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In a randomized trial, patients with type 2 diabetes, hypertriglyceridemia, and low HDL cholesterol who received pemafibrate did not have fewer cardiovascular events, although some lipid levels decreased.

In a phase 2b trial involving patients with hypertriglyceridemia, the use of olezarsen (which targets APOC3 mRNA) for 6 months reduced triglyceride levels by approximately 50% as compared with placebo.

The results of this phase 3 trial of the effect of olezarsen, a drug that targets APOC3 mRNA, on plasma triglyceride levels and acute pancreatitis in familial chylomicronemia syndrome support further clinical research.

Weekly doses of an antisense inhibitor of apolipoprotein C-III (APOC3) in persons with severe or uncontrolled hypertriglyceridemia resulted in a reduction in APOC3 and triglyceride levels at the end of 13 weeks. Elevated triglyceride levels are associated with several pathologic conditions, including insulin resistance, the metabolic syndrome, diabetes, cardiovascular disease, and hereditary disorders, such as the familial chylomicronemia syndrome, familial combined hyperlipidemia, and familial hypertriglyceridemia. 1 , 2 Patients with triglyceride levels above 2000 mg per deciliter (22.6 mmol per liter), measured at the peak of abdominal pain, are at high risk for pancreatitis. 3 , 4 Current guidelines from the Endocrine Society and the European Atherosclerosis Society recommend that fasting triglyceride levels should be maintained at values below 1000 mg per deciliter (11.3 mmol per liter) or 10 mmol per liter, respectively, to prevent intermittent . . .

Approximately 25% of US adults are estimated to have hypertriglyceridemia (triglyceride [TG] level ≥150 mg/dL [≥1.7 mmol/L]). Elevated TG levels are associated with increased cardiovascular disease (CVD) risk, and severe hypertriglyceridemia (TG levels ≥500 mg/dL [≥5.6 mmol/L]) is a well-established risk factor for acute pancreatitis. Plasma TG levels correspond to the sum of the TG content in TG-rich lipoproteins (TRLs; ie, very low-density lipoproteins plus chylomicrons) and their remnants. There remains some uncertainty regarding the direct causal role of TRLs in the progression of atherosclerosis and CVD, with cardiovascular outcome studies of TG-lowering agents, to date, having produced inconsistent results. Although low-density lipoprotein cholesterol (LDL-C) remains the primary treatment target to reduce CVD risk, a number of large-scale epidemiological studies have shown that elevated TG levels are independently associated with increased incidence of cardiovascular events, even in patients treated effectively with statins. Genetic studies have further clarified the causal association between TRLs and CVD. Variants in several key genes involved in TRL metabolism are strongly associated with CVD risk, with the strength of a variant's effect on TG levels correlating with the magnitude of the variant's effect on CVD. TRLs are thought to contribute to the progression of atherosclerosis and CVD via a number of direct and indirect mechanisms. They directly contribute to intimal cholesterol deposition and are also involved in the activation and enhancement of several proinflammatory, proapoptotic, and procoagulant pathways. Evidence suggests that non-high-density lipoprotein cholesterol, the sum of the total cholesterol carried by atherogenic lipoproteins (including LDL, TRL, and TRL remnants), provides a better indication of CVD risk than LDL-C, particularly in patients with hypertriglyceridemia. This article aims to provide an overview of the available epidemiological, clinical, and genetic evidence relating to the atherogenicity of TRLs and their role in the progression of CVD.

The prevalence of metabolic syndrome has markedly increased worldwide. However, studies in the United States show that it has remained stable or slightly declined in recent years. Whether this applies to other countries is presently unclear. We examined the trends in the prevalence of metabolic syndrome and its components in Korea. The prevalence of metabolic syndrome and its components was estimated in adults aged >30 years from the Korean National Health Insurance Service data from 2009 to 2013. The revised National Cholesterol Education Program criteria were used to define metabolic syndrome. Approximately 10 million individuals were analyzed annually. The age-adjusted prevalence of metabolic syndrome increased from 28.84% to 30.52%, and the increasing trend was more prominent in men. Prevalence of hypertriglyceridemia, low HDL-cholesterol, and impaired fasting plasma glucose significantly increased. However, the prevalence of hypertension decreased in both genders. The prevalence of abdominal obesity decreased in women over 50 years-of-age but significantly increased in young women and men (<50 years). The prevalence of metabolic syndrome is still increasing in Korea. Trends in each component of metabolic syndrome are disparate according to the gender, or age groups. Notably, abdominal obesity among young adults increased significantly; thus, interventional strategies should be implemented particularly for this age group.

Hypertriglyceridemia (HTG) represents a major health problem with prevalence exceeding 30% in the U.S. The present study aims to assess the effect of elevated serum triglyceride (TG) levels on the severity of acute pancreatitis (AP). Prospectively enrolled AP patients were categorized into normal, mild, moderate, and severe/very severe categories based on their TG levels and compared in respect to demographics, comorbidities, and clinical outcomes. Multivariate analysis determined whether elevated TG levels were independently associated with persistent organ failure. Two hundred and one out of 400 AP patients had serum TGs measured within 72 h of presentation, of which 115 had normal TG levels and 86 HTG (20 mild, 41 moderate, and 25 severe/very severe). Patients with HTG were of younger age (44 vs. 52 years), predominantly male (65% vs. 45%), obese (57% vs. 34%), diabetic (38% vs. 17%), and developed more frequently persistent organ failure (40% vs. 17%) compared with those with normal TGs (P<0.02). The rate of persistent organ failure increased proportionally with HTG severity grades (17% when normal TGs, 30% in mild, 39% in moderate, and 48% in severe/very severe HTG, Ptrend<0.001). On multivariate analysis controlling for age, gender, body mass index, diabetes, and alcohol etiology, moderate HTG (odds ratio (OR), 2.6; P=0.04) and severe/very severe HTG (OR, 4.9; P=0.009) were independently associated with persistent organ failure. Elevated serum TGs in AP patients are independently and proportionally correlated with persistent organ failure regardless of etiology. TG-mediated lipotoxicity may be an attractive target to design novel interventions for severe AP.

