The relation between VLDL-cholesterol and risk of cardiovascular events in patients with manifest cardiovascular disease

Heidemann, Britt E; Koopal, Charlotte; Bots, Michiel L.; Asselbergs, Folkert W.; Westerink, Jan; Visseren, Frank L J

doi:10.1016/j.ijcard.2020.08.030

Cited by 24 publications

(16 citation statements)

References 38 publications

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“…It is possible that under conditions of marked LDL-C reduction, a larger proportion of non-HDL-C resides in the pool of triglyceride-rich lipoproteins, which in turn may be less strongly associated with cardiovascular risk than LDL particles. 32 Pharmacological lowering of atherogenic lipids with high-intensity statin therapy reduces the risk of MACE after an ACS. 8,9,11,12,33 Despite achievement of a conventional LDL-C goal with statins, there is substantial residual risk for recurrent MACE after ACS that may be reduced with intensified lipid lowering with ezetimibe or a PCSK9 inhibitor.…”

Section: Discussionmentioning

confidence: 99%

Apolipoprotein B, Residual Cardiovascular Risk After Acute Coronary Syndrome, and Effects of Alirocumab

et al. 2022

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Background: Apolipoprotein B (apoB) provides an integrated measure of atherogenic risk. Whether apoB levels and apoB lowering hold incremental predictive information on residual risk after acute coronary syndrome beyond that provided by low-density lipoprotein cholesterol is uncertain. Methods: The ODYSSEY OUTCOMES trial (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab) compared the proprotein convertase subtilisin/kexin type 9 inhibitor alirocumab with placebo in 18 924 patients with recent acute coronary syndrome and elevated atherogenic lipoproteins despite optimized statin therapy. Primary outcome was major adverse cardiovascular events (MACE; coronary heart disease death, nonfatal myocardial infarction, fatal/nonfatal ischemic stroke, hospitalization for unstable angina). Associations between baseline apoB or apoB at 4 months and MACE were assessed in adjusted Cox proportional hazards and propensity score–matched models. Results: Median follow-up was 2.8 years. In proportional hazards analysis in the placebo group, MACE incidence increased across increasing baseline apoB strata (3.2 [95% CI, 2.9–3.6], 4.0 [95% CI, 3.6–4.5], and 5.5 [95% CI, 5.0–6.1] events per 100 patient-years in strata <75, 75–<90, ≥90 mg/dL, respectively; P trend <0.0001) and after adjustment for low-density lipoprotein cholesterol ( P trend =0.035). Higher baseline apoB stratum was associated with greater relative ( P trend <0.0001) and absolute reduction in MACE with alirocumab versus placebo. In the alirocumab group, the incidence of MACE after month 4 decreased monotonically across decreasing achieved apoB strata (4.26 [95% CI, 3.78–4.79], 3.09 [95% CI, 2.69–3.54], and 2.41 [95% CI, 2.11–2.76] events per 100 patient-years in strata ≥50, >35–<50, and ≤35 mg/dL, respectively). Compared with propensity score–matched patients from the placebo group, treatment hazard ratios for alirocumab also decreased monotonically across achieved apoB strata. Achieved apoB was predictive of MACE after adjustment for achieved low-density lipoprotein cholesterol or non–high-density lipoprotein cholesterol but not vice versa. Conclusions: In patients with recent acute coronary syndrome and elevated atherogenic lipoproteins, MACE increased across baseline apoB strata. Alirocumab reduced MACE across all strata of baseline apoB, with larger absolute reductions in patients with higher baseline levels. Lower achieved apoB was associated with lower risk of MACE, even after accounting for achieved low-density lipoprotein cholesterol or non–high-density lipoprotein cholesterol, indicating that apoB provides incremental information. Achievement of apoB levels as low as ≤35 mg/dL may reduce lipoprotein-attributable residual risk after acute coronary syndrome. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01663402.

