Myocardial Infarction Due to Coronary Embolism

Myocardial infarction due to coronary embolism is infarction from occlusion of a coronary artery by material from outside the coronary tree, in patients whose coronary arteries are otherwise free of significant atherosclerosis. It is rare, accounting for about 3% of acute infarcts, but it is probably under diagnosed.

Sources are the left atrium and appendage in atrial fibrillation (the commonest), left ventricular thrombus after anterior infarction or in dilated cardiomyopathy, vegetations of infective or non-bacterial endocarditis, mechanical or bioprosthetic valve thrombus, atrial myxoma, papillary fibroelastoma, calcific valve debris, paradoxical embolism through a patent foramen ovale or atrial septal defect, iatrogenic embolism (catheter related thrombus, air, device), and aortic atheroma.

Hypercoagulable states (antiphospholipid syndrome, malignancy, nephrotic syndrome, inherited thrombophilia) add to the risk. Left main and left anterior descending arteries are most often involved because of their flow, and multiple vessel emboli occur.

Mortality is higher than in atherothrombotic infarction (about 10 to 30%), and recurrence is common if the source is not treated.

Pathophysiology.

An embolus lodges at a coronary bifurcation or in a distal vessel and causes abrupt occlusion without prior collateral development, so the infarct is usually large for the vessel size.

Embolisation to other organs (brain, kidneys, spleen, limbs) often coexists, and the diagnosis may be missed if attention stays on the heart alone.

In paradoxical embolism, venous thrombus crosses the interatrial septum when right sided pressures rise, for example in pulmonary embolism or during Valsalva.

Acute chest pain, dyspnoea, syncope, arrhythmia or shock in a patient with atrial fibrillation (especially with inadequate anticoagulation), recent anterior infarction, prosthetic valve, endocarditis, cancer or previous embolic events. Signs of other emboli (stroke, limb ischaemia, abdominal pain, haematuria) and of the source (murmur, fever, irregular pulse, deep vein thrombosis) are clues.

• ECG: ST elevation or depression in the territory of the vessel, and atrial fibrillation or other arrhythmia.
• Troponin; D-dimer is non-specific.
• Coronary angiography: abrupt cut off of a coronary artery (often with a convex meniscus), a filling defect, in an otherwise angiographically normal or minimally diseased tree, with normal flow in other vessels. Intracoronary imaging (optical coherence tomography or intravascular ultrasound) shows thrombus without a ruptured plaque.
• Search for the source: transthoracic and transoesophageal echocardiography (left atrial appendage, left ventricular thrombus, valves, vegetation, mass, septal defect with agitated saline), CT or MRI, blood cultures, ambulatory ECG monitoring for atrial fibrillation, venous duplex of the legs, antiphospholipid antibodies and thrombophilia tests, and cancer screening when indicated.
• Imaging of other organs where embolism is suspected (brain, abdomen).

Differential diagnosis.

• Atherothrombotic infarction and plaque erosion.
• Spontaneous coronary artery dissection and coronary spasm.
• Takotsubo syndrome and myocarditis.
• Thrombosis in situ in hypercoagulable states, and coronary ectasia with thrombus.

Reperfusion.

• Primary percutaneous coronary intervention is preferred. Techniques are aspiration thrombectomy (selective use), balloon angioplasty with or without stenting (stenting is often unnecessary when there is no underlying lesion), and intracoronary glycoprotein IIb/IIIa inhibitor (tirofiban 25 microgram/kg bolus over 3 minutes then 0.15 microgram/kg/min, or eptifibatide 180 microgram/kg bolus then 2 microgram/kg/min). Reduce tirofiban to half the dose, and eptifibatide infusion to 1 microgram/kg/min, when creatinine clearance is under 30 mL/min and under 50 mL/min respectively.
• Avoid systemic fibrinolysis in suspected infective endocarditis, atrial myxoma and aortic dissection because of haemorrhage and further embolisation. In other cases it is used only when primary intervention is not available.
• Unfractionated heparin 70 to 100 units/kg intravenous bolus during intervention (60 units/kg with glycoprotein IIb/IIIa inhibitor), then infusion 12 to 15 units/kg/h (maximum 1000 units/h) to aPTT 1.5 to 2.5 times control.
• Aspirin 150 to 300 mg orally loading dose then 75 to 100 mg daily, and a P2Y12 inhibitor (ticagrelor 180 mg loading dose then 90 mg twice daily) when a stent is placed or the thrombus is extensive; duration is by indication.

Treat the source.

• Non-valvular atrial fibrillation: apixaban 5 mg orally twice daily (2.5 mg twice daily if two of age 80 or over, weight 60 kg or under, creatinine 133 micromol/L or over), or rivaroxaban 20 mg once daily with the evening meal (15 mg when creatinine clearance is 15 to 49 mL/min), long term. Warfarin (INR 2.0 to 3.0) for mechanical valves (INR 2.5 to 3.5 for mitral and high risk aortic valves) and for rheumatic mitral stenosis. Do not cardiovert atrial fibrillation lasting over 48 hours without 3 weeks of anticoagulation or exclusion of atrial appendage thrombus by transoesophageal echocardiography. Left atrial appendage occlusion when long term anticoagulation is contraindicated.
• Left ventricular thrombus: warfarin (INR 2.0 to 3.0) or apixaban 5 mg twice daily for at least 3 to 6 months, with repeat imaging.
• Infective endocarditis: antibiotics by organism and early surgery for large mobile vegetations (10 mm or more) with embolism; avoid anticoagulation for embolism prevention in native valve disease.
• Atrial myxoma or fibroelastoma: urgent surgical resection.
• Paradoxical embolism: treat venous thrombosis with anticoagulation (apixaban 10 mg twice daily for 7 days then 5 mg twice daily, for at least 3 months), then close the patent foramen ovale or septal defect.
• Antiphospholipid syndrome: warfarin to INR 2.0 to 3.0 (higher range in arterial events by specialist decision); avoid direct oral anticoagulants in triple positive disease.

Heart failure and arrhythmia. Treat by usual practice for the ventricular function. Beta blockers, ACE inhibitors and mineralocorticoid antagonists when ejection fraction is 40% or under.

Monitoring. Continuous ECG for 48 to 72 hours, troponin, echocardiography at 24 to 48 hours and at 1 and 3 months, INR or renal function by anticoagulant, repeat imaging of the source.

Referral and escalation. Immediate cardiology and catheter laboratory activation. Refer urgently to cardiac surgery for endocarditis, tumour, or prosthetic valve thrombosis, and to neurology and vascular services when there are multiple emboli.

Special groups.

• Pregnancy: mechanical valve thrombosis and paradoxical embolism are the main concerns; use low molecular weight heparin, with warfarin avoided from 6 to 12 weeks; direct oral anticoagulants are contraindicated.
• Kidney impairment: adjust direct oral anticoagulants by creatinine clearance, and limit contrast.
• Older adults: bleeding risk assessment for combined antithrombotic therapy.
• Region specific: rheumatic mitral stenosis with atrial fibrillation and poorly monitored warfarin is a frequent source in sub-Saharan Africa.