Atherosclerotic cardiovascular disease (ASCVD) risk calculators estimate the 10-year incident risk of myocardial infarction (MI), coronary artery disease (CAD) death, or stroke; however, they lack comprehensiveness and accuracy. Carotid intima-media thickness (CIMT) is a surrogate marker that may improve risk estimation acumen. The objective of this study was to derive ASCVD risk scores from historical data and determine whether these risk scores are associated with the history of subclinical CAD and CIMT.
View Article and Find Full Text PDFObjective: Coronary artery disease (CAD) prediction remains inconsistent with many unappreciated risk factors. Haptoglobin genotype determines the haptoglobin protein's effectiveness to bind free hemoglobin and prevent oxidative stress, a contributor to atherosclerosis. The haptoglobin 2-2 genotype increases the prevalence of cardiovascular disease (CVD) approximately five times compared to the 1-1 genotype in individuals with diabetes.
View Article and Find Full Text PDFThe complex interplay of increased atherogenic lipoproteins, inflammation, and immune activation hallmarks the pathogenesis of atherosclerotic cardiovascular disease (ASCVD). Atherosclerotic cardiovascular disease remains a leading cause of death, yet risk estimator tools lack comprehensiveness for genetic/inflammatory biomarkers associated with ASCVD. Unexplained ASCVD risk necessitates a better understanding of primary, secondary, and tertiary prevention variables.
View Article and Find Full Text PDFHealthcare workers experience moral injury (MI), a violation of their moral code due to circumstances beyond their control. MI threatens the healthcare workforce in all settings and leads to medical errors, depression/anxiety, and personal and occupational dysfunction, significantly affecting job satisfaction and retention. This article aims to differentiate concepts and define causes surrounding MI in healthcare.
View Article and Find Full Text PDFClin Med Insights Cardiol
April 2023
Background: Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of death worldwide and is poorly predicted with current risk estimation tools. The biological mechanisms relating ASCVD risk factors to oxidative stress (OS) and how this accumulates ASCVD risk are misunderstood.
Purpose: To develop a comprehensive conceptual model explaining how expanded clinical, social, and genetic ASCVD risk factors accumulate ASCVD risk through OS.