Red cell distribution width (RDW) has been shown to predict adverse outcomes in specific scenarios. We aimed to assess the association between RDW and all-cause death and a clinically relevant composite endpoint in a population with various clinical manifestations of cardiovascular diseases. We retrospectively analyzed 700 patients (median age 72.7 years [interquartile range, IQR, 62.6–80]) admitted to the Cardiology ward between January and November 2016. Patients were divided into tertiles according to baseline RDW values. After a median follow-up of 3.78 years (IQR 3.38–4.03), 153 (21.9%) patients died and 247 (35.3%) developed a composite endpoint (all-cause death, acute coronary syndromes, transient ischemic attack/stroke, and/or thromboembolic events). With multivariate Cox regression analysis, the highest RDW tertile was independently associated with an increased risk of all-cause death (adjusted hazard ratio [HR] 2.73, 95% confidence interval [CI] 1.63–4.56) and of the composite endpoint (adjusted HR 2.23, 95% CI 1.53–3.24). RDW showed a good predictive ability for all-cause death (C-statistics: 0.741, 95% CI 0.694–0.788). In a real-world cohort of patients, we found that higher RDW values were independently associated with an increased risk of all-cause death and clinical adverse cardiovascular events thus proposing RDW as a prognostic marker in cardiovascular patients.

Vitamin D deficiency has a pathogenetic and prognostic role in coronary artery disease and a key role in pain transmission. Diabetic patients have a higher risk of silent myocardial ischemia (SMI) due to diabetic neuropathy. We evaluated the correlation between SMI and Vitamin D serum levels in type 2 diabetic patients and assessed whether SMI patients had a worse survival rate than their symptomatic counterpart. We enrolled 253 patients admitted in our Cardiology Unit and compared them with 50 healthy volunteers. We created three sub-groups: symptomatic MI group (125, 32.4%); SMI group (78, 25.7%), and no-MI group (50, 41.9%). 25(OH)D levels (nmol/L) were lower in the SMI group (34.9 ± 5.8) compared to those in the symptomatic MI (49.6 ± 6.1; p = 0.01), no MI (53.1 ± 6.2; p = 0.001), and control groups (62.1 ± 6.7; p = 0.0001). 25(OH)D levels predicted SMI in diabetic patients, with an inverted odds ratio of 1.11 (p = 0.01). Symptomatic MI group survival was higher than the SMI one (6-year survival rate: 83 vs. 69%; p = 0.01). Diabetic patients with SMI had a higher mortality risk and showed lower 25(OH)D levels than the symptomatic group. This suggests the crucial role that vitamin D has in the pathogenesis of SMI.

Long COVID-19 (LC) is a poorly understood, multifactorial condition that persists for at least three months following SARS-CoV-2 infection. The underlying pathophysiological mechanisms responsible for the wide range of associated symptoms—including fatigue, brain fog, and respiratory issues—remain unclear. However, emerging evidence suggests that the reactivation of latent viral infections, such as Epstein-Barr virus, cytomegalovirus, and varicella-zoster virus, may significantly contribute to the complexity of LC. These latent viruses can be reactivated by SARS-CoV-2, contributing to a chronic inflammatory state that prolongs symptomatology. This review confirms the potential involvement of latent viral infections in LC and examines whether these infections play an independent role or act synergistically with other factors. In addition, recent studies have highlighted viral persistence and immune dysregulation as key elements in LC. Our findings suggest that preventative strategies, including vaccination and antiviral treatments during the acute phase of COVID-19, show potential in reducing LC risk by preventing viral reactivation. However, tailored diagnostic and therapeutic strategies targeting these latent infections are urgently needed. Identifying biomarkers of viral reactivation, particularly for high-risk populations, could be considered another effective strategy to mitigate LC severity. Further research is crucial to better understand the interactions between SARS-CoV-2 and latent infections, and to improve the prevention and treatment of LC.

Il cor triatrium destro (CTD), anomalia congenita in cui l’atrio sinistro è settato da una membrana in due parti, è un rilievo estremamente raro: in centri ad alti volumi la prevalenza è inferiore allo 0.01% (1). Il cor triatriatum destro è spesso associato ad alter anomalie congenite quali anomalie della valvola polmonare, il ventricolo destro ipoplasico, l’anomalia di Ebstein, i difetti del setto inter–atriale (DIA) (2,3). Quando la settazione è incompleta può essere asintomatico e riscontrato accidentalmente all’esame ecocardiografico (4). Descrizione del caso: A dicembre 2022 un uomo di 55 anni, affetto da fibrillazione atriale parossistica e sintomatico per cardiopalmo e dispnea (EHRA II),si ricoverava per ablazione dell’aritmia. Non venivano rilevati segni di scompenso cardiaco e gli esami del sangue erano normali. All’esame obiettivo si auscultava un soffio sistolico continuo. All’esame ecocardiografico (TTE) si evidenziava un DIA ed una membrana che divideva in modo incompleto l’atrio destro in due parti. Si sospettava un CTD o una valvola di Eustachio prominente. All’ecocardiogramma trans esofageo 3D (TEE) si mostrava una membrana non ostruttiva che divideva l’atrio destro in una camera superiore ed una camera inferiore, compatibile con CTD (Figura 1 e 3). Si confermava la lieve dilatazione dell’atrio destro ed il DIA ostium secundum (Figura 2 e 3) con un flusso eccentrico di 0.7 cm2 di area, shunt sinistro – destro non significativo (Qp/Qs 0.9). Non si indicava la chiusura ma follow–up clinico ed ecocardiografico poichè la funzione e le dimensioni del ventricolo destro e le pressioni polmonari erano normali. Per il riscontro di una formazione trombotica nell’auricola sinistra, ridotte velocità di svuotamento e smock–effect, si indicava una strategia e l‘ablazione veniva posticipata.

BACKGROUND: Vitamin D deficiency has a pathogenetic and prognostic role in coronary artery disease. Moreover, Vitamin D has a key role in pain modulation and transmission. Diabetic patients have a high risk of silent myocardial ischemia (SMI), due to diabetic neuropathy. We aimed to evaluate the correlation between SMI and Vitamin D serum levels in a population of type 2 diabetic patients and to assess whether SMI patients had a worse survival than their symptomatic counterpart.METHODS: In this retrospective, cross-sectional, observational study, we enrolled 253 patients admitted in Policlinico of Modena Hospital and compared them with 50 healthy volunteers. We divided the 253 patients into three sub-groups: symptomatic MI group (125, 32.4%); SMI (78, 25.7%), and no-MI one (50, 41.9%). The entire population had a 25-hydroxyvitamin D (25(OH)D) measurement. RESULTS: 25(OH)D levels (nmol/l) were lower in SMI group (34.9 ± 5.8) respect to symptomatic MI (49.6 ± 6.1; p = 0.01); no MI (53.1 ± 6.2; p = 0.001) and control group (62.1 ± 6.7; p = 0.0001). 25(OH)D level was the only independent variable able to influence the development of SMI in diabetic patients, with an inverted odd-ratio of 1.11 (p = 0.01). Symptomatic MI group had better survival than SMI one (6-year survival rate: 83 vs. 69%; p = 0.01)CONCLUSIONS: Type 2 diabetic with SMI had a higher mortality risk and showed lower 25(OH)D levels than the symptomatic group. This suggests the crucial vitamin D role in the pathogenesis of SMI.