Background: Ezetimibe demonstrates decreasing visceral fat and improving insulin sensitivity in animals and humans. We first reported simvastatin dose-dependently worsens insulin sensitivity. Whether ezetimibe may compensate untoward effects of simvastatin, depending on dosages of simvastatin have not been investigated in patients with hypercholesterolemia, compared with simvastatin alone. Methods: This was a randomized, single-blind, placebo-controlled, parallel study. Age, sex, and body mass index were matched among groups. Fifty-one in each group were given placebo, ezetimibe 10 mg combined with simvastatin 10 mg (Vyto10), ezetimibe 10 mg combined with simvastatin 20 mg (Vyto20), or simvastatin 20 mg alone (Simva20), respectively daily for 2 months. Results: Placebo therapy did not significantly change insulin and insulin sensitivity and adiponectin levels and visceral fat area (VFA) and VFA/subcutaneous fat area (SFA) relative to baseline measurements. Vyto10 therapy significantly decreased CRP and insulin levels and increased adiponectin levels and insulin sensitivity, and reduced VFA, VFA/SFA, and blood pressure. Vyto20 therapy did not significantly change insulin levels and insulin sensitivity and adiponectin levels but significantly reduced CRP levels and VFA, VFA/SFA, and blood pressure. Simva20 therapy significantly decreased adiponectin levels and insulin sensitivity but did not significantly change VFA, VFA/SFA, and blood pressure. Of note, these different effects of each therapy were significant by ANOVA. Conclusions: Vyto10, Vyto20, and Simva20 showed significant reduction of LDL cholesterol levels and improvement of flow-mediated dilation in patients with hypercholesterolemia. However, Vyto10, Vyto20, and Simva20 showed significantly differential metabolic effects, depending on dosages of simvastatin.
Residual cardiovascular risk and failure of high density lipoprotein cholesterol raising treatment have refocused interest on targeting hypertriglyceridemia. Hypertriglyceridemia, triglyceride-rich lipoproteins, and remnant cholesterol have demonstrated to be important risk factors for cardiovascular disease; this has been demonstrated in experimental, genetic, and epidemiological studies.Fibrates can reduce cardiovascular event rates with or without statins.High dose omega-3 fatty acids continue to be evaluated and new specialized targeting treatment modulating triglyceride pathways, such as inhibition of apolipoprotein C-III and angiopoietin-like proteins, are being tested with regard to their effects on lipid profiles and cardiovascular outcomes.In this review, we will discuss the role of hypertriglyceridemia, triglyceride-rich lipoproteins and remnant cholesterol on cardiovascular disease, and the potential implications for treatment stargeting hypertriglyceridemia. (
Short stature is reportedly associated with cardiovascular disease (CVD). However, the mechanism underlying this intriguing epidemiological finding is unclear. Pulse wave velocity (PWV), a marker of vascular stiffness, is a predictor of future CVD. Therefore, PWV may be affected by height even before overt CVD occurs. Here, we investigated the association between adult height and PWV in subjects without overt CVD.A total of 1019 subjects (48 ± 12 years old; 509 men, 21 with diabetes mellitus, 209 with hypertension) without overt CVD were enrolled, all of whom underwent brachial-ankle PWV (baPWV) measurements. The subjects were divided into 3 groups by height. A multiple regression model was used to estimate baPWV values among heights after the adjustment for confounders.Mean baPWV value was highest in the group with the shortest height for both sexes (both P < .001). Bivariate correlation analysis between height and baPWV showed significant correlations in men (r = -0.131, P = .003) and women (r = -0.180, P < .001). In the multiple regression analysis with adjustment for identified confounders, group height was a predictor of baPWV (P for trend = .003) in younger men (<50 years old) but not in older men, while group height was correlated with baPWV in older women (≥50 years old, P for trend = .014) but not in younger women.Height is inversely correlated with baPWV in subjects without overt CVD, especially in younger men and older women. This may explain the historical epidemiological observation of an inverse relationship between height and CVD.
