An Uncommon Cause of Acute Coronary Syndrome: The Essence of a Broad-Minded Approach

INTRODUCTION

Acute coronary syndrome (ACS) can occur due to a variety of etiologies such as plaque rupture, plaque erosion, vasospasm, and embolism. Identifying the exact mechanism of ACS is vital for appropriate management and to prevent inappropriate interventions. This case highlights the need for extensive evaluation and astute clinical sense in managing such cases, which not only avoided the patient being on long-term dual antiplatelet therapy but also prevented possible intervention-related complications and future cerebrovascular events too.

CASE REPORT

A 42-year-old female with no risk factors for coronary artery disease and no previously known heart disease presented to the emergency with acute onset retrosternal chest pain, constricting type and of moderate intensity that had started 5 h back. Her pulse rate was 70/min, and blood pressure was 140/90 mmHg. The electrocardiogram showed sinus rhythm with ST depression in leads V4 to V6. Trop T was positive. The patient was diagnosed with a case of nonST-elevation ACS. Echocardiography revealed rheumatic heart disease (RHD) with severe mitral stenosis (MS)/moderate mitral regurgitation (MR) with a mitral valve area of 1.38 cm², mean gradient across the mitral valve being 11 mmHg, and dilated left atrium [Figure 1 and Video 1]. There was no regional wall abnormality and LV systolic function was normal. The patient received medical treatment in the emergency following which there was a significant reduction in chest pain.

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Figure 1: (a) Transthoracic echocardiogram showing severe MS with MVA=1.38 cm2 by planimetry (b) Continuous wave Doppler across mitral valve showing mean pressure gradient of 11 mmHg across mitral valve (c) Colour Doppler across mitral valve showing moderate mitral regurgitation.

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Next day, the patient was taken up for coronary angiography and possible revascularization. 6F right radial artery access was taken. A coronary angiogram was done using 6F TIG catheter. Coronary angiogram revealed total occlusion of the distal circumflex artery (LCX) at the level of 2^nd obtuse marginal (OM2) flow, with total occlusion of the terminal OM and TIMI I flow in OM2 [Figure 2a and Video 2]. The rest of the coronaries did not show any obstructive disease. After seeing the angiogram, the initial thought was to go ahead with percutaneous coronary intervention of the LCX. But after carefully looking into the angiogram, we noticed a small old organized clot in the distal left anterior descending artery (LAD) [Figure 2b and Video 3], raising suspicion of coronary embolism. The presence of severe MS and the fact that coronary artery disease is less prevalent among patients with RHD further strengthened the suspicion of embolism as the etiology of ACS rather than atherosclerosis. However, transthoracic echocardiography did not show any clot and she was not in atrial fibrillation (AF). Therefore, it was decided to defer coronary revascularization at that point in time as the patient was angina free and echocardiography did not show any regional wall motion abnormality. The patient underwent transesophageal echocardiography which showed a clot at the tip of the left atrial appendage (LAA) [Figure 3a and Video 4] and reduced LAA velocity [Figure 3b]. Findings of moderate MR and severe rheumatic MS were also noted on TEE [Figure 3c and d, respectively].

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Figure 2: (a) Initial coronary angiogram in RAO view showing total occlusion of distal LCX at the level of 2^nd obtuse marginal and total occlusion of terminal OM with retrograde filling through collaterals from left anterior descending artery (LAD), (b) Coronary angiogram in AP cranial view showing organized clot in distal LAD with normal flow. (RAO: Right anterior oblique, LCX: Left circumflex artery, OM: Obtuse marginal, AP: Anterior-posterior.)

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Figure 3: (a) Trans-oesophageal echocardiogram showing left atrial appendage (LAA) clot (b) Pulsed wave Doppler showing reduced LAA velocity (c) Colour Doppler showing moderate mitral regurgitation with vena contracta (VC) of 0.275 cm (d) Continuous wave Doppler across mitral valve showing mean pressure gradient of 15 mmHg suggestive of severe mitral stenosis.

