Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Classify an intracardiac mass as thrombus, tumour, vegetation or mimic and act on embolic, obstructive and infective risk before tissue certainty.
'Cardiac mass' is an imaging description, not a diagnosis. The practical differential is thrombus, infection, benign or malignant tumour, and pseudomass such as trabeculation, crista terminalis, Chiari network, lipomatous septum or artefact.
Multimodality imaging should answer a decision: TOE for a valve/LAA/device question, contrast echo for cavity definition and vascularity, CMR for tissue, CT for calcification/coronary/surgical anatomy, and FDG-PET/CT for selected infection or malignancy.
Management is cause-led. Thrombus needs indication-specific anticoagulation and repeat imaging; vegetation needs cultures, antimicrobials and an Endocarditis Team; tumour needs surgical/oncology review and histology.
Blood stasis, endocardial injury and hypercoagulability favour thrombus: commonly the left-atrial appendage in AF, an akinetic LV apex after infarction, or the right atrium around a catheter.
Bloodstream organisms may adhere to endocardium, particularly where there is pre-existing injury, prosthetic material or a device lead, and become embedded in platelet-fibrin material. Bacteraemia, valve destruction and embolic features raise the probability.
Primary benign tumours are uncommon; atrial myxoma and valvular papillary fibroelastoma are recognisable patterns. Imaging suggests probability, while histopathology establishes tumour identity when tissue is obtained.
Cardiac metastases are more common than primary malignant cardiac tumours. Known cancer, broad infiltration, rapid growth, multiple lesions or pericardial invasion should prompt an oncological tissue strategy.
Stasis and endocardial injury favour coagulation, infection can build platelet-fibrin vegetations, and neoplastic cells may proliferate within or spread to cardiac tissue. These are alternative origins, so location and clinical setting shape the initial probability.
Attachment, mobility, size and composition influence whether a component fragments, sending material to systemic arteries from the left heart or pulmonary arteries from the right. A right-to-left shunt can alter this usual destination.
A large or mobile mass may intermittently block a valve, inflow or outflow tract, producing positional symptoms, syncope, pulmonary congestion or sudden haemodynamic collapse.
Vegetation can destroy a valve or extend into peri-annular tissue, while malignancy can invade myocardium, conduction tissue or pericardium, causing failure, arrhythmia or effusion.
LAA filling defect with AF/mitral stenosis or laminated/apical mass with recent anterior MI, aneurysm or severe LV dysfunction.
A serpiginous mobile right-heart mass with DVT/acute RV strain suggests thrombus in transit; a line-associated mass may be thrombus, fibrin sheath or infection.
Fever, positive cultures, new regurgitation, prosthetic/device infection, peripheral emboli or immune phenomena plus an irregular oscillating valve/device mass.
A mobile LA septal stalk mass suggests myxoma; a small frond-like valve lesion may be papillary fibroelastoma, but imaging appearance is not histology.
Positional syncope, acute valve obstruction, stroke/limb ischaemia, coronary embolism or a highly mobile left-sided mass requires urgent surgical/embolism assessment.
Broad-based infiltration, rapid growth, multiple lesions, pericardial invasion/effusion, known cancer or constitutional symptoms requires urgent cardio-oncology and tissue strategy.
A mass in a stasis site, relevant AF, infarction or ventricular dysfunction, and absent perfusion or enhancement favour thrombus; organised thrombus may show peripheral enhancement and remain uncertain.
An oscillating valve or device mass with fever, positive cultures, new regurgitation or embolic phenomena favours endocarditis. A negative initial TTE does not exclude it.
A left-atrial septal stalk suggests myxoma, while enhancement, vascularity, infiltration or known cancer raises tumour probability. Histology is definitive when tissue can be obtained safely; imaging alone estimates probability.
Trabeculation, crista terminalis, Chiari network, lipomatous hypertrophy of the interatrial septum and redundant tissue have characteristic locations and relationships to adjacent anatomy; multiplanar expert imaging helps prevent unnecessary treatment.
Reverberation disappears or changes in another plane, while slow left-atrial-appendage filling may resolve on delayed CT. Confirmation with a second plane or modality is essential.
Left-sided thrombus, vegetation or tumour fragments can occlude cerebral, coronary, mesenteric or limb arteries, causing stroke, infarction or acute limb ischaemia.
Right-heart thrombus, particularly a mobile thrombus in transit, can embolise into the pulmonary circulation and cause acute RV failure, hypoxaemia or obstructive shock.
A mobile atrial tumour or large mass can intermittently obstruct mitral, tricuspid or outflow blood flow, leading to positional syncope, pulmonary oedema or sudden death.
Vegetation may perforate a leaflet, cause severe regurgitation or form an abscess that disrupts conduction. Heart failure or uncontrolled infection can require urgent surgery.
Malignancy can impair contractility, provoke arrhythmia, compress coronary structures or cause a pericardial effusion and tamponade, often signalling advanced disease.
An LV apical mass in an akinetic aneurysm is thrombus until disproved; an LA septal stalk mass suggests myxoma; an upstream valve mass with bacteraemia suggests vegetation.
Spontaneous echo contrast and early CT filling defects require TOE or delayed CT interpretation before cancelling procedures or committing to long treatment.
Chronic fibrosis and neovascularisation can blur the classic non-enhancing rule, so integrate perfusion, location and interval change.
Blood cultures and echo are complementary; prior antibiotics can sterilise cultures and a valve mass can be sterile non-bacterial thrombotic endocarditis.
Imaging estimates probability and operability; even a textbook-looking myxoma can prove sarcoma or thrombus.
Calling every mobile echo structure thrombus and starting anticoagulation before considering vegetation or tumour.
Calling a valve mass infective endocarditis without cultures and clinical criteria—or excluding endocarditis after one negative TTE.
Using early-phase CT LAA filling defect as definite thrombus without delayed imaging/TOE.
Assuming lack of enhancement is absolute proof of thrombus or enhancement absolute proof of tumour.
Observing an obstructive or embolising presumed myxoma while waiting for diagnostic certainty.
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A patient with fever and embolic stroke has a mobile mitral-valve mass on TTE. They are haemodynamically stable and have not received antibiotics. What is the best next step?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem ·
Never use a fixed dose without INR monitoring. Review bleeding, pregnancy, liver disease, diet and interacting medicines; the target differs with valve type/site and a new interacting medicine warrants early INR recheck.
Not for mechanical valves or moderate-to-severe rheumatic mitral stenosis. Check Cockcroft-Gault creatinine clearance, hepatic function, bleeding and CYP3A4/P-gp interactions; do not underdose from age alone, and avoid use below creatinine clearance 15 mL/min because there is no clinical experience.