121 research outputs found

    Expert opinion of the Heart Failure Association of the Polish Society of Cardiology, the College of Family Physicians in Poland, and the Polish Society of Family Medicine on the peri discharge management of patients with heart failure

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    Despite advances in the treatment of heart failure (HF), the rate of hospitalisation for exacerbations of the disease remains high. One of the underlying reasons is that recommended guidelines for the management of HF are still too rarely followed in daily practice. Disease exacerbation requiring inpatient treatment is always a factor that worsens the prognosis, and thus signals disease progression. This is also a key moment when therapy should be modified for HF exacerbation, or initiated in the case of newly diagnosed disease. Inpatient treatment and the peri‑discharge period is the time when the aetiology and mechanism of HF decompensation should be established. Therapy should be individualised based on aetiology, HF phenotype, and comorbidities; it should take into account the possibilities of modern treatment. According to the recommendations of the European Society of Cardiology (ESC), patients with HF should receive multidisciplinary management. Cooperation between the various members of the multidisciplinary team taking care of patients with HF improves the efficiency and quality of treatment. This document expands and details the information on the peri‑discharge management of HF contained in the 2021 ESC guidelines and the 2022 American Heart Association (AHA)/American College of Cardiology (ACC)/Heart Failure Society of America (HFSA) guidelines

    Rationale and design of the ESC Heart Failure III Registry - Implementation and discovery

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    AIMS Heart failure outcomes remain poor despite advances in therapy. The European Society of Cardiology Heart Failure III Registry (ESC HF III Registry) aims to characterize HF clinical features and outcomes and to assess implementation of guideline-recommended therapy in Europe and other ESC affiliated countries. METHODS Between 1 November 2018 and 31 December 2020, 10 162 patients with chronic or acute/worsening HF with reduced, mildly reduced, or preserved ejection fraction were enrolled from 220 centres in 41 European or ESC affiliated countries. The ESC HF III Registry collected data on baseline characteristics (hospital or clinic presentation), hospital course, diagnostic and therapeutic decisions in hospital and at the clinic visit; and on outcomes at 12-month follow-up. These data include demographics, medical history, physical examination, biomarkers and imaging, quality of life, treatments, and interventions - including drug doses and reasons for non-use, and cause-specific outcomes. CONCLUSION The ESC HF III Registry will provide comprehensive and unique insight into contemporary HF characteristics, treatment implementation, and outcomes, and may impact implementation strategies, clinical discovery, trial design, and public policy

    Association of Mitochondrial DNA Variations with Lung Cancer Risk in a Han Chinese Population from Southwestern China

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    Mitochondrial DNA (mtDNA) is particularly susceptible to oxidative damage and mutation due to the high rate of reactive oxygen species (ROS) production and limited DNA-repair capacity in mitochondrial. Previous studies demonstrated that the increased mtDNA copy number for compensation for damage, which was associated with cigarette smoking, has been found to be associated with lung cancer risk among heavy smokers. Given that the common and “non-pathological” mtDNA variations determine differences in oxidative phosphorylation performance and ROS production, an important determinant of lung cancer risk, we hypothesize that the mtDNA variations may play roles in lung cancer risk. To test this hypothesis, we conducted a case-control study to compare the frequencies of mtDNA haplogroups and an 822 bp mtDNA deletion between 422 lung cancer patients and 504 controls. Multivariate logistic regression analysis revealed that haplogroups D and F were related to individual lung cancer resistance (OR = 0.465, 95%CI = 0.329–0.656, p<0.001; and OR = 0.622, 95%CI = 0.425–0.909, p = 0.014, respectively), while haplogroups G and M7 might be risk factors for lung cancer (OR = 3.924, 95%CI = 1.757–6.689, p<0.001; and OR = 2.037, 95%CI = 1.253–3.312, p = 0.004, respectively). Additionally, multivariate logistic regression analysis revealed that cigarette smoking was a risk factor for the 822 bp mtDNA deletion. Furthermore, the increased frequencies of the mtDNA deletion in male cigarette smoking subjects of combined cases and controls with haplogroup D indicated that the haplogroup D might be susceptible to DNA damage from external ROS caused by heavy cigarette smoking
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