Background and Objectives: This study aimed to investigate the novel adiponectin–resistin (AR) index as a predictor of the development of metabolic syndrome (MetS) in individuals with type 2 diabetes mellitus (T2DM). MetS is common in T2DM and increases cardiovascular risk. Adiponectin and resistin, adipokines with opposing effects on insulin sensitivity and inflammation, make the AR index a potential marker for metabolic risk. Materials and Methods: This prospective observational study included 80 T2DM participants (ages 30–60) from Sarajevo, Bosnia and Herzegovina, over 24 months. The participants were divided into two groups: T2DM with MetS (n = 48) and T2DM without MetS (n = 32). Anthropometric data, biochemical analyses, and serum levels of adiponectin and resistin were measured at baseline and every six months. The AR index was calculated using the formula AR = 1 + log10(R) − 1 + log10(A), where R and A represent resistin and adiponectin concentrations. Logistic regression identified predictors of MetS. Results: T2DM patients who developed MetS showed a significant decline in adiponectin levels (40.19 to 32.49 ng/mL, p = 0.02) and a rise in resistin levels (284.50 to 315.21 pg/mL, p = 0.001). The AR index increased from 2.85 to 2.98 (p = 0.001). The AR index and resistin were independent predictors of MetS after 18 months, with the AR index showing a stronger predictive value (p = 0.007; EXP(B) = 1.265). Conclusions: The AR index is a practical marker for predicting MetS development in T2DM participants, improving metabolic risk stratification. Incorporating it into clinical assessments may enhance early detection and treatment strategies.

Background Acute pancreatitis (AP) is a condition with various etiological factors, marked by the sudden onset of inflammation in the pancreatic tissue. Predicting the severity and potential mortality of AP involves analyzing clinical data alongside laboratory tests and imaging. Among several grading methods with strong predictive capabilities for illness severity and mortality, the Bedside Index for Severity in Acute Pancreatitis (BISAP) score is notable. This study aims to explore the potential role of laboratory markers, specifically red cell distribution width (RDW), RDW/platelet (PLT) ratio, and mean platelet volume (MPV), in predicting disease severity, with patients being stratified according to the BISAP scoring system. Materials and methods This research included 161 patients hospitalized at Cantonal Hospital Zenica in Zenica, Bosnia and Herzegovina, with a diagnosis of AP. The BISAP score was determined based on laboratory and radiological analyses. This score was used to evaluate potential correlations between laboratory findings such as RDW, RDW/PLT ratio, and MPV. Results The age range was significantly higher in patients with BISAP scores ≥3 (68 years, 64-76) compared to those with BISAP scores <3 (59.5 years, 42.75-69) (p = 0.000). RDW values were also significantly higher in patients with BISAP scores ≥3 (15.6%, 14-16.9) compared to those with BISAP scores <3 (13.5%, 13-14.1) (p = 0.000). Hospital stay duration was significantly longer for patients with BISAP scores ≥3 (9 days, 6-11) compared to those with BISAP scores <3 (5 days, 5-7) (p = 0.000). Additionally, the RDW/PLT ratio was significantly lower in patients with BISAP scores <3 (0.063 ± 0.02) compared to those with BISAP scores ≥3 (0.09 ± 0.059) (p = 0.012). Conclusion Our results indicate a significant difference in RDW/PLT ratios between patient severity groups based on BISAP scores (scores <3 vs. ≥3). This suggests that the RDW/PLT ratio may serve as a useful predictor for assessing the severity of AP. However, further research is needed to explore the full potential of the RDW/PLT ratio in evaluating AP patients.

Heart failure (HF) and atherosclerosis represent two major cardiovascular diseases that are intricately linked, both contributing significantly to global morbidity, mortality, and healthcare burden. Despite substantial progress in diagnostic methods and therapeutic strategies, the overall impact of these conditions remains considerable. This is largely due to their complex and overlapping pathophysiological mechanisms, persistent residual atherosclerotic risk, and the ongoing challenges associated with implementing guideline-directed medical therapy for HF in routine clinical practice. Recent advancements in the management of diverse HF phenotypes, lipid abnormalities, atherosclerotic cardiovascular disease (ASCVD), and obesity have facilitated the adoption of multidrug regimens. These include beta-blockers, renin-angiotensin-aldosterone system inhibitors, and sodium-glucose cotransporter 2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1), which have collectively improved outcomes in HF populations. This review aims to elucidate the shared pathophysiological mechanisms linking these conditions and to examine their clinical overlap with ischemic heart disease, cerebrovascular disease, peripheral arterial disease, dyslipidemia, and obesity.

