Stroke in young adults is associated with significant morbidity, and its prevalence is rising in the United States. This is partly attributed to a rise in the prevalence of traditional risk factors including hypertension, hypercholesterolemia, obesity, diabetes mellitus, smoking and heart disease. In addition, there are non-modifiable risk factors comprising migraine, pregnancy and postpartum state, illicit drug use, oral contraceptives and hypercoagulable state. The mechanisms causing stroke in young adults are unique and include cervical dissection, cardioembolic phenomenon, vasculitis and vasculopathy, connective tissue disease, patent foramen ovale and cerebral venous thrombosis. The diagnosis of stroke in the young population can be challenging given its myriad clinical presentations. In this document, we provide an overview of the epidemiology of stroke in young adults, explore mechanisms that may explain increasing rates of stroke in this population, and provide a critical updated overview of the existing literature on the management and prevention of stroke in young adults.

Cardiac amyloidosis (CA) is caused by deposition of amyloid fibrils in the myocardium and has two main subtypes, transthyretin cardiac amyloidosis (ATTR) and immunoglobulin light chain cardiac amyloidosis (AL). ATTR is further differentiated into wild-type (wtATTR) and hereditary (hATTR), depending on the absence or presence of mutation in the transthyretin gene. The increased recognition of disease with the improvement in diagnostic armamentarium and serendipitous advancements in the therapeutic landscape have changed the status of CA from being a rare and untreatable disease to being a not-so-rare and treatable disease. Both ATTR and AL have certain clinical aspects that can provide early clues for the disease. While electrocardiography followed by echocardiography and subsequently cardiac magnetic resonance can raise suspicion for CA, the definitive diagnosis of ATTR is non-invasively established by bone scintigraphy while that of AL always needs histological confirmation. Severity of CA can be gauged by serum biomarker-based staging of both ATTR and AL. ATTR therapies work by silencing or stabilizing TTR or by degrading amyloid fibrils, while AL is managed with anti-plasma cell therapies and autologous stem cell transplant.