Systemic amyloidosis is a rare protein misfolding and deposition condition that causes
slow organ failure. Each of the more than 15 exclusive sorts of systemic amyloidosis, which encourage
amyloid production and tissue deposition, is introduced by a unique precursor protein.
Amyloidosis can affect various organs, including the heart, kidneys, liver, nerves, gastrointestinal
tract, lungs, muscles, skin, and soft tissues. It can either be acquired or hereditary. Insidious
and doubtful signs often cause a put-off in diagnosis. In the closing decade, noteworthy progressions
have been made in the identity, prediction, and handling of amyloidosis. Shotgun proteomics
based on mass spectrometry has revolutionized amyloid typing and enabled the identification
of novel amyloid forms. It is critical to correctly identify the precursor protein implicated in
amyloidosis because the kind of protein influences the proper treatment strategy. Cardiac amyloidosis
is a disorder characterized by the systemic accumulation of amyloid protein in the myocardium's
extracellular space, which causes a variety of symptoms. The buildup of amyloid aggregates
precipitates myocardial thickening and stiffening, culminating in diastolic dysfunction
and, in due course, heart failure. We examine every kind of systemic amyloidosis in this text to
offer practitioners beneficial equipment for diagnosing and treating those unusual diseases. This
review presents a comprehensive analysis of cardiac amyloidosis and consolidates current methods
for screening, diagnosis, evaluation, and treatment alternatives.
