Coronary Embolism

Coronary embolism is occlusion of a coronary artery by material that arises from another site, in a vessel that is normal or has only mild disease. It is diagnosed by exclusion, after atherothrombosis, dissection and spasm have been considered.

It accounts for about 3% of acute coronary syndromes in registries and probably more at autopsy, because emboli often lyse before angiography. The left anterior descending artery is the commonest site. More than one vessel is affected in a substantial minority.

Most emboli arise in the heart. Atrial fibrillation is the leading source, usually without adequate anticoagulation.

Others are left ventricular thrombus, rheumatic mitral stenosis, prosthetic valve thrombosis, infective endocarditis, non-bacterial thrombotic endocarditis, cardiac tumours (myxoma, papillary fibroelastoma), cardiomyopathy, and paradoxical embolism through a patent foramen ovale or atrial septal defect.

Procedural embolism (calcific debris, thrombus or air) follows catheterisation, PCI, valve implantation and cardiac surgery. Hypercoagulable states also contribute. In sub-Saharan Africa, rheumatic mitral stenosis with atrial fibrillation is an important cause.

Pathophysiology. The embolus lodges at a bifurcation or where the vessel tapers. Collateral supply is poor in a previously normal artery, so the infarct is large for the territory. Fragmentation and spontaneous lysis can restore flow within hours to days, which explains normal angiograms done late.

Emboli to the brain, kidneys, spleen, limbs and gut often occur at the same time.

• Chest pain and dyspnoea, with ST elevation or non-ST elevation presentation.
• A patient with atrial fibrillation, rheumatic mitral stenosis or a prosthetic valve who is not adequately anticoagulated.
• Concurrent embolism: stroke or transient ischaemic attack, acute limb ischaemia, renal infarction (flank pain, haematuria), splenic infarction, mesenteric ischaemia.
• Fever, a new murmur and embolic stigmata (endocarditis). A young patient with few risk factors.
• Cardiogenic shock, ventricular arrhythmia or heart block in large infarcts.

Red flags.

• Embolic stroke or other concurrent systemic embolism
• Fever, a new regurgitant murmur or vegetation
• Mechanical valve with subtherapeutic INR
• Mobile left atrial, left ventricular or valve mass
• Cardiogenic shock or ventricular arrhythmia

• ECG and high sensitivity troponin.
• Coronary angiography. An abrupt cut off with a convex or dome shaped end, often distal or at a bifurcation, in an otherwise smooth artery with no atherosclerosis in the other vessels. Optical coherence tomography shows intraluminal thrombus and excludes plaque rupture or erosion.
• Source search. Transthoracic then transoesophageal echocardiography (left atrial appendage, left ventricular thrombus, valve vegetation or thrombus, tumour, septum) with an agitated saline study for a shunt. Prolonged rhythm monitoring for atrial fibrillation.
• Systemic embolism. CT or MRI of the brain, and imaging of the abdomen and limbs by symptoms. Venous duplex of the legs.
• Laboratory. Full blood count, blood cultures (3 sets), antiphospholipid antibodies, thyroid function, lipids, creatinine, INR.

Differential diagnosis.

• Plaque rupture or erosion (type 1 myocardial infarction)
• Spontaneous coronary artery dissection
• Coronary vasospasm
• In situ thrombosis from a hypercoagulable state
• Takotsubo syndrome and myocarditis
• Aortic dissection with coronary involvement
• Type 2 myocardial infarction
• Pulmonary embolism

Emergency reperfusion for ST elevation or ongoing ischaemia.

• Aspirin 300 mg orally once, then 75 to 100 mg daily (usual maximum 325 mg daily).
• Primary PCI is preferred. Give unfractionated heparin 70 to 100 units/kg intravenously (activated clotting time 250 to 350 seconds). Thrombus aspiration or mechanical thrombectomy suits fresh, plaque free embolic thrombus, with balloon angioplasty alone where flow is restored. Stent only for dissection or a residual flow limiting lesion.
• Intracoronary or intravenous tirofiban for a large residual thrombus burden or no reflow, 25 microgram/kg intravenously over 3 minutes, then 0.15 microgram/kg/min for up to 18 hours (halve the infusion at creatinine clearance 60 mL/min or less), with platelets at 2 to 6 hours and daily.
• Systemic fibrinolysis is avoided with recent embolic stroke (haemorrhagic transformation) and with endocarditis (septic embolism and haemorrhage).

Anticoagulation after reperfusion. 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, no fixed maximum. Check platelets on days 5 to 14 for heparin induced thrombocytopenia. Reduce or withhold with active bleeding. Then long term therapy by source:

• Atrial fibrillation: 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. Long term. Reduce or avoid with strong dual CYP3A4 and P-glycoprotein inhibitors (ketoconazole, ritonavir).
• Rheumatic mitral stenosis with atrial fibrillation: warfarin to an INR of 2.0 to 3.0. Direct oral anticoagulants are not used. Warfarin 5 mg orally once daily at the start (2 to 3 mg in older adults, liver impairment or interacting drugs), no fixed maximum, INR every 2 to 3 days at the start, weekly until stable, then every 4 to 12 weeks.
• Mechanical valve: warfarin to an INR of 3.0 (2.5 to 3.5) for mitral or tricuspid valves and for aortic valves with risk factors, and 2.5 (2.0 to 3.0) for a bileaflet aortic valve without risk factors.
• Left ventricular thrombus: anticoagulation for at least 3 months with repeat imaging.
• Infective endocarditis: intravenous antibiotics chosen by culture, with early surgery for vegetation over 10 mm with a recent embolic event, or over 30 mm. Anticoagulation is not started.
• Cardiac tumour: surgical excision.
• Paradoxical embolism: anticoagulation for venous thrombosis, with closure of the patent foramen ovale considered when criteria are met (age 18 to 60 years, no other cause after full workup).
• Hypercoagulable state: therapy by cause with haematology.

After a stent. Oral anticoagulation plus clopidogrel 75 mg orally once daily for 6 to 12 months, with aspirin for at most 1 week after PCI. Use pantoprazole 40 mg once daily for gastric protection.

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). Mechanical valves need a specialist plan.
• Region: where INR monitoring is poor, time in range is low and embolic risk is high, so prioritise adherence support and point-of-care testing.

Monitoring. Echocardiography (transoesophageal where needed) after 3 months of anticoagulation for thrombus resolution. Ambulatory ECG for atrial fibrillation. Creatinine and haemoglobin at least yearly on apixaban. INR every 4 to 12 weeks once stable. Bleeding review at each visit.

Referral and escalation. Refer to cardiology and a heart team, and to cardiac surgery for tumour, endocarditis or valve thrombosis. Urgent for shock, ongoing ischaemia, mobile intracardiac mass or concurrent stroke.