Distal embolization, such as plaque debris and thrombus during percutaneous coronary and carotid interventions, often lead to virtually untreatable small vessel occlusions and the no-reflow phenomenon, which may cause periprocedural end organ ischemia and infarction. This is clinically important as the one-year mortality is doubled in patients with a periprocedural myocardial infarction. To prevent a distal embolization a number of distal protection devices have been developed, with others still under development, such as a balloon occlusion device (PercuSurge GuardWire), numerous filter devices (FilterWire EX, AngioGuard, Mednova Neuroshield, AccuNet) and a catheter occlusion device (Parodi Anti-Emboli System). The usefulness and roles of distal protection devices, for
Although soluble suppression of tumorigenicity 2 (sST2) in serum is known to be associated with ischemic heart disease and heart failure, data regarding its prognostic impact in ST-segment elevation myocardial infarction (STEMI) is limited. We evaluated the prognostic impacts of serum sST2 and other serum biomarkers in STEMI patients undergoing primary percutaneous coronary intervention (PCI).Consecutive all 323 patients with STEMI that underwent primary PCI were enrolled. Blood tests and samples were obtained in an emergency room. The primary endpoint was 1-year major adverse cardiovascular and cerebrovascular events (MACCEs), defined as a composite of cardiovascular death, non-fatal MI, non-fatal stroke, and ischemia-driven revascularization.Mean age was 59.1±13.1 years (men 84%). MACCE (20 cardiovascular deaths, 7 non-fatal MI, 4 non-fatal stroke, 7 ischemia-driven revascularizations) occurred in 38 patients (12%). After adjusting for confounding factors, Cox regression analysis revealed that high serum sST2 (>75.8 ng/mL mean value, adjusted hazard ratio 2.098, 95% CI 1.008-4.367, p = 0.048) and high serum NT-proBNP level (>400 pg/mL, adjusted hazard ratio 2.606, 95% CI 1.086-6.257, p = 0.032) at the time of presentation independently predicted MACCE within a year of primary PCI. Furthermore, when high serum sST2 level was combined with high serum NT-proBNP level, the hazard ratio of MACCE was highest (adjusted hazard ratio 7.93, 95% CI 2.97-20.38, p<0.001).Elevated serum levels of sST2 or NT-proBNP at the time of presentation were found to predict 1-year MACCE independently and elevated serum levels of sST2 plus NT-proBNP were associated with even poorer prognosis in patients with STEMI undergoing primary PCI.
Two decades ago, it was recognized that lipoprotein(a) (Lp(a)) concentrations were elevated in patients with cardiovascular disease (CVD). However, the importance of Lp(a) was not strongly established due to a lack of both Lp(a)-lowering therapy and evidence that reducing Lp(a) levels improves CVD risk. Recent advances in clinical and genetic research have revealed the crucial role of Lp(a) in the pathogenesis of CVD. Mendelian randomization studies have shown that Lp(a) concentrations are causal for different CVDs, including coronary artery disease, calcified aortic valve disease, stroke, and heart failure, despite optimal low-density lipoprotein cholesterol (LDL-C) management. Lp(a) consists of apolipoprotein (apo) B100 covalently bound to apoA. Thus, Lp(a) has atherothrombotic traits of both apoB (from LDL) and apoA (thrombo-inflammatory aspects). Although conventional pharmacological therapies, such as statin, niacin, and cholesteryl ester transfer protein, have failed to significantly reduce Lp(a) levels, emerging new therapeutic strategies using proprotein convertase subtilisin-kexin type 9 inhibitors or antisesnse oligonucleotide technology have shown promising results in effectively lowering Lp(a). In this review we discuss the revisited important role of L(a) and strategies to overcome residual risk in the statin era.
'%3e%3cg id='b'%3e%3cpath id='a' stroke='%23000' stroke-width='2' d='M-6-25H6m-12 3H6m-12 3H6'/%3e%3cuse xlink:href='%23a' y='44'/%3e%3c/g%3e%3cpath stroke='%23fff' d='M0 17v10'/%3e%3ccircle r='12' fill='%23cd2e3a'/%3e%3cpath fill='%230047a0' d='M0-12A6 6 0 0 0 0 0a6 6 0 0 1 0 12 12 12 0 0 1 0-24z'/%3e%3c/g%3e%3cg transform='rotate(-123.69)'%3e%3cuse xlink:href='%23b'/%3e%3cpath stroke='%23fff' d='M0-23.5v3M0 17v3.5m0 3v3'/%3e%3c/g%3e%3c/svg%3e)