Left Ventricular Thrombus

Left ventricular (LV) thrombus is a mass of thrombus attached to the endocardium of the left ventricle, usually at the apex. It forms where wall motion is poor and stasis is greatest.

The commonest setting is anterior myocardial infarction with apical akinesis or aneurysm. Incidence has fallen with primary PCI to about 4 to 6%, and is higher (up to 10 to 15% by cardiac MRI) with large anterior infarcts and ejection fraction under 40%.

Other causes are dilated cardiomyopathy with ejection fraction under 30%, takotsubo syndrome, peripartum cardiomyopathy, myocarditis, left ventricular non-compaction, hypertrophic cardiomyopathy with an apical aneurysm, Chagas disease, amyloidosis, endomyocardial fibrosis and Loeffler endocarditis, antiphospholipid syndrome, and malignancy.

Without treatment the risk of embolism is high, in older studies 10 to 15%, with most events in the first 3 months. Stroke and systemic embolism are the major complications. In the tropics, endomyocardial fibrosis and Chagas disease are important causes.

Pathophysiology. The three elements are stasis in akinetic or aneurysmal segments, endocardial injury, and a prothrombotic state after infarction. Thrombus forms within days to 2 weeks after infarction, mostly in the first 2 weeks.

• Often asymptomatic and found on imaging.
• Embolism: stroke or transient ischaemic attack, acute limb ischaemia, renal infarction (flank pain, haematuria), splenic infarction, mesenteric ischaemia, and coronary embolism.
• Features of the underlying disease: heart failure, previous infarction, cardiomyopathy.

Red flags.

• Embolic stroke or other systemic embolism
• Mobile or protruding thrombus
• Ejection fraction under 30% with apical aneurysm
• Thrombus on dual antiplatelet therapy after infarction, or after stent implantation
• Antiphospholipid syndrome or a prosthetic valve

• Echocardiography with an ultrasound contrast agent. Contrast shows a filling defect and greatly improves detection over unenhanced imaging (sensitivity rises from about one third to over 90%). Thrombus is a discrete echo dense mass, distinct from the endocardium, seen in two views, next to an akinetic or dyskinetic segment. Record size, mobility (mobile or protruding thrombus has the highest embolic risk) and site.
• Cardiac MRI with late gadolinium enhancement. The reference test: thrombus appears as a dark, non-enhancing mass against enhancing myocardium, with sensitivity about 88% and specificity about 99%. It also shows scar and the cause.
• Cardiac CT with delayed phase imaging when MRI is not possible.
• Embolic workup when indicated: brain imaging, vascular imaging, and renal or abdominal imaging.
• Laboratory. Full blood count, creatinine, INR, antiphospholipid antibodies, natriuretic peptide, and eosinophil count when Loeffler endocarditis is possible.

Differential diagnosis.

• Trabeculations and left ventricular non-compaction
• Papillary muscle and false tendons
• Apical hypertrophic cardiomyopathy
• Cardiac tumours (myxoma, fibroma, metastasis)
• Vegetation
• Near field imaging artefact
• Endomyocardial fibrosis with overlying thrombus

Anticoagulation for at least 3 months is the treatment. Start without delay. Evidence from randomised studies and registries shows direct oral anticoagulants perform at least as well as warfarin, and warfarin remains the best studied option.

