Objectives: Postinfarction left ventricular free-wall rupture (LVFRW) is a rare, unpredictable, and often fatal complication of acute myocardial infarction. We reviewed our surgical experience with post-infarction LVFWR over 25 years to identify risk factors for in-hospital mortality.
Methods: Seventy-two consecutive patients with LVFWR who underwent surgical repair between 1994 and 2023 were retrospectively analyzed.
Non-tuberculous mycobacteria (NTM) is gaining clinical recognition as a recently emerging pulmonary pathogen. complex (MAC), the most common NTM, is the cause of pulmonary MAC disease. Currently, the macrolide azithromycin (AZM) is the standard first-line antibiotic for treatment of the disease.
View Article and Find Full Text PDFBackground And Aims: Addition of the PCSK9 inhibitor, evolocumab, to statin therapy promoted coronary plaque stabilization after an acute coronary syndrome. While apolipoprotein B (ApoB) has been proposed as a goal for lipid-lowering therapy in the prevention of cardiovascular disease, its association with plaque stability has not been studied.
Methods: The High-Resolution Assessment of Coronary Plaques in a Global Evolocumab Randomized Study (HUYGENS) used serial optical coherence tomography to assess coronary plaque phenotypes in patients with non-ST elevation myocardial infarction treated with evolocumab plus statin or placebo plus statin for 52 weeks.
Purpose: This study aimed to investigate the potential therapeutic effects of 5-aminolaevulinic acid (5-ALA) combined with sodium ferrous citrate (SFC) on kidney injury and fibrosis in a mouse model of unilateral ureteral obstruction (UUO)-induced chronic kidney disease (CKD).
Methods: A murine UUO model was used to mimic human CKD. The mice received daily intragastric administration of 5-ALA/SFC for 7 and 14 consecutive days.
Background: The ongoing residual cardiovascular risks despite lowering low-density lipoprotein cholesterol (LDL-C) levels suggest the need to identify additional drivers associated with atherosclerosis. Circulating lipoprotein(a) [Lp(a)]promotes formation of foam cells via its proatherogenic properties. However, whether a lower Lp(a) level in combination with favorable LDL-C control could induce a more stable form of disease remains unknown.
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