scholarly journals LIPOPROTEIN(A) INTERACTIONS WITH LOW-DENSITY LIPOPROTEIN CHOLESTEROL AND OTHER CARDIOVASCULAR RISK FACTORS: A CASE-ONLY STUDY OF PREMATURE ACS

2015 ◽  
Vol 31 (10) ◽  
pp. S296
Author(s):  
M. Afshar ◽  
L. Pilote ◽  
L. Dufresne ◽  
J. Engert ◽  
G. Thanassoulis
Keyword(s):  
Risk Factors ◽  
Cardiovascular Risk ◽  
Cardiovascular Risk Factors ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Lipoprotein A

scholarly journals Independent role of low-density lipoprotein cholesterol in subclinical coronary atherosclerosis in the absence of traditional cardiovascular risk factors

2019 ◽  
Vol 20 (8) ◽  
pp. 866-872 ◽  
Author(s):  
Ki-Bum Won ◽  
Gyung-Min Park ◽  
Yu Jin Yang ◽  
Soe Hee Ann ◽  
Yong-Giun Kim ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Risk ◽  
Cardiovascular Risk Factors ◽  
Coronary Atherosclerosis ◽  
Subclinical Atherosclerosis ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol

Abstract Aims Individuals without traditional cardiovascular risk factors (CVRFs) still experience adverse events in clinical practice. This study evaluated the predictors of subclinical coronary atherosclerosis in individuals without traditional CVRFs. Methods and results A total of 1250 (52.8 ± 6.5 years, 46.9% male) asymptomatic individuals without CVRFs who underwent coronary computed tomographic angiography for a general health examination were analysed. The following were considered as traditional CVRFs: systolic/diastolic blood pressure ≥140/90 mmHg; fasting glucose ≥126 mg/dL; total cholesterol ≥240 mg/dL; low-density lipoprotein cholesterol (LDL-C) ≥160 mg/dL; high-density lipoprotein cholesterol <40 mg/dL; body mass index ≥25.0 kg/m2; current smoking status; and previous medical history of hypertension, diabetes, and dyslipidaemia. Subclinical atherosclerosis, defined as the presence of any coronary plaque, was present in 20.6% cases; the incidences of non-calcified, calcified, and mixed plaque were 9.6%, 12.6%, and 2.6%, respectively. Multivariate regression analysis showed that LDL-C level [odds ratio (OR): 1.008; 95% confidence interval (CI): 1.001–1.015], together with age (OR: 1.101; 95% CI: 1.075–1.128) and male sex (OR: 5.574; 95% CI: 3.310–9.388), was associated with the presence of subclinical atherosclerosis (All P < 0.05). LDL-C level was significantly associated with an increased risk of calcified plaques rather than non-calcified or mixed plaques. Conclusion LDL-C, even at levels currently considered within normal range, is independently associated with the presence of subclinical coronary atherosclerosis in individuals without traditional CVRFs. Our results suggest that a stricter control of LDL-C levels may be necessary for primary prevention in individuals who are conventionally considered healthy.

scholarly journals Persistent arterial wall inflammation in patients with elevated lipoprotein(a) despite strong low-density lipoprotein cholesterol reduction by proprotein convertase subtilisin/kexin type 9 antibody treatment

2018 ◽  
Vol 40 (33) ◽  
pp. 2775-2781 ◽  
Author(s):  
Lotte C A Stiekema ◽  
Erik S G Stroes ◽  
Simone L Verweij ◽  
Helina Kassahun ◽  
Lisa Chen ◽  
...  
Keyword(s):  
Cardiovascular Risk ◽  
Arterial Wall ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Lipid Lowering ◽  
Controlled Study ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Lipoprotein A

