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Heart Rate Variability and Eating Disorders
Published in Herbert F. Jelinek, David J. Cornforth, Ahsan H. Khandoker, ECG Time Series Variability Analysis, 2017
Changes in the autonomic function in the cardiovascular system can be assessed from various aspects of the electrocardiogram (ECG). The simplest of these is measurement of QT intervals. Bradycardia is a common observation in AN patients with longer QT and corrected QT intervals (QTc) than in age- and sex-matched controls and regression to the mean with recovery (Cooke and Chambers 1995). Here correction for heart rate was done as it most often is, using Bazett's correction (QTc=QT/sqrtRR), although some controversy exists as to the reliability of this correction in all cases and it can overestimate the number of patients with QT prolongation (Sagie et al. 1993). A meta-analysis of 10 studies, which examined heart rate and alterations in QT interval, found that while the QTc intervals tended to be longer in AN patients than in the corresponding controls, these differences did not reach statistical significance (Lesinskiene et al. 2008). QT interval prolongation may not have such good predictive value in recognizing patients who are at particular risk of sudden death (Jauregui-Garrido and Jauregui-Lobera 2012). QT intervals in patients with eating disorders are generally <600 ms, a duration that has been clearly associated with significant risk of sudden death (Jackman et al. 1988). While QT interval duration alone may not have good predictive power, Jáuregui-Garrido suggests that increased QT interval dispersion may be an independent predictor of sudden cardiac death, provided it can be measured with sufficient reliability (Jauregui-Garrido and Jauregui-Lobera 2012).
Cytochromes P450, Cardiovascular Homeostasis and Disease
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
Chin Eng Ong, Amelia Dong, Boon Hooi Tan, Yan Pan
EETs also play a key role in ischemia-reperfusion injury (IRI), a condition of exacerbated myocardial damage induced by tissue reperfusion and blood flow restoration after an infarction event (Yellon and Hausenloy, 2007). Studies in recent years demonstrate the protective role of EETs on the heart from IRI (see Fig. 15.2). EETs, when injected directly to the coronary circulation, significantly decreased infarct size and myocardial remodeling in animal IRI models (Gross et al., 2007). Another study showed that EETs or a dual-acting compound possessing EET mimetic and sEH inhibitory properties was able to reduce infarct size and preserve left ventricular developed pressure (LVDP) when administered to isolated mouse hearts (Batchu et al., 2011). The attenuation of deleterious electrocardiographic changes (such as ST elevation and QT prolongation) and mitochondrial damage (increased mitochondrial T-tube fragmentation and swelling) were also noted following ischemia-reperfusion of the isolated perfused heart (Batchu et al., 2009; Katragadda et al., 2009). Acutely, EETs attenuate apoptosis, preserve mitochondrial structure and function, and promote pro-survival signaling. Chronically, EETs are able to prevent adverse remodeling and help maintain systolic function. These protective effects were blocked by the EET antagonist 14,15-epoxyeicosa-5(Z)-enoic acid. Multiple pathways have been associated with cardioprotective effects of EETs including those of sarcolemmal and mitochondrial potassium channels, p42/p44 mitogen-activated protein kinase (MAPK), and phosphoinositide-3-kinase–protein kinase B (PI3K-AKT) signaling (Katragadda et al., 2009; Seubert et al., 2004), all of which are important components of cardioprotective mechanisms.
COVID-19;-The origin, genetics,and management of the infection of mothers and babies
Published in Egyptian Journal of Basic and Applied Sciences, 2020
Hassan Ih El-Sayyad, Yousef Ka Abdalhafid
The mechanisms of the antiviral actions of both drugs are not understood. However, in vitro studies have shown, a basic lysosomotropic drugs with a pKa of _9.5. They become trapped in acidic endosomes, alkalinizing the organelle, and thereby interfere with the pH-dependent entry of CoVs, through the endolysosomal pathway [114]. Chloroquine may also interfere with glycosylation of the ACE2 CoV cell membrane receptor, thus preventing its binding and cellular entry [115]. When deciding to use a particular medication for SARS-CoV2 during pregnancy, advantages, and potential adverse effects should be taken into account in each individual case. Consequently, even if this drug is not assigned to any FDA category, the effects of its administration during pregnancy are mild and there is no evidence of damage for the fetus or preterm delivery risk. Although kalil et al. [116] reported that chloroquine and hydroxychloroquine are highly tolerated. There are some recorded side effects such as retinopathy, hyperglycemia, neurologic effects, and QT prolongation predicting sign of cardiotoxicity. Other authors such as Divala et al. [117] mentioned that There was no evidence that chloroquine was associated with birth weight, gestational age, neonatal growth, and development, neurological development, and visual acuity in infants.