Thinking Outside the ‘Cage’

Acute coronary syndrome (ACS) consists of clinical suspicion of myocardial ischemia or laboratory confirmation of myocardial infarction (MI). ACS includes 3 major entities: non-ST elevation MI (NSTEMI), unstable angina, and ST-elevation MI (STEMI). ACS usually occurs as a result of a reduced supply of oxygenated blood to the myocardium, which is caused by restriction or occlusion of at least 1 of the coronary arteries. This alteration in blood flow is commonly secondary to a rupture of an atherosclerotic plaque or spontaneous dissection of a coronary artery. In rare cases, this reduction in blood flow is caused by a coronary embolism (CE) arising from a prosthetic heart valve.^1,2

One of the first descriptions of CE was provided by Rudolf Virchow in the 1850s from postmortem autopsy findings.³ At that time, these coronary findings were associated with intracardiac mural thrombus or infective endocarditis. During the 1940s, CE was described in living patients who had survived a MI, and outcomes were not as catastrophic as originally believed. In the 1960s, a higher than usual association between prosthetic valves and CE was suspected and later confirmed by the invention and implementation of coronary angiography. Multiple studies have been published that confirm the association between prosthetic valves (especially in the mitral position), atrial fibrillation (AF), and a higher than usual rate of CEs.^4,5

Discussion

The prevalence of this disease has varied during the years. Data from autopsies of patients with ACS and evidence of thromboembolic material in coronary arteries originally estimated a prevalence as high as 13%.^6,7 After the invention of diagnostic angiography, consensus studies have established the prevalence to be approximately 3% in patient with ACS.¹ The prevalence may be higher in patient with significant risk factors that may increase the probability of CEs, like prosthetic heart valves and AF.²

In 2015 Shibata and colleagues proposed a scoring system for the diagnosis of CE. The scoring system consisted of major and minor criteria.⁶ Diagnosis of CE is established by ≥ 2 major criteria; 1 major and 2 minor; or ≥ 3 minor criteria. This scoring system increases the diagnostic probability of the disease.^1,6

The major criteria are angiographic evidence of coronary artery embolism and thrombosis without atherosclerotic components (met by this patient); concomitant coronary emboli in multiple coronary vascular territories; concomitant systemic embolization without left ventricular thrombus attributable to acute MI; histological evidence of venous origin of coronary embolic material; and evidence of an embolic source based on transthoracic echocardiography, transesophageal echocardiography, computed tomography, or magnetic resonance imaging.^1,6 The minor criteria are 25% stenosis on coronary angiography except for the culprit lesion (met by this patient); presence of emboli risk factors, such as prosthetic heart valve (met by this patient); and AF.^1,6

Management of CE remains controversial; aspiration of thrombus may be considered in the acute setting and with evidence of a heavy thrombus formation. This may allow for restoration of flow and retrieval of thrombus formation for histopathologic evaluation. However, it is important to mention that in the setting of STEMI, aspiration has been shown to increase risk of stroke and lead to increased morbidity. If aspiration of thrombus provides good restoration of flow, there is no need for further percutaneous intervention. Benefits of aspiration in low thrombus burden are not well established and do not provide any additional benefit compared with those of anticoagulation.^6-11

Anticoagulation should be initiated in patients with AF and low bleeding risk, even when CHA₂DS₂-VASc (congestive heart failure, hypertension, aged ≥ 75 years, diabetes mellitus, stroke or transient ischemic attack, vascular disease, aged 65 to 74 years, sex category) score is low. In patients with prolonged immobilization, recent surgery, pregnancy, use of oral contraceptives/tamoxifen, or other reversible risks, 3 months of anticoagulation has been shown to be sufficient. In the setting of active cancer or known thrombophilia, prolonged anticoagulation is recommended. Thrombophilia testing is not recommended in the setting of CE.¹