Kounis syndrome (KS) describes the occurrence of acute coronary syndromes precipitated by allergic, hypersensitivity, or anaphylactic reactions and represents a unique intersection between immunologic activation and cardiovascular disease. The epidemiology of KS is likely underestimated due to diagnostic overlap with other cardiac and allergic conditions and limited awareness across medical specialties. This narrative review focuses on the distinctive features of KS in special populations, emphasizing how patients’ age, comorbidities, immune status, and vascular substrate modify presentation, diagnosis, and outcomes. In elderly patients, polypharmacy, increased plaque vulnerability, and endothelial dysfunction favor Type II and III KS. Pediatric cases, although rare, are predominantly Type I and strongly associated with food allergies, insect stings, vaccines, and antibiotics, with under-recognition driven by diagnostic bias and ethical concerns surrounding invasive testing. Patients with coronary stents, cardiac devices, chronic kidney disease, and those receiving dialysis exhibit heightened susceptibility due to chronic inflammation, foreign-body hypersensitivity, and prothrombotic states. Pregnancy and the peripartum period represent a unique immuno-hemodynamic milieu in which Th2 immune shift, increased coronary vasoreactivity, and obstetric triggers can compromise both maternal and fetal perfusion. Additional risk modulation is observed in atopic individuals, asthmatics, patients with autoimmune, inflammatory, oncologic, psychiatric, and neurodevelopmental conditions, as well as in COVID-19 and post-infectious states. We propose a host-modified framework for KS that complements traditional classification by integrating immune phenotype and vascular substrate, enabling improved risk stratification and personalized preventive strategies.

Introduction: Diabetes mellitus is associated with systemic complications, including the development of pulmonary injury, characterized mainly by excessive accumulation of extracellular matrix components and inflammatory cell infiltration in lung tissue. This process is driven by oxidative stress and chronic inflammation, both caused and exacerbated by hyperglycemia. N-acetylcysteine (NAC) and glycine, known for their antioxidant and anti-inflammatory effects, offer potential therapeutic benefits in mitigating diabetes-induced lung injury. Objective: The study aimed to investigate the effects of supplementation by either NAC or glycine or their combination on reducing lung injury in rats with type 1 diabetes Materials and methods: The study used 30 adult Wistar albino rats (10 weeks old, weighing between 180 g and 380 g). Six of them were used as controls, while 24 adult rats (10 weeks old, 180-380 g) with type 1 diabetes, induced through a single intraperitoneal injection of streptozotocin (STZ) at a dose of 55 mg/kg, were randomly assigned to four experimental groups: control (CTL), diabetic (Db), NAC treatment (diabetic+NAC), glycine treatment (diabetic+glycine), and combined NAC and glycine treatment (diabetic+NAC+glycine). NAC (100 mg/kg) and glycine (250 mg/kg) were administered orally for 12 weeks. At the end of the study, lung tissues were collected for histopathological examination. Qualitative, semi-quantitative, and stereological histological analysis was used to analyze structural changes in the lung tissue. Semi-quantitative scoring was carried out to evaluate the extent of inflammation, while stereological analysis was performed to determine the volume density of alveolar spaces and septal connective tissue. The semi-quantitative scoring included scores ranging from 0 (absent), 1 (minimal), 2 (mild), 3 (moderate), to 4 (severe). Results: Qualitative histological analysis revealed pronounced inflammation and fibrosis in the lungs of untreated diabetic rats, characterized by thickened alveolar septa and immune cell infiltration. Both treatments with NAC and glycine individually reduced inflammation and fibrosis compared to untreated diabetic rats. The greatest improvement was observed in the NAC+glycine group, where the alveolar structure appeared almost normal, with minimal inflammation. Semiquantitative analysis showed statistically significant differences in peribronchial and peribrochiolar infiltrates between the diabetic group (2.16±0.47) and the control group (0.33±0.21, p=0.026). The combination of NAC and glycine significantly reduced peribronchial and peribronchiolar infiltrates (0.33±0.33, p=0.026) compared to the diabetic group. Similarly, septal inflammatory infiltrates were significantly lower in the NAC+glycine group (1±0.36) compared to diabetic rats (3.33±0.33, p=0.004). Total airway inflammatory infiltration was also significantly reduced in the NAC+glycine group (1.33±0.33, p=0.002) compared to the diabetic group (5.5±0.5). Conclusion: As the combination of NAC and glycine demonstrated protective effects against lung inflammation and fibrosis in diabetic rats, a synergistic effect of NAC and glycine in mitigating pulmonary complications associated with type 1 diabetes may be suggested. These findings warrant further exploration of the combination for managing diabetic lung disease and potentially other fibrotic conditions.

Aim To compare the impact of electrical cardioversion (ECV) and pharmacological cardioversion (PCV) on left atrial size (LA) and left ventricular ejection fraction (LVEF), as well as to identify predictors of rhythm disorder recurrence in patients with atrial fibrillation (AF) or atrial flutter (AFL).Methods A prospective observational cohort study was conducted on 105 patients with persistent AF or AFL at the University Clinical Centre Tuzla. The patients were divided into two groups: 53 underwent ECV and 52 received PCV. Demographic and clinical data, including ECG and transthoracic echocardiography, were collected. Follow-up assessments were conducted at 7 days, 1 month, and subsequently every 3 months for a year.Results Baseline characteristics were similar between the groups. Recurrence of rhythm disorder within one year was observed in 52.4% of cases, with ECV showing a slightly lower, though not significantly different, primary failure rate at 7 days compared to PCV (13.2% vs. 23.1%). Significant predictors of recurrence included longer duration of disorder (p<0.001), hypertension (p=0.016), lack of pre-cardioversion amiodarone (p=0.027), and larger LA (p<0.001). Both ECV and PCV significantly reduced LA over time, with no significant differences in LVEF between groups.Conclusion Both ECV and PCV are effective in restoring sinus rhythm, with a trend towards lower recurrence in the ECV group. Predictors such as disorder duration, hypertension, lack of pre-cardioversion amiodarone, and LA should be considered when planning cardioversion to optimize patient outcomes.