A 65-Year-Old Man with Coronary Artery Embolism and Acute Inferior Myocardial Infarction Following Cardioversion for Ventricular Tachycardia

Introduction

The risk of thromboembolism following cardioversion have been studied in patients with atrial fibrillation, with studies evaluating the protocols recommended for prevention of such complications. However, this has not been evaluated in ventricular arrythmias. Overall, the incidence of thromboembolic complications in atrial fibrillation is 6–7% without anticoagulation and only 0.5–1.6% if patients receive adequate anticoagulation. The incidence of coronary artery embolism is 0.4%, but this has only been examined in atrial fibrillation [1].

The American Heart Association (AHA) recommended the use of direct-current synchronized cardioversion for treatment of hemodynamically unstable ventricular tachycardia. However, cardioversion is typically used in acute settings and may not be the best first-line treatment for all cases of ventricular tachycardia [2]. In a hemodynamically stable patient with ventricular tachycardia, the first-line treatment in achieving sinus rhythm is intravenous antiarrhythmics. If this fails, emergency electrical cardioversion may be performed with no prior anticoagulation required. The success rate of termination of the arrhythmia is 95% [3].

Arrhythmias are a possible complication of electrical cardioversion. Fortunately, the arrhythmias are mostly benign, like sinus tachycardia or non-sustained ventricular tachycardia, but ventricular fibrillation may be apparent in some patients. Cardioversion is also reported to be associated with pulmonary or systemic thromboembolism, especially anticoagulation was not performed prior to the procedure [3].

Although rare, direct-current (DC) cardioversion can lead to embolization to the coronary arteries. Most emboli travel to the brain, causing stroke; this is due to the characteristic of the circulatory system. For instance, the embolism usually travels to the aorta rather than the coronary arteries due to the lumen size difference and the increase in vascular resistance in the aorta. Additionally, the ostia of coronary arteries are partially covered with aortic valves and the Valsalva sinus, making it more difficult for emboli to enter. Lastly, emboli usually travel in the circulation in systole, while coronary flow usually occurs in diastole. These factors make thromboembolism complications usually occur in the central nervous system rather than the coronary arteries [4].

This case report details the history of a 65-year-old man who presented with acute myocardial infarction following DC cardioversion of ventricular tachycardia, highlighting the uniqueness of the case and treatment of the patient.

Case Report

A 65-year-old Bahraini man with previously diagnosed hypertension, chronic kidney disease, diabetes mellitus, dyslipidemia, and monomorphic ventricular tachycardia presented to the Emergency Department with symptoms of epigastric pain, palpitations, and 3 episodes of vomiting on the day of presentation. The symptoms were sudden in onset and were continuous in nature. He was tachycardic, with a heart rate of 206 beats per minute, and he was afebrile, with temperature of 37.1°C, and was maintaining saturation on room air with 96% peripheral oxygen saturation. Physical examination results were otherwise unremarkable.

He had been admitted to the hospital in 2021 with similar symptoms and was diagnosed with ventricular tachycardia and reduced ejection fraction heart failure (25–30%). He was offered an implantable cardiac defibrillator but refused. He was prescribed the following oral drugs on discharge: empagliflozin 110 mg, amiodarone 200 mg, atorvastatin 40 mg, carvedilol 25 mg 2 times a day, spironolactone 25 mg, furosemide 40 mg, and valsartan 80 mg. However, he was not compliant with his medications and had stopped using amiodarone for 6 months.

As part of the initial investigations, he underwent electrocardiography (ECG), which revealed wide complex tachycardia -monomorphic ventricular tachycardia (Figure 1). Thus, chemical cardioversion was started with 150 mg amiodarone 2 times, which failed, requiring electrical cardioversion with 360 Joles. A subsequent ECG showed bradycardia of 40–46 beats per minutes, and no ST-T wave changes suggestive of ischemia, with negative troponin marker. He was seen by a cardiologist was counseled about receiving an implantable cardiac defibrillator.

