The Role of Fasting LDL-C Levels in Their Non-fasting Reduction in Patients With Coronary Heart Disease.
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ABSTRACT:
SUBMITTER: Lin Q
PROVIDER: S-EPMC8241924 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:This study aimed to compare the percentage attainment of fasting and non-fasting LDL-C and non-HDL-C target levels in coronary heart disease (CHD) patients receiving short-term statin therapy. This study enrolled 397 inpatients with CHD. Of these, 197 patients took statins for <1 month (m) or did not take any statin before admission (CHD1 group), while 204 patients took statins for ≥1 m before admission (CHD2 group). Blood lipid levels were measured at 0, 2, and 4 h after a daily breakfast. Non-fasting LDL-C and non-HDL-C levels significantly decreased after a daily meal (P < 0.05). Both fasting and non-fasting LDL-C or non-HDL-C levels were significantly lower in the CHD2 group. The percentage attainment of LDL-C <1.4 mmol/L at 2 and 4 h after a daily breakfast was significantly higher than that during fasting (P < 0.05), but the percent attainment of non-fasting non-HDL-C <2.2 mmol/L was close to its fasting value (P > 0.05). Analysis of c-statistic showed that non-fasting cut-off points for LDL-C and non-HDL-C were 1.19 and 2.11 mmol/L, corresponding to their fasting goal levels of 1.4 and 2.2 mmol/L, respectively. When post-prandial LDL-C and non-HDL-C goal attainments were re-evaluated using non-fasting cut-off points, there were no significant differences in percentage attainment between fasting and non-fasting states. Non-HDL-C is more stable than LDL-C in assessing the percent attainment of non-fasting lipid for coronary heart disease patients. If we want to use LDL-C to assess the percent attainment of post-prandial blood lipids, we may need to determine a lower non-fasting cut-off point.
| S-EPMC8049565 | biostudies-literature
Project description:Background and aimsMany traditional assessments of risk for coronary heart disease (CHD) and diabetes require laboratory studies performed after an 8-h fast. We assessed whether metabolic-syndrome (MetS) severity would remain linked to future CHD and diabetes even when assessed from non-fasting samples.Methods and resultsParticipants in the Atherosclerosis Risk in Communities study were assessed at 4 visits and followed for 20-years of adjudicated CHD outcomes. We used Cox proportional-hazard models (for 20-year CHD outcomes) and logistic regression (for 9-year diabetes outcomes) to compare incident disease risk associated with a race/ethnicity-specific MetS-severity Z-score (MetS-Z) calculated in participants who were fasting (≥8 h) or non-fasting. All analyses were adjusted for sex, race, education, income and smoking. MetS Z-scores were overall similar between participants who were always fasting vs. those non-fasting at Visits 1-3 (all values -0.1 to 0.4), while MetS-Z for participants who were non-fasting at Visit-4 were higher at each visit. Baseline MetS-Z was linked to future CHD when calculated from both fasting and non-fasting measurements, with hazard ratio (HR) for fasting MetS-Z 1.53 (95% confidence interval [CI] 1.42, 1.66) and for non-fasting 1.28 (CI 1.08, 1.51). MetS-Z at Visit-1 also remained linked to future diabetes when measured from non-fasting samples, with odds ratio for fasting MetS-Z 3.10 (CI 2.88, 3.35) and for non-fasting 1.92 (CI 1.05, 3.51).ConclusionsMetS-Z remained linked to future CHD and diabetes when assessed from non-fasting samples. A score such as this may allow for identification of at-risk individuals and serve as a motivation toward interventions to reduce risk.
| S-EPMC7393664 | biostudies-literature
Project description:BackgroundCoronary heart disease (CHD) patients with standard low-density lipoprotein cholesterol (LDL-C) remain at risk of cardiovascular events, making it critical to explore new targets to reduce the residual risk. The relationship between β-sheet conformation and CHD is gaining attention. This study was designed to compare the coronary lesions in CHD patients with varying LDL-C and evaluate whether serum β-sheets are associated with coronary damage.MethodsTwo hundred and one patients diagnosed with stable CHD were recruited and divided into four groups according to LDL-C. Baseline information, coronary lesion-related indicators, and peripheral blood samples were collected. Serum β-sheet content was determined by thioflavin T fluorescence.ResultsThe baseline information was comparable in CHD patients with different LDL-C. No difference was found in indicators relevant to coronary lesions among groups. The content of β-sheet was negatively correlated with LDL-C. Multiple linear regression revealed that serum β-sheet was positively correlated with coronary lesion when risk factors such as age, smoking, and LDL-C were controlled.ConclusionsThis is the first study that reports the serum β-sheet levels of CHD patients being gradually increased with decreasing LDL-C when coronary lesions were comparable. Serum β-sheet might exacerbate the coronary lesions in CHD patients independent of known risk factors such as LDL-C.
