Pathophysiology of LV Remodeling Following STEMI

Central Illustration. Serial Diffusion Tensor CMR Scans Were Performed on 100 Reperfused Patients With STEMI at 1 Week and 12 Months Acutely infarcted myocardium had higher mean diffusivity (MD) and lower fractional anisotropy (FA), suggesting that diffusion becomes more unrestricted and isotropic from edema and cardiomyocyte disorganization than remote myocardium. The myocardial sheetlets are unable to adopt their usual orientation in systole, as suggested by low absolute secondary eigenvector angle (E2A) values, and they have fewer myocytes with right-handed orientation (RHM) on helix angle maps, thus highlighting the early loss of organization among subendocardial myocytes. Acute infarct fractional anisotropy and secondary eigenvector angle were independently associated with adverse left ventricular (LV) remodeling at 12 months, with better accuracy than other cardiac magnetic resonance (CMR)–derived biomarkers. DT = diffusion tensor; STEMI = ST-segment elevation myocardial infarction.

Figure 1. Flowchart of Study Enrollment From the 150 enrolled patients, 100 completed early and 12-month scans. CMR = cardiac magnetic resonance; DT = diffusion tensor; ICD = implantable cardioverter-defibrillator; MRI = magnetic resonance imaging; STEMI = ST-segment elevation myocardial infarction.

Figure 2. Representative CMR Images of 2 Separate Patients (A) Short-axis images obtained from the early and 12-month scans of a 70-year-old man who initially presented with anterior ST-segment elevation and underwent primary PCI to his left anterior descending artery. His acute LVEF remained severely impaired (30%) at 12 months, but his LVEDV increased from 172 mL to 228 mL, thus fulfilling the criteria for adverse remodeling. In the early scan, LGE demonstrated transmural infarction of basal anterior and septal walls. Corresponding areas on diffusion tensor maps show high MD, low FA, low E2A, and reduction of RHM (red and orange pixels). By 12 months, the anterior and septal walls have thinned and remain transmurally infarcted. MD was increased in areas corresponding to scar, which in the absence of edema is suggestive of expansion in ECV. FA remained low, indicating underlying collagen deposition and cardiomyocyte disorganization. The E2A remained low, suggesting the myocardial sheetlets were unable to adopt their usual systolic configuration, and the relative absence of RHM suggests loss of organization among subendocardial myocytes. (B) Short-axis images of a 65-year-old man who also…

Figure 3. Correlations Between Early DT-CMR Parameters and LV Size at 12 Months (A) Increased MD, (B) decreased FA, (C) decreased absolute E2A, and (D) decreased proportions of RHM in acutely infarcted myocardium were associated with the degree of serial increase in body surface area (BSA)–indexed left ventricular end-diastolic volume (LVEDVi) over 12 months following STEMI. LV = left ventricular; other abbreviations as in Figures 1 and 2.

Figure 4. ROC Curves for Prediction of Adverse LV Remodeling and LVEF <35% at 12 Months Comparison of receiver-operating characteristic (ROC) curves with 95% CIs of diffusion tensor CMR parameters, acute LVEF, acute infarct size, and infarct ECV. The absolute E2A had the highest area under the curve for predicting adverse remodeling. Abbreviations as in Figures 1 to 3.

Figure 5. Relationship Between Tissue Characteristics of Chronic Infarct, Adjacent, and Remote Regions With Serial Change in LV Size (A) Increased MD, (B) decreased FA, (C) decreased absolute E2A, and (D) decreased proportions of RHM in acutely infarcted myocardium were all associated with lower LVEF at 12 months following STEMI. Abbreviations as in Figures 1 to 3.