Thrombotic Occlusion of a Large Septal Perforator Presenting as ST-Segment Elevation in V1-V2 and Treated with Aspiration Thrombectomy: A Brief Review of the Literature

ABSTRACT: The interventricular septum constitutes approximately one-third of the mass of the left ventricle, and the bulk of the anterior septum is supplied by septal branches of the left anterior descending coronary artery. Ischemia of the interventricular septum results in angina, infarction, biventricular failure and ventricular arrhythmias. While the majority of septal infarctions are due to occlusions of the proximal left anterior descending coronary artery, a large first septal branch thrombosis can rarely be the culprit. Given the paucity of data pertaining to septal perforator disease, a thorough discussion on septal perforator coronary artery interventions and an illustrative case will be provided. J INVASIVE CARDIOL 2011;23:E255–E259 Key words: septal myocardial infarction; interventricular septum; septal branch percutaneous interventions; septal perforator; septal branch; aspiration thrombectomy ————————————————————

While the vast majority of septal myocardial infarctions (MI) are a product of occlusions in the proximal segment of the left anterior descending (LAD) coronary artery, a thrombosis of a large septal branch can rarely be the culprit. The incidence of septal branch occlusion resulting in ST-segment elevation is unknown. However, septal myocardial infarctions are quite common and lead to angina, biventricular failure and arrhythmias.¹ Although septal branches of the LAD supply the bulk of the interventricular septum (IVS), there is a paucity of data pertaining to the efficacy and safety of septal branch interventions.² These branches are frequently ignored as potential targets for revascularization secondary to the fact that they are surgically inaccessible, usually small in caliber (1.5–2.0 mm in diameter), and have an acutely angulated vessel origin.^1–3 Septal perforators are also associated with high restenosis rates after angioplasty due to their increased elasticity, and septal branch disease usually involves the ostium and functions as a branch ostial stenosis, which limits the role for stenting and prevents the delivery of bulky devices.^1,3

We present a patient with ST-segment elevation in V1 and V2 secondary to a proximal thrombotic occlusion of a large septal branch with thrombolysis in myocardial infarction (TIMI)-0 flow. After aspiration thrombectomy using a low-profile catheter, there was restoration of TIMI-3 flow, normalization of the ST-segments, and resolution of her severe chest pain. The patient also had normal septal wall motion on her echocardiogram prior to discharge.

Case Report. A 78-year-old African American female presented to the emergency department with severe chest pain at rest. Past medical history was notable for coronary artery disease, hypertension, hyperlipidemia and impaired glucose tolerance. The patient underwent stenting of her LAD coronary artery in January of 2009 due to exertional angina.

Her physical examination was normal, and her electrocardiogram showed normal sinus rhythm and ST-segment elevation in leads V1 and V2 (Figure 1A). The patient was treated with aspirin and clopidogrel and brought emergently to the catheterization lab. Coronary angiography revealed a right dominant system with mild coronary calcification. There was a moderate proximal right coronary artery stenosis and minimal left circumflex disease. The LAD was a large-caliber vessel with a widely patent proximal stent with mild in-stent restenosis. The stent was located approximately 1–2 mm after the origin of the first septal branch, which had a thrombotic occlusion with TIMI-0 flow distally (Figure 2A). The mid-LAD had a 60–70% stenosis distal to the stent, and the remainder of the LAD and its diagonal branches had minor luminal irregularities.

Using a 6 French (Fr) EBU Launcher 4.0 guide catheter (Medtronic Vascular, Minneapolis, Minnesota), bivalirudin, and Integrilin double bolus and infusion, two 0.01" Asahi Prowater guidewires (Abbott Laboratories, Abbott Park, Illinois), were placed in the distal LAD and into the first septal branch without difficulty. A Pronto low-profile (LP) catheter (Vascular Solutions, Minneapolis, Minnesota) was carefully placed just proximal to the thrombotic occlusion, and after continuous negative suction (aspiration) was applied, the Pronto LP catheter was slowly advanced across the lesion. After several additional passages were performed, the 100% thrombotic stenosis was converted to a 10–20% residual stenosis, and there was restoration of TIMI-3 flow (Figure 2B). No stent was deployed.