| S-EPMC9395970 | biostudies-literature
Project description:Statins lower low-density lipoprotein cholesterol (LDL-C) and improve clinical outcomes in patients with atherosclerotic cardiovascular disease (CVD). Patients with acute coronary syndromes (ACS) often do not achieve LDL-C targets despite potent statin treatment, and have a particularly high risk of early recurrent events. Evolocumab, a proprotein convertase subtilisin/kexin type (PCSK9)-inhibitor resulting in rapid, marked LDL-C reduction, has been studied in hypercholesterolemic subjects without CVD and stabilized patients with CVD; the feasibility, safety, and efficacy of this treatment initiated in the acute phase of ACS remain unknown. We report the design of evolocumab for early reduction of LDL-cholesterol levels in patients with ACS (EVOPACS), a phase-3, multicenter, randomized, double-blind, placebo-controlled trial to assess the feasibility, safety, and LDL-C-lowering efficacy of evolocumab on top of atorvastatin 40 mg in patients with ACS. The primary endpoint is percent change in LDL-C from baseline to 8 weeks. Secondary endpoints are adverse events and serious adverse events. Against a background of beneficial cardiovascular effects of statins beyond LDL-C lowering and in view of preclinical evidence of similar effects of PCSK9 inhibition, the study will also address a variety of exploratory endpoints including the change in C-reactive protein and other inflammatory biomarkers; platelet reactivity; and occurrence of contrast-induced acute kidney injury and myocardial injury in patients undergoing cardiac catheterization. An intracoronary imaging sub-study will investigate the change from baseline in the lipid core burden index in non-culprit lesions, as assessed by serial near-infrared spectroscopy. Recruitment began in January 2018 and enrollment of 308 patients is planned.
| S-EPMC6490138 | biostudies-literature
Project description:Coronary heart disease (CHD) patients who have undergone percutaneous coronary intervention (PCI) have higher rates of depression than the general population. However, few researchers have assessed the impact of depression on the secondary prevention of CHD in China.The main purpose of this investigation was to explore the relationship between depression and secondary prevention of CHD in Chinese patients after PCI.This descriptive, cross-sectional one-site study recruited both elective and emergency PCI patients one year after discharge. Data from 1934 patients were collected in the clinic using questionnaires and medical history records between August 2013 and September 2015. Depression was evaluated by the 9-item Patient Health Questionnaire. Secondary prevention of CHD was compared between depression and non-depression groups.We found that depression affected secondary prevention of CHD in the following aspects: lipid levels, blood glucose levels, smoking status, physical activity, BMI, and rates of medication use.Depressive patients with CHD are at increased risk of not achieving the lifestyle and risk factor control goals recommended in the 2006 AHA guidelines. Screening should focus on patients after PCI because treating depression can improve outcomes by improving secondary prevention of CHD.
