scholarly journals An update on the measurement and management of cholesterol with specific reference to secondary prevention of cardiovascular disease (CVD)

2018 ◽  
Vol 60 (1) ◽  
pp. 15-21 ◽  
Author(s):  
Muhammed Vally ◽  
F Kathrada ◽  
N Butkow
Keyword(s):  
Cardiovascular Disease ◽  
Secondary Prevention ◽  
Serum Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Current Evidence ◽  
Total Serum ◽  
Specific Reference ◽  
Prevention Of Cardiovascular Disease

Cardiovascular disease remains the largest contributor to non-communicable adverse disease outcomes. Treatment and prevention of cardiovascular disease have evolved at a dramatic pace in the last 40 years. Serum-cholesterol has emerged as the dominant risk factor for coronary artery disease and events. The link between serum-cholesterol and arterial atherosclerosis is well documented. The attainment of cholesterol goals has historically concentrated on low-density lipoprotein cholesterol (LDL-C) levels. Current evidence and guidelines have shifted to the attainment of non-HDL-C target levels which represent a more thorough inclusion of small dense atherogenic particles. Methods to reduce serum-cholesterol mainly centre around the use of the HMG CoA-reductase inhibitors also known as the statins. High intensity statins like atorvastatin (80 mg) and rosuvastatin (40 mg) are now the preferred starting therapies to lower cholesterol by at least 40–50% in patients with established cardiovascular disease as secondary prevention. In the event of failure of these medications, evidence suggests that the addition of ezetimibe may enhance the total serum-lowering levels to 50–60%. New therapies aimed at inhibiting PCSK9 revealed exciting new targets for LDL-C lowering, but the high cost of these antibodies could preclude access to this therapeutic intervention. Aggressive pursuit of lower LDL-C or non-high-density lipoprotein cholesterol (non-HDL-C) levels may reduce the incidence of secondary myocardial infarctions, strokes and death from cardiovascular disease.

scholarly journals Low-density lipoprotein cholesterol lowering therapy for the secondary prevention of atherosclerotic cardiovascular disease

2020 ◽  
Vol 2020 (3) ◽  
Author(s):  
Parth N Patel ◽  
Robert P Giugliano
Keyword(s):  
Cardiovascular Disease ◽  
Secondary Prevention ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Blood Cholesterol ◽  
Atherosclerotic Cardiovascular Disease ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Lowering Therapy

Atherosclerotic cardiovascular disease (ASCVD) is highly prevalent and a major contributor to morbidity and mortality worldwide. Elevated blood cholesterol is a key driver of risk for atherosclerotic events, and patients with established ASCVD comprise a specific high-risk population in which low-density lipoprotein cholesterol (LDL-C) lowering therapy is strongly endorsed by multiple guidelines. An increasing number of medications across several pharmacologic classes are available today in clinical practice. Therefore, guidance on the appropriate use of these interventions is necessary for cost-effective solutions to managing residual atherothrombotic risk. In this review we summarize the key evidence supporting LDL-C lowering as described in the most recent 2018 multi-society Blood Cholesterol Guidelines, and provide a framework for optimizing LDL-C lowering therapy in secondary prevention populations.

Effect of serum lipoprotein(a) on estimation of low-density lipoprotein cholesterol by the Friedewald formula

1994 ◽  
Vol 40 (4) ◽  
pp. 571-573 ◽  
Author(s):  
K M Li ◽  
D E Wilcken ◽  
N P Dudman
Keyword(s):  
Serum Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Total Serum ◽  
Total Serum Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Lipoprotein A ◽  
Friedewald Formula

Abstract The calculation of serum low-density lipoprotein cholesterol (LDL-C) by the Friedewald formula does not account for the cholesterol associated with lipoprotein(a) [Lp(a)]. To quantify the contribution of Lp(a) cholesterol to total serum cholesterol, we measured concentrations of serum Lp(a) by an ELISA and concentrations of other serum lipids and lipoproteins by standard assays in 23 normolipemic women, ages 50-60 years. In measuring serum high-density lipoprotein we found that polyethylene glycol 6000 precipitated > 99.8% of all Lp(a). When serum Lp(a) concentrations were < or = 300 mg/L, 301-600 mg/L, and > 600 mg/L, the uncorrected serum LDL-C was overestimated, respectively, by a mean of 4.1% (n = 7), 8.5% (n = 8), and 21.4% (n = 8). Serum Lp(a) concentrations were positively correlated with percentage overestimation (P < 0.001), but were not correlated with either corrected or uncorrected serum LDL-C. We conclude that the Friedewald formula should be modified to take into account the contribution of Lp(a) cholesterol to total serum cholesterol.

Eligibility for PCSK9 inhibitors based on the 2019 ESC/EAS and 2018 ACC/AHA guidelines

2020 ◽  
pp. 204748732094010
Author(s):  
Konstantinos C Koskinas ◽  
Baris Gencer ◽  
David Nanchen ◽  
Mattia Branca ◽  
David Carballo ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
High Risk ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Atherosclerotic Cardiovascular Disease ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Coronary Syndrome ◽  
Coronary Syndromes

Aims The 2018 American College of Cardiology (ACC)/American Heart Association (AHA) and 2019 European Society of Cardiology (ESC)/European Atherosclerosis Society (EAS) lipid guidelines recently updated their recommendations regarding proprotein convertase subtilisin/kexin-9 inhibitors (PCSK9i). We assessed the potential eligibility for PCSK9i according to the new guidelines in patients with acute coronary syndromes. Methods and results We analysed a contemporary, prospective Swiss cohort of patients hospitalised for acute coronary syndromes. We modelled a statin intensification effect and an incremental ezetimibe effect on low-density lipoprotein-cholesterol levels among patients who were not on high-intensity statins or ezetimibe. One year after the index acute coronary syndrome event, treatment eligibility for PCSK9i was defined as low-density lipoprotein-cholesterol of 1.4 mmol/l or greater according to ESC/EAS guidelines. For ACC/AHA guidelines, treatment eligibility was defined as low-density lipoprotein-cholesterol of 1.8 mmol/l or greater in the presence of very high-risk atherosclerotic cardiovascular disease, defined by multiple major atherosclerotic cardiovascular disease events and/or high-risk conditions. Of 2521 patients, 93.2% were treated with statins (53% high-intensity statins) and 7.3% with ezetimibe at 1 year, and 54.9% had very high-risk atherosclerotic cardiovascular disease. Low-density lipoprotein-cholesterol levels less than 1.8 mmol/l and less than 1.4 mmol/l at 1 year were observed in 37.5% and 15.7% of patients, respectively. After modelling the statin intensification and ezetimibe effects, these numbers increased to 76.1% and 49%, respectively. The proportion of patients eligible for PCSK9i was 51% according to ESC/EAS criteria versus 14% according to ACC/AHA criteria. Conclusions In this analysis, the 2019 ESC/EAS guidelines rendered half of all post-acute coronary syndrome patients potentially eligible for PCSK9i treatment, as compared to a three-fold lower eligibility rate based on the 2018 ACC/AHA guidelines.

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