RESUMEN
Endogenous endophthalmitis is a rare condition that carries a high risk of vision loss. Risk factors for developing endogenous endophthalmitis include having a systemic source of infection and one or more risk factors for immunosuppression. We present a case of a 34-year-old man with methicillin-resistant Staphylococcus aureus bacteremia and COVID-19 pneumonia who was treated with corticosteroids and subsequently developed endogenous endophthalmitis.
RESUMEN
Background Transcatheter aortic valve replacement (TAVR) is increasingly utilized for most patients with symptomatic severe aortic stenosis. TAVR is linked to enhanced long-term cardiac hemodynamics, reversal of left ventricle (LV) hypertrophy, and improved aortic valve gradients. We present a retrospective observational study assessing cardiac remodeling and valvular flow patterns post-TAVR. Methods Retrospective echocardiographic data were collected, evaluating cardiac function and valvular flow patterns before and after TAVR at a single institution. Data was compiled and statistically analyzed using a paired t-test evaluating variations at approximately 30 days and one-year post-TAVR. Results On echocardiogram 30 days and one-year post-TAVR, there was a reduction in LV mass index from 132 g/m² to 110 g/m² (95%CI: 98-122; p=0.01) and 118 g/m² (95%CI: 102-133; p=0.03), and a reduction in relative wall thickness from 0.54 to 0.49 (95%CI: 0.46-0.52; p=0.05) and 0.44 (95%CI: 0.38-0.49; p=0.03), respectively. Doppler velocity indices (DVI) increased from 0.24 to 0.61 (95%CI: 0.49-0.73; p<0.001) and 0.57 (95%CI: 0.48-0.65; p<0.001). Expected improvement in aortic valve velocities and gradients were observed post-TAVR. Conclusions Following TAVR, LV remodeling can be observed as early as 30 days. This is demonstrated by a reduction in LV mass index and relative wall thickness in conjugation with an anticipated improvement in valvular flow patterns and flow across the aortic valve.
RESUMEN
Stress-induced cardiomyopathy (SIC) is associated with varying etiologies. We present a case of a 65-year-old female with recurrent SIC secondary to seizures who presented in cardiogenic shock requiring mechanical circulatory support using an Impella CP via the right axillary approach.
RESUMEN
Long noncoding RNAs (lncRNAs) are emerging regulators of biological processes in the vessel wall; however, their role in atherosclerosis remains poorly defined. We used RNA sequencing to profile lncRNAs derived specifically from the aortic intima of Ldlr -/- mice on a high-cholesterol diet during lesion progression and regression phases. We found that the evolutionarily conserved lncRNA small nucleolar host gene-12 (SNHG12) is highly expressed in the vascular endothelium and decreases during lesion progression. SNHG12 knockdown accelerated atherosclerotic lesion formation by 2.4-fold in Ldlr -/- mice by increased DNA damage and senescence in the vascular endothelium, independent of effects on lipid profile or vessel wall inflammation. Conversely, intravenous delivery of SNHG12 protected the tunica intima from DNA damage and atherosclerosis. LncRNA pulldown in combination with liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis showed that SNHG12 interacted with DNA-dependent protein kinase (DNA-PK), an important regulator of the DNA damage response. The absence of SNHG12 reduced the DNA-PK interaction with its binding partners Ku70 and Ku80, abrogating DNA damage repair. Moreover, the anti-DNA damage agent nicotinamide riboside (NR), a clinical-grade small-molecule activator of NAD+, fully rescued the increases in lesional DNA damage, senescence, and atherosclerosis mediated by SNHG12 knockdown. SNHG12 expression was also reduced in pig and human atherosclerotic specimens and correlated inversely with DNA damage and senescent markers. These findings reveal a role for this lncRNA in regulating DNA damage repair in the vessel wall and may have implications for chronic vascular disease states and aging.