AbstractAimsSubjects with lipoprotein(a) [Lp(a)] elevation have increased arterial wall inflammation and cardiovascular risk. In patients at increased cardiovascular risk, arterial wall inflammation is reduced following lipid-lowering therapy by statin treatment or lipoprotein apheresis. However, it is unknown whether lipid-lowering treatment in elevated Lp(a) subjects alters arterial wall inflammation. We evaluated whether evolocumab, which lowers both low-density lipoprotein cholesterol (LDL-C) and Lp(a), attenuates arterial wall inflammation in patients with elevated Lp(a).Methods and resultsIn this multicentre, randomized, double-blind, placebo-controlled study, 129 patients {median [interquartile range (IQR)]: age 60.0 [54.0–67.0] years, Lp(a) 200.0 [155.5–301.5] nmol/L [80.0 (62.5–121.0) mg/dL]; mean [standard deviation (SD)] LDL-C 3.7 [1.0] mmol/L [144.0 (39.7) mg/dL]; National Cholesterol Education Program high risk, 25.6%} were randomized to monthly subcutaneous evolocumab 420 mg or placebo. Compared with placebo, evolocumab reduced LDL-C by 60.7% [95% confidence interval (CI) 65.8–55.5] and Lp(a) by 13.9% (95% CI 19.3–8.5). Among evolocumab-treated patients, the Week 16 mean (SD) LDL-C level was 1.6 (0.7) mmol/L [60.1 (28.1) mg/dL], and the median (IQR) Lp(a) level was 188.0 (140.0–268.0) nmol/L [75.2 (56.0–107.2) mg/dL]. Arterial wall inflammation [most diseased segment target-to-background ratio (MDS TBR)] in the index vessel (left carotid, right carotid, or thoracic aorta) was assessed by 18F-fluoro-deoxyglucose positron-emission tomography/computed tomography. Week 16 index vessel MDS TBR was not significantly altered with evolocumab (−8.3%) vs. placebo (−5.3%) [treatment difference −3.0% (95% CI −7.4% to 1.4%); P = 0.18].ConclusionEvolocumab treatment in patients with median baseline Lp(a) 200.0 nmol/L led to a large reduction in LDL-C and a small reduction in Lp(a), resulting in persistent elevated Lp(a) levels. The latter may have contributed to the unaltered arterial wall inflammation.

scholarly journals The Association of Lipoprotein(a) and Intraplaque Neovascularization in Patients With Carotid Stenosis: A Retrospective Study

2021 ◽  
Author(s):  
Shuang Xia ◽  
Weida Qiu ◽  
Liwen Li ◽  
Bo Kong ◽  
Lan Xu ◽  
...  
Keyword(s):  
Risk Factors ◽  
Carotid Stenosis ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Binary Logistic Regression ◽  
Plasma Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Lipoprotein A

Abstract Background: Lipoprotein(a) is increasingly recognised as a major risk factor for atherothrombotic cardiovascular disease. We examined whether plasma lipoprotein(a) concentrations were associated with intraplaque neovascularization (IPN) levels in patients with carotid stenosis and in terms of increasing plaque susceptibility to haemorrhage and rupture. Methods: We included 85 patients diagnosed with carotid stenosis as confirmed using carotid ultrasound who were treated at Guangdong General Hospital. The IPN level was determined using contrast-enhanced ultrasound through the movement of the microbubbles. Univariate and multivariate binary logistic regression analyses were used to determine whether lipoprotein(a) affected IPN levels, and whether lipoprotein(a), cholesterol, triglyceride, and low-density lipoprotein cholesterol affected IPN levels, respectively. Results: Lipoprotein(a) was a significant predictor of higher IPN levels in binary logistic regression before adjusting for other risk factors (P = 0.031, odds ratio [OR]: 1.238, 95% confidence interval [CI]: 1.020,1.503) whereas cholesterol, triglyceride, and low-density lipoprotein cholesterol were not predicators of IPN in univariate analysis. After adjusting for other risk factors, including age, diabetes mellitus, and smoking status, lipoprotein(a) remained statistically significant in predicting IPN (P = 0.012, OR: 1.335, 95% CI: 1.065,1.674). Conclusions: Plasma lipoprotein(a) concentrations were found to be independently associated with higher IPN levels in patients with carotid stenosis, but not cholesterol, triglyceride, or low-density lipoprotein cholesterol. Lowering plasma lipoprotein(a) levels may decrease the risk of cardiovascular and cerebrovascular events.

scholarly journals Assessing the Accuracy of Estimated Lipoprotein(a) Cholesterol and Lipoprotein(a)‐Free Low‐Density Lipoprotein Cholesterol

2022 ◽  
Author(s):  
Weili Zheng ◽  
Michael Chilazi ◽  
Jihwan Park ◽  
Vasanth Sathiyakumar ◽  
Leslie J. Donato ◽  
...  
Keyword(s):  
High Density Lipoprotein ◽  
Particle Number ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Interquartile Range ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Lipoprotein A ◽  
C 50

