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Cardiovascular Engineering

Cardiovascular Engineering - Poster Session A

Poster H9 - Cardiac Strain MRI Analysis Shows Improved Cardiac Function after Myocardial Infarction in Pigs

Thursday, October 24, 2024
10:00 AM - 11:00 AM EST
Location: Exhibit Hall E, F & G

Introduction:  Cardiac injuries such as myocardial infarctions (MI) can result in the loss of cardiomyocytes, formation of large fibrotic scars, increased stiffness, and impaired relaxation of the left ventricle. Due to the limited regenerative capabilities of the heart, most cardiac tissue is lost after acute MI and is not recoverable. Such adverse changes to the heart post-MI paired with no long term recovery of cardiomyocytes can be fatal and lead to heart failure. In the past synthetic cardiac stromal cells (synCSCs) have demonstrated much progress in improving cardiac function and repair post-MI. Further research has also demonstrated the effectiveness of embedding these synCSC particles in hyaluronic acid (HA) hydrogels, resulting in the creation of injectable Artificial Cardiac Patch (iArtCP). While various methods have been utilized to analyze the efficacy of this novel therapeutic, this study will provide a new perspective in analyzing cardiac repair and function through MRI analysis of cardiac strain. Various methods of myocardial strain will be analyzed and an overview of different types of strains such as Longitudinal, Circumferential and Radial will be discussed.

Materials and

Methods:  The porcine models were separated into three groups: induced MI (negative control), induced MI with Hyaluronic Acid gel (negative control), and MI with the iArtCP treatment. Cardiac function and health were primarily analyzed through magnetic resonance imaging (MRI) across the groups at various time points. Each group was studied longitudinally with images acquired at Pre-MI, Day 3, and Day 29 post-MI time points (Figure 1). At each MRI session, short and long-axis MRI cine sequences were taken. Cine sequences were used to calculate left ventricular ejection fraction (LVEF), stroke volume, and left ventricular fractional shortening (LVFS). LVEF is the percentage of blood ejected by the heart per beat, calculated by identifying and measuring end-diastolic and end-systolic volumes of the left ventricle (LVEDV and LVESV): LVEF = (LVEDV–LVESV)/LVEDV. The shortening of the cardiac muscles was analyzed by measuring the internal diameter of the left ventricle during systolic and diastolic phases (LVIDs and LVIDd): LVFS = (LVIDd – LVIDs) / LVIDd. Cine sequences were also used to measure myocardial strain (MS) within a cardiac cycle: MS=(L-Lo)/Lo. MS was analyzed in three perspectives: longitudinal, circumferential and radial. Longitudinal strain was measured from the apex to the mitral valve, circumferential strain along the left ventricle's perimeter, and radial strain by thickness changes using the short-axis cine view (Figure 2). Stroke volume was calculated by finding the difference in LVEDV and LVESV. All measurements were taken using the OsiriX DICOM (Pixmeo). Statistical analysis was performed using a two-way ANOVA test, followed by the Bonferroni test.

Results, Conclusions, and Discussions: After a myocardial infarction, the necrosis can lead to loss of cardiomyocyte function and myocardial fiber shortening. Such changes in the cardiac environment can lead to reduced cardiac output and strain within the left ventricle. By analyzing cardiac strain overtime, it enables us to study the health of myocardial fibers in effectively pumping blood to the rest of the body. Myocardial Strains in the longitudinal, radial and circumferential directions indicated the degree of deformation of myocardial fibers within each cardiac cycle. At Day 28, the treatment group (MI+iArtCP) had significantly improved cardiac strain both compared to itself from Day 3 as well as across the negative controls on Day 28 (Figure 3). Analysis of left ventricular ejection fraction (LVEF) and fractional shortening (LVFS) also showed improvement in cardiac function as LVEF and LVFS measurements were significantly elevated in the treatment group in comparison to itself on Day 3 and the controls on Day 28 (Figure 4). All together, improvements across several factors indicate that cardiac function was effectively improved Post-MI and that the analysis of myocardial strain is an effective tool in analyzing cardiac repair. Limitations within the study include small sample size and limited duration to fully study the long-term effects of the therapeutics. Variable image quality, noise and operator dependency are limitations in obtaining MRI sequences. Despite these limitations myocardial strain measures are valuable in revealing cardiac function and health and have strong translational prospects as these methods can easily be implemented in clinical settings.

Acknowledgements (Optional):