Rare Coronary Embolism Secondary to Cardioversion of Atrial Fibrillation

The diagnosis and management of myocardial infarction with nonobstructive coronary arteries (MINOCA) are difficult due to its variable presentations, different causes, and challenging diagnostic approaches. Cardiac imaging modalities including cardiac magnetic resonance (CMR) are very useful tools for diagnosing and managing MINOCA. Myocardial infarction (MI) can be caused by coronary emboli that can be contributed to atrial fibrillation (AF). Rarely, coronary embolism with resultant MINOCA can occur after direct current cardioversion (DCCV) even in fully anticoagulated patients. We present a rare case of a coronary embolism following DCCV as well as a CMR finding of microvascular obstruction (MVO), which has not previously been reported after DCCV. This case also emphasizes the value of obtaining a CMR for patients with MINOCA.


Introduction
Determining the precise etiologyofmyocardialinfarction with nonobstructive coronary arteries (MINOCA) can be challenging. Cardiac magnetic resonance (CMR) imaging is very helpful in diagnosing, treating, and risk-stratifying patients withMINOCA. Cardiac emboli are one of the causes of myocardial infarction (MI), and atrial fibrillation (AF) accounts forapproximately15% of cardiacemboli [1].It is exceedingly rare to have cardiac emboli after directcurrentcardioversion (DCCV) in adequately anticoagulatedpatients [2].

Case Presentation
A 51-year-old man with a past medical history of paroxysmal AF, hypertension, and morbid obesity presented to the emergency department with worsening dyspnea and lower extremity edema and was hospitalized forde novoacute decompensated heart failure (ADHF). He was noted to be in AF with a rapid ventricular response. Transthoracic echocardiography revealedsevere systolic dysfunctionwith a left ventricular ejection fraction (LVEF) of 20-25%. Coronary angiography demonstrated only minimal luminal coronary artery disease( Figure 1). Differential diagnoses of this non-ischemic cardiomyopathy includedtachycardiomyopathy. He underwent a transesophageal echocardiogram (TEE), which ruled out left atrial appendage (LAA) thrombus. Synchronized direct current cardioversion (DCCV) was successful in converting AF into normal sinus rhythm (NSR), but the patient reverted to AF within 24 hours.He was started onsotaloland apixaban and was cardioverted again while on antiarrhythmics after four weeks of anticoagulation, and NSR was sustained.

FIGURE 1: Coronary angiography demonstrated only minimal luminal coronary artery disease
Three months after the patient was diagnosed withheart failure with reducedejection fraction(HFrEF), CMR was performed using a 1.5 T scanner (Signa Artist, GE Medical Systems, Milwaukee, WI). Retrospective ECGgated breath-hold steady-state free precession cine images were obtained in short-axis slices at 10 mm intervals (slice thickness of 6 mm, 4 mm gap) and two-chamber, three-chamber, and four-chamber views. This revealed normal left ventricular size and ejection fraction and a hypokinetic basal anterolateral segment. Gadolinium-based contrast agent (MultiHance, Bracco Diagnostics, Princeton, NJ) was injected in a 15-mmol bolus and late gadoliniumenhancement(LGE)images were acquired 10 minutes later by using an inversion recovery gradient echo sequence. This revealed dense transmural hyperenhancement in the basal anterolateral myocardium with centralhypoenhancementconsistent with microvascularobstruction (MVO, Figure 2). Moreover, the focal nature of hyperenhancement and the absence of wavefront phenomenon were more consistent with an embolic infarct.In hindsight, this patient met the criteria for MINOCA and was found to have evidence of MI secondary tocoronaryembolism,likely after DCCV ( Table 1).In this case report, we highlightthe role of CMR in MINOCA and the rare finding of MVO post-DCCV.

Discussion
In order to diagnoseMINOCA,three criteria must be met: diagnosis of acuteMI, ruling outflowlimitingcoronary artery disease using invasive angiography or coronary CT angiography (CCTA), and absence of obvious causes of acute MI. Differential diagnoses of MINOCA include plaque erosion or rupturewith spontaneous recanalization, coronary embolism, spontaneous coronary artery dissection, microvascular disease, stresscardiomyopathy, and myocarditis. Due to thebroad differential diagnosis of MINOCA, treatment and prognosis vary remarkably [3,4]. CMR is apowerfultool in assessing patients withMIdue to its ability to diagnose acute and chronic MI,narrow thedifferentialdiagnosis, and determine the prognosis by assessing the scar burden. In patients with MINOCA, CMR should be obtained within seven days of presentationandpreferably not in the first 24 hours to improve the diagnosticaccuracy [3].CMR protocol should include cine assessment of cardiac function and structure, T2 assessment of myocardial edema, andLGEto assessformacroscopic scar/fibrosis/infiltrative disease(both pattern and extent) [3].
LGE technique can be helpful in broadly categorizing MINOCA into ischemic versus non-ischemichyperenhancement patterns.IschemicMINOCA will have a subendocardialor transmuralLGE pattern versus mid-myocardial or subepicardial in non-ischemic causessuch asviralmyocarditis [5]. Moreover,CMR can help categorize the type of ischemic LGE pattern based on appearance, as embolic infarcts often display a wedge-shaped hyperenhancementpatternand theabsence of wavefront phenomenonwith a predominance of scar in thesubepicardiumrather thansubendocardium [6].It is important to differentiate this atypical infarct pattern fromcommonnon-ischemic etiologies.
MVOis seen following coronary reperfusion therapy, especially after prolongedmyocardial ischemia.Itis caused bymicrovascular damage impairing blood flowthroughdamaged capillariesand is the CMRvisualrepresentation ofthe no-reflow phenomenon [7,8]. On early or late gadolinium enhancement, MVO is seen as a dark central (hypoenhanced) focus withinhyperenhancedmyocardialscar, which is due to the inabilityof gadoliniumto penetratethe damaged microvasculature. Correlated myocardial segments with MVO are more likely to have remodeling, wall-thinning, and poor functional recovery [9]. Identification of MVO can predict the risk of left ventricular remodeling and future risk of major adverse cardiac events; MVO on LGE is more prognostic than on early gadoliniumenhancement [8,10]. MVO is typically seenafterMIbutmay be iatrogenic such as after catheterablation ofventricular tachycardia [8].
AF, infective endocarditis, and prosthetic valve thrombosis are the most common causes of coronary emboli; AF accounts for about 15% of coronary emboli [1]. Coronary embolism after DCCV of AF is exceedingly rare andseldom reported [2].

Conclusions
This case illustratesthe importance of obtaining CMR in patients with MINOCA.Although ourpatient did not present withsymptoms of anMI, CMR was able to identifyasilent embolicinfarctafter DCCV for AF.Despite its paucity, DCCV in AF patients can cause coronaryembolism even in fully anticoagulated patients.

Additional Information Disclosures
Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work.