Search Results (216)

Background: Patients with type 2 diabetes mellitus (T2DM) who present with ST-segment elevation myocardial infarction (STEMI) remain at high risk of adverse remodeling after reperfusion. This observational study examined whether pre-admission glucose-lowering therapy class was associated with six-month left ventricular (LV) reverse remodeling and myocardial work recovery. Methods: We analyzed 253 patients with STEMI, baseline LV ejection fraction ≤ 50%, successful primary PCI, and complete baseline and six-month echocardiography. The primary inferential analyses focused on 75 patients with T2DM, grouped according to pre-admission therapy with SGLT-2 inhibitors, GLP-1 receptor agonists, DPP-4 inhibitors, or conventional therapy; non-diabetic patients were retained as a descriptive reference group. Clinical outcome, propensity-score, subgroup, and mediation analyses were considered exploratory because of small subgroup and event counts. Results: SGLT-2 inhibitor and GLP-1 receptor agonist exposure was associated with larger improvements in LVEF, LV volumes, and global work efficiency than DPP-4 inhibitors or conventional therapy. Crude MACE rates were highest in the conventional-therapy group, but event estimates were imprecise and confounded by baseline risk, revascularization status, and discharge therapy. Conclusions: In patients with T2DM recovering from STEMI, pre-admission exposure to SGLT-2 inhibitors and, to a lesser extent, GLP-1 receptor agonists was associated with more favorable structural and myocardial work recovery. These hypothesis-generating findings should be interpreted as associations and require confirmation in adequately powered prospective studies. Full article

Tryptophan (TRP) metabolism has emerged as a critical interface linking inflammation, immune regulation, oxidative stress, and cellular energetics. The kynurenine pathway, the predominant route of TRP degradation, is highly responsive to inflammatory stimuli and generates a spectrum of bioactive metabolites with divergent and context-dependent biological effects. Indoleamine 2,3-dioxygenase 1 (IDO1)-mediated TRP catabolism integrates immune activation with downstream metabolic signaling, influencing redox homeostasis, endothelial function, and mitochondrial energetics, in part by regulating nicotinamide adenine dinucleotide (NAD⁺) synthesis. Alterations in TRP metabolism are consistently observed across cardiometabolic diseases, including obesity, type 2 diabetes (T2D), atherosclerosis, myocardial infarction (MI), and heart failure with preserved ejection fraction (HFpEF), where they are associated with disease severity and adverse outcomes. Importantly, emerging data suggest that cardiometabolic phenotypes are determined not by pathway activation alone, but by the relative distribution of flux across downstream metabolic branches. Depending on the tissue compartment and stage of the disease, different biological effects may be contributed by redox-active kynurenine 3-monooxygenase (KMO)/3-hydroxykynurenine (3-HK)/quinolinic acid (QA) pathways, 3-hydroxyanthranilic acid (3-HAA)-mediated lipid and inflammasome regulation, microbiome-derived indoles, and NAD⁺-generating pathways. This review synthesizes current evidence using a branch-specific and context-dependent framework. We discuss the utility and limitations of the kynurenine-to-tryptophan ratio (KTR) as an upstream biomarker, the need for downstream metabolite panels, and therapeutic opportunities aimed at pathway modulation rather than broad inhibition. Future studies integrating temporal profiling, spatial and cell-specific approaches, large-animal models, and pathway-informed clinical trials will be essential to define causal mechanisms and enable precision therapeutic translation. Full article

Background: Myocardial fibrosis plays a key role in adverse remodeling after ST-segment-elevated myocardial infarction (STEMI). The effect of sodium–glucose cotransporter 2 inhibitors (SGLT2is) on myocardial fibrosis deposition among patients with STEMI undergoing primary percutaneous coronary intervention (pPCI) is unclear. Objectives: To assess the effects of SGLT2is on myocardial fibrosis among patients with STEMI undergoing pPCI. Methods: Patients with STEMI undergoing pPCI with left ventricular ejection fraction ≤ 50% were randomized to dapagliflozin 10 mg or placebo. The primary endpoint was cardiac magnetic resonance (CMR)-derived 6-month changes in remote myocardium extracellular volume (ECV) fraction from baseline. Secondary endpoints included changes in CMR-derived myocardial volumes, change in serum fibrosis biomarker levels, and adverse events. Multivariable adjustment for infarction location and diabetes status was performed as sensitivity. The study was halted prematurely due to slow recruitment. Results: Fifty-two patients underwent randomization between May 2021 and April 2024 and completed follow-up. At 6 months, dapagliflozin resulted in a non-significant reduction in ECV change compared to placebo (−0.39 [4.7] vs. 1.43 [5.7]; difference: −1.82 [−4.86; 1.23]; p-value = 0.235) while also leding to a higher degree of reduction in N-terminal pro-peptide of type III collagen (−177.0 pg/mL [416.1] vs. 3.6 pg/mL [553.8]; p-value = 0.208). No significant differences in other biomarkers or adverse events were noted in the main analysis. After adjustment, dapagliflozin was associated with increased reduction in left ventricular end-systolic volume (−4.02 mL [7.4] vs. 0.10 mL [10.1]; difference: −4.92 [−9.8; −0.1]; p-value = 0.047). Conclusions: In STEMI patients undergoing pPCI, dapagliflozin did not result in a significant reduction in ECV or biomarkers of fibrosis at 6 months. Full article

