HF-ETIO — Specialist FULLPAGE (v7.1, no-debug)

Prerequisite

Confirmed HF diagnosis (symptoms/signs + natriuretic peptides + echocardiography or equivalent)

Dynamic workflow: start with ECG/Echo only → Rank → follow suggested investigations → add new findings → Rank again.

Demographics

Sex:

History

Baseline priors emphasize the most common causes: ischemic, idiopathic/primary DCM, hypertension, and valvular disease. Highly specific findings can outrank priors (e.g., eosinophilia → eosinophilic myocarditis; amyloid strain pattern).

Presentation & Labs

Chest pain at onset

Troponin rise/dynamics

TSH elevation

Infectious serology positive (HIV/Chagas/Lyme)

Iron overload/hemochromatosis (high ferritin/TSAT/genetics)

Eosinophilia (eosinophilic myocarditis/HES)

Viral prodrome

Age ≥ 65 years

Echocardiography

Coronary anatomy/ischemia

Significant stenosis (CTA/ICA)

Angiographically normal coronaries

Ischemia on stress test (SPECT/Stress-echo/CMR)

Cardiac MR / Nuclear

LGE ischemic pattern (subendocardial/territorial)

LGE myocarditis pattern (subepicardial/mid + edema)

Diffuse subendocardial LGE / high T1 (amyloid)

Typical DCM pattern (mid-wall septal LGE; ring-like in some genetic forms e.g., DSP)

Takotsubo pattern (apical/variant ballooning, minimal LGE)

FDG-PET uptake suggestive of sarcoid

No LGE

Pulmonary thromboembolism

History of DVT/PE

CTPA positive for acute PE

V/Q scan suggestive of CTEPH (mismatched perfusion defects)

Amyloid & infiltrative/storage

Click “Rank etiologies”, then click any ranked item to view typical features and tests.

Ranked etiologies (probable)

Select findings and click “Rank etiologies”.

Suggested next investigations

Explanations for symptoms & findings

Presentation & symptoms — chest pain patterns

Pericarditis: Classically sharp and pleuritic; improves by sitting up and leaning forward and is exacerbated by inspiration, lying supine, and deglutition.
Myocarditis: Often mimics acute coronary syndrome (pressure-like/anginal). When the pericardium is also involved, the pain may take on a pericarditic character.
Myocardial infarction: Typically anginal; however, concomitant pericardial involvement may produce features reminiscent of pericarditis.

Failure phenotype & ECG

ECG changes (pericarditis pattern): PR-segment depression and diffuse, concave (“saddleback”) global ST‑segment elevations.
Pathological Q waves: >40 ms (1 mm) wide, >2 mm deep, or >25% of QRS depth; seen in V1–V3.
Deep, narrow Q-waves (inferior/lateral): may be suggestive of HCM.
Low QRS voltage: All limb-lead QRS <5 mm, or all precordial-lead QRS <10 mm.
LVH voltage criteria: e.g., Sokolow–Lyon: S in V1 + tallest R in V5 or V6 >35 mm.
Epsilon wave (ARVC): Small deflection at the end of QRS; best seen in ST segment of V1–V2, often present V1–V4.
Prolonged QTc: In addition to congenital/drug causes, can be seen in Takotsubo syndrome and myocarditis.
RV infarction clues: Inferior ST-elevation pattern (III > II) with ST elevation in V1 and in right-sided leads (V3R–V4R) supports RV involvement.
S1Q3T3 pattern: prominent S in lead I, Q wave and T inversion in lead III; classic but neither sensitive nor specific for PE.

Presentation & labs

CRP elevated: Supports an inflammatory process; increases likelihood of myocarditis or pericarditis.
Viral prodrome (myocarditis): Recent respiratory or gastrointestinal illness; myocarditis typically follows by ≈2–4 weeks.
Eosinophilic myocarditis: Often with peripheral eosinophilia, but up to 25% lack eosinophilia (possible underdiagnosis).
Serology: Routine viral serology not recommended, except HIV and HCV. Target bacterial tests to suspicion (e.g., Borrelia, rickettsial infections, Trypanosoma cruzi).

Echocardiography

Constrictive physiology: Septal bounce, respiratory septal shift, and Doppler evidence of constriction; chronic pericardial disease can mimic restrictive cardiomyopathy.
Pericardial effusion: Supports pericardial involvement in the right context.
Consider amyloidosis: Increased thickness of the interatrial septum, AV valves and/or RV free wall.
HCM: Wall thickness >14 mm in ≥1 LV segment not fully explained by loading; LVOTO ≥30 mmHg at rest/exercise, asymmetric hypertrophy, or patchy mid‑wall LGE in the most hypertrophied segment further suggest HCM.

