Cardiac amyloidosis was long considered rare and untreatable, but both assumptions have given way, and the disease is now recognized as an underdiagnosed and increasingly treatable cause of heart failure. The available therapies work by slowing amyloid deposition, so their benefit depends on early diagnosis, yet the condition is still identified late and usually only after referral for specialized imaging. Artificial intelligence has started to shorten this path. Models built on the electrocardiogram and the echocardiogram detect amyloid infiltration with high accuracy and have reached external validation, while artificial-intelligence-based analysis of heart sound, the cheapest and most widely available cardiac signal, has not yet been directly evaluated in this disease. The physiological rationale for studying it is strong, because a ventricle stiffened by amyloid is expected to alter the low-frequency diastolic sounds that reflect ventricular compliance, although whether these changes are specific to amyloidosis remains unknown. This review brings together the acoustic manifestations of cardiac amyloidosis, the signal-processing and machine learning methods relevant to heart sounds, the clinical evidence across imaging and acoustic modalities, and the practical and equity questions that deployment raises. Heart sound analysis remains the most scalable and least explored opportunity in the field. We outline the mechanistic rationale, the available methods, the lessons from the more mature electrocardiographic and echocardiographic literature, and a set of minimum design requirements for a first disease-specific study.

Giant cell arteritis (GCA) is the most common primary systemic vasculitis of older adults and has traditionally been framed as an ophthalmologic emergency. Its most serious consequences, however, occur in the cardiovascular system, often years after inflammatory markers have normalized. In contemporary matched population cohorts, patients with GCA carry an approximately two-fold excess risk of aortic aneurysm; the historical Olmsted County cohort reported a 17-fold excess of thoracic aortic aneurysm with wide confidence limits, and the characteristic latency to aneurysm is five to ten years. Patients also face elevated risks of aortic dissection, myocardial infarction, stroke, venous thromboembolism, and heart failure that cluster within the first year of diagnosis, when vascular inflammation is most active. This narrative review, based on a structured search of PubMed/MEDLINE and Google Scholar through September 2026 with independent verification of every cited estimate, synthesizes current evidence on the full spectrum of cardiac and aortic complications of GCA, including aortitis, aneurysm and dissection, coronary arteritis, valvular disease, pericarditis, myocarditis, and conduction disease. We trace their common origin to the immunopathology of the arterial wall, where dendritic cell activation, Th1/Th17 polarization, and maladaptive vascular remodeling produce occlusion in medium-sized arteries and dilation in the aorta. We examine current diagnostic modalities, from the ultrasound-based fast-track clinic, which has reduced permanent visual loss by half or more in observational cohorts, to FDG-PET/CT, in which aortic uptake at diagnosis is associated with subsequent aortic dilation. We review treatment after the GiACTA and SELECT-GCA trials in the light of the 2025 European Alliance of Associations for Rheumatology (EULAR) recommendations, the unresolved role of antiplatelet and statin therapy, and the surgical and endovascular management of GCA-related aortopathy. We suggest that the organization of care, as well as the limitations of drug therapy, may contribute to the residual mortality of GCA, a hypothesis that has not been tested; distinguish recommendations that are supported by current guidelines from those that are our own proposals; and outline a cardio-rheumatology pathway in which baseline vascular phenotyping informs individualized aortic surveillance. GCA is a disease whose natural history often begins in the rheumatology clinic and ends in the cardiac operating room without prior surveillance.