Background: The advanced lung cancer inflammation index (ALI) is an independent prognostic biomarker used to assess inflammation and nutritional status in various cancers, heart failure, and acute coronary syndromes. This study investigates the prognostic significance of ALI in patients experiencing ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI), comparing its predictive abilities with the established Neutrophil-Lymphocyte Ratio (NLR). Methods: We conducted a retrospective analysis of 1171 patients from the Matrix Registry, encompassing demographic and clinical data for STEMI cases treated with pPCI, and ALI was determined using the formula [serum albumin (g/dL) × body mass index (kg/m²)]/NLR at the time of hospital admission. The primary outcome was all-cause mortality. Results: Of the 1171 patients, 86 died during the follow-up period. Univariate analysis identified age, female gender, smoking, hypertension, diabetes, prior myocardial infarction (PMI), lower left ventricular ejection fraction (LVEF), and reduced ALI as factors associated with mortality. Multivariate analysis confirmed age (HR: 1.1, 95% CI: 1.05–1.11, p < 0.001) and PMI (HR: 2.4, 95% CI: 1.4–4.3, p = 0.001) as prominent independent predictors, alongside ALI (HR: 0.95, 95% CI: 0.92–0.97, p < 0.001) and LVEF (HR: 0.98, 95% CI: 0.97–0.99, p = 0.04). An ALI cut-off of ≤10 indicated a higher mortality risk (HR: 2.3, 95% CI: 1.5–3.7, p < 0.001). The area under the curve for ALI (0.732) surpassed that for NLR (0.685), demonstrating ALI’s superior predictive capability. Conclusions: ALI is an independent prognostic factor for all-cause mortality in STEMI patients undergoing pPCI, showing greater discriminatory power than NLR, particularly in patients with ALI values ≤ 10, who face a 2.3-fold higher mortality risk.

Uric acid (UA) is a potent endogenous antioxidant. However, high concentrations of this molecule have been associated with cardiovascular disease (CVD) and renal dysfunction, involving mechanisms that include oxidative stress, inflammatory processes, and endothelial injury. Experimental and in vitro results suggest that this biomarker behaves like other antioxidants, which can shift from the physiological antioxidant action to a pro-oxidizing effect according to their level and to microenvironment conditions. However, data on patients (general population or CAD cohorts) are controversial, so the debate on the role of hyperuricemia as a causative factor for CVD is still ongoing. Increasing evidence indicates UA as more meaningful to assess CVD in women, even though this aspect needs deeper investigation. It will be important to identify thresholds responsible for UA “biological shift” from protective to harmful effects in different pathological conditions, and according to possible gender-related differences. In any case, UA is a low-tech and inexpensive biomarker, generally performed at patient’s hospitalization and, therefore, easily accessible information for clinicians. For these reasons, UA might represent a useful additive tool as much as a CV risk marker. Thus, in view of available evidence, progressive UA elevation with levels higher than 6 mg/dL could be considered an “alarm” for increased CV risk.

Coronavirus disease 2019 (COVID-19) has quickly become a worldwide health crisis. Although respiratory disease remains the main cause of morbidity and mortality in COVID patients, myocardial damage is a common finding. Many possible biological pathways may explain the relationship between COVID-19 and acute myocardial infarction (AMI). Increased immune and inflammatory responses, and procoagulant profile have characterized COVID patients. All these responses may induce endothelial dysfunction, myocardial injury, plaque instability, and AMI. Disease severity and mortality are increased by cardiovascular comorbidities. Moreover, COVID-19 has been associated with air pollution, which may also represent an AMI risk factor. Nonetheless, a significant reduction in patient admissions following containment initiatives has been observed, including for AMI. The reasons for this phenomenon are largely unknown, although a real decrease in the incidence of cardiac events seems highly improbable. Instead, patients likely may present delayed time from symptoms onset and subsequent referral to emergency departments because of fear of possible in-hospital infection, and as such, may present more complications. Here, we aim to discuss available evidence about all these factors in the complex relationship between COVID-19 and AMI, with particular focus on psychological distress and the need to increase awareness of ischemic symptoms.

