scholarly journals Dyslipidemia Management in Patients with Coronary Artery Disease. Data from the POLASPIRE Survey

2021 ◽  
Vol 10 (16) ◽  
pp. 3711
Author(s):  
Piotr Jankowski ◽  
Paweł Kozieł ◽  
Małgorzata Setny ◽  
Marlena Paniczko ◽  
Maciej Haberka ◽  
...  

Lipid-lowering in patients with coronary artery disease (CAD) is related to a lower risk of cardiovascular events. We evaluated factors related to the management of hypercholesterolemia in patients with established CAD. Patients were interviewed 6–18 months after hospitalization for an acute coronary syndrome (ACS) or a myocardial revascularization procedure. Statins were prescribed at discharge to 94.4% of patients, while 68.1% of the patients hospitalized for an ACS were prescribed a high-dose statin. Hospitalization in a teaching hospital, percutaneous coronary intervention, cholesterol measurement during hospitalization and the male sex were related to prescription of statins at discharge. The intensity of lipid-lowering therapy in the post-discharge period increased in 17.3%, decreased in 11.7%, and did not change in 71.0% of the patients. The prescription of a lipid-lowering drug (LLD) at discharge (odds ratio 5.88 [95% confidence intervals 3.05–11.34]) and a consultation with a cardiologist (2.48[1.51–4.08]) were related to the use of LLDs, while age (1.32 [1.10–1.59] per 10 years), loneliness (0.42[0.19–0.94]), professional activity (1.56[1.13–2.16]), and diabetes (1.66[1.27–2.16]) were related to achieving an LDL cholesterol goal 6–18 months after discharge. In conclusion, health-system-related factors are associated with the LLD utilization, whereas mainly patient-related factors are related to the control of hypercholesterolemia following hospitalization for CAD.

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.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
H Yamamoto ◽  
H Otake ◽  
T Shinke ◽  
T Yamashita ◽  
H Kawamori ◽  
...  

Abstract Background Diabetes mellitus has been known as an important factor of coronary artery disease (CAD) progression despite of widespread with lipid-lowering therapy. Although we have reported that large glucose fluctuation is associated with the development of cardiovascular disease in both diabetes mellitus (DM) and non-DM patients, the underlying mechanisms remain unclear. Monocytes play a key role for atherosclerotic plaque formation. Monocytes in human peripheral blood are divided into three subsets: CD14++CD16− monocytes, CD14++CD16+ monocytes, and CD14+CD16++ monocytes. The CD14++CD16+ monocyte subset has recently received attention because it is reported to be associated with future cardiovascular events such as acute myocardial infarction. However, their impact on coronary plaque vulnerability in coronary artery disease (CAD) patients with or without DM remains unclear. Purpose The aim of this study was to investigate the impact of CD14++CD16+ monocyte levels on coronary plaque vulnerability and glucose fluctuation in stable CAD patients with well-regulated lipid levels. Methods This prospective observational study included 50 consecutive patients with CAD (DM [n=22], Non-DM [n=28]), receiving lipid-lowering therapy and undergoing coronary angiography and optical coherence tomography (OCT). Patients were divided into 3 tertiles according to the CD14++CD16+ monocyte percentages assessed by flow cytometry. Standard OCT parameters including lipid arc, lipid length, fibrous cap thickness (FCT) on lipid rich plaque, were assessed for 97 angiographically intermediate lesions (diameter stenosis: 30–70%). The presence of thin-cap fibroatheroma (TCFA), defined as a thin fibrous cap (<65μm) overlying a lipid-rich plaque (>90°), was also assessed. Daily glucose fluctuation assessed by using continuous glucose monitoring system was analyzed by measuring the mean amplitude of glycemic excursion (MAGE). Results CD14++CD16+ monocytes negatively correlated with FCT on lipid rich plaque (r=0.508, p<0.01) (Figure. 1). The presence of thin-cap fibroatheroma (TCFA) was increased stepwise according to the tertile of CD14++CD16+ monocytes (0 [tertile 1] vs. 5 [tertile 2] vs. 10 [tertile 3], p<0.01). CD14++CD16+ monocytes were a significant determinant of TCFA (OR 1.279, p=0.001). Although CD14++CD16+ monocytes were not significantly correlated with MAGE in DM patients (r=0.259, p=0.244), a significant relationship was found between CD14++CD16+ monocytes and MAGE in non-DM patients (r=0.477, p=0.018) (Figure 2). Conclusions CD14++CD16+ monocytes were associated with coronary plaque vulnerability in CAD patients with well-regulated lipid levels both in DM and non-DM patients. Cross-talk between glucose fluctuation and CD14++CD16+ monocytes may enhance plaque vulnerability, particularly in non-DM patients. CD14++CD16+ monocytes could be a possible therapeutic target for coronary plaque stabilization.


Atherosclerosis: pathophysiology 212Development of atherosclerotic plaques 214Epidemiology 216Assessment of atherosclerotic risk 218Risk factors for coronary artery disease 220Hypertension 226Treatment of high blood pressure 228Combining antihypertensive drugs 230Lipid management in atherosclerosis 232Lipid-lowering therapy 236When to treat lipids ...


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