This year promises to be an important turning point for the Pacific Lipid Association (PLA). Our goal is to reinvigorate our membership through greater opportunities to serve the PLA and National Lipid Association (NLA). This can only be done by improving member communication and engaging our membership in activities that are both personally rewarding and promote the mission and goals of the PLA/NLA.
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CASE STUDY
This case has unanswered questions but shows how a cardiologist and nurse practitioner who became certified lipid specialists create a team approach for their patient.
MS. TAYLOR AND DR. GREENFIELD:
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Inflammation is a dynamic process with many interconnected signaling pathways involving multiple classes of cells by which the human body responds to pathogen exposure and/or tissue damage, playing a central role in all stages of atherosclerosis. (1) Cholesterol crystals directly activate nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome and interleukin 1 beta (IL-1β) production.
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Along with lipid accumulation, inflammation plays a key role in the development of atherosclerosis.(1) Perhaps 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG CoA reductase) inhibitors (statins) are effective in the prevention of atherosclerotic cardiovascular disease (ASCVD) because they significantly decrease low-density lipoprotein (LDL) particles and inflammation.
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Atherosclerosis is widely recognized as a chronic inflammatory disorder. Therapies with anti-inflammatory effects in patients with an increased inflammatory status can reduce cardiovascular events, as the CANTOS study showed.(1) Inflammatory markers are an essential tool for evaluating a patient’s inflammatory state. The question is: which biomarker is best?
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Differentiating Biological Targets for Cardiovascular Risk Reduction from Risk Assessment Tools
Cardiovascular disease (CVD) remains the leading cause of mortality across the globe. The cornerstones of CVD prevention and treatment are accurate risk assessment — such that the intensity of preventive treatment matches the magnitude of absolute risk — and targeting biological markers that are known to mediate CV risk, respectively.
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Introduction
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The “response to retention” model of atherosclerosis holds up as the present and best narrative explanation for the initiation and propagation of atherosclerotic cardiovascular disease (ASCVD).(1) As you know, this model posits that the passage of apolipoprotein B (apoB)-containing lipoproteins (LP) triggers the initiation of the atheroma.
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I am honored to have the opportunity to work with you all in promoting education, service and quality improvement efforts in clinical lipidology and preventive cardiology as this year’s President of the Pacific Lipid Association.
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“Knowing is not enough; we must apply. Willing is not enough; we must do.” This remark by Goethe introduces readers to the rationale for the Institute of Medicine of the National Academies Committee on Standards for Developing Trustworthy Clinical Practice Guidelines: Guidelines We Can Trust 2011.
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President, National Lipid Association Director, Division of Cardiology
Advocate Lutheran General Hospital
Co-Director, Cardiology Service Line
Advocate Medical Group
Clinical Associate Professor
Loyola Stritch School of Medicine
Park Ridge, IL
Diplomate, American Board of Clinical Lipidology


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