Thrombotic Occlusion of a Septal Perforator Causing ST-Segment Elevation Myocardial Infarction

Abstract

Septal branches of the left anterior descending artery constitute the blood supply to the interventricular septum. Ischemia of the septal artery can have consequences of angina, arrhythmia, infarction, and ventricular dysfunction. However, percutaneous intervention of the septal perforator artery cannot only be technically challenging, but also poorly studied.

Case 

A 54-year-old female with history of coronary artery disease, diabetes, hypertension, and dyslipidemia presented to the emergency room with chest heaviness. The patient had previously undergone stenting of her right posterior descending artery one year prior using a drug-eluting stent.

Physical exam was remarkable for a tachycardic patient in mild respiratory distress. Electrocardiogram revealed ST-segment elevation in V1-V3 (Figure 1). The patient was brought emergently to the catheterization laboratory, where angiography revealed a large left anterior descending (LAD) artery and first septal perforator (SP) branch with an ostial 100% thrombotic occlusion (Figure 2).  

Using a 6 French EBU 3.5 guide (Medtronic), the left main coronary artery was engaged. A 0.014” Prowater guidewire (Abbott) was placed into the distal first SP, while a second 0.014” Kinetix guidewire (Boston Scientific) was used to secure position in the distal LAD. A ClearWay 1.0 x 10 mm perfusion balloon (Atrium) was used to infuse a single bolus of eptifibatide (9 cc) at the ostium of the occluded SP branch. An Apex 2.0 x 8 mm balloon (Boston Scientific) was used to pre-dilate the lesion (Figure 3) into the anterior and posterior bifurcation branches. Final images confirmed excellent angiographic result and TIMI-3 flow into the LAD and SP branches (Figure 4). The remainder of the hospital course was unremarkable, with complete resolution of ST-segment changes on the electrocardiogram. The patient was discharged home in 2 days on dual antiplatelet therapy indefinitely.

Discussion

The interventricular septum encompasses one-third of the left ventricle and plays a major role in ventricular function.¹ The septal branches of the LAD supply a majority of the anterior portion of the interventricular septum.² In addition, blood supply to the atrio-ventricular node, the His bundle, and its proximal left and right bundles comes from the atrioventricular (AV) nodal artery and the first SP.³ Up to 30% of patients may have a large first SP.⁴ While the size and anatomy of septal branches differs, the distribution supplied can be extensive and occlusion of a large SP can cause significant myocardial ischemia.⁵ Anginal symptoms can also result from coronary spasm of the septal branch.⁸ Septal infarction is most commonly caused by LAD occlusion, which occurs in 18% of patients from plaque shift during LAD intervention.⁶ However, isolated occlusion of the first SP may cause clinical ischemia, infarction, arrhythmia and congestive heart failure.^1-4,7,9 Electrocardiogram may show ST-segment elevation in leads V1-V3.⁸ Occlusion of the first SP following LAD or septal intervention has also been shown to induce complete and delayed heart block.^3,7,9 Multiple prior reports have shown transient complete heart block following jailing of first SP during coronary intervention.¹⁰

SP intervention has gained popularity in regards to nonsurgical reduction of septal thickness in patients with hypertrophic obstructive cardiomyopathy.¹¹ However, PCI of SP has rarely been described, because of technical difficulties in revascularization. SP are not amenable to bypass surgery, given their depth and location beneath epicardial arteries.^1-2,4 Furthermore, SP enter the heart at acute right angles and therefore make stenting difficult due to small size and sharp angles of origin.^2,4 Given these technical challenges, failed intervention may result in acute vessel closure.⁴

Balloon angioplasty has been implemented with success in several instances of SP occlusion. Vermuri et al¹ described the acute and long-term outcomes of 21 patients with a 95% success rate: 95% had event-free survival over 18-month follow-up; 86% were free from angina; and 83% of patients with congestive heart failure demonstrated improvement of functional class. Topaz et al presented similar success in a case study of 11 patients.¹² A common complication of SP intervention includes restenosis: Topaz demonstrated a 27% restenosis rate after SP angioplasty. One proposed reason for the high restenosis rate is compression of SP by the interventricular septum, causing increased elastic recoil.⁸ Incidence of acute septal closure has not been well studied. One small study reported that 1 out of 11 patients had acute vessel closure.¹⁰ Ostial septal branch lesions carry even greater risk of closure. Another potential sequelae of acute closure following angioplasty of the first SP is a resultant ventricular septal defect, although the incidence of this is also unknown.^2,4 

Stent implantation in the septal artery has been shown to prevent elastic recoil, intimal hyperplasia and reduction in restenosis.⁸ Stent implantation has also been shown to relieve anginal symptoms and restore hemodynamic stability.¹² The major difficulty in stenting the septal artery lies in the aforementioned acute right angle takeoff of the SP from the LAD, and the small vessel size, which makes stent deployment difficult.² In addition, stenting of the first SP may not be prudent in the case of a patent LAD, because stent deployment may result in extension into the LAD and subsequent occlusion.¹³ Rotational atherectomy has shown some success in debulking septal artery obstructive disease prior to balloon angioplasty.² However, the small size of the septal branches, as well as angulated origins, makes rotational atherectomy challenging.² There was also one reported case of aspiration thrombectomy of a thrombotic occlusion of a large SP with residual stenosis of 10-20%.⁴ Although there is controversy related to SP angioplasty and stenting, there is perhaps greater success to be gained with adjunctive mechanical thrombectomy devices, as well as development of lower profile catheters to accommodate the technically challenging aspects of SP intervention.

Herein, we present a rare case of an acute SP thrombotic occlusion resulting in ST-segment elevation myocardial infarction and successfully treated with selective glycoprotein IIb/IIIa receptor inhibitor infusion and angioplasty. 

The authors can be contacted via Dr. Jon George at georgej@deborah.org.

Disclosure: Dr. Marreddy reports no conflicts of interest regarding the content herein. Dr. George reports he is a consultant for Boston Scientific and receives research support from Atrium Medical.

References

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