Valentina Valenti

Background/Objectives: Anemia and renal impairment are key predictors of adverse outcomes in acute coronary syndromes (ACSs). The hemoglobin-to-creatinine (Hb/Cr) ratio combines these parameters into a simple index. This study aimed to evaluate its prognostic value at discharge in patients with ST-elevation myocardial infarction (STEMI). Methods: The primary endpoint was one-year all-cause mortality; secondary endpoints included major bleeding and the composite of all-cause mortality or reinfarction. Optimal Hb/Cr cut-off values were identified using Liu’s method. Multivariable logistic regression and propensity score matching were used to assess associations with outcomes. Results: We analyzed 11,236 STEMI patients from the PRAISE registry with available hemoglobin and creatinine values at discharge. The optimal cut-points were 13.68 for mortality and 14.42 for secondary endpoints. Patients were stratified into low (p < 0.001). Conclusions: The Hb/Cr ratio is independently associated with one-year adverse outcomes in STEMI and may serve as a simple marker of increased vulnerability. Prospective studies are needed to validate its clinical utility.

Acute chest pain (ACP) is a frequent cause of Emergency Department (ED) admissions, with millions of cases reported globally each year. Timely and accurate diagnosis is crucial due to the wide range of underlying causes, such as acute coronary syndrome (ACS), pulmonary embolism (PE), aortic dissection, and others. Misdiagnosis can lead to missed life-saving interventions or, alternatively, unnecessary hospitalizations, escalating healthcare costs. While risk stratification tools like the HEART, GRACE, and TIMI scores are useful, additional imaging is often required to achieve diagnostic precision. Coronary computed tomography angiography (CCTA) has shown significant potential in enhancing diagnostic accuracy and improving patient outcomes. In this review, we explore the challenges physicians encounter when evaluating ACP in the ED, emphasizing the utility of CCTA as a key diagnostic tool. Additionally, we present a clinical case that illustrates how CT scan effectively aids in diagnosing patients with ambiguous symptoms, with CT imaging playing a pivotal role in identifying the underlying pathology.

Background. Oxidative stress and inflammation are typically implied in atherosclerosis pathogenesis and progression, especially in coronary artery disease (CAD). Our objective was to investigate the oxidative stress and inflammation burden directly associated with atherosclerotic plaque in patients with stable coronary disease undergoing coronary artery bypass graft (CABG) surgery. Specifically, markers of oxidative stress and inflammation were compared in blood samples obtained from the atherosclerotic left anterior descending artery (LAD) and blood samples obtained from the healthy left internal thoracic artery (LITA), used as a bypass graft, within the same patient. Methods. Twenty patients scheduled for off-pump CABG were enrolled. Blood samples were collected from the LITA below anastomosis and the LAD below the stenosis. Samples were analysed for oxidative stress (sNOXdp, H₂O₂, NO) and inflammation markers (TNFα, IL-6, IL-1β, IL-10). Results. The analysis showed a significant increase in oxidative stress burden in the LAD as compared to LITA, as indicated by higher sNOX2-dp and H₂O₂ levels and lower NO levels (p < 0.01). Also, pro-inflammatory cytokines were increased in the LAD as compared to the LITA, as indicated by higher TNFα and IL-6 amounts (p < 0.01). On the other hand, no significant differences could be seen regarding IL-1β and IL-10 levels between the two groups. Conclusions. The oxidative stress and inflammatory burden are specifically enhanced in the LAD artery of stable coronary patients compared to systemic blood from the LITA of stable coronary patients.

We have described a clinical case with atypical onset of sarcoidosis. A young patient presented to the emergency room with acute heart failure and severe cardiac dysfunction simulating dilated cardiomyopathy or severe myocarditis. Hypoxic respiratory failure refractory to oxygen therapy was treated with steroids. The diagnosis was made by a multidisciplinary team who decided to perform EndoBronchial UltraSound-guided TransBronchial Needle Aspiration (EBUS TBNA) in addition to a cardiac MRI. The result was to obtain, in this case, a prompt therapeutic response in order to preserve the patient cardiac function.

Cardiotoxicity has emerged as a major side effect of doxorubicin (DOX) treatment, affecting nearly 30% of patients within 5 years after chemotherapy. Heart failure is the first non-cancer cause of death in DOX-treated patients. Although many different molecular mechanisms explaining the cardiac derangements induced by DOX were identified in past decades, the translation to clinical practice has remained elusive to date. This review examines the current understanding of DOX-induced cardiomyopathy (DCM) with a focus on mitochondria, which were increasingly proven to be crucial determinants of DOX-induced cytotoxicity. We discuss DCM pathophysiology and epidemiology and DOX-induced detrimental effects on mitochondrial function, dynamics, biogenesis, and autophagy. Lastly, we review the current perspectives to contrast the development of DCM, which is still a relatively diffused, invalidating, and life-threatening condition for cancer survivors.

Background: Aging is an independent risk factor for cardiovascular diseases. The autophagy process may play a role in delaying aging and improving cardiovascular function in aging. Data regarding autophagy in atrial fibrillation (AF) patients are lacking. Methods: A post hoc analysis of the prospective ATHERO-AF cohort study, including 150 AF patients and 150 sex- and age-matched control subjects (CS), was performed. For the analysis, the population was divided into three age groups: 70 years. Oxidative stress (Nox2 activity and hydrogen peroxide, H₂O₂), platelet activation (PA) by sP-selectin and CD40L, endothelial dysfunction (nitric oxide, NO), and autophagy parameters (P62 and ATG5 levels) were assessed. Results: Nox2 activity and H₂O₂ production were higher in the AF patients than in the CS; conversely, antioxidant capacity was decreased in the AF patients compared to the CS, as was NO production. Moreover, sP-selectin and CD40L were higher in the AF patients than in the CS. The autophagy process was also significantly impaired in the AF patients. We found a significant difference in oxidative stress, PA, NO production, and autophagy across the age groups. Autophagy markers correlated with oxidative stress, PA, and endothelial dysfunction in both groups. Conclusions: This study provides evidence that the autophagy process may represent a mechanism for increased cardiovascular risk in the AF population.

Cardiovascular disease is the leading cause of death in western countries. Among cardiovascular diseases, myocardial infarction represents a life-threatening condition predisposing to the development of heart failure. In recent decades, much effort has been invested in studying the molecular mechanisms underlying the development and progression of ischemia/reperfusion (I/R) injury and post-ischemic cardiac remodeling. These mechanisms include metabolic alterations, ROS overproduction, inflammation, autophagy deregulation and mitochondrial dysfunction. This review article discusses the most recent evidence regarding the molecular basis of myocardial ischemic injury and the new potential therapeutic interventions for boosting cardioprotection and attenuating cardiac remodeling.