01OverviewDefinition, clinical context and the essential points that orientate the chapter.
'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.
Key points
- First exclude artefact and normal variants, then classify by chamber, attachment, mobility, haemodynamic effect, vascularity and clinical setting.
- Thrombus favours stasis sites: LAA in AF/mitral stenosis, LV apex after MI or severe dysfunction, and right atrium around lines or with venous thromboembolism.
- Vegetation is an infected endocardial mass—usually mobile on a valve or device—with fever, bacteraemia, valve destruction or embolic/immunological features.
- Tumour is less common than thrombus; atrial myxoma often arises by a stalk from the interatrial septum, while metastases are more common than primary malignant cardiac tumours.
- TTE is the entry test; TOE is superior for valves, prostheses, device leads, LAA and small posterior lesions.
- CMR characterises tissue and perfusion; thrombus usually lacks perfusion/enhancement, whereas tumour often enhances, although organised thrombus can be complex.
- Never anticoagulate an unidentified mass reflexively: vegetation, vascular tumour, recent haemorrhagic embolus and dissection carry different hazards.
- A mass that shrinks on effective anticoagulation supports thrombus, but interval response must not delay surgery for obstruction, embolisation or suspected malignancy.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Intracardiac thrombus
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.
Infective vegetation
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.
Benign primary tumour
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.
Malignant or metastatic tumour
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.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Distinct origins: thrombus, infection or tumour
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.
- 2Outcome branch: embolisation
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.
- 3Outcome branch: intracardiac obstruction
A large or mobile mass may intermittently block a valve, inflow or outflow tract, producing positional symptoms, syncope, pulmonary congestion or sudden haemodynamic collapse.
- 4Lesion-specific branch: destruction or invasion
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.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
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.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Comprehensive TTE with ultrasound contrast when neededFirst step - Why
- Confirm the mass, location, attachment, mobility, haemodynamic effect and cavity opacification.
- Interpretation and limitations
- Contrast distinguishes thrombus from poorly seen myocardium and can assess perfusion; a screening/handheld finding must be followed by formal imaging.
- 02
TOE - Why
- Resolve valves, prostheses, peri-annular structures, device leads, atrial septum and LAA.
- Interpretation and limitations
- A negative TTE does not exclude endocarditis or LAA thrombus when suspicion is high; repeat TOE/imaging if the clinical trajectory remains convincing.
- 03
CMR with first-pass perfusion and LGE - Why
- Characterise composition, vascularity, invasion and extracardiac extension.
- Interpretation and limitations
- No perfusion or LGE strongly favours thrombus; heterogeneous enhancement/invasion favours tumour, but chronic organised thrombus can enhance peripherally.
- 04
ECG-gated cardiac CT - Why
- Define calcification, fat, LAA/coronary anatomy, prosthetic/perivalvular infection and surgical relationships.
- Interpretation and limitations
- Delayed CT improves LAA thrombus specificity by distinguishing slow flow; CT may miss small vegetations better seen on TOE.
- 05
Three sets of peripheral blood cultures before antibiotics - Why
- Test suspected infective vegetation and guide antimicrobial therapy.
- Interpretation and limitations
- Obtain before antibiotics when clinically feasible and do not wait for a fever spike; after cultures, do not delay treatment in sepsis or unstable infection.
- 06
Targeted staging: FBC/CRP, renal/liver/coagulation, DVT/PE imaging, CT body or FDG-PET/CT - Why
- Define infection, embolic source, malignancy and treatment safety.
- Interpretation and limitations
- Select from the working diagnosis; PET uptake can support active infection/tumour but is non-specific and requires anatomical correlation.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Thrombus
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.
Infective vegetation
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.
Cardiac tumour
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.
Normal variant or pseudomass
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.
Artefact or slow-flow defect
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.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01ClassifyNew intracardiac massFirst stepMass or filling defect on echo, CT or CMR.+
- 1Confirm it in a second plane/modality and compare prior imaging; map chamber, attachment, mobility, obstruction and embolic risk while excluding artefact/normal variants.
- 2Ask immediately about AF/MI/LV dysfunction, venous catheters/DVT, fever/cultures/procedures, cancer and constitutional or embolic symptoms.
- 3Choose TOE for valve/LAA/device targets, CMR for tissue and CT for calcification/coronary or surgical anatomy; do not order every modality without a decision question.
- 4DefinitiveIf haemodynamic, embolic or septic instability exists, treat the leading emergency in parallel rather than awaiting definitive histology.
02ThrombusLikely intracardiac thrombusMass in a stasis/catheter location with non-enhancing imaging or a thromboembolic context.+
- 1Identify the substrate and concurrent emergency: acute MI/LV aneurysm, AF/mitral stenosis, severe cardiomyopathy, catheter, cancer or PE with thrombus in transit.
- 2Start therapeutic anticoagulation when benefit outweighs bleeding, selecting drug, INR target and duration by indication, valves, renal function, pregnancy and antiplatelet needs; LV thrombus use may be off-label and specialist-led.
- 3For haemodynamically unstable PE/right-heart thrombus in transit, activate a PE response team and select reperfusion—thrombolysis, surgical embolectomy or catheter therapy—by shock, bleeding and anatomy.
