrillation/flutter, and right or left bundle branch block (iii) At baseline, associations between ApoA-IV and variables reflecting atherosclerotic disease were weaker than those for congestive heart failure (iv) Each 10 mg dl-1 increase in ApoA-IV concentration was associated with an 11% reduced risk of death during the observation period () (v) A significant association between ApoA-IV and all-cause mortality was found in the nonwasting group (, 95% CI: 0.84–0.96, ) (vi) In patients with , there was a relationship between ApoA-IV concentrations and death from cardiac causes (, 95% CI: 0.80–0.98, ), sudden cardiac death (, 95% CI: 0.72–0.95, ), and combined cerebrovascular events (, 95% CI: 0.73–0.96, ) (vii) Atherogenic events (fatal and nonfatal myocardial infarction or cardiovascular interventions), which were included in the overall group with cardiac events, were not associated with ApoA-IV concentration (, 95% CI: 0.92–1.05, )
(i) CKD and CVD groups revealed accumulation of two proteins: ApoA-IV and α-1-microglobulin (ii) The results showed that at least two processes differentially contribute to the plaque formation in CKD- and CVD-mediated atherosclerosis (iii) The downregulation and upregulation of ApoA-IV in CVD and CKD groups suggested that substantial differences exist in the efficacy of cholesterol transport in both groups of patients
(i) The ratio of ApoB/ApoA-I was a strong predictor of myocardial infarction, both among subjects with and without renal dysfunction (, 95% CI: 2.25–4.91 and , 95% CI: 2.54–3.26, , respectively)
Cross-sectional observational CARE FOR HOMe Cross-sectional observational LURIC
PCSK9
(i) Acute myocardial infarction (ii) Surgical or interventional coronary/cerebrovascular/peripheral-arterial revascularization (iii) Stroke with (iv) Amputation above the ankle or death of any cause, cardiovascular death (v) Death immediately after intervention to treat CHD (vi) Fatal stroke (vii) Other causes of death due to CHD
443 1450
443 1450
G1-G4 G1-G4
—
(i) Kaplan-Meier analysis demonstrated no significant association between tertiles of PCSK9 and CV outcomes (). Separate analyses stratified by statin intake did not yield different results (statin users: ; statin nonusers: ) (ii) In multivariate analyses, we adjusted for confounders; PCSK9 was not an independent predictor of CV events () (iii) In Kaplan-Meier analysis, tertiles of PCSK9 were not associated with cardiovascular deaths (). Separate analyses stratified by statin intake did not yield different results (no statin: ; statin: )