Cardiovascular disease is traditionally interpreted through macrocirculatory parameters such as cardiac output, vascular resistance, and epicardial coronary anatomy. However, clinical outcomes frequently diverge from predictions based solely on these indices, particularly in syndromes such as heart failure with preserved ejection fraction (HFpEF), cardiogenic shock, and sepsis-associated myocardial dysfunction. Increasing evidence suggests that the integrity of the microvascular–immune interface plays a central role in determining tissue perfusion and cardiovascular resilience. This review proposes a staged framework of cardiovascular decompensation centered on progressive failure of this interface. In Stage 1, chronic cardiometabolic and inflammatory stress produces a primed but compensated microvascular state characterized by endothelial activation, glycocalyx vulnerability, pericyte remodeling, platelet sensitization, and reduced lymphatic reserve. Perfusion is preserved at rest, but vasodilatory reserve and microvascular stability are reduced, narrowing the effective perfusion window under physiologic stress. In Stage 2, acute insults such as infection, ischemia, or neurohumoral activation precipitate threshold instability within the microcirculation. Perfusion becomes governed by the arterial pressure–critical closing pressure (Pa − Pcrit) relationship rather than traditional arterial–venous gradients. As this window narrows, segmental capillary derecruitment and heterogeneous flow emerge, producing loss of hemodynamic coherence in which systemic blood pressure and cardiac output may appear preserved despite impaired tissue perfusion. In Stage 3, inflammatory amplification and immunothrombotic processes consolidate microvascular dysfunction. Pericyte contraction, endothelial injury, cytokine escalation, and neutrophil extracellular trap formation promote platelet–fibrin deposition and capillary obstruction, transforming reversible conductance failure into structural microvascular impairment. This framework provides a unifying physiologic lens for diverse cardiovascular syndromes, including Type 2 myocardial infarction, HFpEF decompensation, and cardiogenic shock. It also suggests that therapeutic efficacy may depend less on macrocirculatory normalization alone and more on preserving microvascular integrity before immunothrombotic consolidation occurs. Although this model remains hypothesis-generating, it highlights the microvascular–immune interface as a central determinant of cardiovascular stability and a potential target for future precision hemodynamic and immunomodulatory strategies. Full article

Background: Lipoprotein(a) (Lp(a)) is a genetically determined lipoprotein associated with atherosclerotic cardiovascular disease (ASCVD). Its prognostic role in type 2 diabetes mellitus (T2DM) remains unclear. We aimed to evaluate the association of Lp(a) with first myocardial infarction (MI), cardiovascular (CV) mortality, and all-cause mortality, with a focus on sex differences. Methods: We retrospectively analysed patients with T2DM and no prior MI who were hospitalised between 2000 and 2018 and had baseline Lp(a) measurements. Patients were followed until MI, death, or the end of 2023. Lp(a) was categorised as ≤50, 51–90, and >90 mg/dL. Cox proportional hazards models were adjusted for low-density lipoprotein cholesterol, arterial hypertension, and estimated glomerular filtration rate < 60 mL/min/1.73 m², with attained age used as the time scale. Results: A total of 2967 patients (37.5% women) were included. During follow-up, 12.5% of patients experienced MI, 36.4% died from CV causes, and 68.8% died from any cause. A significant interaction between Lp(a) and sex was observed for MI. In sex-specific analyses, Lp(a) > 50 mg/dL was associated with a higher risk of first MI in women (51–90 mg/dL: HR 1.79, 95% CI 1.07–2.99; >90 mg/dL: HR 2.67, 95% CI 1.66–4.32), whereas no significant association was observed in men. Elevated Lp(a) ≥ 50 mg/dL was also associated with higher CV mortality overall (51–90 mg/dL: HR 1.42, 95% CI 1.07–1.89; >90 mg/dL: HR 1.38, 95% CI 1.01–1.91), without a significant interaction with sex. No significant associations were observed for all-cause mortality. Conclusions: In patients with T2DM, elevated Lp(a) > 50 mg/dL was associated with increased risk of first MI, predominantly in women, and with higher CV mortality overall. Lp(a) may serve as a valuable marker for CV risk stratification in this population. Full article

