Cardiac sarcoidosis (CS) and inherited cardiomyopathies (inherited CM) are associated with advanced heart failure, cardiac conduction defects, ventricular arrhythmias and sudden cardiac death. Both conditions can have similar clinical presentations. Differentiating between the two disease cohorts is important in delivering specific management to patients, such as immunosuppressive therapy for CS patients and genetic screening for inherited CM. In this review, we examined the existing evidence on the overlap between CS and common inherited CM, such as hypertrophic cardiomyopathy, arrhythmogenic cardiomyopathy, restrictive cardiomyopathy and dilated cardiomyopathy. In patients where both CS and inherited CM were implicated, CS tended to be diagnosed much later, often when patients presented with complications warranting a workup or cardiac histological confirmation. CS can masquerade as an inherited CM, leading to delays in the instigation of CS therapy. Confirmed dual pathology overlap between inherited CM and CS is rarer. Advanced cardiac imaging, such as cardiovascular magnetic resonance, plays an important role in the clinical workup of both CS and inherited CM. However, findings on cardiac imaging alone often cannot differentiate between the two conditions. Definitive differentiation between CS and inherited CM requires both clinical experience and, at times, a myocardial biopsy.

Coronavirus disease 19 (COVID-19) is responsible for one of the worst pandemics in human history. The causative virus, the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), can invade host cells in multiple organs by binding the angiotensin-converting enzyme (ACE) II expressed on the cell surface. Once inside the host cell, viral replication takes place, leading to cellular disruption and the release of signal molecules that are recognised by the innate immune system. Innate immunity activation leads to the release of proinflammatory cytokines and primes the adaptive immune system. The proinflammatory environment defends against further viral entry and replication. SARS-CoV-2 infection is thought to lead to myocardial injury through several mechanisms. Firstly, direct viral-mediated cellular invasion of cardiomyocytes has been shown in in vitro and histological studies, which is related to cellular injury. Secondly, the proinflammatory state during COVID-19 can lead to myocardial injury and the release of protein remnants of the cardiac contractile machinery. Thirdly, the hypercoagulable state of COVID-19 is associated with thromboembolism of coronary arteries and/or other vascular systems. COVID-19 patients can also develop heart failure; however, the underlying mechanism is much less well-characterised than for myocardial injury. Several questions remain regarding COVID-19-related heart failure, including its potential reversibility, the role of anti-viral medications in its prevention, and the mechanisms underlying heart failure pathogenesis in long COVID-19. Further work is required to improve our understanding of the mechanism of cardiac sequelae in COVID-19, which may enable us to target SARS-CoV-2 and protect patients against longer-lasting cardiovascular complications.