Cardiac Amyloidosis: An Updated Review for Pharmacists, Nursing, and Radiologists.

Abstract: Background: Cardiac amyloidosis is an infiltrative cardiomyopathy caused predominantly by misfolded immunoglobulin light chains (AL) or transthyretin (ATTR), leading to diastolic dysfunction, conduction disease, and heart failure. Early recognition remains challenging due to overlap with common conditions. Aim: To provide an updated, practice-oriented synthesis for pharmacists, nurses, and radiologists/nuclear medicine physicians on epidemiology, pathophysiology, diagnostic pathways, and therapeutics. Methods: Narrative review and critical integration of contemporary consensus algorithms and modality-specific evidence regarding electrocardiography, echocardiography (strain), cardiac magnetic resonance (LGE, T1/ECV), bone–avid scintigraphy (Tc-PYP with SPECT/CT), endomyocardial biopsy, genotyping, and disease-modifying therapy. Results: Hallmark features include voltage–mass discordance, apical-sparing strain, diffuse subendocardial/transmural LGE with elevated native T1/ECV and reversed nulling order, and grade 2–3 Tc-PYP uptake (with negative monoclonal screen) confirming ATTR. Management is phenotype-specific: clone-directed therapy (e.g., Dara-CyBorD, ASCT) for AL; TTR stabilization (tafamidis) and silencers (for neuropathy) for ATTR. Across phenotypes, diuretics/MRAs anchor volume control; β-blockers and RAAS inhibitors are often poorly tolerated; anticoagulation is frequently indicated. Role-specific contributions—medication safety/access (pharmacists), surveillance and self-management support (nurses), protocolized imaging and reporting (radiology/nuclear)—shorten time-to-diagnosis and improve outcomes. Conclusion: Implementing a structured diagnostic algorithm and phenotype-tailored therapy within an interprofessional model materially improves safety, timeliness, and quality of care in cardiac amyloidosis.