scholarly journals Lipid lowering to delay the progression of coronary artery disease

Heart ◽  
2003 ◽  
Vol 89 (4) ◽  
pp. 451-458 ◽  
Author(s):  
M. D Feher
2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
KA Krychtiuk ◽  
M Lenz ◽  
P Hohensinner ◽  
K Distelmaier ◽  
L Schrutka ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): FWF Background and aims Proprotein convertase subtilisin/kexin type-9 (PCSK9) is an enzyme promoting the degradation of low-density lipoprotein receptors (LDL-R) in hepatocytes. Inhibition of PCSK9 has emerged as a novel target for lipid-lowering therapy. Monocytes are crucially involved in the pathogenesis of atherosclerosis and can be divided into three subsets. The aim of this study was to examine whether circulating levels of PCSK9 are associated with monocyte subsets. Methods We included 69 patients with stable coronary artery disease. PCSK9 levels were measured and monocyte subsets were assessed by flow cytometry and divided into classical monocytes (CD14++CD16-; CM), intermediate monocytes (CD14++CD16+; IM) and non-classical monocytes (CD14 + CD16++; NCM). Results Mean age was 64 years and 80% of patients were male. Patients on statin treatment (n = 55) showed higher PCSK9-levels (245.4 (206.0-305.5) ng/mL) as opposed to those without statin treatment (186.1 (162.3-275.4) ng/mL; p = 0.05). In patients on statin treatment, CM correlated with circulating PCSK9 levels (R = 0.29; p = 0.04), while NCM showed an inverse correlation with PCSK9 levels (R=-0.33; p = 0.02). Patients with PCSK9 levels above the median showed a significantly higher proportion of CM as compared to patients with PCSK-9 below the median (83.5 IQR 79.2-86.7 vs. 80.4, IQR 76.5-85.2%; p = 0.05). Conversely, PCSK9 levels >median were associated with a significantly lower proportion of NCM as compared to those with PCSK9 <median (10.2, IQR 7.3-14.6 vs. 14.3, IQR 10.9-18.7%; p = 0.02). In contrast, IM showed no association with PCSK-9 levels. Conclusions We hereby provide a novel link between PCSK9 regulation, innate immunity and atherosclerotic disease in statin-treated patients.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Joost Besseling ◽  
Gerard K Hovingh ◽  
John J Kastelein ◽  
Barbara A Hutten

Introduction: Heterozygous familial hypercholesterolemia (heFH) is characterized by high levels of low-density lipoprotein cholesterol (LDL-C) and increased risk for premature coronary artery disease (CAD) and death. Reduction of CAD and mortality by statins has not been properly quantified in heFH. The aim of the current study is to determine the effect of statins on CAD and mortality in heFH. Methods: All adult heFH patients identified by the Dutch FH screening program between 1994 and 2014 and registered in the PHARMO Database Network were eligible. Of these patients we obtained hospital, pharmacy (in- and outpatient), and mortality records in the period between 1995 and 2015. The effect of statins (time-varying) on CAD and all-cause mortality was determined using a Cox proportional hazard model, while correcting for the use of other lipid-lowering therapy, thrombocyte aggregation inhibitors, antihypertensive and antidiabetic medication (all time-varying). Furthermore, we used inverse probability for treatment weighting (IPTW) to account for differences between statin-treated and untreated patients regarding history of CAD before follow-up, age at start of follow-up and age of screening, as well as body mass index, LDL-C and triglycerides. Results: Of the 25,479 identified heFH patients, 11,021 gave informed consent to obtain their medical records, of whom 2,447 could be retrieved. We excluded 766 patients younger than 18. The remaining 1,681 heFH patients comprised our study population and these had very similar characteristics as compared to the 23,798 excluded FH patients, e.g. mean (SD) LDL-C levels were 214 (74) vs. 203 (77) mg/dL. Among 1,151 statin users, there were 133 CAD events and 15 deaths during 10,115 statin treated person-years, compared to 17 CAD events and 9 deaths during 4,965 person-years in 530 never statin users (combined rate: 14.6 vs. 5.2, respectively, p<0.001). After applying IPTW to account for indication bias and correcting for use of other medications, the hazard ratio of statin use for CAD and all-cause mortality was 0.61 (0.40 - 0.93). Conclusions: In heFH patients, statins lower the risk for CAD and mortality by 39%.


2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Steven R Gundry ◽  
Jean Epstein

Introduction: Coronary Artery Disease (CAD) is thought to be progressive; standard treatment protocols call for instituting a low fat/low cholesterol diet program, exercise, and lipid lowering agents. This results in an approximate 30-40% new event rate in 5 yrs. We evaluated our treatment strategy to reverse CAD with The Corus Score (CS) (Cardiodx, Redwood City, Ca), proven to quantify coronary artery obstructive plaque by the expression of 23 genes. Methods: Based upon using a Lectin-limited diet to prevent/reverse Metabolic Syndrome and CAD, we have enrolled and followed 800 pts (aged 42-89 yrs) with known CAD, defined as previous MI, stent, CABG, or positive stress test/angiogram, positive CS greater than 30, into a physician coached program, which reduces grains, legumes, nightshades, seeded vegetables, Casein A1 milk, (the all lectin containing food groups),and fruits; emphases consumption a liter of olive oil/wk, large amts of green vegetables, and 4 oz amts of proteins, avoiding commercial poultry (Matrix Protocol). All Apo E 4 genotypes avoided animal fats and cheeses. Pts were instructed to take 4,000 mg of high DHA fish oil, 200mg of Grape Seed Extract, and 25 mg of Pycnogenol per day, and consume polyphenol rich coffee and/or teas and 1 oz dark chocolate/day. Diets/supplements were individualized based on results of Advanced Cardiovascular Risk Markers (ACRM), which were sent to two core labs. Yearly assessment of CAD severity was measured by Corus Score (possible range 1-40). Any score above 30 was assessed by Nuclear Stress testing. Results: Pts have been followed for 1.5 to 6 years (mean 4.5 yrs). Only 6/800 pts (0.5%) have received a new stent, all 6 had rising Corus scores: two also had a rising Lp-PLA2, 2 had rising Cardiac Troponin I levels; one pt required CABG: . There have been no MI’s, unstable angina. Corus scores at baseline decreased from 34+/-4 (range 6-36) to 24+/-3, P<0.01. Only 64/800 pts (8%) had a rise in Corus scores/ 736/800 pts’ CS declined or remained stable (92%). Only 6/64 Corus scores had positive Stress tests. Conclusions: Simple Nutrigenomic-based dietary interventions, based upon ACRM's and Corus Scores, represents a quantum leap forward in preventing/modifying Cardiovascular events in known CAD patients.


2020 ◽  
Vol 1 (3-4) ◽  
pp. 150-153
Author(s):  
Chandramukhi Sunehra ◽  
Krishnaswamy Raghu

A young, 18-year-old lady presented with history of chest pain on exertion typical of angina. General examination revealed multiple tendon xanthomas. Systemic examination was unremarkable. Electrocardiogram showed segment (ST) depression in inferior and lateral leads. Echocardiogram revealed normal left ventricular systolic function and no left ventricular regional wall motion abnormalities. Diastolic flow turbulence was noted in the left main coronary artery and proximal left anterior descending artery on color Doppler interrogation across the coronary arteries. Lipid profile showed unusually high total cholesterol and low-density lipoprotein cholesterol. Subsequent evaluation with coronary angiogram revealed triple vessel coronary artery disease. The patient underwent coronary artery bypass surgery and is on antiplatelet and lipid-lowering drug therapy.


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