MAO-B-specific inhibition, either in knockout (KO) mice or pharmacologically, preserves left ventricular function and reduces cardiac fibrosis after myocardial infarction or pressure overload. We investigated whether stimulation of MAO-B in cardiac fibroblasts provokes ROS production and myofibroblast development. Fibroblast-specific MAO-B knockdown (KD) mice were created by crossing Col1a2CreERT mice with MAO-B^fl/fl mice. The KD was induced by tamoxifen injection. Fibroblasts of KD mice and wild types (WTs) were isolated and reduced MAO-B expression in KD fibroblasts was confirmed. In isolated mitochondria from the left ventricle of these mice, ROS production was reduced under stimulation with the specific MAO-B substrate β-phenylethylamine (PEA). Mitochondrial ROS production in fibroblasts, detected by MitoSox Red staining, increased under PEA (1000 µM) stimulation only in WT fibroblasts. mRNA of the marker genes for myofibroblast differentiation, Col1a1 and periostin, increased 2- or 3-fold, respectively, in WT but not in MAO-B KD fibroblasts. The enhanced migration potential under PEA was reduced in MAO-B KD fibroblasts. In conclusion, stimulation of MAO-B in cardiac fibroblasts leads to the formation of mitochondrial ROS, enhancement of myofibroblast marker gene expression and migration of the cells. Excessive fibrosis caused by elevated MAO-B activity in myocardial infarction can therefore contribute to cardiac dysfunction. Full article

Background: Pacemakers enable continuous long-term surveillance of atrial fibrillation detected by implanted devices. Circulating biomarkers reflecting endothelial dysfunction, inflammation, and myocardial stress may help identify patients at risk for atrial fibrillation (AF) progression and higher arrhythmic burden. Methods: This analysis included patients from the prospective ACaSA study (NCT05127720) with a dual chamber pacemaker (Microport^® BOREA DR or TEO DR) and monitored weekly via remote monitoring technology (SMARTVIEW^®). Individuals with permanent AF or single-chamber systems were excluded. Baseline plasma concentrations of angiopoietin-2 (ANGPT2), growth differentiation factor-15 (GDF-15), fibroblast growth factor-23 (FGF-23), bone morphogenetic protein-10 (BMP10), and tumor necrosis factor–related apoptosis-inducing ligand receptor-2 (TRAIL-R2) were quantified using enzyme-linked immunosorbent assays. N-terminal pro-B-type natriuretic peptide (NT-proBNP) was measured using electrochemiluminescence immunoassay. Biomarkers were log₂-transformed, with values below assay detection limits imputed at half the lower limit of detection. Two endpoints were assessed following a 30-day blanking period: (1) progression to persistent AF, defined as ≥7 consecutive days with >99% daily AF burden, analyzed using Cox regression; and (2) AF burden, calculated as total AF time normalized to monitored days and categorized as <25%, 25–75%, or >75%, analyzed using multinomial logistic regression. Multivariable models were adjusted for age, sex, heart failure, diabetes, and prior myocardial infarction; Cox models were limited to age, sex, and heart failure due to fewer events. Results: A total of 223 patients were included (median age 75 years; 37.2% women). During follow-up, 28 patients (13.3%) progressed to persistent AF. Higher baseline ANGPT2 was the strongest predictor of progression (HR per doubling 1.83, 95% CI 1.27–2.66, p = 0.001), followed by GDF-15 (HR 1.52, 95% CI 1.03–2.24, p = 0.036). In the burden analysis, ANGPT2 demonstrated a pronounced graded relationship with arrhythmic load, with markedly increased odds of high (>75%) AF burden (OR 8.31, 95% CI 2.63–26.26, p < 0.001). GDF-15 independently predicted both medium (OR 2.05, p = 0.025) and high burden (OR 2.32, p = 0.037). NT-proBNP displayed a borderline association with high burden (OR 2.02, p = 0.061). No significant associations were observed for FGF-23, BMP10, or TRAIL-R2. Conclusions: In continuously monitored pacemaker patients, ANGPT2 and GDF-15 emerged as key biomarkers associated with AF disease severity. ANGPT2 was strongly linked to both progression to persistent AF and high AF burden, whereas GDF-15 consistently predicted higher AF burden and also contributed to risk of progression. These findings highlight endothelial and inflammatory pathways as potential markers of atrial disease progression. Full article

