Excessive inflammation and impaired healing of cardiac tissue following a myocardial infarction (MI) can drive the development of heart failure. Cardiac repair begins immediately after the onset of MI and continues for months. The repair process can be divided into the following 3 overlapping phases, each having distinct functions and sequelae: the inflammatory phase, the proliferative phase, and the maturation phase. Macrophages, neutrophils, and lymphocytes are present in the myocardium throughout the repair process and govern the duration and function of each of these phases. However, changes in the functions of these cell types across each phase are poorly characterized. Numerous immunomodulatory therapies that specifically target inflammation have been developed for promoting cardiac repair and preventing heart failure after MI. However, these treatments have been largely unsuccessful in large‐scale clinical randomized controlled trials. A potential explanation for this failure is the lack of a thorough understanding of the time‐dependent evolution of the functions of immune cells after a major cardiovascular event. Failure to account for this temporal plasticity in cell function may reduce the efficacy of immunomodulatory approaches that target cardiac repair. This review is concerned with how the functions of different immune cells change with time following an MI. Improved understanding of the temporal changes in immune cell function is important for the future development of effective and targeted treatments for preventing heart failure after MI.

Background: Percutaneous closure of patent foramen ovale (PFO) and atrial septal defects (ASD) is being more commonly performed due to changes in international guidelines supporting its use. This study was performed to determine the clinical outcomes, safety and cost implications of same-day discharge (SDD) following such procedures and place this in an Australian context. Methods: This was a retrospective, observational study of patients undergoing elective percutaneous PFO or ASD closure at St. George Hospital, Australia between January 2011 and January 2020. Primary outcomes included 30-day major adverse cardiovascular endpoints (MACE) and readmission to hospital within 30 days. Results: Twenty-four patients were included in the primary analysis. Ten (41.7%) patients underwent elective ASD closure while 14 (58.3%) underwent PFO closure. Among the 24 patients who underwent elective percutaneous closure of structural heart disease, 23 patients (95.8%) were managed with SDD. There were no MACE outcomes at 30 days. No patients were re-admitted to hospital at 30 days following these procedures. When compared to overnight admission to hospital post-elective percutaneous structural heart condition closure, SDD yielded a cost saving of AUD 5999 per case. Conclusion: SDD following elective percutaneous closure of ASD and PFO was demonstrated to be a safe and effective strategy for managing patients. With more widespread use, it can lead to significant cost savings for hospitals without compromising patient care.

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