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Section: Discussionmentioning

confidence: 99%

Apolipoprotein B, Residual Cardiovascular Risk After Acute Coronary Syndrome, and Effects of Alirocumab

et al. 2022

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“…Emerging evidence suggested that TG and TGRLs played a causal role in development of CAD. 28,29 Due to the complex interaction of lipoprotein metabolism, the TG to HDL-C ratio has been regarded as a more practical indicator to mirror plasma atherogenicity than individual lipid values. 30 AIP was derived from the ratio of TG/HDL-C.…”

Section: Discussionmentioning

confidence: 99%

Association of Atherogenic Index of Plasma With Angiographic Progression in Patients With Suspected Coronary Artery Disease

et al. 2022

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The present study aimed to explore the correlation of atherogenic index of plasma (AIP) with angiographic progression of coronary artery disease (CAD). AIP was defined as the base 10 logarithm of the ratio of the triglyceride to high-density lipoprotein cholesterol concentration. The extent of coronary lesion was assessed by the Gensini Score (GS) system and angiographic progression was defined as the GS rate of change per year >1 point. A total of 896 patients with suspected CAD who underwent coronary computed tomography angiography twice at intervals of >6 months were included. Baseline AIP was positively correlated with remnant cholesterol (r = .644, P < .001). When patients were assigned into four groups according to baseline AIP quartiles, the incidence of CAD progression significantly increased across the quartiles of AIP (Q1 [lowest]: 23.7 vs Q2: 29.9 vs Q3: 33.9 vs Q4 [highest]: 34.8%; P = .042). After multivariate adjustment, the odds ratio for CAD progression was 1.89 when comparing the highest to the lowest quartile of AIP (95% confidence interval: 1.18–3.02; P = .008). Therefore, AIP was independently correlated with angiographic progression of CAD beyond conventional risk factors, suggesting that AIP may play a role in early risk stratification as a simple surrogate of residual risk.

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“…Furthermore, a proportion of arterial plaque cholesterol is derived from VLDL and its residue IDL in patients with mild-to-moderate HTG ( Gill et al, 2021 ). Of note, plasma VLDL cholesterol (VLDL-C) is an increased risk factor for major adverse CVD events, independent of the established risk factors such as LDL-C ( Heidemann et al, 2021 ). It seems that the remnant cholesterol, but not TG, in TGRL particles is a causal factor of atherosclerosis ( Jørgensen et al, 2013 ; Varbo and Nordestgaard, 2016 ; Dron and Hegele, 2020 ).…”

Section: Tgrl and Atherosclerosismentioning

confidence: 99%

Triglyceride and Triglyceride-Rich Lipoproteins in Atherosclerosis

Zhang

Yin

Qiao

et al. 2022

Front. Mol. Biosci.

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Cardiovascular disease (CVD) is still the leading cause of death globally, and atherosclerosis is the main pathological basis of CVDs. Low-density lipoprotein cholesterol (LDL-C) is a strong causal factor of atherosclerosis. However, the first-line lipid-lowering drugs, statins, only reduce approximately 30% of the CVD risk. Of note, atherosclerotic CVD (ASCVD) cannot be eliminated in a great number of patients even their LDL-C levels meet the recommended clinical goals. Previously, whether the elevated plasma level of triglyceride is causally associated with ASCVD has been controversial. Recent genetic and epidemiological studies have demonstrated that triglyceride and triglyceride-rich lipoprotein (TGRL) are the main causal risk factors of the residual ASCVD. TGRLs and their metabolites can promote atherosclerosis via modulating inflammation, oxidative stress, and formation of foam cells. In this article, we will make a short review of TG and TGRL metabolism, display evidence of association between TG and ASCVD, summarize the atherogenic factors of TGRLs and their metabolites, and discuss the current findings and advances in TG-lowering therapies. This review provides information useful for the researchers in the field of CVD as well as for pharmacologists and clinicians.

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The relation between VLDL-cholesterol and risk of cardiovascular events in patients with manifest cardiovascular disease

Cited by 24 publications

References 38 publications

Apolipoprotein B, Residual Cardiovascular Risk After Acute Coronary Syndrome, and Effects of Alirocumab

Apolipoprotein B, Residual Cardiovascular Risk After Acute Coronary Syndrome, and Effects of Alirocumab

Association of Atherogenic Index of Plasma With Angiographic Progression in Patients With Suspected Coronary Artery Disease

Triglyceride and Triglyceride-Rich Lipoproteins in Atherosclerosis

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