CLINICIAN GUIDE · CARDIOMYOPATHY & CARDIAC AMYLOIDOSIS · SECTION 1 OF 3

Understanding myocardial disease

Recognize major myocardial patterns and AL versus ATTR amyloidosis.

Cardiomyopathy describes a myocardial disorder

The heart muscle may be enlarged, thickened, scarred, or unusually stiff. Phenotype is a starting point; the underlying cause determines treatment and family implications.

Dilated

Enlargement and reduced systolic function may occur

Hypertrophic

Unexplained thickening; obstruction and arrhythmic risk vary

Restrictive/infiltrative

Impaired filling; EF may initially remain preserved

Arrhythmogenic

Myocardial disease with important arrhythmic risk

Enlarged ventricular chambers with reduced systolic function — A reduced-EF phenotype example. Appearance alone does not establish the cause.

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Amyloidosis: protein deposition in the heart

AL arises from immunoglobulin light chains associated with a plasma-cell disorder. ATTR arises from transthyretin and can be hereditary or wild type. Distinguishing them promptly is essential because treatments differ.

Deposits can impair relaxation and eventually pumping function, with AF and conduction disease. Preserved EF does not establish benign disease.

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Clues that warrant a closer look

Unexplained wall thickening or HFpEF with atypical features.
Bilateral carpal tunnel history, spinal stenosis, neuropathy, or orthostasis.
Unexpected conduction disease, arrhythmias, or family cardiomyopathy/sudden death.
Low EKG voltage relative to wall thickness or apical-sparing strain.

These are clues, not diagnostic criteria. Absence of low voltage does not exclude amyloidosis; apical sparing alone does not prove it.

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Clinical references

Adult clinician education · References reviewed October 11, 2026.