Spontaneous coronary artery dissection presenting as massive brain stroke: Happy landing with percutaneous coronary intervention

Sanjay Kumar Sharma; Rajiv Motiani

doi:10.4103/jcpc.jcpc_25_22

CASE REPORT

Year : 2022 | Volume : 11 | Issue : 4 | Page : 102-104

Spontaneous coronary artery dissection presenting as massive brain stroke: Happy landing with percutaneous coronary intervention

Sanjay Kumar Sharma¹, Rajiv Motiani²
¹ Department of Cardiology, Neo Hospital, Noida, Uttar Pradesh, India
² Department of Neurology, Neo Hospital, Noida, Uttar Pradesh, India

Date of Submission	16-Sep-2022
Date of Decision	17-Nov-2022
Date of Acceptance	18-Nov-2022
Date of Web Publication	21-Jan-2023

Correspondence Address:
DM, SCAI, FESC, FIMSA Sanjay Kumar Sharma
Department of Cardiology, Neo Hospital, D-170A, Sector 50, Noida - 201 301, Uttar Pradesh
India

Source of Support: None, Conflict of Interest: None

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DOI: 10.4103/jcpc.jcpc_25_22

Abstract

Spontaneous coronary artery dissection (SCAD) presenting as stroke is indeed an extremely rare scenario. We hereby describe our experience of a case of SCAD in a 29-year-old man who presented with a massive brain stroke. Based on the neurological findings, the diagnosis of left hemiparesis, left upper motor neuron facial palsy, and acute right middle cerebral artery infarct was made. Coronary angiography displayed a large type B dissection along with heavy burden of thrombus and intimal hematoma in proximal to the mid-left anterior descending artery (LAD). SCAD of the LAD was managed with percutaneous coronary intervention using a provisional stenting approach with two overlapping drug-eluting stents. With this case, the author would like to outline vital clinical insights for clinicians managing such a challenging and perplexing patient cohort.

Keywords: Left anterior descending artery, percutaneous coronary intervention, spontaneous coronary artery dissection, stroke

How to cite this article:
Sharma SK, Motiani R. Spontaneous coronary artery dissection presenting as massive brain stroke: Happy landing with percutaneous coronary intervention. J Clin Prev Cardiol 2022;11:102-4

How to cite this URL:
Sharma SK, Motiani R. Spontaneous coronary artery dissection presenting as massive brain stroke: Happy landing with percutaneous coronary intervention. J Clin Prev Cardiol [serial online] 2022 [cited 2023 Jun 8];11:102-4. Available from: https://www.jcpconline.org/text.asp?2022/11/4/102/368354

Introduction

Spontaneous coronary artery dissection (SCAD) is a potentially life-threatening condition, albeit a rare one. SCAD implies the creation of a false lumen around the true lumen in the tunica media of the coronary artery, which leads to compression of the true lumen, resulting in myocardial infarction (MI). It predominantly affects young females, constituting approximately 87%–95% of all cases, with a mean age at diagnosis of the index event between 44 and 53 years.^[1] Paradoxically, the manifestation of SCAD with signs and symptoms of stroke remains extremely rare among young adult men. We herein report such a gut-wrenching case.

Case Report

A 29-year-old non diabetic, normotensive man presenting with facial deviation, and left-sided weakness for almost 3 h associated with slurred speech along with severe chest pain. Looking at the signs and symptoms of cardiogenic shock along with a massive brain stroke, wherein noradrenaline and dopamine infusions were immediately started with a large inotropic support. Noncontract head CT displayed a large area of wedge-shaped subtle hypodensity with blurring of gray-white matter interface in the right fronto- and temporoparietal region, suggesting acute infarct [Figure 1]a. Brain magnetic resonance imaging (MRI) showed a large acute infarct in the right fronto-parieto-temporal region involving the right basal ganglia and the horizontal segment of the right middle cerebral artery (MCA) lost normal flow void, raising suspicion of thrombosis. Neck MRI angiography revealed a short segment atheromatous thickening in the right internal carotid artery (ICA) origin causing about 50%–55% stenosis. Laboratory results were all within normal limits, except for cardiac troponin T and I. These findings are consistent with the diagnosis of left hemiparesis, left upper motor neuron facial palsy, and acute right MCA infarct.

In view of the presenting complaint of chest pain and elevated cardiac troponin levels, he was further referred to cardiologist. A family history of coronary artery disease (CAD), diabetes, and hypertension was noncontributory. Apart from smoking, there were no other cardiovascular risk factors. Electrocardiographic findings include normal sinus rhythm, right bundle branch block, and ST-elevation V2–V5, were consistent with cardiogenic shock [Figure 1b. Echocardiography displayed akinetic mid-anterior septum and apex, regional wall motion abnormalities, dilation of the left atrium/left ventricle, severe mitral regurgitation, moderate tricuspid regurgitation, severe left ventricular systolic dysfunction (ejection fraction, 25%), and grade-III diastolic dysfunction. The patient was clinically diagnosed with ST-elevation MI. Coronary angiography demonstrated a large type B dissection along with a heavy burden of thrombus and intimal hematoma in proximal to the mid-left anterior descending artery (LAD) [Figure 2]a [Supplementary Video 1]. The diagnosis of a single-vessel CAD with severe left ventricular dysfunction was made. Provisional stenting or T and small protrusion (TAP) technique has been proposed to treat LAD dissection, and ultimately it was planned to perform provisional stenting using two overlapping drug-eluting stents.

