Background: Acute myocarditis is characterized by heterogeneous inflammatory myocardial involvement, and cardiac magnetic resonance (CMR)-derived late gadolinium enhancement (LGE) is an important marker of myocardial injury. However, the relationship between systemic inflammatory burden and quantitative CMR-defined myocardial involvement remains insufficiently characterized. We aimed to evaluate the association between inflammatory indices, particularly the systemic inflammation response index (SIRI), and the presence and extent of LGE in patients with acute myocarditis. Methods: This retrospective single-center observational cohort study included clinically suspected acute myocarditis patients who underwent CMR within 4 weeks of symptom onset. Patients were classified according to the presence or absence of LGE on CMR. Inflammatory indices, including the SIRI, systemic immune–inflammation index (SII), multi-inflammatory indices (MII-I and MII-II), and stress hyperglycemia ratio (SHR), were calculated from admission laboratory parameters. Receiver operating characteristic (ROC) analysis, logistic regression, linear regression, and hurdle Poisson regression analyses were performed. Results: LGE was present in 62 patients (36.5%). Patients with LGE demonstrated significantly higher inflammatory markers and inflammatory index values. Among all evaluated biomarkers, the SIRI demonstrated the highest discriminatory performance for LGE detection (AUC: 0.944, 95% CI: 0.897–0.973; cut-off > 1.33; sensitivity 93.5%; specificity 85.2%; p < 0.001). In multivariable logistic regression analysis, the SIRI remained independently associated with LGE presence (OR: 4.538, 95% CI: 2.570–8.011; p < 0.001). The SIRI was also independently associated with both log-transformed LGE percentage and the number of involved myocardial segments. Conclusions: Higher SIRI levels were associated with both the presence and extent of CMR-defined myocardial involvement in patients with acute myocarditis and may reflect the burden of early inflammatory myocardial injury. However, these findings should be interpreted cautiously given the retrospective single-center design and require confirmation in larger prospective multicenter studies before potential clinical application.

Background/Objectives: Hypertrophic cardiomyopathy (HCM) is characterized by myocardial hypertrophy and fibrosis, while low-grade systemic inflammation may contribute to adverse myocardial remodeling. We investigated the relationship between routinely available inflammatory and nutritional indices and late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) and explored a simple biomarker–structural score for identifying patients with LGE positivity. Methods: This retrospective, cross-sectional, single-center study included 197 adults with HCM who underwent CMR and laboratory testing within one week. Ten inflammatory and nutritional indices were evaluated, with Benjamini–Hochberg false-discovery rate (FDR) correction for multiple comparisons. LGE-positive patients were additionally stratified by scar burden. Multivariable logistic regression examined laboratory and structural correlates of LGE. An exploratory 0–5 biomarker–structural score assigned one point each for albumin < 40 g/L, erythrocyte sedimentation rate (ESR) ≥ 5 mm/h, hs-Troponin T ≥ 14 ng/L, NT-proBNP ≥ 125 pg/mL, and interventricular septal thickness (IVS) ≥ 1.8 cm. Discrimination was assessed by ROC analysis, and internal stability was examined using 1000 bootstrap resamples. Results: Among 197 patients, 127 (64.5%) were LGE-positive. After FDR correction, higher NLR × CRP index, CAR, and PLR × CRP index and lower PNI were associated with LGE positivity, while the NLR × CRP index, CAR, and PNI remained associated with increasing LGE burden. Lower albumin, higher ESR, NT-proBNP ≥ 125 pg/mL, and greater IVS thickness were independently associated with LGE positivity. The exploratory five-component score yielded an AUC of 0.818, with a mean bootstrap AUC of 0.820. Conclusions: In HCM, routinely available inflammatory and nutritional indices were associated with LGE-defined myocardial scar, with the NLR × CRP index, CAR, and PNI showing the most consistent relationships with LGE burden. A simple exploratory score integrating inflammatory/nutritional status, systemic inflammation, myocardial injury, hemodynamic stress, and septal hypertrophy showed an apparent AUC of 0.818 for LGE positivity, supporting further evaluation in independent HCM cohorts.

We aimed to evaluate left atrial appendage functions (LAA) derived by speckle tracking echocardiography in patients with mild to severe mitral regurgitatio