Left Ventricular Adverse Remodeling in Ischemic Heart Disease: Emerging Cardiac Magnetic Resonance Imaging Biomarkers

Abstract

Post-ischemic left ventricular (LV) remodeling is a biologically complex process involving myocardial structure, LV shape, and function, beginning early after myocardial infarction (MI) and lasting until 1 year. Adverse remodeling is a post-MI maladaptive process that has been associated with long-term poor clinical outcomes. Cardiac Magnetic Resonance (CMR) is the best tool to define adverse remodeling because of its ability to accurately measure LV end-diastolic and end-systolic volumes and their variation over time and to characterize the underlying myocardial changes. Therefore, CMR is the gold standard method to assess in vivo myocardial infarction extension and to detect the presence of microvascular obstruction and intramyocardial hemorrhage, both associated with adverse remodeling. In recent times, new CMR quantitative biomarkers emerged as predictive of post-ischemic adverse remodeling, such as T1 mapping, myocardial strain, and 4D flow. Additionally, CMR T1 mapping imaging may depict infarcted tissue and assess diffuse myocardial fibrosis by using surrogate markers such as extracellular volume fraction, which may predict functional recovery or risk stratification of remodeling. Finally, there is emerging evidence supporting the utility of intracavitary blood flow kinetic energy and hemodynamic features assessed by the 4D flow CMR technique as early predictors of remodeling.

Keywords: 4D flow; adverse remodeling; cardiac magnetic resonance imaging; feature-tracking myocardial strain; left ventricular remodeling; myocardial infarction; surgical ventricular restoration.

Figure 1

Apical post-infarction aneurysm and intracavitary thrombus. The cine-MR image acquired on the vertical long-axis view (A) showed aneurysmal remodeling of the apex with a homogenous hypointense thrombus adhered to the wall (*, size of 4 × 2.5 cm). On the LGE image (B), the mass appeared markedly hypointense compared to the ventricular blood pool and was surrounded by an enhanced infarcted LV wall (transmural LGE pattern, arrowheads).

Figure 2

Cardiac magnetic resonance images of LV anterior myocardial infarction due to left anterior descending artery occlusion, acquired during the subacute phase (A–F) and six-month FU (G–I). T2-w STIR (A) and LGE (B) images acquired on the mid-ventricular short axis view show myocardial edema (white arrowhead) and necrosis (black arrowhead), respectively, of the antero-septal wall. Cine MR images acquired in four-chamber view (C) show thickening of the damaged LV apical wall due to post-ischemic edema and the presence of a tiny apical thrombus (red arrow). Areas of increased myocardial T1, reduced circumferential strain (CS), and expansion of extracellular volume fraction (ECV) well match the infarcted region, respectively, on the native nT1 (D), CS (E), and ECV (F) maps. FU images demonstrate disappearance of myocardial edema on STIR images (G), persistence and shrinkage of the scar on LGE images (H), and adverse LV remodeling with thinning of the infarcted walls and rounding of the apex as for aneurysmal evolution (black arrows, I). LV: left ventricle; STIR: short tau inversion recovery; LGE: late gadolinium enhancement.

Figure 3

A color-coded 4D flow vector map at mid-diastole demonstrates the intracavitary flow with the generation of a large mid-ventricular vortex in patients with post-ischemic LV dilation.

Figure 4

Cardiac MR imaging of a 72-year-old man with an occluded left anterior descendent coronary artery treated with a by-pass and surgical ventricle restoration. Two-chamber cine true fast imaging with steady-state free precession sequence in the end-systolic phase before (A) and six months after surgery (B).

Figure 5

CMR imaging biomarkers in the risk prediction of adverse remodeling.