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Little is known about the etiology of acute liver failure (ALF) in Latin America. The objective of this paper is to investigate the main etiologies of ALF in Brazil, including Drug Induced Liver Injury (DILI) using stringent causality criteria.
All the cases of individuals who underwent liver transplantation (LT) in 12 centers in Brazil for ALF were reviewed. When DILI was stated as the cause of ALF, causality criteria were applied on site by the main investigator in order to rule out other etiologies.
325 individuals had ALF mainly for unknown reasons (34%), DILI (27%) and AIH (18%). Reassessment of the 89 cases of DILI, using stringent causality criteria, revealed that in only 42 subjects could DILI be confirmed as the cause of ALF. Acetaminophen (APAP) toxicity (n=3) or DILI due to herbal and dietary supplements (HDS) (n=2) were not commonly observed.
Undetermined etiology and DILI are the main causes of ALF in Brazil. However, APAP toxicity and DILI due to HDS are mostly uncommon.
Undetermined etiology and DILI are the main causes of ALF in Brazil. However, APAP toxicity and DILI due to HDS are mostly uncommon.
The relationship between obesity and arterial stiffness is complex, with a potential interaction by age (inverse association at younger age and positive at older age) and conflicting reports on the effect of lifestyle-based weight loss on arterial stiffness. Little is understood about post-bariatric surgery changes in arterial stiffness. This study aimed to examine post-bariatric surgery changes in arterial stiffness and identify factors associated with greater changes in arterial stiffness.
In 72 patients (mean age 44.5 years, 72.2% female), we evaluated two arterial stiffness measures, cardio-ankle vascular index (CAVI) and heart-ankle pulse wave velocity (haPWV), one month prior to and 6 months after bariatric surgery. Another follow-up visit was conducted 12 months after bariatric surgery in a subset of 58 participants.
Six months after bariatric surgery, an evident decrease was seen in body mass index, heart rate, and systolic blood pressure. In contrast, both CAVI and haPWV significantly increased at 6 months (+0.64 [0.42, 0.87] and +0.24 [0.04, 0.44] m/s, respectively). Among 58 patients with relevant data, CAVI and haPWV remained elevated 12 months after bariatric surgery (+0.80 [0.53, 1.07] and +0.40 [0.17, 0.62] m/s, respectively). Being non-diabetic and having larger decreases in post-surgery heart rate were independently associated with greater increases in post-surgical CAVI.
Arterial stiffness measures, CAVI and haPWV, were elevated after bariatric surgery despite other favorable cardiometabolic changes. Further studies are necessary to elucidate the underlying mechanism and prognostic implications of this elevation in arterial stiffness measures after bariatric surgery.
Arterial stiffness measures, CAVI and haPWV, were elevated after bariatric surgery despite other favorable cardiometabolic changes. Further studies are necessary to elucidate the underlying mechanism and prognostic implications of this elevation in arterial stiffness measures after bariatric surgery.
Shocks near defibrillation threshold (nDFT) strength commonly extinguish all ventricular fibrillation (VF) wavefronts, but a train of rapid, well-organized postshock activations (PAs) typically appears before sinus rhythm ensues. If one of the PA waves undergoes partial propagation block (wavebreak), reentry may be induced, causing VF to reinitiate and the shock to fail.
The purpose of this study was to determine whether wavebreak leading to VF reinititation following nDFT shocks occurs preferentially at the right ventricular insertion (RVI), which previous studies have identified as a key site for wavebreak.
We used panoramic optical mapping to image the ventricular epicardium of 6 isolated swine hearts during nDFT defibrillation episodes. After each experiment, the hearts were fixed and their geometry scanned with magnetic resonance imaging (MRI). The MRI and mapping datasets were spatially coregistered. For failed shocks, we identified the site of the first wavebreak of a PA wave during VF reinitiation.
We recorded 59 nDFT failures. In 31 of these, the first wavebreak event occurred within 1 cm of the RVI centerline, most commonly on the anterior side of the right ventricular insertion (aRVI) (23/31). The aRVI region occupies 16.8% ± 2.5% of the epicardial surface and would be expected to account for only 10 wavebreaks if they were uniformly distributed. By χ
analysis, aRVI wavebreaks were significantly overrepresented.
The anterior RVI is a key site in promoting nDFT failure. Targeting this site to prevent wavebreak could convert defibrillation failure to success and improve defibrillation efficacy.
The anterior RVI is a key site in promoting nDFT failure. Targeting this site to prevent wavebreak could convert defibrillation failure to success and improve defibrillation efficacy.
Atrial fibrillation (AF) and heart failure (HF) often accompany one another, and each is independently associated with poor outcomes. However, the association between AF burden and outcomes is poorly understood.
The purpose of this study was to describe the association between device-based AF burden and HF clinical outcomes.
We used a nationwide, remote monitoring database of cardiac implantable electronic devices (CIEDs) linked to Medicare claims. We included patients with nonpermanent AF, undergoing new CIED implant, stratified by baseline HF. The outcomes were new-onset HF, HF hospitalization, and all-cause mortality at 1 and 3 years.
We identified 39,710 patients who met inclusion criteria (25,054 with HF; 14,656 without HF). Patients with HF were younger (mean age 76.3 vs 78.5 years; P <.001), more often male (65% vs 54%; P <.001), and had higher mean CHA
DS
-VASc scores (5.4 vs 4.1; P <.001). Among those without HF, increasing device-based AF burden was significantly associated with increased risk of new-onset HF (adjusted hazard ratio [HR] 1.09 per 10% AF burden; 95% confidence interval [CI] 1.06-1.12; P <.001) and all-cause mortality (adjusted HR 1.05 per 10% AF burden; 95% CI 1.01-1.10; P = .012). Lanraplenib mouse Among patients with HF, increasing AF burden was significantly associated with increased risk of HF hospitalization (adjusted HR 1.05 per 10% AF burden; 95% CI 1.04-1.06; P <.001) and all-cause mortality (adjusted HR 1.06 per 10% AF burden; 95% CI 1.05-1.08; P <.001).
Among older patients with AF receiving a CIED, increasing AF burden is significantly associated with increasing risk of adverse HF outcomes and all-cause mortality.
Among older patients with AF receiving a CIED, increasing AF burden is significantly associated with increasing risk of adverse HF outcomes and all-cause mortality.
Website: https://www.selleckchem.com/products/lanraplenib.html
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