Objectives: Malperfusion is a major determinant of outcome in acute type A aortic dissection (ATAAD), yet its heterogeneous patterns and prognostic impact remain incompletely defined. We investigated the association between malperfusion burden, territory-specific involvement, and early outcomes after emergency ATAAD repair. Methods: We performed a retrospective single-center study including 483 consecutive patients undergoing emergency surgery for ATAAD (2010–2022). Malperfusion was classified by coronary, visceral, and peripheral territories and stratified as none, single-territory, or multidistrict (≥2 territories). The primary outcome was in-hospital mortality. Secondary outcomes included stroke, renal replacement therapy, peri-procedural myocardial infarction, major vascular events, and a composite endpoint of major adverse events (MAEs). Multivariable logistic regression identified independent predictors. Results: Overall, 68.5% of the population were male with a mean age of 65.4 ± 12.1 years. Malperfusion was present in 151 patients (31.3%), including 131 (27.1%) with single-territory and 20 (4.1%) with multidistrict involvement. In-hospital mortality increased stepwise with malperfusion burden (12.7%, 19.8%, and 50.0%; p < 0.001). MAEs occurred in 36.6% of patients, with a similar gradient (31.2%, 46.2%, and 65.0%, p < 0.001). In multivariable analysis, preoperative shock, neurological deficit, descending aortic involvement, and redo surgery were independent predictors of MAEs, whereas malperfusion burden showed an attenuated association after adjustment. Territory-specific analyses revealed strong associations between coronary malperfusion and peri-procedural myocardial infarction, visceral malperfusion and postoperative dialysis, and peripheral malperfusion and major vascular events. Conclusions: Malperfusion burden is associated with worse early outcomes after ATAAD repair but largely reflects underlying clinical severity. Distinct malperfusion territories confer specific postoperative risks, supporting a pattern-based approach to perioperative risk stratification. Full article

Acute myocardial infarction (AMI) results from a lack of oxygen supply to the myocardium, leading to the loss of cardiomyocytes and their replacement with fibrotic scar tissue. This process is closely associated with the development of heart failure. Regenerative medicine has emerged as a promising strategy to enhance treatment outcomes in severe cases of heart failure. This study aimed to evaluate myocardial regeneration after AMI using a biomaterial composed of mononuclear stem cells and human amniotic membrane. A total of 120 Wistar rats were subjected to experimentally induced AMI. On the 7th day post-infarction, rats with an ejection fraction of <50% on echocardiography were randomized into four groups: (1) control; (2) stem cells; (3) amniotic membrane; and (4) amniotic membrane combined with stem cells. On the 30th day, the surviving animals underwent a second echocardiographic evaluation and were subsequently euthanized. The group treated with the combination of amniotic membrane and stem cells showed reduced systolic and diastolic ventricular volumes. Histological analysis revealed that these animals exhibited less fibrosis and a lower percentage of type I collagen. Based on the results of the study, it was concluded that the combination of human amniotic membrane and mononuclear stem cells decreased ventricular volumes and myocardial fibrosis, suggesting more favorable ventricular remodeling in this experimental model. Full article

Background and Objectives: During the past 25 years, a significant body of research has been conducted reporting on the salutary effects of the Mediterranean diet and extra-virgin olive oil, one of its main components. The initial studies were epidemiological observations on populations with very low mortality rates due to significant reductions in myocardial infarction fatalities. Population-based studies demonstrated that the Mediterranean diet with olive oil consumption is associated with a lower prevalence of cardiovascular and cerebrovascular disease, obesity, arthritis, and cancer. Materials and Methods: In this narrative review, we present recent studies on the effects of extra-virgin olive oil and the Mediterranean diet—compared with various other diets—on several vascular risk factors, including hypertension, hyperlipidemia, type 2 diabetes mellitus, and obesity, as well as their impact on cognitive decline and dementia. Results: This diet has been shown to improve cognitive function in patients with mild cognitive impairment, Alzheimer’s disease, vascular cognitive impairment, and vascular dementia. The main mechanisms responsible for cognitive improvement include control of arterial hypertension by reducing systolic and diastolic blood pressure, lowering triglycerides and low-density lipoprotein cholesterol and increasing high-density lipoprotein cholesterol, along with improvement in fasting glucose, insulin levels, and hemoglobin A1c in subjects with type 2 diabetes mellitus, as well as lowering body mass index and obesity. Conclusions: The Mediterranean diet and olive oil induce—along with prevention of cardiovascular disease and stroke—a significant improvement of vascular risk factors, slowing the progression of both vascular dementia and Alzheimer’s disease. There is a need for additional placebo-controlled clinical trials to confirm the supportive nutritional role of extra-virgin olive oil in age-associated cognitive decline in the elderly. Full article

