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Cracking the Code of Calcification: How Presence and Burden among Intracranial Arteries Influence Stroke Incidence and Recurrence.
AJNR Am J Neuroradiol
January 2025
University of Padova (M.C.); University of Bologna (M.O.A.); Department of Radiology (R.C, R.S., L.S.), Azienda Ospedaliero Universitaria (A.O.U.) di Cagliari, Cagliari, Sardegna, Italy; Department of Neurology and Stroke Program (S.C.), University of Maryland School of Medicine, Baltimore, Maryland, United States; CVPath Institute (R.V.), Gaithersburg, Maryland, United States; Department of Radiology (G.DR.), Azienda San Camillo Forlanini, Rome, Lazio, Italy; Department of Epidemiology (D.B.), Erasmus Medical Center, Rotterdam, South Holland, Netherlands; Department of Radiology and Nuclear Medicine (D.B.), Erasmus Medical Center, Rotterdam, South Holland, Netherlands; Mayo Clinic (L.S.), Rochester, Minnesota, United States.
Background: Intracranial atherosclerosis accounts for about 8% of all strokes in Western societies but the influence of arterial calcification on plaque instability is a topic on ongoing debate.
Purpose: Explore the association between the presence and burden of calcium in atherosclerotic plaques among intracranial arteries with the risk of clinical or silent stroke events through a systematic review and meta-analysis.
Data Sources: Adhering to PRISMA guidelines, studies from PubMed and Embase were analyzed up to May 2024.
Clinical Diagnosis and Differential Diagnosis Between CSF1R- and AARS2-Related Leukoencephalopathy.
J Mol Neurosci
January 2025
Department of Neurology, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Science/Peking Union Medical College, Beijing, 100730, China.
CSF1R-related leukoencephalopathy (CSF1R-L) and AARS2-related leukoencephalopathy (AARS2-L) were two disease entities sharing similar phenotype and even pathological changes. Although clinically, radiologically, and pathologically similar, they were caused by mutation of two different genes. As the rarity of the two diseases, the differential diagnosis of them was difficult.
View Article and Find Full Text PDFCardiovascular-Liver-Metabolic Health: Recommendations in Screening, Diagnosis, and Management of Metabolic Dysfunction-Associated Steatotic Liver Disease in Cardiovascular Disease via Modified Delphi Approach.
Circulation
January 2025
Division of Cardiology, Department of Medicine, Emory Clinical Cardiovascular Research Institute; and Emory University School of Medicine, Atlanta, GA (L.S.S.).
There is a new awareness of the widespread nature of metabolic dysfunction-associated steatotic liver disease (MASLD) and its connection to cardiovascular disease (CVD). This has catalyzed collaboration between cardiologists, hepatologists, endocrinologists, and the wider multidisciplinary team to address the need for earlier identification of those with MASLD who are at increased risk for CVD. The overlap in the pathophysiologic processes and parallel prevalence of CVD, metabolic syndrome, and MASLD highlight the multisystem consequences of poor cardiovascular-liver-metabolic health.
View Article and Find Full Text PDFA Novel Polymer Film to Develop Heart Valve Prostheses.
Polymers (Basel)
November 2024
Icon Lab Gmbh Ltd., 1 Barrikad St., Nizhny Novgorod 603003, Russia.
Polymer heart valves are a promising alternative to bioprostheses, the use of which is limited by the risks of calcific deterioration of devitalized preserved animal tissues. This is especially relevant in connection with the increasingly widespread use of transcatheter valves. Advances in modern organic chemistry provide a wide range of polymers that can replace biological material in the production of valve prostheses.
View Article and Find Full Text PDFThe Role of Dietary Magnesium in Cardiovascular Disease.
Nutrients
December 2024
Center for Magnesium Education and Research, Pahoa, HI 96778, USA.
In the past 20 years, a large number of epidemiological studies, randomized controlled trials, and meta-analyses have found an inverse relationship between magnesium intake or serum magnesium and cardiovascular disease, indicating that low magnesium status is associated with hypertension, coronary artery calcification, stroke, ischemic heart disease, atrial fibrillation, heart failure, and cardiac mortality. Controlled metabolic unit human depletion-repletion experiments found that a mild or moderate magnesium deficiency can cause physiological and metabolic changes that respond to magnesium supplementation, which indicates that these types of deficiencies or chronic latent magnesium deficiency are contributing factors to the occurrence and severity of cardiovascular disease. Mechanisms through which a mild or moderate magnesium deficiency can contribute to this risk include inflammatory stress, oxidative stress, dyslipidemia and deranged lipid metabolism, endothelial dysfunction, and dysregulation of cellular ion channels, transporters, and signaling.
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