scholarly journals Triglyceride and Small Dense LDL-Cholesterol in Patients with Acute Coronary Syndrome

2021 ◽  
Vol 10 (19) ◽  
pp. 4607
Author(s):  
Masakazu Hori ◽  
Teruhiko Imamura ◽  
Nikhil Narang ◽  
Hiroshi Onoda ◽  
Shuhei Tanaka ◽  
...  

Background: Small dense LDL-cholesterol is an established risk factor for atherosclerosis but is not routinely measured in daily practice. The association between small dense LDL-cholesterol and triglyceride, which in turn is routinely measured, in patients with acute coronary syndrome remains unknown. Methods: Consecutive patients with acute coronary syndrome who were admitted to our institute were prospectively included, and serum samples were obtained on admission. The association between small dense LDL-cholesterol and triglyceride was investigated. Results: Among 55 patients (median 71 years old, 64% men), median (interquartile range) small dense LDL-cholesterol was 23.6 (17.0, 36.0) and triglyceride was 101 (60, 134) mg/dL. Triglyceride level correlated with small dense LDL-cholesterol (r = 0.67, p < 0.001) and was an independent determinant of small dense LDL-cholesterol together with body mass index (p = 0.010 and p = 0.008, respectively). Those with high triglyceride and high body mass index had a 3-fold level of small dense LDL-cholesterol compared with those with low triglyceride and low body mass index (45.8 [35.0, 54.0] mg/dL versus 15.0 [11.6, 23.7] mg/dL, p = 0.001). Conclusions: Triglyceride level was a major determinant of small dense LDL-cholesterol in patients with acute coronary syndrome. Triglyceride level might be a useful and practical biomarker for risk stratification for patients with acute coronary syndrome together with body mass index.

2011 ◽  
Vol 412 (15-16) ◽  
pp. 1423-1427 ◽  
Author(s):  
Yoshifumi Fukushima ◽  
Satoshi Hirayama ◽  
Tsuyoshi Ueno ◽  
Tomotaka Dohi ◽  
Tetsuro Miyazaki ◽  
...  

Author(s):  
Nobuaki Kobayashi ◽  
Yusaku Shibata ◽  
Osamu Kurihara ◽  
Takahiro Todoroki ◽  
Masayuki Tsutsumi ◽  
...  

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Shao-Yuan Chuang ◽  
Jonathan Jiunn-Horng Chen ◽  
Chih-Cheng Wu ◽  
Wen-Harn Pan

Few studies examine the association between serum uric acid (SUA) and acute coronary syndrome (ACS). We aimed to investigate the association between SUA and ACS in a prospective study of ethnic Chinese. Enrolled were 128569 adults ≥ 20 yrs from 4 MJ Health Checkup Clinics in Taiwan during 1994 –1996, excluding those with heart disease, stroke, renal disease and cancer disease. All physical examination, biochemical test and structured questionnaire were executed in standardized central labs. ACS was defined by main ICD-9 of 410 – 414 from claim data of National Health Insurance for hospitalization and from Death certification registry. Cox proportional hazard model was used to estimate the hazard ratios (HRs) between levels of SUA and ACS events. A total of 2049 subjects (Men: 1239/Women: 810) developed ACS during the period from baseline to Dec.31.2002. Men had higher ACS incidence than women (2.84 vs. 1.61 per 1000 person-years [PY]; p < .0001). Independent risk factors of ACS unfolded from this study included age, male sex, waist circumference, body mass index, triglycerides, total-cholesterol, hypertension, diabetes, uric acid, and current smoking. The crude incidences of ACS were 1.27, 2.06, 3.27 and 4.61 per 1000 PY in that order for four consecutive SUA groups (group1: <5.0 mg/dl; group 2: 5.0 – 6.9 mg/dl; group 3: 7.0 – 8.9 mg/dl; group 4: ≥9.0 mg/dl) (p-value for trend <.0001). Compared to group1, the multi-variate adjusted HRs (95% Confidence intervals) were 1.14 (0.92, 1.42) for group 2, 1.38 (1.10, 1.72) for group 3 and 1.38 (1.10, 1.72) for group 4 among men, and 1.03 (0.87, 1.22), 1.30 (1.05, 1.62) and 1.43 (0.99, 2.05) among women after adjusting for age, systolic/diastolic BP, body mass index, triglycerides, total cholesterol, diabetes, smoking, alcohol drinking, physical activity, and occupation. One standard deviation increase in SUA corresponded to around 30% ACS risk increase in women (HR=1.33; 1.04 –1.70) and 60% in men (HR=1.59; 1.25–2.03). Baseline SUA level independently predicts the development of ACS and should be considered as a potential risk factor of ACS.