Later in the day he developed severe epigastric pain, with 3 episodes of vomiting. ECG showed inferior wall myocardial infarction (Figure 2) that was not present initially and was continuous in nature, with non-subsiding pain.

Thus, he was started on 300 mg oral aspirin orally (PO) and 600 mg oral Plavix and was referred to the Cardiac Center for a coronary angiogram, which showed occlusion of the distal left anterior descending artery, distal ramus, distal left circumflex/posterior descending artery dominant circumflex, and distal right coronary artery, with no significant atherosclerosis, indicating a dominant left system and a small, non-dominant right coronary artery (Figure 3).

An angiogram done in 2021 was normal; thus, clot embolization into the coronaries was reported.

After the coronary angiogram, he was started on 7 ml/hr IV integrilin at continuous infusion and unfractionated heparin 5000 iu/MI intravenous (acute coronary syndrome protocol). A transesophageal echocardiogram showed left ventricular ejection fraction of 40%, and akinetic posterior, inferior, and lateral segments. There was no left ventricular thrombus or left ventricular scar, which was confirmed by a contrast echocardiogram. Also, a small patent foramen ovale with left-to-right shunt and moderate mitral regurgitation was seen. He did not have clinical signs and symptoms of deep venous thrombosis, and paradoxical embolism was ruled out (Videos 1, 2).

Laboratory tests revealed a high white blood cell count of 17×109/L, with 81.1% neutrophils and 11.5% lymphocytes, and the rest of the complete blood count was normal. He had normal thyroid function test results, while his brain natriuretic peptide (BNP) level was high (1191.9 PG/ml). His troponin levels were high, at 1.09 ug/L, which increased to 1.71 ug/L on day 2. His creatinine kinase – myocardial band (CK – Mb) was initially 45.7 IU/L, which then changed to 35.6 IU/L. His baseline renal function test results were abnormal, with no signs of acute kidney injury. His electrolytes and magnesium levels were within normal range. Other markers were initially normal, then became deranged from day 2 with levels of aspartate aminotransferase 128 IU/L, lactate dehydrogenase 221 IU/L, and creatine kinase 233 IU/L, which subsequently rose to 1535 IU/L.

Unfortunately, day 2 of admission, he had hematuria, with kidney ureter and bladder ultrasound revealing a large right-sided staghorn calculus; thus, infusions were stopped and he was re-started on the infusions after the hematuria resolved.

He also had an episode of paroxysmal atrial fibrillation that resolved spontaneously and was switched to an unfractionated heparin atrial fibrillation protocol.

During admission, he was started on oral medications: aspirin 75 mg, clopidogrel 75 mg, atorvastatin 40 mg, furosemide 40 mg, pantoprazole 40 mg, amiodarone 300 mg 2 times a day, concor 2.5 mg, and sacubitril/valsartan 100 mg 2 times a day. A repeat angiogram was done 72 hours after the first angiogram, revealing improvement in the occlusion.

Patient was counseled regarding implantable cardiac defibrillator implantation but refused and thus was loaded with amiodarone 400 mg 3 times a day orally for one week followed by 400 mg 2 times a day orally for one week then 400 mg once a day orally for one week then 200 mg once a day to continue orally.

Patient was discharged on apixaban 2.5 mg 2 times a day orally due to development of atrial fibrillation. He was continued on the following oral medications: Plavix 75 mg, Lipitor 40 mg, Lasix 40 mg, pentazole 40 mg, amiodarone (dose as above), concor 2.5 mg and Entresto 100 mg 2 times a day. On follow up, he was doing well, with no further episodes of ventricular tachycardia or acute myocardial infarction.