Atherosclerosis, manifesting as acute myocardial infarction, stroke and peripheral artery disease, is the main cause of death worldwide. Conventional risk factors contributing to the development and progression of atherosclerosis are well established, including diabetes mellitus, hypertension, hypercholesterolemia, smoking and obesity. In recent decades, other lipid molecules have been identified as risk factors for atherosclerosis and arterial calcification, including lipoprotein (a) and apolipoproteins. Despite the available evidence for the association between those biomarkers and atherosclerosis in the general population, their impact on diabetic patients is incompletely characterized. This review aims to summarize the current evidence on the relationship between lipoprotein (a), apolipoproteins and atherosclerotic cardiovascular disease in diabetic patients. By integrating genetic, epidemiological, and mechanistic data, this review highlights the dual and context-dependent associations of lipoprotein (a) with incident type 2 diabetes and atherosclerotic cardiovascular risk, supporting more nuanced interpretation of Lp(a) in diabetes-related risk assessment. Full article

Background: Manganese (Mn) is an essential trace element with antioxidant properties; however, excessive exposure may contribute to inflammation and vascular dysfunction. Hair analysis provides an indicator of long-term Mn exposure. This study evaluated the relationship between hair Mn levels, acute coronary syndrome (ACS), coronary artery disease (CAD) severity, and cardiovascular risk factors, with particular emphasis on metabolic status in a cardiometabolic population. Methods: Hair Mn concentration was measured using inductively coupled plasma optical emission spectrometry (ICP-OES) in 80 patients (mean age 67 ± 11 years; 28.8% women) undergoing coronary angiography for suspected ACS. Final diagnoses included stable CAD (N = 42) and ACS [ST-elevation myocardial infarction (STEMI) N = 17, non-ST-elevation myocardial infarction (NSTEMI) N = 12, and unstable angina (UA) N = 9]. CAD severity was quantified using the SYNTAX score and the Coronary Artery Surgery Study Score (CASSS). Associations with clinical variables were assessed using non-parametric tests and Spearman correlations. The median SYNTAX score was 13.8 (range 0.0–68.5), and the median hair Mn concentration was 0.22 ppm (range 0.01–1.65). Results: SYNTAX scores were higher in ACS than in stable CAD (p = 0.027), with the highest values observed in NSTEMI. Hair Mn levels did not differ among diagnostic groups and showed no association with CASSS or SYNTAX (R = −0.11; p = 0.348). No differences were detected with respect to sex, smoking, prior myocardial infarction, hypertension, hyperlipidemia, or type 2 diabetes. A modest inverse correlation was observed between hair Mn and body mass index (BMI) in unadjusted analysis (R = −0.25; p = 0.03), but this association was not robust after correction for multiple comparisons, suggesting a potential exploratory link between manganese homeostasis and cardiometabolic status. Conclusions: Although hair Mn concentration was not associated with angiographic indices of CAD severity or ACS subtypes, the observed relationship with BMI may indicate a role of Mn homeostasis in cardiometabolic regulation. Larger prospective studies are required to clarify these associations. Full article

