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Atrial cardiomyopathy refers to structural and electrical remodelling of the atria, which can lead to impaired mechanical function. While historical studies have implicated atrial fibrillation as the leading cause of cardioembolic stroke, atrial cardiomyopathy may be an important, underestimated contributor. To date, the relationship between atrial cardiomyopathy, atrial fibrillation, and cardioembolic stroke remains obscure. This review summarizes the pathogenesis of atrial cardiomyopathy, with a special focus on neurohormonal and inflammatory mechanisms, as well as the role of adipose tissue, especially epicardial fat in atrial remodelling. It reviews the current evidence implicating atrial cardiomyopathy as a cause of embolic stroke, with atrial fibrillation as a lagging marker of an increased thrombogenic atrial substrate. Finally, it discusses the potential of antithrombotic therapy in embolic stroke with undetermined source and appraises the available diagnostic techniques for atrial cardiomyopathy, including imaging techniques such as echocardiography, computed tomography, and magnetic resonance imaging as well as electroanatomic mapping, electrocardiogram, biomarkers, and genetic testing. More prospective studies are needed to define the relationship between atrial cardiomyopathy, atrial fibrillation, and embolic stroke and to establish a prompt diagnosis and specific treatment strategies in these patients with atrial cardiomyopathy for the secondary and even primary prevention of embolic stroke.

BackgroundCancer and ischemic heart disease are the leading causes of mortality. The optimal management for patients with concomitant acute myocardial infarction (AMI) and cancer remains challenging.ObjectiveTo evaluate in-hospital and 1-year adverse outcomes in cancer patients receiving percutaneous coronary intervention (PCI) to treat AMI.MethodsThis was a single-center, retrospective cohort study, patients with cancer admitted to The First Affiliated Hospital of Xi’an Jiaotong University for AMI and discharged between January 2015 and June 2020 were analyzed. The outcomes were all-cause mortality at 1-year follow up and incidence of in-hospital adverse events, including arrhythmias, heart failure, major bleeding, stroke, and all-cause death.ResultsA total of 119 patients were included, of these, 68 (57.1%) received PCI (PCI group) and 51 (42.9%) did not (non-PCI group). Patients in the PCI group had a lower incidence of in-hospital arrhythmias (22.1 vs. 39.2%; p = 0.042), major bleeding (2.9 vs. 15.7%; p = 0.013), and all-cause mortality (1.5 vs. 11.8%; p = 0.018) than those in non-PCI group. On 1-year follow-up, the PCI group had a lower all-cause mortality than the non-PCI group (log-rank test = 14.65; p < 0.001). Multivariable Cox regression showed that PCI is an independent protective factor (adjusted HR = 0.503 [0.243–0.947], p = 0.045) for cancer patients who have concomitant AMI.ConclusionCancer patients receiving PCI for AMI had a lower risk of in-hospital adverse events and mortality as well as 1-year all-cause mortality compared to those who refused PCI. Our study therefore supports the use of PCI to improve prognosis of this selected group of patients.

Hypertrophic cardiomyopathy (HCM) is a genetic disease of the cardiac sarcomere with an autosomal dominant pattern of inheritance. Patients with HCM are at high risk of developing atrial fibrillation (AF) particularly in the setting of advanced diastolic dysfunction and left atrial enlargement. AF is a marker of increased mortality and morbidity and results in a significant reduction in quality of life. Antiarrhythmic medications improve symptoms and reduce AF recurrence, but few are safe and there exists little data to guide their long-term use in HCM. Non-pharmacologic approaches have emerged and have equal or greater efficacy than pharmacologic approaches. Although these approaches are promising, the long-term impact on atrial function needs to be carefully studied as it may impact quality of life in patients that age in the setting of a progressive diastolic disease disorder. Nonetheless, with the significant impact of AF in HCM, rhythm control strategies are often required. The understanding of rhythm control strategies in HCM, an often rapidly progressive diastolic dysfunction disorder, may provide insight in how to treat the much more prevalent AF patient with hypertensive cardiomyopathy. Regardless of treatment strategy (rhythm or rate control) patients are a moderate to high risk of thromboembolism and until data are available to suggest otherwise require long-term warfarin anticoagulation.