Ectopic fat obesity and triglycerides are risk factors for diabetes and multiple cardiovascular diseases. However, there have been limited studies on the association between triglycerides and ectopic fat obesity. The purpose of this study was to explore the association between triglycerides and ectopic fat obesity. In this cross-sectional study, we retrospectively analyzed 15464 adult participants recruited by Murakami Memorial Hospital (8430 men and 7034 women, average age of 43.71 ± 8.90). All patients were divided into two groups according to the threshold used to diagnose hypertriglyceridemia. The logistic regression model was used to analyze the association between triglycerides and the risk of ectopic fat obesity, and the generalized additive model was used to identify the nonlinear association. In this study population, the prevalence of ectopic fat obesity was 17.73%. After adjusting other covariables, triglycerides were positively correlated with the risk of ectopic fat obesity (OR: 1.54, 95% CI:1.41-1.69, P<0.0001). Through smooth curve fitting, we found that there was an inverted U-shaped curve association between triglycerides and ectopic fat obesity. This association remained unchanged even if the adjusted covariables were removed from the model, and the inflection point of the curve was 3.98. When triglyceride levels were ≤3.98, triglycerides were positively correlated with the risk of ectopic fat obesity (OR:1.784, 95% CI:1.611-1.975, P<0.0001). When triglyceride levels were >3.98 (right side of the inflection point), there was a negative correlation (OR:0.519, 95% CI:0.333-0.810, P = 0.0039). Our research showed that there is a significant association between triglycerides and ectopic fat obesity. This relation is not a simple linear relationship but instead an inverted U-shaped curve association.

Abstract Background Multifactorial chylomicronemia syndrome (MCS) is a severe form of hypertriglyceridemia (hyperTG) associated with an increased risk of acute pancreatitis. However, the risk of acute pancreatitis is very heterogenous in MCS. Previous studies suggested that inflammation might promote disease progression in hyperTG-induced acute pancreatitis. Objective To determine if low-grade inflammation is associated with acute pancreatitis in MCS. Methods This study included 102 subjects with MCS for whom high-sensitivity C-reactive protein (hsCRP) concentration was measured at their first visit at the Montreal Clinical Research Institute. Results Patients with MCS who had a previous history of acute pancreatitis had a significant higher hsCRP concentration (4.62 mg/L vs 2.61 mg/L; P = .003), and high hsCRP concentration (≥ 3 mg/L) was independently associated with acute pancreatitis prevalence (P < .05). Up to 64% of the variability in acute pancreatitis prevalence was explained by the maximal triglycerides (TG) concentration, hsCRP concentration, the presence of rare variants in TG-related genes, and fructose intake, based on a stepwise multivariate regression model (P < .0001). Conclusion This retrospective study showed for the first time that hsCRP concentration is strongly associated with acute pancreatitis prevalence in MCS. It also suggests that low-grade inflammation may be a driver of acute pancreatitis in severe hypertriglyceridemia. Prospective studies could help determine the causality of this association and assess whether medication known to reduce low-grade inflammation could help prevent acute pancreatitis in individuals with severe hypertriglyceridemia.

AMR101 is an ω-3 fatty acid agent containing ≥96% pure icosapent-ethyl, the ethyl ester of eicosapentaenoic acid. The efficacy and safety of AMR101 were evaluated in this phase 3, multicenter, placebo-controlled, randomized, double-blinded, 12-week clinical trial (ANCHOR) in high-risk statin-treated patients with residually high triglyceride (TG) levels (≥200 and <500 mg/dl) despite low-density lipoprotein (LDL) cholesterol control (≥40 and <100 mg/dl). Patients (n = 702) on a stable diet were randomized to AMR101 4 or 2 g/day or placebo. The primary end point was median percent change in TG levels from baseline versus placebo at 12 weeks. AMR101 4 and 2 g/day significantly decreased TG levels by 21.5% (p <0.0001) and 10.1% (p = 0.0005), respectively, and non-high-density lipoprotein (non-HDL) cholesterol by 13.6% (p <0.0001) and 5.5% (p = 0.0054), respectively. AMR101 4 g/day produced greater TG and non-HDL cholesterol decreases in patients with higher-efficacy statin regimens and greater TG decreases in patients with higher baseline TG levels. AMR101 4 g/day decreased LDL cholesterol by 6.2% (p = 0.0067) and decreased apolipoprotein B (9.3%), total cholesterol (12.0%), very-low-density lipoprotein cholesterol (24.4%), lipoprotein-associated phospholipase A2 (19.0%), and high-sensitivity C-reactive protein (22.0%) versus placebo (p <0.001 for all comparisons). AMR101 was generally well tolerated, with safety profiles similar to placebo. In conclusion, AMR101 4 g/day significantly decreased median placebo-adjusted TG, non-HDL cholesterol, LDL cholesterol, apolipoprotein B, total cholesterol, very-low-density lipoprotein cholesterol, lipoprotein-associated phospholipase A2, and high-sensitivity C-reactive protein in statin-treated patients with residual TG elevations.