The leaflets of the mitral valve interact with the mitral jet and significantly impact diastolic flow patterns, but the effect of mitral valve morphology and kinematics on diastolic flow and its implications for left ventricular function have not been clearly delineated. In the present study, we employ computational hemodynamic simulations to understand the effect of mitral valve leaflets on diastolic flow. A computational model of the left ventricle is constructed based on a high-resolution contrast computed-tomography scan, and a physiological inspired model of the mitral valve leaflets is synthesized from morphological and echocardiographic data. Simulations are performed with a diode type valve model as well as the physiological mitral valve model in order to delineate the effect of mitral-valve leaflets on the intraventricular flow. The study suggests that a normal physiological mitral valve promotes the formation of a circulatory (or “looped”) flow pattern in the ventricle. The mitral valve leaflets also increase the strength of the apical flow, thereby enhancing apical washout and mixing of ventricular blood. The implications of these findings on ventricular function as well as ventricular flow models are discussed.
Individuals widely use non-nutritive sweeteners (NNS) in attempts to lower their overall daily caloric intake, lose weight, and sustain a healthy diet. There are insufficient scientific data that support the safety of consuming NNS. However, recent studies have suggested that NNS consumption can induce gut microbiota dysbiosis and promote glucose intolerance in healthy individuals that may result in the development of type 2 diabetes mellitus (T2DM). This sequence of events may result in changes in the gut microbiota composition through microRNA (miRNA)-mediated changes. The mechanism(s) by which miRNAs alter gene expression of different bacterial species provides a link between the consumption of NNS and the development of metabolic changes. Another potential mechanism that connects NNS to metabolic changes is the molecular crosstalk between the insulin receptor (IR) and G protein-coupled receptors (GPCRs). Here, we aim to highlight the role of NNS in obesity and discuss IR-GPCR crosstalk and miRNA-mediated changes, in the manipulation of the gut microbiota composition and T2DM pathogenesis.
Background-Catheter ablation of ventricular tachycardia (VT) is still one of the most challenging procedures in cardiac electrophysiology, limited, in part, by unmappable arrhythmias that are nonsustained or poorly tolerated. Calculation of the inverse solution from body surface potential mapping (sometimes known as ECG imaging) has shown tremendous promise and can rapidly map these arrhythmias, but we lack quantitative assessment of its accuracy in humans. We compared inverse solution mapping with computed tomography-registered electroanatomic epicardial contact catheter mapping to study the resolution of this technique, the influence of myocardial scar, and the ability to map VT. Methods and Results-For 4 patients undergoing epicardial catheter mapping and ablation of VT, 120-lead body surface potential mappings were obtained during implantable defibrillator pacing, catheter pacing from 79 epicardial sites, and induced VT. Inverse epicardial electrograms computed using individualized torso/epicardial surface geometries extracted from computed tomography images were compared with registered electroanatomic contact maps. The distance between estimated and actual epicardial pacing sites was 13±9 mm over normal myocardium with no stimulus-QRS delay but increased significantly over scar (P=0.013) or was close to scar (P=0.014). Contact maps during right ventricular pacing correlated closely to inverse solution isochrones. Maps of inverse epicardial potentials during 6 different induced VTs indicated areas of earliest activation, which correlated closely with clinically identified VT exit sites for 2 epicardial VTs. Conclusions-Inverse solution maps can identify sites of epicardial pacing with good accuracy, which diminishes over myocardial scar or over slowly conducting tissue. This approach can also identify epicardial VT exit sites and ventricular activation sequences. (Circ Arrhythm Electrophysiol. 2012;5:1001-1009.)
Moderate (32°C) therapeutic hypothermia demonstrated superior and near-complete cardioprotection compared with 35°C and control, warranting further investigation into clinical applications.
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