Seo JH, Abd T, George RT, Mittal R. A coupled chemo-fluidic computational model for thrombogenesis in infarcted left ventricles. Am J Physiol Heart Circ Physiol 310: H1567-H1582, 2016. First published March 25, 2016; doi:10.1152/ajpheart.00855.2015.-A coupled chemo-fluidic computational model for investigating flowmediated thrombogenesis in infarcted left ventricles (LVs) is proposed. LV thrombus (LVT) formation after the acute myocardial infarction (AMI) may lead to thromboembolic events that are associated with high mortality and morbidity, and reliable stratification of LVT risk is the key to managing the treatment of AMI patients. There have been several studies emphasizing the importance of LV blood flow patterns on thrombus formation; however, given the complex interplay between ventricular flow dynamics and biochemistry of thrombogenesis, current understanding is mostly empirical. In the present model, blood flow in the LV is obtained by solving the incompressible Navier-Stokes equations, and this is coupled to the biochemical modeling of the coagulation cascade, platelet activation, and fibrinogen polymerization. The coupled model is used to examine the effect of ventricular flow patterns on thrombogenesis in modeled ventricles. It is expected that the method developed here will enable in-depth studies of thrombogenesis in patient-derived infarcted LV models. computational hemodynamics; cardiac flow; intraventricular flow; blood clot; coagulation cascade; biochemical reaction NEW & NOTEWORTHY A computational method that simultaneously resolves the left ventricular flow patterns as well as the biochemical coagulation cascade (CC) is proposed. The method enables a clear identification of the effect of flow patterns on left ventricular thrombogenesis and suggests a metric quantitatively correlated to thrombogenic risk.ONE OF THE MOST FEARED COMPLICATIONS for patients with acute myocardial infarction (AMI) is the occurrence of thromboembolic events associated with left ventricular (LV) thrombus (LVT) formation (11) and cardioembolic strokes, which account for 20 -30% of all ischemic strokes (25,27,33). The identification of high-risk patients and the pharmacological prevention of LVT formation are the keys to preventing these embolic events. Thrombus formation results from the combination of disturbed blood flow patterns, endothelial injury, and hypercoagulability of the endothelium. After AMI, LV regional wall akinesia or dyskinesia changes the patterns of blood flow in the LV, and this can result in local stasis of blood flow (3). Prolonged ischemia also leads to subendocardial tissue injury with inflammatory changes and may lead to the development of a LV aneurysm (30, 34), which may cause further abnormalities in LV flow. Furthermore, patients with acute coronary syndrome show a hypercoagulable state with increased concentrations of prothrombin and fibrinopeptide (11). The above prerequisites in the LV with AMI lead to the formation of LVT composed of fibrin, platelets, and red blood cells.Risk factors f...
Pharmacogenetics uses the genetic variation in metabolic pathways to identify groups of patients who may respond differently in terms of therapeutic and adverse effects. Much clinical interest lies in drug metabolism and the opportunity to improve prescribing efficacy and safety. Owing to widespread use and increasing concern regarding side effects, statins are of significant interest in this area. Among other benefits, statins have been shown to improve lipid profiles and reduce coronary heart disease event rates in many populations. However, variability in drug response exists, and genetic variability may be a contributing factor. Our primary goal is to feature the most important genes involved in lipid metabolism, clinical outcomes, and statin-induced side effects, highlighting genome-wide association studies and the candidate gene approach.
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