Cardiac Amyloidosis
A group of infiltrative cardiomyopathies in which misfolded protein deposits in the myocardium cause progressive heart failure. Increasingly recognised and now treatable.
Cardiac amyloidosis results from extracellular deposition of misfolded protein (most commonly light-chain AL or transthyretin ATTR) in the myocardium. The result is biventricular wall thickening, restrictive physiology, and progressive heart failure.
Echocardiographic clues include increased LV wall thickness disproportionate to ECG voltage, biatrial enlargement, restrictive diastolic filling, and the "apical-sparing" pattern on speckle-tracking strain (apical strain preserved while basal and mid segments are abnormal).
The emergence of disease-modifying therapy, tafamidis for ATTR, daratumumab-based regimens for AL, has made earlier and more accurate diagnosis clinically actionable. AI-assisted echo enables population-level screening for the imaging phenotype.