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Real-world medical user profile, treatment method styles along with patient-reported outcomes inside a subset involving HR+/HER2- advanced breast cancer patients along with poor prognostic elements: files via a global review.
Introduction Inherited cardiovascular diseases are an important cause of sudden cardiac death (SD). The use of risk scores identify high risk patients who would benefit from an implantable cardioverter-defibrillators (ICDs). The development of automated devices for out-of-hospital cardiac arrest improves early resuscitation. The objective of the study is to quantify prevented SD and the neurological recovery of patients with inherited cardiovascular diseases. Methods Two hundred fifty-seven cases of SD (age 42 ± 18 years, 79.4% men) of non-ischemic cardiac cause were prospectively collected during the study period (2009-17). Fifty three (20.6%) had a resuscitated cardiac arrest (RCA) (age 40 ± 18 years, 64.2% male). Epidemiological, clinical and autopsy aspects were analyzed. Prevented SD was defined as a combination of RCA and appropriate ICD therapy cases. Results An autopsy was performed in 157/204 (77.0%) cases who died. There were 19 (12.1%) cases with a negative autopsy. The diagnosis of cardiomyopathy and channelopathy was 58.0 and 18.7%, respectively. Female sex and confirmed or suspected channelopathy were associated with successful resuscitation. The percentage of prevented SD remained low during the study period (mean 35.6%). 60.4% of RCA cases presented good neurological outcome. There was no association between neurological recovery and therapeutic hypothermia, but there was association with time of resuscitation (min). Conclusion A fifth part of non-ischemic cardiac arrests were resuscitated. Female sex and channelopathies were more prevalent among RCA. Two thirds of RCA had a good neurological recovery.Recent evidence indicates that a large proportion of deaths from coronavirus disease 2019 (COVID-19) can be attributed to cardiovascular disease, including acute myocardial infarction, arrhythmias and heart failure. Indeed, severe infection increases the risk of heart failure among patients with COVID-19. In most patients, heart failure arises from complex interactions between pre-existing conditions, cardiac injury, renin-angiotensin system activation, and the effects of systemic inflammation on the cardiovascular system. In this review, we summarize current knowledge regarding pathogen-driven heart failure occurring during treatment for COVID-19, the potential effects of commonly used cardiovascular and anti-infective drugs in these patients, and possible directions for establishing a theoretical basis for clinical treatment.Peroxiredoxin 2 (PRDX2), an inhibitor of reactive oxygen species (ROS), is potentially involved in the progression of atherosclerosis (AS). The aim of this study was to explore the role and mechanism of PRDX2 in AS. The expression of PRDX2 was evaluated in 14 human carotid artery tissues with or without AS. The results showed that the positive reaction of PRDX2 was observed in the carotid artery vascular smooth muscle cells (CAVSMCs). To assess the mechanism by which PRDX2 may function in AS, the CAVSMCs were transfected with pEX4-PRDX2 and si-PRDX2. The catalase, hydrogen peroxide (H2O2) scavenger, was used to further confirm that PRDX2-induced inhibitory effects might be mediated through reducing ROS levels. Phenotype alteration and functional testing included transcription testing, immunostaining, and expression studies. The drug of MAPK signaling pathway inhibitors SB203580, SP600125, and PD98059 was used to evaluate the underlying mechanism. In this study, we found that the protein level of PRDX2 and the level of H2O2 were higher in the human AS carotid artery tissues than in the normal carotid artery tissues, accompanied with the activation of MAPK signaling pathway. The up-regulation of PRDX2 in the CAVSMCs significantly decreased the expression of ROS, collagen type I (COL I), collagen type III (COL III), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) and inhibited the proliferation, migration, and transformation of the CAVSMCs. The up-regulation of PRDX2 reversed the effect of the CAVSMCs treated with tumor necrosis factor-α (TNF-α). In addition, PRDX2 down-regulation promoted the protein levels of p-p38, p-JNK, and p-ERK, which was confirmed in relevant MAPK inhibitor treatment experiments. Our results suggest a protective role of PRDX2, as a scavenger of ROS, in AS progression through inhibiting the VSMC phenotype alteration and function via MAPK signaling pathway.Thrombotic angiopathy is a pathologic description to describe endothelial injury, and with sufficient and sustained injury can lead to exposure of underlying tissue factor and the deposition of associated fibrin material. We present briefly a case of an 87-year-old woman with mitral valve regurgitation and atrial fibrillation undergoing mitral valve annuloplasty, Cox-maze procedure, and excision of the left atrial appendage. Pathologic examination of the excised atrial appendage revealed commonly encountered cardiomyocyte hypertrophy and endocardial fibroelastosis, however also showed a non-occlusive, acute thrombotic angiopathy involving epicardial veins. The surgical and immediate post-operative course was unremarkable; however, 3 weeks after discharge, the patient would develop a fatal pulmonary embolism. While fibrin thrombosis developing within the atrial appendage chamber is a recognized concern in the setting of atrial fibrillation, the significance of an acute thrombotic angiopathy involving epicardial veins of the atrial appendage is less clear although in the presented case was the sole potential harbinger of a subsequent fatal thrombotic event.Introduction Patients with type 2 diabetes mellitus are at high risk to develop vascular complications resulting in high morbidity and mortality. Cocoa flavanols are promising nutraceuticals with possible beneficial vascular effects in humans. However, limited research is currently available on the vascular effects in a diabetic population with inconsistent results. Possible reasons for this inconsistency might be heterogeneity in the given intervention (dose per time and day, single dose vs. split-dose, placebo formula) and the studied population (blood pressure at baseline, duration of diabetes, use of vasoactive antihypertensive and antidiabetic drugs, sex). Inavolisib Therefore, we aimed to develop a randomized, double-blinded, placebo-controlled cross-over trial to investigate whether cocoa flavanols have an acute impact on blood pressure and vascular reactivity in patients with type 2 diabetes with and without arterial hypertension. Methods and Analysis We will include participants in four groups (i) patients with type 2 diabetes without arterial hypertension, (ii) patients with type 2 diabetes with arterial hypertension and 1 antihypertensive drug, (iii) non-diabetic participants with essential hypertension and 1 antihypertensive drug, and (iv) healthy controls.
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