Dataset Information

Transforming a pre-existing MRI environment into an interventional cardiac MRI suite.

ABSTRACT:

Aims

To illustrate the practical and technical challenges along with the safety aspects when performing MRI-guided electrophysiological procedures in a pre-existing diagnostic magnetic resonance imaging (MRI) environment.

Methods and results

A dedicated, well-trained multidisciplinary interventional cardiac MRI team (iCMR team), consisting of electrophysiologists, imaging cardiologists, radiologists, anaesthesiologists, MRI physicists, electrophysiological (EP) and MRI technicians, biomedical engineers, and medical instrumentation technologists is a prerequisite for a safe and feasible implementation of CMR-guided electrophysiological procedures (iCMR) in a pre-existing MRI environment. A formal dry run "mock-up" to address the entire spectrum of technical, logistic, and safety issues was performed before obtaining final approval of the Board of Directors. With this process we showed feasibility of our workflow, safety protocol, and bailout procedures during iCMR outside the conventional EP lab. The practical aspects of performing iCMR procedures in a pre-existing MRI environment were addressed and solidified. Finally, the influence on neighbouring MRI scanners was evaluated, showing no interference.

Conclusion

Transforming a pre-existing diagnostic MRI environment into an iCMR suite is feasible and safe. However, performing iCMR procedures outside the conventional fluoroscopic lab, poses challenges with technical, practical, and safety aspects that need to be addressed by a dedicated multi-disciplinary iCMR team.

SUBMITTER: Bijvoet GP

PROVIDER: S-EPMC8456838 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background: Cardiac bridging integrator 1 (cBIN1) organizes transverse tubule (t-tubule) membrane calcium handling microdomains required for normal beat-to-beat contractility. cBIN1 is transcriptionally reduced in heart failure (HF). We recently found that cBIN1 pretreatment can limit HF development in stressed mice. Here, we aim to explore whether cBIN1 replacement therapy can improve myocardial function in continuously stressed hearts with pre-existing HF. Methods: Adult male mice were subjected to sham or transverse aortic constriction (TAC) surgery at the age of 8-10 weeks old. Adeno-associated virus 9 (AAV9) transducing cBIN1-V5 or GFP-V5 (3 × 1010 vg) was administered through retro-orbital injection at 5 weeks post-TAC. Mice were followed by echocardiography to monitor cardiac function until 20 weeks after TAC. Overall survival, heart and lung weight (LW), and HF incidence were determined. In a second set of animals in which AAV9-cBIN1 pretreatment prevents HF, we recorded cardiac pressure-volume (PV) loops and obtained myocardial immunofluorescence imaging. Results: The overall Kaplan-Meir survival of AAV9-cBIN1 mice was 77.8%, indicating a significant partial rescue between AAV9-GFP (58.8%) and sham (100%) treated mice. In mice with ejection fraction (EF) ≥30% prior to AAV9 injection at 5 weeks post-TAC, AAV9-cBIN1 significantly increased survival to 93.3%, compared to 62.5% survival for AAV9-GFP treated mice. The effect of exogenous cBIN1 was to attenuate TAC-induced left ventricular (LV) dilation and prevent further HF development. Recovery of EF also occurs in AAV9-cBIN1-treated mice. We found that EF increases to a peak at 6-8 weeks post-viral injection. Furthermore, PV loop analysis identified that AAV9-cBIN1 increases both systolic and diastolic function of the post-TAC hearts. At the myocyte level, AAV9-cBIN1 normalizes cBIN1 expression, t-tubule membrane intensity, and intracellular distribution of Cav1.2 and ryanodine receptors (RyRs). Conclusions: In mice with pre-existing HF, exogenous cBIN1 can normalize t-tubule calcium handling microdomains, limit HF progression, rescue cardiac function, and improve survival.