Background/Objectives: While acute cardiac injury during COVID-19 is well-documented, the long-term risk of new-onset heart failure (HF) in survivors remains a critical clinical concern. This study aims to quantify the risk of new-onset heart failure during a 25 months prognostic follow-up period following recovery from SARS-CoV-2. Methods: We conducted a systematic review and meta-analysis of nine high-quality studies (n > 400,000 survivors) in accordance with PRISMA 2020 guidelines. Databases including PubMed/MEDLINE and Scopus were searched through January 2026. A quantitative meta-analysis was performed on six studies using a random-effects model to pool adjusted hazard ratios (aHR). Results: The pooled analysis revealed a significant 35% increased risk of new-onset heart failure following COVID-19 recovery (aHR 1.35; 95% CI: 1.14–1.60; p = 0.001). Significant heterogeneity was observed (I² = 92.62%), reflecting diverse risk profiles among survivors. The risk was most pronounced in immunocompromised kidney transplant recipients (aHR 2.32) and younger adults under the age of 65 (aHR 1.53). Subclinical myocardial damage, characterized by reduced left ventricular longitudinal strain, was identified even in survivors who experienced mild initial infections. Conclusions: COVID-19 recovery serves as a significant independent risk factor for chronic heart failure, emphasizing that cardiovascular impact extends far beyond the acute phase. These findings necessitate the implementation of structured cardiovascular monitoring and biomarker screening for at least one year post-infection to address this emerging chronic disease burden.

Background/Objectives: Viral respiratory tract infections (VRTIs) in patients with diabetes mellitus (DM) are characterized by a severity gap rather than an infection gap. This review synthesizes evidence from the 2023–2026 respiratory seasons to provide a post-pandemic framework for managing the synergistic metabolic and viral threats in this population. Materials and Methods: A scoping review of literature from PubMed, Scopus, and Embase (2023–2026) was conducted, focusing on clinical outcomes and mechanistic interactions between DM and emerging respiratory pathogens. Results: Recent data identify human Metapneumovirus (hMPV) and adenovirus as significant threats to diabetic hosts, with mortality risks equivalent to seasonal influenza (HR 1.00 for hMPV vs. influenza). The two-hit model combines a baseline of innate immune paralysis, characterized by impaired neutrophil chemo-taxis and mechanical SP-D dysfunction, with a cellular signaling environment primed for cytokine overreaction by epigenetic metabolic memory. The stress hyperglycemia ratio (SHR) has emerged as a promising predictor of mortality compared to absolute glucose or HbA1c, with a proposed threshold of ≥1.14 identifying patients at 3.5-fold increased risk for mechanical ventilation. Precision management should consider the prudent suspension of SGLT2 inhibitors to mitigate euglycemic DKA risks and considering the early use of GLP-1 receptor agonists for their hypothesized pulmonary anti-inflammatory properties. Conclusions: Closing the mortality gap may require a shift from generic viral care to a precision model that treats metabolic susceptibility with high clinical priority alongside the treatment of the viral pathogen.

Background: Adults hospitalized with COVID-19, influenza A/B, or respiratory syncytial virus (RSV) frequently receive empirical antibiotics, but antibiotic prescribing, confirmed bacterial co-infection, antimicrobial resistance (AMR), and outcomes have not been jointly synthesized across these infections. Methods: We conducted a PRISMA 2020 systematic review and meta-analysis of 39 studies including 839,531 hospitalized adults. Random-effects models with Freeman–Tukey double-arcsine transformation pooled prevalence estimates; sensitivity and publication-bias analyses were performed where appropriate. Results: Pooled antibiotic use was 62.56% (95% CI, 53.75–70.97%) for COVID-19, 57.48% (25.76–86.09%) for influenza A/B, and 76.03% (67.62–83.53%) for RSV, with very high heterogeneity. Confirmed bacterial co-infection was lower: 5.31% (3.43–7.56%), 18.66% (9.98–29.30%), and 24.36% (18.53–30.70%), respectively. Prescribing-to-confirmed infection ratios ranged from 3.0 to 46.2. AMR evidence was restricted to COVID-19 studies and was dominated by carbapenem-resistant Gram-negative organisms, mainly in secondary, ICU-associated, or healthcare-associated infections. Confirmed bacterial complications were associated with ICU admission, longer hospitalization, and higher mortality. Conclusions: Antibiotic prescribing exceeded confirmed bacterial infection across all viral groups, but estimates require cautious interpretation due to heterogeneity, diagnostic uncertainty, observational evidence, and the absence of low-risk-of-bias studies. The evidence base was dominated by COVID-19 cohorts, while influenza A/B and RSV data, especially virus-specific AMR evidence, remain limited. COVID-19-specific AMR findings should not be generalized to influenza A/B or RSV. Virus-specific stewardship should prioritize rapid diagnostics, systematic sampling, reassessment, and de-escalation when bacterial infection is not confirmed.