Background Accurate measurement of the cholesterol within lipoprotein(a) (Lp[a]‐C) and its contribution to low‐density lipoprotein cholesterol (LDL‐C) has important implications for risk assessment, diagnosis, and treatment of atherosclerotic cardiovascular disease, as well as in familial hypercholesterolemia. A method for estimating Lp(a)‐C from particle number using fixed conversion factors has been proposed (Lp[a]‐C from particle number divided by 2.4 for Lp(a) mass, multiplied by 30% for Lp[a]‐C). The accuracy of this method, which theoretically can isolate “Lp(a)‐free LDL‐C,” has not been validated. Methods and Results In 177 875 patients from the VLDbL (Very Large Database of Lipids), we compared estimated Lp(a)‐C and Lp(a)‐free LDL‐C with measured values and quantified absolute and percent error. We compared findings with an analogous data set from the Mayo Clinic Laboratory. Error in estimated Lp(a)‐C and Lp(a)‐free LDL‐C increased with higher Lp(a)‐C values. Median error for estimated Lp(a)‐C <10 mg/dL was −1.9 mg/dL (interquartile range, −4.0 to 0.2); this error increased linearly, overestimating by +30.8 mg/dL (interquartile range, 26.1–36.5) for estimated Lp(a)‐C ≥50 mg/dL. This error relationship persisted after stratification by overall high‐density lipoprotein cholesterol and high‐density lipoprotein cholesterol subtypes. Similar findings were observed in the Mayo cohort. Absolute error for Lp(a)‐free LDL‐C was +2.4 (interquartile range, −0.6 to 5.3) for Lp(a)‐C<10 mg/dL and −31.8 (interquartile range, −37.8 to −26.5) mg/dL for Lp(a)‐C≥50 mg/dL. Conclusions Lp(a)‐C estimations using fixed conversion factors overestimated Lp(a)‐C and subsequently underestimated Lp(a)‐free LDL‐C, especially at clinically relevant Lp(a) values. Application of inaccurate Lp(a)‐C estimations to correct LDL‐C may lead to undertreatment of high‐risk patients.

scholarly journals Gender Difference in Blood Pressure Control and Cardiovascular Risk Factors with Diagnosed Hypertension

2021 ◽  
pp. 275-280
Author(s):  
Tarique Shahzad Chachar ◽  
Ummama Laghari ◽  
Ghullam Mustafa Mangrio ◽  
Abdul Ghaffar Dars ◽  
Ruqayya Farhad ◽  
...  
Keyword(s):  
Risk Factors ◽  
Blood Pressure ◽  
Cardiovascular Risk ◽  
Cardiovascular Risk Factors ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Pressure Control ◽  
Health Sciences ◽  
Low Density Lipoprotein Cholesterol ◽  
Male And Female

Objective: Our study was designed to compare the gender difference in Blood Pressure Control and Cardiovascular Risk Factors in patients of Liaquat University of Medical and Health Sciences Jamshoro Pakistan. Methodology: This cross-sectional study was conducted in  Liaquat University of Medical and Health Sciences Jamshoro Pakistan from December 2019 to December 2020. Blood pressure was measured twice by trained physicians using aneroid sphygmomanometers after a standardized protocol. Patients were asked to sit with both feet on the floor for ≥5 minutes before the first BP measurement. Both the two BP measurements were taken 60 seconds apart.  For this research we defined hypertension as systolic BP ≥140 mm Hg, diastolic BP ≥90 mm Hg. Results:  We conducted a comparison between Hypertensive and nonhypertensive participants of the male and female groups. High blood pressure increased the level of uric acid in both male and female groups (351 ± 92 vs 303 ± 75). We observed that the hypertensive male population reported a high prevalence of cardiovascular risk factors due to  increase amount of total cholesterol level, triglyceride and low-density lipoprotein cholesterol (5.45 ± 1.01, 1.42 ±  0.85,  2.56 ± 0.70) than females (5.15 ± 0.91, 1.29 ± 0.87, 2.30 ± 0.63). Conclusion: Our results concluded that the male hypertensive population is more prone to future cardiovascular risk due to increased amount of total cholesterol levels, triglycerides, and low-density lipoprotein cholesterol, and sex hormones (androgens).

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