Coronary anatomy / ischemia

Significant stenosis, stress‑induced ischemia, or ischemic LGE supports an ischemic etiology. Normal coronaries favor non‑ischemic causes (myocarditis, Takotsubo, genetic DCM) in the right context.
Right ventricular infarction: Often accompanies inferior MI (RCA). Consider recording right-sided leads (V3R–V4R) when inferior ST-elevation is present to assess RV involvement.

Cardiac MR / CT / Nuclear

Pericardial imaging: CT — thickening/calcification supports chronic disease or constriction. CMR — pericardial LGE, edema and/or thickening compatible with active pericardial inflammation.
Myocardial patterns: Ischemic LGE (subendocardial/territorial), myocarditis‑type LGE (subepicardial/mid‑wall + edema), diffuse subendocardial LGE/high T1 (amyloid), mid‑wall septal LGE or ring‑like scars (DCM/genetic, e.g., DSP), minimal LGE with edema and typical ballooning (Takotsubo).

Pulmonary vasculature / thromboembolism

In right-sided HF, consider acute pulmonary embolism or chronic thromboembolic pulmonary hypertension (CTEPH).
Clues: acute dyspnea and pleuritic chest pain, hypoxemia, RV strain on ECG (RBBB/right axis), RV dilation/dysfunction and PH on echo.
Imaging: CTPA for acute PE; V/Q scanning for suspected CTEPH. Right heart catheterization can support diagnosis and hemodynamic assessment.
McConnell’s sign: classically described in acute PE, but may also be seen in right ventricular infarction; interpret in clinical context.

Amyloid & infiltrative/storage

Red flags: marked LV wall thickness with low voltages, apical‑sparing GLS, neuropathy/proteinuria or abnormal light chains, bone tracer uptake ≥2 (ATTR), CMR diffuse subendocardial LGE/high T1. Consider Fabry, iron overload, sarcoidosis, and other storage diseases when appropriate.

Myocarditis — additional notes

Recurrent myocarditis may represent the “hot phase” of certain cardiomyopathies (e.g., desmoplakin‑related ARVC), linking inflammatory episodes to scar evolution and arrhythmic risk.

General note on co‑existing etiologies

Multiple conditions can coexist or interact. Hypertension or diabetes may precipitate, unmask, or aggravate dilated cardiomyopathy; AF/atrial flutter can cause or worsen heart failure yet does not exclude other etiologies. Identifying one mechanism does not rule out additional concurrent causes — a layered diagnostic approach is often necessary.

Peripartum cardiomyopathy (PPCM)

Peripartum cardiomyopathy is defined as HF with reduced left ventricular ejection fraction (LVEF) <45%, without any other cause of HF, that occurs mainly during the peripartum period or in the months following delivery, termination, or miscarriage.^[3]

Genetic counseling and testing should be considered in women with PPCM.

References

1) López‑Ayala JM, et al. Genetics of myocarditis in arrhythmogenic right ventricular dysplasia. Heart Rhythm. 2015;12:766–773. doi:10.1016/j.hrthm.2015.01.001.
2) Schulz‑Menger J, et al. 2025 ESC Guidelines for the management of myocarditis and pericarditis. European Heart Journal. 2025; ehaf192. https://doi.org/10.1093/eurheartj/ehaf192.
3) Bauersachs J, König T, van der Meer P, Petrie MC, Hilfiker‑Kleiner D, Mbakwem A, et al. Pathophysiology, diagnosis and management of peripartum cardiomyopathy: a position statement from the Heart Failure Association of the European Society of Cardiology study group on peripartum cardiomyopathy. Eur J Heart Fail. 2019;21:827–43. doi:10.1002/ejhf.1493.

Disclaimer

Educational use only. This tool is intended for informational and educational purposes only. It does not replace professional medical judgement, clinical guidelines, or individualized patient care.

No patient‑identifiable information should be entered. Use of this tool is at the user’s own risk. The authors and publishers disclaim any liability for decisions or outcomes resulting from its use.

Heart diagnosis — Etiology workup in established heart failure

Prerequisite

Demographics

Failure phenotype & ECG

History

Presentation & Labs

Echocardiography

Coronary anatomy/ischemia

Cardiac MR / Nuclear

Pulmonary thromboembolism

Amyloid & infiltrative/storage

Disclaimer

All possible causes (alphabetical)