| S-EPMC5739347 | biostudies-literature
Project description:To date there is no clear explanation as to how Chlamydia pneumoniae heat shock protein 60 (cHSP60) gets activated either through TLR-2/4, MAPKinase (p38/JNK/ERK), apoptotic/antiapoptotic, chemokines and inflammatory cytokines pathways leading to coronary artery disease (CAD). Hence to better understanding towards cHSP60 signaling in CAD patients, we performed experiments at RNA levels in cHSP60 positive and negative groups of CAD patients. For the determination of positivity for C. pneumoniae, Helicobacter pylori, Cytomegalovirus and Herpes Simplex Virus in atheromatous plaque multiplex Real Time PCR was performed. Monoplex Real Time PCR was also performed with 16S rRNA and HSP60 gene Chlamydia pneumoniae. Further study was performed only on cHSP60 positive (negative for H. pylori, CMV & HSV-1) and cHSP60 negative (also negative for H. pylori, CMV & HSV-1) CAD patients. 1. Patients Forty patients (28 males, 12 females) in age group (51±13 year) attending Department of Cardio Thoracic & Vascular Surgery, Safdarjung Hospital, New Delhi from September 2007 to April 2008 were enrolled in the study. These patients had manifestations of CAD and were undergoing open by-pass heart surgery. Prior written consent was obtained from each patient. The study received clearance from Ethical committee, Safdarjung hospital. Patients who had a recent acute coronary syndrome or transient ischemic attack were not included in our study. 2. Atheroma collection and handling Atheromatous tissue were collected in aseptic conditions and placed in 30 ml transport medium immediately upon resection. Three types of transport medium were used for tissue: viz. Dulbecco?s phosphate-buffered saline (PBS; Gibco Life Technologies, Paisley, Scotland) for DNA, RNA later (Ambion Inc., Woodward st. Austin, Texas, USA) for RNA and optimum cutting temperature compound (Sigma, St. Louis, MO, USA) for protein. 3. Atheroma DNA & RNA isolation and testing Total DNA was isolated for checking the positivity for C. pneumoniae from atheromatous plaques as described earlier [1]. Total RNA from the atheroma samples were isolated using RNeasy fibrous tissue mini kit (Qiagen Sciences, Maryland, USA) and the concentration was determined by a RNA dye-binding assay (Pico-Green, Molecular Probes, Eugene, OR). For cDNA synthesis, RETRO script (Ambion Inc., Woodward st. Austin, Texas, USA) was used as per manufacturer instructions. For detecting positivity for C. pneumoniae, Helicobacter pylori, Cytomegalovirus and Herpes Simplex Virus in atheromatous plaques, multiplex RT-PCR was performed [as describe in reference 1]. Monoplex RT PCR amplification primers and probes were custom designed by Applied Biosystems (Foster City, CA, USA). Briefly, sequences for the 16S rRNA and HSP60 gene of the organisms of interest were aligned and inspected for regions of conserved and variable sequences. 4. Microarray experiment Further study was performed only on cHSP60 positive (negative for H. pylori, CMV & HSV-1) and cHSP60 negative (also negative for H. pylori, CMV & HSV-1) CAD patients. cHSP60 positive samples represented the test samples and cHSP60 negative samples represented the control samples. 3 samples were analysed: samples 17 and 23 were biological replicates of test samples and also performed in duplicate as technical replicates, and sample 26 was a control sample and was also performed in duplicate as a technical replicate. Reference 1. Hem C Jha, Pragya Srivastava, Aabha Divya , Jagdish Prasad, Aruna Mittal. Prevalence of Chlamydophila pneumoniae is higher in aorta and coronary artery than in carotid artery of coronary artery disease patients. APMIS, 2009: 117 (12): 905-911.
2010-05-16 | E-GEOD-19590 | biostudies-arrayexpress
Project description:BackgroundChronic kidney disease (CKD) patients have an increased risk for coronary artery disease (CAD) and myocardial infarction. Therefore, there is a need to identify CKD patients at high risk of CAD. Coronary angiography, the gold standard for detecting CAD, carries a risk of serious adverse events.MethodsHere, we assessed the validity of a novel non-invasive reflectance mode photoplethysmography (PPG) sensor for the evaluation of CAD in patients with advanced CKD. PPG signals were generated using green and infrared wavelengths and recorded from fingers of 98 patients. The detected signal has the shape of the pulse wave contour carrying information about the vascular system, that is, arterial stiffness. We studied four patient groups: (i) controls-patients without CKD or CAD; (ii) CKD alone; (iii) CAD alone (confirmed by coronary angiography); and (iv) CKD and CAD combined.ResultsWith advancing age, we observed a steeper ascending signal during systole and greater signal decline during diastole (infrared wavelength: Slopes 4-6, P = 0.002, P = 0.003 and P = 0.014, respectively; green wavelength: Slopes 2-3, P = 0.006 and P = 0.005, respectively). Presence of CAD was associated with a slower signal decline during diastole in CKD patients compared with those without CAD (infrared wavelength: Slope 1, P = 0.012). CKD was associated with lower blood volume amplitude during each cardiac cycle compared with those without CKD (R-value, P = 0.022).ConclusionsPPG signal analyses showed significant differences between our groups, and it may be a potentially useful tool for the detection of CAD in CKD patients.
