Background/Objectives: Ventricular recovery after ST-segment elevation myocardial infarction (STEMI) is commonly assessed using either structural (volumetric) or functional (ejection-fraction) criteria, although these may capture different aspects of recovery. We examined whether their cross-classification identifies distinct recovery patterns and whether myocardial mechanics and left atrial function provide additional information. Methods: We prospectively followed 101 patients with first STEMI and single-vessel coronary artery disease treated with PCI. Echocardiography was performed 12–24 h after reperfusion and at 12 ± 2 months. Structural recovery (≥15% reduction in 3D LV end-systolic volume) and functional recovery (≥5-point absolute LVEF increase) were cross-classified into four recovery patterns. Results: Among 53 patients with complete paired measurements, 10 (18.9%) showed concordant recovery, 7 (13.2%) isolated structural recovery, 9 (17.0%) isolated functional recovery, and 27 (50.9%) no recovery; 30.2% therefore showed discordant recovery. The no-recovery group was heterogeneous, including both volumetric deterioration and stable or improving volumes below the recovery threshold. Continuous changes in 3D-ESV and LVEF were only moderately correlated (ρ = 0.353, p = 0.0095), and discordance persisted in sensitivity analyses. Myocardial mechanics and LASR did not differentiate recovery patterns, but several of these baseline markers showed exploratory associations with clinical outcomes after false-discovery-rate correction. Conclusions: Structural and functional recovery after STEMI are complementary rather than interchangeable, and this discordance persisted across extensive sensitivity analyses; however, assignment of individual patients to specific recovery categories remained sensitive to the chosen thresholds and LVEF measurement method. Myocardial mechanics and LASR may provide additional information about clinical expression.

Dilated cardiomyopathy (DCM) is a major cause of heart failure and sudden cardiac death, characterized by left ventricular dilation and systolic dysfunction in the absence of significant coronary or valvular disease. Although traditionally viewed as an idiopathic condition, DCM is now recognized as a genetically driven disorder in a substantial proportion of cases. Pathogenic variants affecting structural, cytoskeletal, desmosomal, and nuclear proteins not only initiate myocardial remodeling but also influence disease progression and arrhythmic vulnerability. Importantly, genetic findings do not merely explain disease etiology but also shape its clinical expression. The specific gene involved, as well as the type of mutation, can influence the pattern of ventricular remodeling, the distribution of myocardial fibrosis, and the degree of electrical instability. Cardiac magnetic resonance has emerged as a central tool in bridging molecular insights with clinical assessment. By enabling accurate evaluation of ventricular volumes and function, as well as detailed tissue characterization through late gadolinium enhancement (LGE) and parametric mapping, cardiac magnetic resonance reveals imaging patterns that often mirror the underlying genetic substrate. The integration of genetic testing and advanced imaging provides a more comprehensive understanding of dilated cardiomyopathy, allowing improved risk stratification and supporting a personalized approach to patient management.