Very late bioresorbable scaffold thrombosis after discontinuation of dual antiplatelet therapy

Inflammation induced by pathogens or of autoimmune origin is particularly harmful to terminally differentiated organs with poor regenerative capacity, such as the heart and brain. Chronic inflammation is thought to impair heart failure, neurodegenerative diseases, and metabolic syndrome. Interestingly, increased resting heart rate has been linked to cognitivedecline after ischaemic stroke. Thisobservation is supportedby animal experiments demonstrating deleterious effects of chronic stress on ischaemic brain injury mediated by increased heart rate. Interestingly, damage to the cerebral insular lobe (or ‘insula’) following stroke or subarachnoid haemorrhage causes autonomic dysfunction and sympathetic overactivation (stress), and may lead to neurocardiogenic damage and troponin elevation. Therefore, not only may subclinical myocardial injury (as reflected by elevated cTnT) lead to cognitive dysfunction, vice versa it is also possible that brain injury (associated with cognitive dysfunction) causes cardiac damage. Finally, we think that an important contribution has been made to the heart and brain interaction. The roles of shared common harmful mechanisms (e.g. autonomic nervous imbalance, inflammation), subclinical (silent) stroke, and white matter disease need to be investigated to uncover the heart of the matter.