scholarly journals Low HDL despite statin-lowered LDL cholesterol levels raises risk of cardiovascular events

2008 ◽  
Vol 5 (2) ◽  
pp. 66-66
2011 ◽  
Vol 26 (S2) ◽  
pp. 1940-1940
Author(s):  
M.-L. Ancelin ◽  
I. Carrière ◽  
J.-P. Boulenger ◽  
A. Malafosse ◽  
R. Stewart ◽  
...  

BackgroundLipids appear to mediate depressive vulnerability in the elderly, however, sex differences and genetic vulnerability have not been taken into account in previous prospective studies.MethodsDepression was assessed in a population of 1040 women and 752 men aged 65 years and over at baseline and after 7-year follow-up. Clinical level of depression (DEP) was defined as having either a score of 16 and above on the Centre for Epidemiology Studies Depression scale or a diagnosis of current major depression on the Mini International Neuropsychiatric Interview. Lipid levels, apolipoprotein E and serotonin transporter linked promoter region (5-HTTLPR) genotypes were evaluated at baseline.ResultsMultivariate analyses adjusted by socio-demographic and behavioral variables, measures of physical health including ischemic pathologies, and genetic vulnerability indicated gender-specific associations between dyslipidemia and DEP, independent of the use of lipid lowering agents or apolipoprotein E status. Men with low LDL-cholesterol levels had twice the risk of prevalent and incident DEP whereas in women low HDL-cholesterol levels were found to be significantly associated with increased prevalent DEP (OR = 1.5) only. A significant interaction was observed between low LDL-cholesterol and 5-HTTLPR genotype, men with s/s or s/l genotype being at increased risk of DEP (OR = 6.0 and 2.7, respectively). No significant gene-environment interaction was observed for women.ConclusionsDEP is associated with higher atherogenic risk in women (low HDL-cholesterol), whereas the reverse is observed in men (low LDL-cholesterol). Late-life depression may have a complex gender-specific etiology involving genetic vulnerability in men.


2016 ◽  
Vol 157 (31) ◽  
pp. 1219-1223 ◽  
Author(s):  
György Paragh ◽  
István Karádi

Considerable evidence suggests that “the lower the better” is a reasonable approach for reducing cardiovascular risk by lowering LDL cholesterol levels. Despite the reduction in cardiovascular events and mortality achieved by statin therapy, significant residual risk remains, especially in severe hereditary hypercholesterolemia, such as familial hypercholesterolemia. Some new strategies to achieve even lower LDL levels are now available, including the addition of cholesterol absorption inhibitor ezetimibe, and the recently available Proprotein convertase subtilisin/kexin type 9 monoclonal antibodies. In addition, new LDL drugs may be effectively administrated in those individuals who are unable to tolerate statins. The authors summarize the efficacy and clinical indications of these new agents and review the currently available guidelines. Orv. Hetil., 2016, 157(31), 1219–1223.


2004 ◽  
Vol 2004 (4) ◽  
pp. 177-184
Author(s):  
Rampratap S. Kushwaha ◽  
Henry C. McGill ◽  
Frederick H. Hausheer

The present studies were conducted to determine whether a synthetic truncated apoC-I peptide that inhibits CETP activity in baboons would raise plasma HDL cholesterol levels in nonhuman primates with low HDL levels. We used 2 cynomolgus monkeys and 3 baboons fed a cholesterol- and fat-enriched diet. In cynomolgus monkeys, we injected synthetic truncated apoC-I inhibitor peptide at a dose of 20 mg/kg and, in baboons, at doses of 10, 15, and 20 mg/kg at weekly intervals. Blood samples were collected 3 times a week and VLDL+LDL and HDL cholesterol concentrations were measured. In cynomolgus monkeys, administration of the inhibitor peptide caused a rapid decrease in VLDL+LDL cholesterol concentrations (30%–60%) and an increase in HDL cholesterol concentrations (10%–20%). VLDL+LDL cholesterol concentrations returned to baseline levels in approximately 15 days. In baboons, administration of the synthetic inhibitor peptide caused a decrease in VLDL+LDL cholesterol (20%–60%) and an increase in HDL cholesterol (10%–20%). VLDL+LDL cholesterol returned to baseline levels by day 21, whereas HDL cholesterol concentrations remained elevated for up to 26 days. ApoA-I concentrations increased, whereas apoE and triglyceride concentrations decreased. Subcutaneous and intravenous administrations of the inhibitor peptide had similar effects on LDL and HDL cholesterol concentrations. There was no change in body weight, food consumption, or plasma IgG levels of any baboon during the study. These studies suggest that the truncated apoC-I peptide can be used to raise HDL in humans.


