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| http://dx.doi.org/10.1097/CM9.0000000000000996 | DOI Listing |
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Non-persistence with multiple secondary prevention medications for peripheral arterial disease among older hypertensive patients.
Front Pharmacol
December 2024
School of Pharmacy, University of Eastern Finland, Kuopio, Finland.
Introduction: The benefit of secondary prevention in hypertensive patients with peripheral arterial disease (PAD) is based on continual simultaneous taking of statins, antiplatelet agents and antihypertensive agents, preferably angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs). Our study was aimed at a) the analysis of the extent of non-persistence with multiple medication classes, and b) identifying factors associated with the likelihood of non-persistence.
Methods: In our cohort study, 3,401 hypertensive patients (1,853 females and 1,548 males) aged ≥65 years treated simultaneously with statins, antiplatelet agents and ACEIs/ARBs and in whom PAD was newly diagnosed during 2012 were analysed.
De Novo Hypercalcaemia in a Patient With Chronic Hypoparathyroidism.
Cureus
December 2024
Endocrinology, Mallow General Hospital/University College Cork, Cork, IRL.
Calcium Homeostasis in the human body is regulated by hormones, including parathyroid hormone and vitamin D3. Dysfunction in the form of hypoparathyroidism causes hypocalcaemia. In patients treated for primary hypoparathyroidism with activated vitamin D replacement, iatrogenic hypercalcaemia can occur.
View Article and Find Full Text PDFAngiotensin Receptor-Neprilysin Inhibitor in Heart Failure Patients With Renal Dysfunction.
Cardiovasc Ther
January 2025
Department of Cardiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Heart failure (HF) and renal dysfunction often coexist and interact in many complex and bidirectional pathways, leading to detrimental effects on patient outcomes. The treatment of HF patients with renal dysfunction presents a significant clinical challenge. Interestingly, sacubitril/valsartan, an angiotensin receptor-neprilysin inhibitor (ARNI), may have beneficial effects on cardiac and renal outcomes in patients with HF with reduced ejection fraction, particularly by slowing the rate of decrease in the estimated glomerular filtration rate compared to a single angiotensin-converting enzyme inhibitor.
View Article and Find Full Text PDFEarly genetic screening and cardiac intervention in patients with cardiomyopathies in a multidisciplinary clinic.
ESC Heart Fail
December 2024
Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada.
Aims: Patients with cardiomyopathies are a heterogeneous group of patients who experience high morbidity and mortality. Early cardiac assessment and intervention with access to genetic counselling in a multidisciplinary Cardiomyopathy Clinic may improve outcomes and prevent progression to advanced heart failure.
Methods And Results: Our prospective cohort study was conducted at a multidisciplinary Cardiomyopathy Clinic with 421 patients enrolled (42.
ATM/ATR-Mediated DNA Damage Response Facilitates SARS-CoV-2 Spike Protein-Induced Syncytium Formation.
J Med Virol
January 2025
Tianjin Key Laboratory of Radiation Medicine and Molecular Nuclear Medicine, State Key Laboratory of Advanced Medical Materials and Devices, Institute of Radiation Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China.
Multinucleated cells are present in lung tissues of patients infected by SARS-CoV-2. Although the spike protein can cause the fusion of infected cells and ACE2-expressing cells to form syncytia and induce damage, how host cell responses to this damage and the role of DNA damage response (DDR) signals in cell fusion are still unclear. Therefore, we investigated the effect of SARS-CoV-2 spike protein on the fusion of homologous and heterologous cells expressing ACE2 in vitro models, focusing on the protein levels of ATR and ATM, the major kinases responding to DNA damage, and their substrates CHK1 and CHK2.
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