Endothelial dysfunction, wall thickening and plaque are progressive manifestations of atherosclerosis. Delayed or absent brachial artery dilation after ischemic stimulus has been associated with severity of extracoronary and coronary atherosclerosis. In the current study, we aimed to verify if delayed or absent dilation associates with critical coronary stenosis. We also evaluated the association between coronary stenosis, carotid artery wall thickness and peripheral artery disease. Endothelial function was investigated by flow-mediated dilation of the brachial artery up to 3 min after ischemia, and patients classified as early, late or no dilators. Coronary angiography was performed through transradial or femoral artery approach. Computerized quantitative angiography was used to obtain percent stenosis of all lesions, while the Gensini score was used to evaluate the severity of coronary atherosclerosis. Seventy-four patients were enrolled. Carotid wall thickness and plaque, and peripheral artery disease were detected by ultrasound. Subjects with critical coronary stenosis showed a higher prevalence of delayed or absent dilation (coronary stenosis ≥70 per cent: late dilators 50 per cent, no dilators 35 per cent; coronary stenosis ≤70 per cent : late dilators 27 per cent, no dilators 6 per cent). The Gensini score was progressively higher in late dilators and no dilators compared with early dilators (early: 4.5±13.5; late 17.5±27.1; no 39.7±55.0; P<0.02). Carotid atherosclerosis and peripheral artery disease were more prevalent in subjects with critical coronary stenosis. Delayed or absent dilation associates with coronary stenosis and different degree of coronary atherosclerosis. The kinetic of arterial dilation seems to be relevant as the magnitude of dilation.
The authors show the direct in vitro action of thyroid hormones on RNA-polymerase activity in rat liver mitochondria. 3,5,3' L-triiodothyronine (L-T3) and 3,5,3',5' L-tetraiodothyronine (L-T4) stimulate mitochondrial RNA synthesis without either increasing the permeability of preswollen mitochondria or stimulating the synthesis of the triphosphate ribonucleotides (NTP's). Thyroid hormones do not directly depress mitochondrial RNA hydrolysis. Studies carried out with structural analogues of thyroid hormones indicate the structural specifications of the regulating system of the mitochondrial RNA-polymerase. L-T3 and L-T4 are also effective 'in vitro' on mitochondria obtained from animals undergoing different hormonal and dietary treatments, with the exceptions of those fed with a hypoprotein diet. Thus, the authors suggest the possible intervention of a specific mitochondrial receptor for L-T3 and L-T4.
Cardiovascular diseases represent, to date, the major cause of mortality worldwide. Diagnosis of the most frequent of such disease, Acute Myocardial Infarction (AMI), requires the evaluation of time-series measurement of specific cardiac biomarkers concentration. The aim of this work is to provide the clinicians with a quantitative tool to analyze such time-series, with the final goal of enhancing the diagnostic and prognostic procedures. The proposed approach is based on a novel dynamical model, which synthetically describes the basic mechanisms underlying cardiac troponin (cTnT) release into the plasma after the onset of AMI. Leveraging tools of system identification and a dataset of AMI patients treated at our University Hospital, the model has been assessed as an effective tool to quantify the characteristic release curves observed under different conditions. Furthermore, it has been shown how the devised approach is also suitable in those cases where only partial measurements are available to the clinician, to recover important clinical information. Finally, an Optimal Experimental Design (OED) analysis has been performed in order to gain insights on how to optimize the experimental data collection phase, with potentially relevant implications on both the quality and cost of the diagnosis procedure.
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