2014 ◽  
Vol 14 (4) ◽  
pp. 271-276 ◽  
Author(s):  
Inna A. Rozumenko ◽  
Victoria Y. Garbusova ◽  
Yurij A. Ataman ◽  
Alexey V. Polonikov ◽  
Alexander V. Ataman

2007 ◽  
Vol 50 (3) ◽  
pp. S73-S74
Author(s):  
B.C. Drumheller ◽  
J. Ayan ◽  
D.A. Peress ◽  
C.I. Song ◽  
M.E. Dubon ◽  
...  

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Se-Jun Park ◽  
Kyoung Hwa Ha ◽  
Dae Jung Kim

Abstract Background The “obesity paradox” has not been elucidated in the long-term outcomes of acute coronary syndrome (ACS). We investigated the association between obesity and cardiovascular (CV) outcomes in ACS patients with and without diabetes. Methods We identified 6978 patients with ACS aged 40–79 years from the Korean National Health Insurance Service-Health Screening Cohort between 2002 and 2015. Baseline body mass index (BMI) was categorized as underweight (< 18.5 kg/m2), normal weight (18.5–22.9 kg/m2), overweight (23.0–24.9 kg/m2), obese class I (25.0–29.9 kg/m2), and obese class II (≥ 30.0 kg/m2). The primary outcome was major adverse CV events (MACE)—CV death, myocardial infarction (MI), and stroke. The secondary outcomes were the individual components of MACE, hospitalization for heart failure (HHF), and all-cause death. Results After adjustment for confounding variables, compared to normal-weight patients without diabetes (reference group), obese class I patients with and without diabetes had a lower risk of MACE, but only significant in patients without diabetes (with diabetes: hazard ratio [HR] 0.95, 95% confidence interval [CI] 0.78–1.14; without diabetes: HR 0.78, 95% CI 0.62–0.97). Obese class II patient with diabetes had a higher risk of MACE with no statistical significance (HR 1.14, 95% CI 0.82–1.59). Underweight patients with and without diabetes had a higher risk of MACE, but only significant in patients with diabetes (with diabetes: HR 1.79, 95% CI 1.24–2.58; without diabetes: HR 1.23, 95% CI 0.77–1.97). Conclusion In ACS patients, obesity had a protective effect on CV outcomes, especially in patients without diabetes.


2021 ◽  
Vol 138 ◽  
pp. 11-19
Author(s):  
Seshika Ratwatte ◽  
Karice Hyun ◽  
Mario D'Souza ◽  
Jennifer Barraclough ◽  
Derek P. Chew ◽  
...  

2009 ◽  
Vol 55 (11) ◽  
pp. 2040-2048 ◽  
Author(s):  
Yen-Hsing Chen ◽  
Timothy G Yandle ◽  
A Mark Richards ◽  
Suetonia C Palmer

Abstract Background: The sources of secretion and clearance of plasma urotensin II (UII) in the human circulation remain uncertain and may be relevant to understanding the role of UII in human physiology and cardiovascular disease. Methods: In 94 subjects undergoing clinically indicated cardiac catheterization, we collected blood samples from arterial and multiple venous sites to measure transorgan gradients of plasma UII immunoreactivity. Results: Net UII release occurred (in descending order of proportional transorgan gradient) across the heart, kidney, head and neck, liver, lower limb, and pulmonary circulations (P &lt; 0.01). Although no specific clearance site was localized, the absence of an overall subdiaphragmatic aorto-caval peptide gradient indicated that there were lower body segment sites of UII clearance as well as secretion. The proportional increase in UII immunoreactivity was significantly correlated across all sites of net peptide release within an individual (P ≤ 0.05). In univariate analyses, mixed venous UII concentrations were correlated with diagnosis of acute coronary syndrome and femoral artery oxygen tension and inversely with systolic blood pressure and body mass index. Diagnosis of acute coronary syndrome and body mass index were independent predictors of mixed venous UII immunoreactivity in multivariate analysis. No correlates of net cardiac UII release were identified. Conclusions: UII is secreted from the heart and multiple other tissues into the circulation. Related increments in UII immunoreactivity across multiple tissue sites suggest that peptide release occurs via a shared mechanism. Increased UII immunoreactivity is observed in subjects with acute coronary syndrome.


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