Background: Medication adherence is a critical component of effective management in type 2 diabetes mellitus (T2DM). Although previous studies have explored the relationship between adherence and clinical outcomes, the strength and consistency of these associations have not been fully elucidated and remain unclear. In particular, evidence derived from patient-reported measures of adherence is limited, and the prognostic significance of adherence as assessed from the patient perspective is not clearly defined. Methods: We conducted a prospective observational cohort study consisting of adult patients with T2DM who received regular outpatient follow-up. Medication adherence was assessed at the time of enrollment using the eight-item Morisky Medication Adherence Scale (MMAS-8) and was categorized as good, moderate, or poor. Participants were subsequently followed for five years to ascertain clinical outcomes. Primary outcomes were assessed longitudinally and included the occurrence of nonfatal myocardial infarction, heart failure, nonfatal stroke, and progression to end-stage kidney disease (ESKD), as well as all-cause mortality. Secondary outcomes included changes in glycated hemoglobin (HbA1c), estimated glomerular filtration rate (eGFR), and low-density lipoprotein (LDL) levels. Results: No statistically significant differences were observed in the incidence of nonfatal myocardial infarction, heart failure, nonfatal stroke, or progression to ESKD across adherence groups. In contrast, all-cause mortality was significantly higher among patients with poor adherence. With respect to metabolic outcomes, HbA1c and eGFR at five years were comparable across adherence groups, whereas LDL levels were significantly higher in patients with poor adherence. Conclusions: Poor medication adherence as assessed at baseline may be related to a higher risk of all-cause mortality and poorer lipid control, while no statistically significant differences were observed for nonfatal cardiovascular or renal outcomes. Full article

Background: Early diagnosis of transthyretin amyloid cardiomyopathy (ATTR-CM) remains challenging. Although ECG and morphological abnormalities at diagnosis are well-described, their temporal evolution has not been systematically evaluated. This study characterized the prevalence and longitudinal progression of electrical and structural cardiac abnormalities preceding ATTR-CM diagnosis. Methods: We retrospectively analyzed patients with confirmed ATTR-CM evaluated at a specialist amyloidosis center between 2006 and 2023. Diagnosis was established by grade 2–3 myocardial uptake on 99mTc-DPD scintigraphy. Standard 12-lead ECGs and transthoracic echocardiograms were reviewed at diagnosis and at baseline, 3–5 years earlier. Results: Sixty-three patients (79% men; mean age 77 ± 8 years) were studied, including 33 (52%) with hereditary ATTR (ATTRv) and 30 (48%) with wild-type ATTR (ATTRwt). Overall, 95% had a NAC score ≤ 2, consistent with less advanced disease at diagnosis. During the prediagnostic phase, 79% of patients exhibited pathological ECGs. Non-specific ST–T abnormalities (40%), prolonged QTc (38%), left-axis deviation (35%), first-degree AV block (33%) and anterior infarction pattern (33%) were each observed in at least one-third of patients. From baseline to diagnosis, significant prolongation was observed in the PR interval (+26 ms), QRS duration (+11 ms), and QTc interval (+22 ms) (p < 0.001 for all), and a leftward shift observed in the electrical axis (−12.03°, p = 0.011). Low voltage was uncommon at both time points. Although interventricular septal thickness increased significantly (+3.42 mm; p < 0.001), left ventricular ejection fraction and dimensions were relatively stable. Conclusions: In this proof-of-concept study, electrical remodeling precedes functional changes and outperforms low voltages to raise clinical suspicion of ATTR-CM. Full article

Chronic rhinosinusitis with nasal polyps (CRSwNP) is a type 2 inflammatory disease effectively treated with dupilumab, a monoclonal antibody that inhibits IL-4 and IL-13 signaling. Dupilumab is an effective treatment for type 2 inflammatory diseases such as CRSwNP. Although efficacy of dupilumab in controlling upper airway inflammation is well established, concerns have emerged regarding its potential cardiovascular effects. Emerging evidence suggests that IL-4/IL-13 signaling plays a protective role in post-myocardial infarction remodeling by promoting anti-inflammatory macrophage polarization, angiogenesis, and controlled fibrosis, especially during the early healing phase. Pharmacological blockade of the IL-4/IL-13 signaling pathway, such as that induced by dupilumab, may theoretically impair myocardial repair mechanisms, particularly in male patients who appear more responsive to these cytokines. Although rare, dupilumab-associated hypereosinophilia and myocarditis have been reported. In patients with pre-existing ischemic heart disease or heart failure, a multidisciplinary risk–benefit evaluation should be considered. Concomitant use of cardioprotective agents such as sacubitril/valsartan or SGLT2 inhibitors may help mitigate potential cardiac risks. Future studies are needed to clarify the safety and therapeutic implications of combining dupilumab with cardiovascular therapies in patients with coexisting CRSwNP and heart disease. This review critically evaluates emerging evidence of potential interference with post-infarction myocardial repair and highlights the importance of a multidisciplinary approach in managing patients with coexisting inflammatory and cardiovascular diseases. The aim of this review is to explore the available data on the cardiovascular impact of dupilumab and to provide possible future perspectives. Full article