The LAD was engaged with 6F XBU 3.5 guiding catheter and the lesion was crossed with 0.014” BMW guidewire. Subsequently, 3.0 mm × 28 mm DES was deployed at 18 atm [[Figure 2]b and Supplementary Video 2]. Considering the need for another stent to cover the ostium of LAD [Figure 2]c, 3.5 mm × 12 mm DES was positioned at the ostial LAD overlapping the proximal stented segment and deployed at 18 atm [Figure 2]d [Supplementary Video 3]. After stenting, TIMI 3 flow was achieved in the LAD vessel [[Figure 2]e and Supplementary Video 4]. The patient was discharged after 5 days of the procedure, at that time, a repeat echocardiogram showed improved LVEF (40%–45%). Repeat coronary angiography after 42 days of percutaneous coronary intervention (PCI) showed normal coronary artery with a patent stent in the LAD with TIMI-3 flow in the main vessel and side branch [[Figure 2]f and Supplementary Video 5].

Figure 1: (a) Noncontract head computed tomography showing a large area of wedge-shaped subtle hypodensity with blurring of gray-white matter interface in the right fronto- and temporoparietal region, (b) Electrocardiographic findings showing normal sinus rhythm, right bundle branch block, ST-Elevation V2–V5

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Figure 2: (a) Angiography showed large type B dissection along with a heavy burden of thrombus and initial hematoma in proximal to mid LAD artery, (b) Deployment of 3.0 mm × 28 mm drug-eluting stent in LAD artery, (c) Angiography revealed need for another stent to cover the ostium of LAD artery, (d) 3.5 mm × 12 mm Drug-eluting stents (DES) was deployed at the ostium of LAD artery overlapping with the proximal stent, (e) Final TIMI flow, (f) Repeat angiography after 42 days of percutaneous coronary intervention revealed normal coronary artery with the patent stent in the LAD artery. LAD: Left anterior descending artery

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Discussion

SCAD remains a less familiar pathology to cardiologists and represents one of the most challenging and extremely arduous therapeutic and diagnostic tasks, especially for interventional cardiologists. The reported prevalence of SCAD ranges from 0.10% to 0.24% among all CAD patients undergoing coronary angiography.^[2]

Several conditions are associated with the development of SCAD, such as fibromuscular dysplasia, chronic inflammatory systemic diseases, hypothyroidism, pregnancy, genetics, emotional stressors, and smoking. Except for smoking, we could not detect any of the predisposing factors in our case. Smoking is a significant risk factor for CAD, so there may be an underlying connection between smoking and SCAD. This hypothesis requires further confirmation with more evidence.^[3]

Stroke is a consequence of embolism from left ventricular clot postinfarct. Nevertheless, so far in the literature, only three SCAD cases have been reported with stroke. In 2010, Rajendra et al.^[4] presented the first case of a middle-aged (56 years) man who had SCAD presenting with stroke. One year later, in 2011, Tariq and Mustafa^[5] reported the second case of a 60-year-old Caucasian man with no significant past medical history who presented with stroke, further diagnostic workup demonstrating MI due to SCAD. In keeping with this, in 2020, Ete et al.^[6] published a case of SCAD in a middle-aged man (49 years) who strangely presented with an ischemic stroke. Collectively, all this evidence provides a clue for stroke as a risky marker that could be identified in patients with SCAD.

The pathogenesis through which SCAD develops stroke yet remains enigmatic. It has been speculated that SCAD causes MI, which leads to the formation of clots in the akinetic left ventricle with possible embolization and thus gives rise to stroke.^[5]

Conservative management of SCAD is recommended in asymptomatic and stable patients, whereas PCI and coronary artery bypass grafting are preferred treatment modalities in acutely ill patients. However, PCI of SCAD poses a great technical challenge: (a) a risk of inserting the guidewire into the false lumen; (b) the dye might not penetrate the false lumen sufficiently; and (c) if an entry point is identified by angiography, a stent can be placed at the proximal entry point to create a sort of seal.^[7] In many circumstances, the dissection is too long for a single stent to be sufficient; in these cases, multiple continuous stents may be employed to hold the dissection in place. Thrombolysis can be catastrophic if administered in the presence of SCAD.^[8] The mainstay of treatment to prevent recurrent thrombosis is anticoagulation. Aspirin and clopidogrel were initiated, without statin therapy. Intra-aortic balloon pump (IABP) and Impella device modalities are widely used in managing cardiogenic shock.

In our case, there was a high chance of neurological worsening with high dose of dual antiplatelet therapy and heparin as both drugs can lead to hemorrhagic transformation; hence, these drugs should be instituted with proper caution. IABP and Impella both device modalities required regular heparin load so that these modalities cannot be preferred in our case. Due to emergency conditions, a simple strategy, rather than a complex one, should be applied, plan A and B should be kept in the mind, and provision stenting is the best option.

Conclusions

This case became more complex due to the young age, an association of LAD dissection with massive brain stroke, and the existing dilemma in the treatment of such entity.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

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