• Warfarin 5 mg orally once daily at the start (2 to 3 mg in older adults, liver impairment or interacting drugs), adjusted to an INR of 2.0 to 3.0, no fixed maximum. INR every 2 to 3 days at the start, weekly until stable, then every 4 to 12 weeks. Bridge until the INR is in range on 2 readings 24 hours apart with unfractionated heparin 80 units/kg intravenous bolus, then 18 units/kg/h, adjusted to anti-Xa 0.3 to 0.7 IU/mL or an aPTT ratio of 1.5 to 2.5 (check platelets on days 5 to 14), or enoxaparin 1 mg/kg subcutaneously every 12 hours (1 mg/kg once daily at creatinine clearance under 30 mL/min).
• Apixaban 5 mg orally twice daily, reduced to 2.5 mg twice daily when at least two of age 80 years or over, weight 60 kg or under and serum creatinine 133 micromol/L or over are present. Also 2.5 mg twice daily at creatinine clearance 15 to 29 mL/min, and avoided under 15 mL/min. Maximum 10 mg daily. Reduce or avoid with strong dual CYP3A4 and P-glycoprotein inhibitors (ketoconazole, ritonavir).
• Rivaroxaban 20 mg orally once daily with the main meal (15 mg at creatinine clearance 15 to 49 mL/min, avoided under 15 mL/min, and contraindicated in moderate or severe liver disease with coagulopathy). Avoid with strong dual CYP3A4 and P-glycoprotein inhibitors.
• Warfarin is preferred in antiphospholipid syndrome (direct oral anticoagulants avoided), mechanical valves, Chagas disease and severe renal impairment, where data on direct oral anticoagulants are limited.
• Antiplatelet therapy after myocardial infarction or PCI. Keep the combination as short as possible. Use an oral anticoagulant with clopidogrel 75 mg once daily for 6 to 12 months, and stop aspirin after 1 to 4 weeks. Ticagrelor and prasugrel are avoided with anticoagulants. Give pantoprazole 40 mg once daily for gastric protection and avoid omeprazole and esomeprazole with clopidogrel.
• Duration and imaging. Repeat contrast echocardiography or MRI at 3 months. Stop when the thrombus has gone and ventricular function has recovered. Continue until resolution if thrombus persists, and long term when severe dysfunction with an apical aneurysm persists, after weighing bleeding risk.
• Prevention after anterior infarction. Routine preventive anticoagulation is not advised. Contrast echocardiography or MRI at 5 to 14 days directs therapy in patients with large apical akinesis or ejection fraction under 35%.
• Embolic events. Treat the event in the usual way. After stroke, start anticoagulation after imaging excludes haemorrhagic transformation, at about 1 day after a transient ischaemic attack, 3 days after a minor stroke, 6 days after a moderate stroke and 12 to 14 days after a major stroke (timing is contested).
• Surgery. Thrombectomy only for refractory embolism or with another surgical indication such as aneurysmectomy. Fibrinolysis is not used.
• Underlying disease. Revascularise ischaemic myocardium and treat heart failure: ramipril 2.5 mg orally once daily, increased every 2 to 4 weeks to 10 mg once daily (maximum 10 mg daily, 5 mg daily at creatinine clearance under 30 mL/min), bisoprolol 1.25 mg once daily increased every 1 to 4 weeks to 10 mg once daily (maximum 10 mg daily in heart failure), spironolactone 25 mg once daily (12.5 mg at eGFR 30 to 49 mL/min/1.73 m2), and dapagliflozin 10 mg once daily (start at eGFR 25 mL/min/1.73 m2 or more, contraindicated in type 1 diabetes), with potassium and creatinine monitoring.
• Specific causes. Loeffler endocarditis and eosinophilic disease need corticosteroids and treatment of the cause, with anticoagulation. Takotsubo thrombus resolves with anticoagulation as ventricular function recovers.

Special groups.

• Pregnancy: warfarin is teratogenic in weeks 6 to 12, and direct oral anticoagulants are avoided in pregnancy and breastfeeding. Use enoxaparin 1 mg/kg subcutaneously every 12 hours with a peak anti-Xa of 0.8 to 1.2 IU/mL 4 to 6 hours after the dose (1 mg/kg once daily at creatinine clearance under 30 mL/min).
• Kidney impairment: reduce apixaban to 2.5 mg twice daily at creatinine clearance 15 to 29 mL/min and avoid it under 15 mL/min, give rivaroxaban 15 mg at creatinine clearance 15 to 49 mL/min and avoid it under 15 mL/min, and check creatinine every 6 months.

Monitoring. Imaging at 3 months, with an earlier scan at 4 to 6 weeks when embolic risk is high. INR every 4 to 12 weeks once stable. Haemoglobin, creatinine and bleeding review at each visit. Echocardiography at 6 months and yearly in persistent dysfunction.

Referral and escalation. Refer to cardiology. Urgent for embolism, mobile thrombus or thrombus that grows on anticoagulation.