Aortic stenosis (AS) and atherosclerosis are progressive cardiovascular conditions that frequently coexist and share multiple clinical and molecular features. Medical therapies have shown effectiveness in preventing and treating atherosclerosis and its consequences. For AS, effective pharmacological therapies remain limited. Understanding the shared risk factors and mechanisms between the two conditions may provide opportunities for therapeutic repositioning in AS. We performed a narrative review focusing on studies published from 2005 to 2025. Inclusion criteria encompassed clinical trials, experimental models, and molecular studies addressing overlapping risk factors, pathological pathways, and treatment approaches for AS and atherosclerosis. AS and atherosclerosis share key risk factors, including age, hypertension, hyperlipidemia, and diabetes. Molecular mechanisms, such as chronic inflammation, endothelial dysfunction, oxidative stress, lipid accumulation, and calcific remodeling, are common to both. Pathways involving the renin-angiotensin system, Notch signaling, and osteogenic mediators contribute to disease progression. Several drug classes, notably proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, lipoprotein(a) (Lp(a)) lowering therapies, anti-inflammatory agents, and immunomodulators, show potential for repositioning in AS management. The substantial overlap in risk factors and molecular mechanisms between AS and atherosclerosis supports a rationale for therapeutic repositioning. Targeting shared pathways could lead to innovative strategies for slowing AS progression and improving patient outcomes.

Background and Objectives: Diastolic dysfunction (DD) is a frequent complication following percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS), potentially contributing to adverse outcomes. This study aimed to investigate the association between post-procedural inflammatory markers and the severity of DD and to propose a preliminary risk score for early prediction. Materials and Methods: We retrospectively analyzed 181 ACS patients undergoing PCI, assessing C-reactive protein (CRP), leukocyte, neutrophil counts, and N-terminal pro-B-type natriuretic peptide (NT-proBNP) measured 24–48 h post-PCI. Echocardiographic DD grading was performed according to ASE/EACVI guidelines. Spearman correlation, ordinal regression, and decision-curve analysis were used to evaluate predictive performance. Results: CRP correlated with DD severity (ρ = 0.232, p = 0.002) and showed a borderline independent association (OR 1.004, 95% CI 0.999–1.009, p = 0.081). NT-proBNP correlated positively with both CRP and DD severity, while leukocyte and neutrophil counts were not significant. A three-parameter risk score (CRP > 10 mg/L, NT-proBNP > 125 pg/mL, age ≥ 65 years) identified patients at higher risk of moderate-to-severe DD (score ≥ 2: sensitivity 62%, specificity 71%). Decision-curve analysis demonstrated clinical utility in guiding post-PCI monitoring. Conclusions: A simple 0–3 point score combining age, CRP, and NT-proBNP showed potential for early identification of patients at risk of moderate-to-severe diastolic dysfunction after PCI. While the model demonstrated acceptable discrimination and calibration, its single-center design, limited sample size, and timing of biomarker assessment warrant cautious interpretation. External validation in larger, multicenter cohorts is required before clinical application.

Background and Objectives: Left ventricular diastolic dysfunction (LVDD) is a known precursor of heart failure with preserved ejection fraction (HFpEF), particularly in patients with metabolic comorbidities. Acute coronary syndrome (ACS) and percutaneous coronary interventions (PCI) may exacerbate LVDD via systemic inflammation. This study aimed to explore the association between post-procedural systemic inflammation and the severity of diastolic dysfunction in patients with ACS and metabolic comorbidities. Materials and Methods: A retrospective observational study was conducted in 181 patients with ACS who underwent PCI. Inflammatory markers (leukocytes, neutrophils, and C-reactive protein [CRP]) measured at 24–48 h post-intervention were analyzed in relation to diastolic dysfunction, assessed by echocardiography. Multivariable ordinal logistic regression and correlation analyses were performed. Results: CRP showed a non-significant trend toward association with more advanced diastolic dysfunction (p = 0.081). Hypertension had a positive but nonsignificant coefficient. Other metabolic comorbidities (diabetes, dyslipidemia, and obesity) were not significantly associated. The correlation between N-terminal pro-B-type natriuretic peptide (NT-proBNP) and troponin was exploratory. NT-proBNP was the only marker significantly correlated with high-sensitivity troponin (TrHS) at 48 h, indicating a link between myocardial injury and wall stress. Conclusions: CRP may be weakly associated with the severity of diastolic dysfunction post-PCI. However, classical metabolic comorbidities were not independently predictive. Post-PCI inflammation showed only modest, non-significant trends toward diastolic impairment, warranting confirmation in larger prospective studies.