- 4Repeat the same high-quality imaging to confirm resolution; persistent/enlarging mass despite verified anticoagulation prompts adherence/interaction review and reconsideration of tumour or surgery.
03InfectionPossible vegetationValve/device mass with clinical or microbiological suspicion of endocarditis.+
- 1Take three peripheral blood-culture sets before antibiotics where feasible, obtain TTE and then TOE when suspicion, prosthesis/device or imaging uncertainty warrants.
- 2After cultures, start syndrome-appropriate IV antibiotics promptly in sepsis/unstable disease and involve microbiology plus the Endocarditis Team; do not biopsy a mobile vegetation percutaneously.
- 3Assess valve dysfunction, abscess, heart failure, conduction change, vegetation mobility/size and cerebral/systemic emboli with CT/PET/MRI as indicated.
- 4EscalationEscalate early for surgery when heart failure, uncontrolled infection, abscess/prosthetic complication or embolic-risk criteria are met; anticoagulation is not started solely to treat vegetation.
04TumourLikely cardiac tumourAttached/enhancing or invasive mass, obstruction, embolism or concerning growth.+
- 1Refer to a cardiac tumour multidisciplinary team; complete CMR/CT staging and assess coronary/valve relationships, embolic and anaesthetic risk.
- 2For a mobile obstructive or embolising presumed myxoma, seek prompt surgical excision rather than observation or empirical anticoagulation.
- 3For suspected malignancy, search for an extracardiac primary and choose the safest site for tissue; avoid intracardiac biopsy when embolic, perforation or bleeding risk is unacceptable.
- 4Use histology to direct oncology/surgical treatment and image relatives only when a syndromic/familial tumour diagnosis supports it.
Key medicines and prescribing safety2 treatments · regimens, roles and cautions+
Warfarin
Typical maintenance 3-9 mg orally once daily, individually titrated; when a VKA is selected for non-mechanical intracardiac thrombus, a common specialist target is INR 2.0-3.0.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.
Apixaban
For licensed NVAF stroke prevention: 5 mg orally twice daily. Use 2.5 mg twice daily when at least two apply—age at least 80 years, weight 60 kg or less, serum creatinine at least 133 micromol/L—or when creatinine clearance is 15-29 mL/min.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.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Systemic embolism
Left-sided thrombus, vegetation or tumour fragments can occlude cerebral, coronary, mesenteric or limb arteries, causing stroke, infarction or acute limb ischaemia.
Pulmonary embolism
Right-heart thrombus, particularly a mobile thrombus in transit, can embolise into the pulmonary circulation and cause acute RV failure, hypoxaemia or obstructive shock.
Valve or chamber obstruction
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.
Valve destruction and invasive infection
Vegetation may perforate a leaflet, cause severe regurgitation or form an abscess that disrupts conduction. Heart failure or uncontrolled infection can require urgent surgery.
Myocardial or pericardial invasion
Malignancy can impair contractility, provoke arrhythmia, compress coronary structures or cause a pericardial effusion and tamponade, often signalling advanced disease.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Record mass dimensions, attachment and mobility in reproducible views; compare with prior studies rather than relying on narrative labels.
- During anticoagulation, track bleeding, FBC, renal/liver function, adherence and interactions; for warfarin, monitor INR to the documented target.
- Repeat echo/CMR/CT at a pre-specified interval to document thrombus response before stopping therapy or proceeding to cardioversion/intervention.
- For possible endocarditis, repeat blood cultures to clearance and reassess fever, CRP, valve function, conduction and embolic complications.
- For tumour, monitor obstruction, embolic symptoms and interval growth while definitive surgery/oncology is arranged—high-risk lesions should not sit on routine surveillance.
- Safety-net sudden focal neurology, limb pain, chest pain, syncope, fever or acute breathlessness as an embolic/infective emergency.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Location changes probability
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.
Slow flow mimics LAA thrombus
Spontaneous echo contrast and early CT filling defects require TOE or delayed CT interpretation before cancelling procedures or committing to long treatment.
Organised thrombus may enhance
Chronic fibrosis and neovascularisation can blur the classic non-enhancing rule, so integrate perfusion, location and interval change.
Culture first, but not culture only
Blood cultures and echo are complementary; prior antibiotics can sterilise cultures and a valve mass can be sterile non-bacterial thrombotic endocarditis.
Pathology is the tumour diagnosis
Imaging estimates probability and operability; even a textbook-looking myxoma can prove sarcoma or thrombus.
11Common pitfallsFrequent interpretation and management errors.
- 01
Calling every mobile echo structure thrombus and starting anticoagulation before considering vegetation or tumour.
- 02
Calling a valve mass infective endocarditis without cultures and clinical criteria—or excluding endocarditis after one negative TTE.
- 03
Using early-phase CT LAA filling defect as definite thrombus without delayed imaging/TOE.
- 04
Assuming lack of enhancement is absolute proof of thrombus or enhancement absolute proof of tumour.
- 05
Observing an obstructive or embolising presumed myxoma while waiting for diagnostic certainty.