Background/Objectives: Patients with diabetes face increased risks during viral respiratory infections. While chronic glycemic control (HbA1c) is a known risk factor, it may fail to capture acute metabolic failure. This study aimed to evaluate the stress hyperglycemia ratio (SHR) at two time points (admission and 72 h) as a prognostic marker. Methods: We conducted a longitudinal analysis of 430 patients (211 with diabetes and 219 without diabetes) hospitalized with viral respiratory infections. The SHR was calculated at admission (SHR_z1) and at 72 h (SHR_z3). The primary outcome was severe clinical deterioration (defined as oxygen requirement >2–HFNO/OTI or mortality). Multivariate logistic regression and ROC curve analysis were used to determine independent predictors and clinical cut-off points. Results: In the global multivariable model (N = 430), continuous SHR_z3 emerged as an independent predictor of severe outcome (OR = 1.86, 95% CI 1.09–3.20, p = 0.0240) alongside chronic glycemic control (HbA1c: OR = 1.41, p < 0.0001) and age (OR = 1.05, p = 0.0001). After stratification, the independent SHR_z3 effect attenuated below statistical significance in both the non-diabetic (p = 0.6168) and diabetic (p = 0.1954) sub-cohorts, while HbA1c (p = 0.0404) and age (p = 0.0036) remained independent predictors within the diabetic subgroup. An exploratory longitudinal phenotype model classifying patients into Stable Normal, Resolvers, Persistent, and Late Spikers showed the highest in-sample discrimination of all models tested (AUC = 0.797, 95% CI 0.756–0.834). Within this model, the Persistent phenotype (SHR ≥ 1.1 sustained at admission and at 72 h) showed a non-significant trend toward higher adjusted odds of severe outcome compared with Stable Normal patients (OR = 1.81, 95% CI 0.91–3.60, p = 0.088) and was associated with a significantly longer hospital stay (Kruskal–Wallis p = 0.004 across phenotypes). Conclusions: Persistent stress hyperglycemia at 72 h is an independent predictor of severe outcome in the unstratified cohort after adjustment for chronic glycemic control, age, and other covariates. Within metabolic strata, the SHR_z3 signal attenuates, and long-standing suboptimal glycemic control (HbA1c) and age dominate, particularly among diabetic patients. Longitudinal SHR trajectories may therefore provide complementary, hypothesis-generating prognostic information when combined with chronic baseline markers, although these findings require external validation in independent cohorts before clinical use.

The introduction of respiratory multiplex PCR in the post-pandemic world has improved the detection of viral infections, whose clinical relevance is still being characterized. Patients with diabetes mellitus (DM) exhibit altered innate immune responses, yet the effect of concurrent viral infection on their inflammatory trajectory and clinical outcomes remains poorly characterized. This study examined whether diabetes is associated with a more pronounced inflammatory response, delayed resolution, and worse multi-organ outcomes during viral respiratory infections. A prospective, longitudinal cohort of 430 hospitalized adults (DM: n = 211; non-DM: n = 219) with PCR-confirmed viral respiratory infections was stratified into four groups by diabetes and co-infection status using a respiratory multiplex PCR panel. Serum IL-6, CRP, NLR, procalcitonin, and urea were measured at admission (Day 1) and at clinical stabilization (Day 6). All variables failed normality testing (Shapiro–Wilk p < 0.0001); non-parametric methods were applied. Receiver operating characteristic (ROC) analysis was used to identify candidate biomarker cutoffs for mortality prediction. SARS-CoV-2 was the predominant pathogen (29.1%). In an exploratory comparison limited by small subgroup sizes (n = 8 vs. n = 14), co-infected diabetic patients had higher baseline inflammatory markers than co-infected non-diabetic patients: median IL-6 32.87 vs. 6.20 pg/mL (Mann–Whitney p = 0.0006) and median CRP 103.83 vs. 23.03 mg/L (p = 0.0012). At the Day 6 checkpoint, co-infected diabetic survivors had higher IL-6 (12.01 vs. 6.13 pg/mL, p = 0.0183) and showed little within-group NLR change (Wilcoxon p = 0.2367); these Day 6 estimates are subject to survivor selection and should be interpreted accordingly. In-hospital mortality was 25.6% in diabetic vs. 3.7% in non-diabetic patients (p < 0.0001). Diabetic patients more frequently required orotracheal intubation (6.4% vs. 1.0%, p = 0.0207) and high-flow nasal oxygen (HFNO) support (7.9% vs. 1.8%, p = 0.0166). In an internal ROC analysis, baseline IL-6 showed the highest discriminatory performance for in-hospital mortality (AUC 0.812, 95% CI 0.772–0.848), with a candidate cutoff of > 55.78 pg/mL (sensitivity 71.0%, specificity 79.1%); IL-6 outperformed CRP (AUC 0.706, DeLong p = 0.0029) and NLR (AUC 0.656, DeLong p = 0.0001). As this cutoff was derived and evaluated in the same cohort, it is reported as exploratory and requires external validation. In this single-center cohort, diabetes was associated with a more pronounced baseline inflammatory profile, slower resolution of the neutrophil-to-lymphocyte ratio, and greater multi-organ involvement during viral respiratory infection, including in the small co-infected subgroup. In the full cohort, diabetes remained associated with higher mortality, IL-6, and CRP after adjustment for age, sex, and BMI; however, the small co-infected subgroups could not be adjusted, so those specific comparisons should be regarded as hypothesis-generating and need confirmation in larger, adequately powered multi-center cohorts.

Chronic obstructive pulmonary disease (COPD) is a chronic progressive respiratory disease characterized by respiratory symptoms and airflow limitation and is one of the leading causes of morbidity and mortality worldwide. The evolution of the disease is associated with episodes of acute exacerbations (AECOPD), characterized by worsening symptoms and accelerated deterioration of lung function. Acute exacerbations of COPD have different severity, being mild, moderate or severe depending on how aggravated the patients’ symptoms are, but they also depend on pulmonary functional and biological changes. Around 70% of AECOPD cases are infectious in nature, through upper or lower respiratory tract infections. Often, exacerbations associated with lower respiratory tract infections are more severe and have a higher risk of unfavorable outcome compared to AECOPD associated with upper respiratory tract infections. Severe exacerbations require hospital management, with most of them being treated in the intensive care unit (ICU). In this narrative review, we evaluated the frequency of different bacterial pathogens involved in severe COPD exacerbations associated with lower respiratory tract infections and the need for treatment in the ICU. Identifying patients with exacerbated COPD at high risk of respiratory infections, especially with Gram-negative bacilli, is extremely important to choose the optimal treatment, thus reducing the risk of death.