Background: Despite advances in reperfusion therapy, ST-segment elevation myocardial infarction (STEMI) remains associated with substantial morbidity and mortality. Early identification of predictors of adverse outcomes is essential for improving risk stratification. Methods: This retrospective study included 512 STEMI patients who underwent coronary revascularization within 6 h of symptom onset. Clinical, laboratory, angiographic and echocardiographic variables were analyzed. The primary endpoint was in-hospital mortality. Secondary outcomes included reduced left ventricular ejection fraction (LVEF < 40%) and moderate-to-severe ischemic mitral regurgitation (IMR). Independent predictors of in-hospital mortality were identified using multivariable logistic regression, while secondary outcomes were described to characterize the study population. Model performance was evaluated using ROC analysis. Results: In-hospital mortality occurred in 9.4% of patients. Reduced LVEF was present in 26.2%, and IMR in 10.9%. Independent predictors of mortality included LVEF < 40% (OR 5.72, 95% CI 2.77–11.80, p < 0.001), IMR (OR 2.61, 95% CI 1.14–5.97, p = 0.023), lower hemoglobin levels (OR 0.74, 95% CI 0.61–0.91, p = 0.003), and reduced glomerular filtration rate (OR 0.96, 95% CI 0.95–0.98, p < 0.001). The model demonstrated good discrimination (AUC 0.88). Complete revascularization was not independently associated with mortality. Conclusions: Left ventricular dysfunction, IMR, anemia, and renal impairment are strong predictors of in-hospital mortality in STEMI patients. Integrating echocardiographic and laboratory parameters may improve early risk stratification and guide clinical decision-making.

Background: Electrocardiographic (ECG) abnormalities are common in acute pulmonary embolism (PE), but the prognostic significance of P wave morphology remains unclear. Early identification of high-risk patients is critical for guiding therapy and monitoring. Methods: We retrospectively analyzed 300 patients with confirmed PE. P wave morphology (normal, biphasic, notched, peaked) was evaluated for association with in-hospital mortality using chi-square and logistic regression, adjusted for age, sex, PESI score, and oxygen saturation. Results: Mortality differed significantly across P wave groups (χ² = 35.3, df = 3, p < 0.001). In univariate analysis, biphasic (OR 15.38, 95% CI 5.02–47.10, p < 0.001) and peaked (OR 7.21, 95% CI 2.35–22.10, p = 0.001) morphologies were strongly associated with mortality, whereas notched P waves were not (OR 1.44, 95% CI 0.16–12.87, p = 0.743). After adjustment, biphasic (OR 14.87, 95% CI 4.77–46.37, p < 0.001) and peaked (OR 6.58, 95% CI 2.11–20.53, p = 0.001) shapes remained independent predictors. Age, sex, PESI score, and oxygen saturation were not significant in multivariable analysis. Conclusions: Biphasic and peaked P wave morphologies on ECG are strong predictors of in-hospital mortality in patients with PE. Routine assessment of P wave shape may provide a simple tool for early risk stratification, warranting validation in prospective cohorts.

Background: Post-infarction heart failure (HF) remains a major contributor to morbidity and mortality despite advances in reperfusion and pharmacological management. However, the combined influence of clinical background, myocardial injury, neuro-hormonal activation, and angiographic disease on HF severity is not fully defined. Methods: We retrospectively analyzed 181 patients with confirmed myocardial infarction treated in a tertiary cardiology center. Demographics, cardiovascular risk factors, prior chronic HF, inflammatory markers (CRP, fibrinogen, ESR, leukocyte indices), and high-sensitivity troponin (hs-Tn) were measured at admission (pre-intervention), immediately after percutaneous coronary intervention (PCI), and at 48 h, angiographic lesion distributions were collected. HF severity was graded on a five-level scale and further dichotomized as no/mild HF (grade 0–1) versus moderate–severe HF (grade ≥ 2). Group comparisons and multivariable logistic regression were used to identify independent determinants of severe HF. Results: Moderate–severe HF occurred in 42.5% of patients (77/181). Compared to HF 0–1, the HF ≥ 2 group was older (64.0 vs. 60.5 years, p = 0.042) and exhibited substantially higher systemic inflammation (CRP 41.5 vs. 9.75 mg/L, p < 0.001; fibrinogen 435 vs. 346 mg/dL, p = 0.0002; ESR 28 vs. 18 mm/h, p = 0.0004). hs-Tn levels and NT-proBNP were significantly elevated in HF ≥ 2 (NT-proBNP 3449 vs. 1243 pg/mL, p = 0.0003), while left ventricular ejection fraction was reduced. Prior HF increased the likelihood of HF ≥ 2 (54.5% vs. 33.7%, p = 0.0078), and conservative therapy was associated with adverse outcomes (87.5% vs. 40.5%, p = 0.0235). In multivariable analysis, NT-proBNP remained the only independent predictor of moderate–severe HF, while CRP showed a positive but non-significant trend after adjustment. Conclusions: Post-MI HF severity reflects the combined influence of myocardial injury, neurohormonal stress, and systemic inflammatory activation. However, in multivariable analysis, NT-proBNP emerged as the dominant independent predictor of moderate–severe HF, while CRP reflected an associated but non-independent inflammatory signal.