Ebstein anomaly (EA) is a rare congenital heart defect that develops as the baby's heart grows in the mother's womb. Researchers aren't sure what risk factors are underlying the defect. However, genetic and environmental factors, family history of heart defects, and the mother's use of certain medications, such as lithium, during pregnancy are believed to play a role.

More than 1 million Americans yearly have a new or recurrent acute myocardial infarction (AMI). Although the mortality rate from AMI has decreased in recent years, post-MI congestive heart failure is increasing due to microvascular obstruction (MVO), ultimately limiting myocardial salvage. We aim to address this unmet need by devising an image-guided therapy called sonoreperfusion (SRP) to resolve MVO by ultrasound-targeted microbubble cavitation (UTMC). In this study, we hypothesized that fibrin-targeted phase shift microbubbles (FTPSMBs; ∼200 nm) (Microvascular Therapeutics, Inc) would improve SRP efficacy compared to fibrin-targeted microbubbles (FTMBs; 1–3 μm) to treat MVO owing to the smaller size and more efficient microthrombi penetration. A rat hindlimb model of MVO was created by directly injecting freshly prepared porcine microthrombi into the left femoral artery under contrast-enhanced ultrasound imaging (CEUS) guidance, and treated with UTMC (1 MHz, 1.5 MPa, 5 ms pulse duration, 5-sec pulse interval) with concomitant administration of FTPSMBs/FTMBs (3 mL/hr). The treatment effect was accessed with CEUS. UTMC with FTPSMBs caused more rapid and complete reperfusion of rat hindlimb following MVO compared with FTMB, likely owing to their small size and more effective thrombus penetration. Studies to explore the underlying molecular mechanisms associated with SRP treatments are underway.

Background: Interstitial myocardial fibrosis is a crucial pathological feature of many cardiovascular disorders. Myocardial fibrosis resulting in extracellular volume (ECV) expansion can be quantified via cardiac MRI (CMR) with T₁ mapping before and after minimally invasive gadolinium (Gd) contrast agent administration. However, longitudinal repetitive ECV measurements are challenging in rodents due to the prolonged scan time with cardiac and respiratory gating that is required for conventional T₁ mapping and the invasive nature of the rodent intravenous lines. Methods: To address these challenges, the objective of this study is to establish a fast, free-breathing, and gating-free ECV procedure using a minimally invasive subcutaneous catheter for in-scanner Gd administration that can allow longitudinal repetitive ECV evaluations in rodent models. This is achieved by the (1) IntraGate sequence for free-breathing, gating-free cardiac imaging; (2) minimally invasive subcutaneous in-scanner Gd administration; and (3) fast T₁ mapping with a varied flip angle (VFA) in conjunction with (4) triple jugular vein blood T₁ normalization. Additionally, full cine CMR (multi-slice short-axis, long-axis 2-chamber, and long-axis 4-chamber) was acquired during the waiting period to assess comprehensive cardiac function and strain. Results: We successfully established a minimally invasive fast ECV quantification protocol to enable longitudinal repetitive ECV quantifications in rodents. Minimally invasive subcutaneous Gd bolus administration induced a reasonable dynamic contrast enhancement (DCE) time course, reaching a steady state in ~20 min for stable T₁ quantification. The free-breathing gating-free VFA T₁ quantification scheme allows for rapid cardiac (~2.5 min) and jugular vein (49 s) T₁ quantification with no motion artifacts. The triple jugular vein T₁ acquisitions (1 pre-contrast and 2 post-contrast) immediately flanking the heart T₁ acquisitions enable accurate myocardial ECV quantification. Our data demonstrated that left-ventricular myocardial ECV quantification was highly reproducible with repeated scans, and the ECV values (0.25) are comparable to reported ranges among humans and rodents. This protocol was successfully applied to the ischemia–reperfusion injury model to detect myocardial fibrosis, which was validated by histopathology. Conclusions: We established a simple, fast, minimally invasive, and robust CMR protocol in rodents that can enable longitudinal repetitive ECV quantification for cardiovascular disease progression. It can be used to monitor disease regression with interventions.