. 2022 May 14;28(1):123–135. doi: 10.1007/s10741-022-10247-5

Table 5.

Endomyocardial biopsy use in challenging clinical scenarios

Clinical scenarios	Key findings	Possible histological diagnosis
Hemodynamically stable non-ischemic DCM not improving after ≥ 3 months of optimal medical therapy	• Family history of CMP or juvenile SCD • Persistently or relapsing increase in serum troponin • Skin abnormalities • Frequent ventricular ectopy or arrhythmias • Myopathy or syndromic features • Chemotherapy	• Myocarditis • Haemochromatosis • Undetermined CMP
Haemodynamically stable patients with clinically suspected AM and normal LVEF	• Persistently or relapsing increase in serum troponin • Development of LV dysfunction • Frequent ventricular ectopy or arrhythmias • Known extracardiac sarcoidosis • Systemic autoimmune disorders	• Lymphocytic myocarditis • GCM • Cardiac sarcoidosis • ENM • Chronic myocarditis
Hemodynamically stable patients with HF and unexplained cardiac hypertrophy	• Family history of CMP or juvenile SCD • Severe cardiac hypertrophy (i.e. > 30 mm) • Stroke or TIA (especially < 40 years) • Renal insufficiency (especially < 40 years) • CTS or polyneuropathy • QRS voltage/LV mass discrepancy • Pericardial effusion • Skin abnormalities • Vitreous abnormalities	• HCM • Fabry disease • Danon disease • PRKAG2 disease • Cardiac amyloidosis
Restrictive cardiomyopathy	• CTS or polyneuropathy • QRS voltage/LV mass discrepancy • Pericardial effusion • Vitreous abnormalities • Skin abnormalities • New-onset diabetes • Anaemia with serum ferritin > 300 ng/mL and transferrin saturation > 55%	• Cardiac amyloidosis • Haemochromatosis • Undetermined CMP
Cardiac mass	• Fever or increased inflammatory markers • Positive blood/urine culture • Atrial roof origin • Ventricular localization • Inconclusive non-invasive assessment	• Vegetation • Primary or secondary cardiac tumour

Clinical scenarios

Key findings

Possible histological diagnosis

Hemodynamically stable non-ischemic DCM not improving after ≥ 3 months of optimal medical therapy

• Family history of CMP or juvenile SCD

• Persistently or relapsing increase in serum troponin

• Skin abnormalities

• Frequent ventricular ectopy or arrhythmias

• Myopathy or syndromic features

• Chemotherapy

• Myocarditis

• Haemochromatosis

• Undetermined CMP

Haemodynamically stable patients with clinically suspected AM and normal LVEF

• Persistently or relapsing increase in serum troponin

• Development of LV dysfunction

• Frequent ventricular ectopy or arrhythmias

• Known extracardiac sarcoidosis

• Systemic autoimmune disorders

• Lymphocytic myocarditis

• GCM

• Cardiac sarcoidosis

• ENM

• Chronic myocarditis

Hemodynamically stable patients with HF and unexplained cardiac hypertrophy

• Family history of CMP or juvenile SCD

• Severe cardiac hypertrophy (i.e. > 30 mm)

• Stroke or TIA (especially < 40 years)

• Renal insufficiency (especially < 40 years)

• CTS or polyneuropathy

• QRS voltage/LV mass discrepancy

• Pericardial effusion

• Skin abnormalities

• Vitreous abnormalities

• HCM

• Fabry disease

• Danon disease

• PRKAG2 disease

• Cardiac amyloidosis

Restrictive cardiomyopathy

• CTS or polyneuropathy

• QRS voltage/LV mass discrepancy

• Pericardial effusion

• Vitreous abnormalities

• Skin abnormalities

• New-onset diabetes

• Anaemia with serum ferritin > 300 ng/mL and transferrin saturation > 55%

• Cardiac amyloidosis

• Haemochromatosis

• Undetermined CMP

Cardiac mass

• Fever or increased inflammatory markers

• Positive blood/urine culture

• Atrial roof origin

• Ventricular localization

• Inconclusive non-invasive assessment

• Vegetation

• Primary or secondary cardiac tumour

AM acute myocarditis, CMP cardiomyopathy, CTS carpal tunnel syndrome, DCM dilated cardiomyopathy, ENM eosinophilic necrotizing myocarditis, GCM giant cell myocarditis, HCM hypertrophic cardiomyopathy, HF heart failure, LV left ventricular, LVEF left ventricular ejection fraction, SCD sudden cardiac death, TIA transient ischemic attack