Background: Frailty is highly common in older patients (pts) undergoing transcatheter aortic valve replacement (TAVR), and it is associated with poor outcomes. The selection of patients who can benefit from this procedure is necessary and challenging. The aim of the present study is to evaluate outcomes in older severe aortic valve stenosis (AS) pts, selected by a multidisciplinary approach for surgical, clinical, and geriatric risk and referred to treatment, according to frailty levels. Methods: A total of 109 pts (83 ± 5 years; females, 68%) with AS were classified by Fried’s score in pre-frail, early frail, and frail and underwent surgical aortic valve replacement SAVR/TAVR, balloon aortic valvuloplasty, or medical therapy. We evaluated geriatric, clinical, and surgical features and detected periprocedural complications. The outcome was all-cause mortality. Results: Increasing frailty was associated with the worst clinical, surgical, geriatric conditions. By using Kaplan–Meier analysis, the survival rate was higher in pre-frail and TAVR groups (p < 0.001) (median follow-up = 20 months). By using the Cox regression model, frailty (p = 0.004), heart failure (p = 0.007), EF% (p = 0.043), albumin (p = 0.018) were associated with all-cause mortality. Conclusions: According to tailored frailty management, elderly AS pts with early frailty levels seem to be the most suitable candidates for TAVR/SAVR for positive outcomes because advanced frailty would make each treatment futile or palliative.

A marked decline in myocardial infarction (AMI) hospitalizations was observed worldwide during the COVID-19 outbreak. The pandemic may have generated fear and adverse psychological consequences in these patients, delaying hospital access. The main objective of the study was to assess COVID fear through the FCV-19S questionnaire (a self-report measure of seven items) in 69 AMI patients (65 ± 11 years, mean ± SD; 59 males). Females presented higher values of each FCV-19S item than males. Older subjects (>57 years, 25th percentile) showed a higher total score with respect to those in the first quartile. The percentage of patients who responded “agree” and “strongly agree” in item 4 (“I am afraid of losing my life because of the coronavirus”) and 3 (“My hands become clammy when I think about the coronavirus”) was significantly greater in the elderly than in younger patients. When cardiovascular (CV) patients were compared to a previously published general Italian population, patients with CV disease exhibited higher values for items 3 and 4. Measures should be put in place to assist vulnerable and high CV risk patients, possibly adding psychologists to the cardiology team.

Background: Atherosclerosis is a chronic inflammatory disease. The balance between pro- and anti-inflammatory factors, acting on the arterial wall, promotes less or more coronary plaque macro-calcification, respectively. We investigated the association between monocyte phenotypic polarization and CTCA-assessed plaque dense-calcium volume (DCV) in patients with stable coronary artery disease (CAD). Methods: In 55 patients, individual DCV component was assessed by quantitative CTCA and normalized to total plaque volume. Flow cytometry expression of CD14, CD16, CD18, CD11b, HLA-DR, CD163, CCR2, CCR5, CX3CR1 and CXCR4 was quantified. Adhesion molecules and cytokines were measured by ELISA. Results: DCV values were significantly associated, by multiple regression analysis, with the expression (RFI) of CCR5 (p = 0.04), CX3CR1 (p = 0.03), CCR2 (p = 0.02), CD163 (p = 0.005) on all monocytes, and with the phenotypic M2-like polarization ratio, RFI CCR5/CD11b (p = 0.01). A positive correlation with the increased expression of chemokines receptors CCR2, CCR5 and CX3CR1 on subsets Mon1 was also present. Among cytokines, the ratio between IL-10 and IL-6 was found to be strongly associated with DCV (p = 0.009). Conclusions: The association between DCV and M2-like phenotypic polarization of circulating monocytes indicates that plaque macro-calcification in stable CAD may be partly modulated by an anti-inflammatory monocyte functional state, as evidenced by cell membrane receptor patterns.