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The patient was continued on parenteral anticoagulation Low molecular weight heparin (LMWH) for 1 week in addition to other treatment for ACS. 48 h Holter did not reveal any episodes of paroxysmal AF/flutter. After a week, a repeat coronary angiogram was done which revealed restoration of blood flow in the distal LCX with some residual occlusion and also improvement in OM2 occlusion [Figure 4a and b and Video 5]. Subsequently, magnetic resonance imaging (MRI) of the brain was also done which showed chronic lacunar infarcts in bilateral cerebellar hemispheres [Figure 5a] and corona radiata [Figure 5b], suggestive of previous silent cerebral embolism. This further added to the suspicion of ACS being cardio-embolic in nature. Subsequently, the patient was started on warfarin 5 mg and LMWH was continued until an INR of 2.5 was achieved. The patient was discharged on clopidogrel 75 mg, warfarin 5 mg, statin, oral penicillin, and beta blocker. She was advised to follow in the outpatient clinic with weekly INR monitoring which was maintained in the range of 2.5–3. There were no episodes of angina after discharge. Repeat angiogram after 6 weeks of discharge showed complete resolution of OM2 occlusion, distal LCX occlusion as well as terminal OM occlusion [Figure 4b and Video 6], hence confirming coronary embolism as the cause of ACS in our patient. The patient was continued on oral anticoagulation along with treatment for RHD-MS/MR. The patient is currently asymptomatic. Figure 6 shows a summary of the timeline of events depicting the clinical presentation of the patient, results of various investigations, treatment given, and the final outcome of the patient.

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Figure 4: (a) Coronary angiogram in RAO view on day 7 showing improvement of blood flow in distal LCX and 2^nd obtuse marginal (OM2), (b) Coronary angiogram in RAO view on day 42 showing complete normalization of blood flow in OM2, distal LCX, and terminal OM. (RAO: Right anterior oblique, LCX: Left circumflex artery, OM: Obtuse marginal).

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Figure 5: (a) MRI brain showing cerebellar lacunar infarcts (white arrows) (b) MRI brain showing corona radiata lacunar infarcts (white arrows).

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Figure 6: Timeline of events starting from the clinical presentation of the patient, results of various investigations, treatment given, and the final outcome.

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DISCUSSION

Coronary artery embolism is an uncommon cause of myocardial infarction.^[1] The first case of coronary embolism was reported by Virchow in 1856.^[2] The coronary arteries are relatively protected anatomically from embolic events.^[3] About 3% of ACS cases may result from coronary embolism.^[4] Here, we presented a rare case of acute coronary syndrome-non ST elevation myocardial infarction (ACSNSTEMI) secondary to coronary embolism due to RHD/severe MS with no evidence of infective endocarditis or AF.

Prizel et al.,^[5] studied a cohort of 55 patients in an autopsy series, with thrombotic material in the coronary arteries but no demonstrable acute plaque rupture, suggesting an embolic source. They constituted around 13% of the acute myocardial infarction cases. Valve disease was an underlying condition in only 22 (40%) of the patients out of which 8 had an abnormal native valve with no evidence of infection (same as our case). Similarly, Murray’s. Hoffman et al.,^[6] in 1956, presented a case report of a 64-year-old male with acute anterolateral wall MI who expired on day 5 of admission. Autopsy findings revealed severe MS and LAA thrombus with embolic masses obstructing both LAD and LCX. The arteriosclerotic changes in the walls of the coronary arteries were minimal and insufficient to explain the massive myocardial infarction, thereby indicating coronary embolism from the left atrium as the cause of ACS and mortality.

Shibata et al.,^[4] did a retrospective analysis of a total of 1776 patients with de novo acute MI over a 12-year period in the National Cerebral and Cardiovascular Center Acute myocardial infarction (AMI) database. This study demonstrated up to 3% prevalence of coronary embolism (n = 52). Diagnosis was made on retrospective examination of diagnostic angiography and subsequent investigation including echocardiography, MRI, and computed tomography. A scoring system was used for the diagnosis of coronary embolism. Majority of the cases with coronary embolism in this series had AF (73%, n = 38). Most had non-valvular AF (n = 30). Eight patients had valvular heart disease (15%). Among the 8 patients with valve disease, 4 had MS and 4 had aortic stenosis. Thus, MS constituted 7.7% of total coronary embolism cases. Our patient had definite coronary embolism as per the scoring system proposed in this study. Furthermore, our case did not have AF which was reported as the most common cause of CE with majority of cases having non-valvular AF. Nevertheless, AF should always be ruled out in coronary embolism cases.^[7]

CONCLUSION

In the presence of RHD and absence of CAD risk factors, coronary embolism should always be kept in mind in ACS cases, even in the absence of atrial fibrillation. This rare case emphasizes the fact that sometimes, even in emergency cases, a good clinical approach and a wait-and-watch policy can be a more rational decision rather than taking aggressive interventional measures.