2015 ◽  
Vol 93 (12) ◽  
pp. 1043-1054 ◽  
Author(s):  
Ulrich Julius

Niacin is an important vitamin (B3) that can be used in gram doses to positively modify pathogenetically relevant lipid disorders: elevated LDL cholesterol, elevated non-HDL cholesterol, elevated triglycerides, elevated lipoprotein(a), and reduced HDL cholesterol. This review reports the latest published findings with respect to niacin’s mechanisms of action on these lipids and its anti-inflammatory and anti-atherosclerotic effects. In the pre-statin era, niacin was shown to have beneficial effects on cardiovascular end-points; but in recent years, two major studies performed in patients whose LDL cholesterol levels had been optimized by a statin therapy did not demonstrate an additional significant effect on these end-points in the groups where niacin was administered. Both studies have several drawbacks that suggest that they are not representative for other patients. Thus, niacin still plays a role either as an additive to a statin or as a substitute for a statin in statin-intolerant patients. Moreover, patients with elevated triglyceride and low HDL cholesterol levels and patients with elevated lipoprotein(a) concentrations will possibly benefit from niacin, although currently the study evidence for these indications is rather poor. Niacin may be useful for compliant patients, however possible side effects (flushing, liver damage) and contraindications should be taken into consideration.


2019 ◽  
Vol 14 (5) ◽  
pp. 476-482 ◽  
Author(s):  
George Ntaios ◽  
Haralampos Milionis

Background Low-density lipoprotein (LDL) cholesterol has been long associated with the risk for ischemic stroke, myocardial infarction, and cardiovascular death. For more than a decade, the main pharmacological option to prevent stroke and myocardial infarction through LDL-cholesterol lowering was the use of statins. During the recent years, two novel classes of drugs have proven their efficacy and safety to reduce LDL-cholesterol and prevent cardiovascular events in large, well-conducted randomized controlled trials: ezetimibe and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors. Aims The present review summarizes the evidence arising from the latest trials of lipid-lowering treatment for cardiovascular outcomes prevention and discusses their implications for secondary prevention strategies in patients with ischemic stroke. Summary of review There is strong evidence which confirms the hypothesis that the lower the LDL-cholesterol, the less frequent the cardiovascular events are and underlines the importance of treating our ischemic stroke patients with intensive statin treatment aiming at low LDL-cholesterol levels. The very low levels of LDL cholesterol seem to be safe, even in the mid/long term but longer follow-up data are needed. Currently there are no tools to reliably predict cardiovascular outcomes in the specific population of ischemic stroke patients. Conclusions Stroke physicians should aim for low LDL-cholesterol levels by intensive statin treatment in all ischemic stroke patients. For those patients who are at the highest risk for recurrent stroke or another cardiovascular event and have unacceptable LDL-cholesterol levels despite intensive statin treatment, PCSK9 inhibitors should be considered.


e-CliniC ◽  
2016 ◽  
Vol 4 (1) ◽  
Author(s):  
Eva Nur Faridah ◽  
Janry A. Pangemanan ◽  
Starry H. Rampengan

Abstract: Acute coronary syndrome (ACS) is due to plaque rupture or erosion of atherosklerosis, including unstable angina pectoris, non-ST elevation myocardial infarction, and ST-elevation myocardial infarction. In indonesia, ACS is still regarded as the highest death contributor. One of the risk factors of ACS is dyslipidemia, that is abnormality condition of lipid in blood. Objective: This study aims to determine description of lipid profile in patients with acute coronary syndrome. Methods: This was a descriptive observational method, based on the secondary data from patients in CVBC Prof. Dr. R. D. Kandou Hospital during January to September 2015. Result: The result showed that from 80 patients of ACS were 37 patients (46,25%) with high total cholsterol levels (≥ 200 mg/dL), 70 patients (87,5%) with low HDL cholesterol levels (≤ 40 - 50 mg/dL), there are 58 patients (72,5%) with high LDL cholesterol levels (> 100 mg/dL) and 32 patients (40%) with high triglycerides levels (≥ 150 mg/dL). Conclusion: Most of ACS patients in this research had high LDL cholesterol levels and low HDL cholesterol levels.Keywords: Acute coronary syndrome, dyslipidemia, lipid profileAbstrak: Sindrom koroner Akut ( SKA ) terjadi karena adanya ruptur atau erosi dari plak aterosklerosis, termasuk angina pektoris tidak stabil, non-ST elevasi miokard infark, dan ST elevasi miokard infark. Di Indonesia, SKA masih di anggap sebagai penyumbang angka kematian tertinggi. Salah satu faktor risiko SKA adalah dislipidemia, yaitu berupa gangguan metabolisme lipid. Tujuan: Penelitian ini bertujuan untuk mengetahui gambaran profil lipid pada penderita sindrom koroner akut. Metode: Penelitian ini bersifat deskriptif observasional dengan menggunakan data sekunder dari penderita SKA di CVBC RSUP. Prof. Dr. R. D. Kandou periode januari – september 2015. Hasil: Hasil penelitian ini menunjukkan dari 80 penderita SKA didapatkan 37 orang (46,25%) adalah penderita yang memiliki kadar kolesterol total tinggi (≥ 200 mg/dL), sebanyak 70 orang (87,5%) memiliki kadar HDL rendah (≤ 40 – 50 mg/dL), adapun yang memiliki kadar LDL tinggi (> 100 mg/dL) yaitu 58 orang (72,5%) dan 32 orang (40%) adalah penderita yang memiliki kadar trigliserida tinggi (≥ 150 mg/dL). Kesimpulan: Penderita sindrom koroner akut dalam penelitian ini sebagian besar memiliki kadar kolesterol LDL yang tinggi dan kadar kolesterol HDL yang rendah.Kata kunci: Sindrom koroner akut, dislipidemia, profil lipid


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