| S-EPMC6671527 | biostudies-literature
Project description:BACKGROUND: Bacterial DNA has been repeatedly detected in atheromatous lesions of coronary heart disease (CHD) patients. Phylogenetic signatures in the atheroma lesions that are similar to those of bacterial biofilms on human barrier organs, including the respiratory or gastrointestinal tract, raise the question of a defective barrier function in CHD. NOD2 plays a major role in defense against bacterial invasion. Genetic variation in the CARD15 gene, which encodes NOD2, was previously shown to result in a barrier defect that causes chronic inflammatory disorders (e.g. Crohn disease). In the present study, we investigated the possible involvement of NOD2/CARD15 in the pathology of CHD by i) analyzing the local expression of NOD2 in atherectomy versus healthy tissue (n = 5 each) using histochemical immunofluorescence and ii) by testing the three major functional CARD15 variants (R702W, G908R and 1007fs) for association with early-onset CHD in 900 German patients and 632 healthy controls. RESULTS: In atherectomy tissue of CHD patients, NOD2 was detected in inflammatory cells at the luminal sides of the lesions. However, the allele and genotype frequencies of the three major CARD15 polymorphisms did not differ between CHD patients and controls. CONCLUSION: The NOD2 up-regulation in atheroma lesions indicates an involvement of this protein in the pathology of CHD. Although NOD2 could be important in local immune response mechanisms, none of the analyzed CARD15 variants seem to play a significant role in the etiology of CHD.
| S-EPMC2204032 | biostudies-literature
Project description:BackgroundHarmful effects of long-term exposure to moderately elevated low-density lipoprotein (LDL)-cholesterol and blood pressure on coronary heart disease (CHD) have not been rigorously examined. We estimated the risk of CHD under long-term exposure to moderately elevated LDL-cholesterol and blood pressure compared with the risk under shorter exposures to higher levels of the same risk factors.MethodsObservational study using data from 2,714 adults in Framingham Offspring Study who were free of existing cardiovascular disease and aged <70 years at baseline (1987-1991). We used the parametric g-formula to estimate 16-year CHD risk under different levels and durations of exposure to LDL-cholesterol (low: <130 mg/dL, moderate: 130 to <160 mg/dL, high 160 to <190 mg/dL, and very high: ?190 mg/dL) and systolic blood pressure (low: <120 mmHg, prehypertension: 120 to <140 mmHg, stage 1 hypertension: 140 to <160 mmHg, and stage 2 hypertension: ?160 mmHg).ResultsThe estimated 16-year CHD risk under exposure to low LDL was 8.2% (95% CI = 7.0-9.6). The 16-year CHD risk under exposure to moderate LDL was 8.9% (7.8-10.1) which was similar to CHD risk under 8 years of low LDL followed by 8 years of high LDL at 9.0% (7.7-10.3); and 12 years of low LDL followed by 4 years of very high LDL at 8.8% (7.6-10.1). The results for blood pressure were similar.ConclusionsLong-term exposure to moderate levels of LDL-cholesterol and blood pressure had a similar impact on CHD risk as shorter exposures to levels considered 'high' per clinical guidelines.
| S-EPMC6066205 | biostudies-literature
Project description:To date there is no clear explanation as to how Chlamydia pneumoniae heat shock protein 60 (cHSP60) gets activated either through TLR-2/4, MAPKinase (p38/JNK/ERK), apoptotic/antiapoptotic, chemokines and inflammatory cytokines pathways leading to coronary artery disease (CAD). Hence to better understanding towards cHSP60 signaling in CAD patients, we performed experiments at RNA levels in cHSP60 positive and negative groups of CAD patients. For the determination of positivity for C. pneumoniae, Helicobacter pylori, Cytomegalovirus and Herpes Simplex Virus in atheromatous plaque multiplex Real Time PCR was performed. Monoplex Real Time PCR was also performed with 16S rRNA and HSP60 gene Chlamydia pneumoniae. Further study was performed only on cHSP60 positive (negative for H. pylori, CMV & HSV-1) and cHSP60 negative (also negative for H. pylori, CMV & HSV-1) CAD patients.
2010-01-06 | GSE19590 | GEO