Takotsubo syndrome is featured by transient left ventricular dysfunction typically triggered by emotional or physical stress. Growing evidence supports a pivotal role of brain-heart interactions in its pathophysiology. Structural neuroimaging studies have identified reduced cortical thickness and gray matter volume in limbic and autonomic regulatory regions, including the insula, cingulate cortex, and amygdala. Functional imaging studies, including 18F-fluorodeoxyglucose (FDG) PET and functional MRI, have demonstrated persistent amygdalar hyperactivity, altered limbic system activity, and widespread hypoconnectivity within autonomic and emotional regulation networks. Importantly, several of these abnormalities appear to persist long after recovery of cardiac function.
Cardiac and neurologic manifestations are common in Fabry disease (FD) and significantly impact prognosis and quality of life. Cardiac involvement includes hypertrophic cardiomyopathy, arrhythmias, and heart failure, while the main neurologic manifestations are cerebrovascular events and peripheral neuropathy. The progressive nature of these manifestations highlights the importance of early detection and management to prevent long-term damage. This article provides an overview of the key cardiac and neurologic manifestations of FD, offers guidance on when cardiologists and neurologists should suspect FD and start diagnostic evaluation, and summarizes the evidence on the role of disease-modifying therapies in managing cardiovascular and neurologic complications.
Heart failure and embolism frequently coexist and share common pathophysiologic mechanisms, including stasis, endothelial dysfunction and inflammation. Their clinical presentations can often be misleading, which makes the diagnostic challenging and mandates appropriate use of different imaging techniques. This article summarizes the pathophysiological links, diagnostic challenges and management strategies of these 2 entities. It also outlines evidence-based and guideline-directed strategies for prevention and treatment, including the role of inflammation, atrial cardiomyopathy and updated anticoagulation recommendations.
Pulmonary hypertension (PH) is a heterogeneous condition defined by an increase in mean pulmonary arterial pressure over 20 mm Hg diagnosed through right heart catheterization. Its global prevalence is around 0.6% to 1%. The prognosis used to be poor but nowadays early diagnosis, risk stratification, and a personalized treatment can significantly enhance the prognosis and quality of life of these patients. PH pathophysiology comprises genetic and environmental factors, such as endothelial dysfunction, smooth muscle cell proliferation, inflammation, thrombosis, and right ventricular remodeling. Especially in pulmonary arterial hypertension, treatment options have been radically altered.
Heart failure (HF) is strongly associated with venous thromboembolism (VTE) through mechanisms of hypercoagulability, venous stasis, and endothelial dysfunction. Patients with HF who develop pulmonary embolism present diagnostic challenges due to overlapping symptoms, and they experience higher risks of mortality and bleeding compared with those without HF. Current evidence highlights HF hospitalization as a major transient risk factor for VTE and chronic HF as an intermediate risk factor for recurrence. This article summarizes the pathophysiological links, prognostic implications, and anticoagulation strategies for patients with HF and VTE.