Discussion

The primary learning outcome from this case report is that the presence of thromboembolism following cardioversion is not only limited to atrial fibrillation but may also be present in patients with ventricular arrhythmia. The diagnosis of coronary embolism is challenging, especially when there is atherosclerosis, as in our patient. However, the treatment approach is life-saving and suspicion must be high, particularly in those with risk factors. The diagnostic criteria for coronary embolism as proposed by Shibati et al is the presence of 2 or more major criteria: evidence of coronary artery embolism without atherosclerosis, concomitant occlusion at other arteries, no attributable left ventricular thrombus, and concomitant systemic embolization, or the presence of 3 minor criteria: less than 25% stenosis on angiography except for the culprit lesion, evidence of an embolic source, and presence of risk factors like atrial fibrillation, prosthetic heart valve, rheumatic heart disease, patent foramen ovale, infective endocarditis, history of cardiac surgery, and hypercoagulable state [5]. Our patient fulfilled 2 major criteria – presence of occlusion in other sites, and evidence of embolism, with no significant atherosclerosis and no left ventricular thrombus.

A systematic review by Diaz et al found the most frequent location of emboli in acute myocardial infarction is the distal portion of coronary arteries, which can cause small transmural infarctions, as seen in our patient [4].

The underlying causes of embolism in the coronary arteries are arrhythmia, with the most common cause being atrial fibrillation, followed by cardiomyopathy and valvular heart disease. Other causes mentioned in the literature include paradoxical embolism through atrial septal defect in a patient with deep vein thrombosis, malignancy, and infective endocarditis [5].

Treatment of coronary embolism initially is the same as for atherosclerotic acute coronary syndrome, which includes antiplatelet therapy, analgesia, and an emergency coronary angiography, as done in our patient. If angiography suggests coronary embolism, options include aspiration thrombectomy, balloon angioplasty, stenting, and intracoronary thrombolytics. This largely depends on the overall complexity of the case. The presence of high thrombus burden suggests the consideration of aspiration thrombectomy, but this is controversial. While this can be helpful in further pathology examination and confirmation of the diagnosis, it may be associated with increased risk of stroke. Intracoronary thrombolytics have been used in some case studies. Infusion of unfractionated heparin, bivalirudin, or glycoprotein IIb/IIIa inhibitors may be useful, especially in vessels with distal embolism, like in our patient. Nevertheless, this might not be helpful in more organized thrombi, like paradoxical embolism. Raphael et al suggested that those with persistent risk factors like our patient require long-term anticoagulation [6–8].

We reviewed the literature for case series or reports on acute coronary embolism after cardioversion in ventricular tachycardia, but found no relevant reports, with most cases involving atrial fibrillation.

In a case presented by Nuqali et al, a 66-year-old man presented to the Emergency Department with atrial fibrillation [9]. He was managed acutely with DC cardioversion after performing transesophageal echocardiogram, with no thrombus being shown. He subsequently developed acute ST segment elevation with stenosis in the left anterior descending distal artery. He underwent aspiration of the thrombus and received intra-coronary nitroglycerin, with complete resolution [9].

A 34-year-old woman with previously diagnosed aortic regurgitation presented with acute inferior myocardial infarction after elective cardioversion for atrial fibrillation. The diagnosis was initially established via ECG and she received thrombolytic therapy followed by coronary bypass graft and aortic valve replacement. Because surgery was planned, the thrombus was not aspirated [10].

Prochanu et al presented a case of embolic acute myocardial infarction following cardioversion, managed through stenting and balloon angiography, with improvement in symptoms and resolution of disease [11].

Most of the cases reported in the literature were managed through intervention. However, the complexity of our patient required him to be on conservative management. For instance, he had multiple comorbidities, including chronic kidney disease, which required cautious use of contrast agent. Fortunately, our patient had complete resolution and was followed up regularly in the clinic with no other acute events.

Conclusions

Electrical cardioversion is a known treatment method used in acute ventricular tachycardia not responding to pharmacological treatment. Embolic myocardial infarction after cardioversion is a very rare complication. Previously reported cases involved atrial fibrillation only. To the best of our knowledge, this is the first reported case of this complication in the absence of specific data on the risk of embolic myocardial infarction after cardioversion in a patient with ventricular tachycardia. Further guidelines are needed on the management and prevention of such complications in ventricular tachycardia patients.