After the percutaneous coronary intervention, the patient was chest pain-free and had normalization of her electrocardiogram (Figure 1B). A transthoracic echocardiogram following the procedure showed normal left ventricular systolic function with an ejection fraction of 60–65% and normal regional wall motion. The patient was discharged to home within 72 hours on maximal medical therapy and was asymptomatic.

Discussion. It is extremely rare for an occlusion of a septal branch artery to cause an acute septal MI in the absence of a LAD thrombosis.⁴ Septal branch disease can certainly cause ischemia, angina, congestive heart failure, conduction abnormalities and arrhythmias,⁵ and while it is a rather unusual cause of infarction, it is imperative that clinicians understand the role and significance of both the IVS and the septal perforator coronary arteries.

The IVS, which constitutes about one-third of the mass of the left ventricle, is a common wall for both the left and right ventricles and is a vital component to left and right ventricular function.³ Septal branches of the LAD supply the majority of the IVS. In fact, the septal branches of the LAD supply two-thirds of the anterior portion of the IVS, while the inferior portion of the septum is supplied by septal branches of the posterior descending coronary artery, which usually arises from the right coronary artery and infrequently from the left circumflex coronary artery.¹ As a result, septal perforators are an important source of collateral blood supply between the right coronary artery and the left system.^1,3 The first septal branch also supplies a significant portion of the conduction system, including the His bundle and the atrioventricular node in 50% of patients.³

The size and anatomy of septal perforators vary widely.² While patients usually have several small-caliber septal branches that are equal in size, a large first septal perforator may be found in approximately 15–30% of patients.^2,3,6 A large first septal perforator coronary artery may have obstructive disease or even coronary artery vasospasm, resulting in angina and significant clinical ischemia.⁷ Infarction of the IVS is usually due to LAD disease, but it can rarely be a product of a discrete stenosis in a large septal perforator.¹ Complete occlusion of a large septal branch may present with angina and ST-segment elevation in leads V1-V3.⁷ It can also present with a right bundle branch block and left axis deviation.⁷

While septal branches supply a large area of distribution and appear to be amenable to revascularization,^1,3 the options are limited as there is no role for bypass surgery of septal branches given their intramyocardial course.^1,3 Septal branches originate below epicardial coronary arteries, enter the heart at right angles, and course throughout the IVS in an anterior to posterior direction.^1–3 Septal perforator percutaneous interventions have recently become more relevant, because these branches are selectively injected with ethanol in the treatment of hypertrophic obstructive cardiomyopathy.² Since the early 1980s, several case reports and a few retrospective series have documented the benefits of angioplasty in this setting as long as the patients are properly selected (Table 1).^{1–3,5,8–13}

The technical success rate of septal branch angioplasty is as high as 95%,^3,8,9 and the rate of acute complications is quite low.⁸ According to the largest series to date, angioplasty of a large septal branch was performed in 21 patients, and it markedly reduced the severity of the stenosis from 89 to 18%.⁸ There was no target lesion revascularization, acute closure, emergency bypass surgery, MI or death, and event-free survival was 95% at 18 months.⁸ At 24 months, there was a marked improvement in anginal class in 86% of patients, and 83% of the patients with congestive heart failure demonstrated an improvement in functional class.⁸

However, angioplasty of septal branches has many limitations. Restenosis occurs in approximately 27% of patients after septal perforator angioplasty,⁹ and there is a 40–50% residual stenosis despite high immediate success rates.¹ This is likely due to the fact that septal perforators are frequently compressed by the myocardium and have increased elastic recoil.² In general, both restenosis rates and target lesion revascularization are much more common after angioplasty alone.¹

As compared to non-ostial disease, angioplasty of branch ostial lesions is also associated with an increased rate of major complications.¹ Abrupt closure occurred in 1 out of 11 patients treated with septal branch angioplasty.^3,9 If acute closure occurs, surgical revascularization is not an option, and bailout stenting of a septal branch might be extremely challenging due to its small size and acutely angulated origin.¹ Another potential but feared complication of septal branch angioplasty is causing a ventricular septal defect, but the incidence of this adverse outcome is unknown.¹

The first published case report demonstrating the safety and benefit for stent implantation in a large septal branch was in 2000.^2–4 Stenting prevents elastic recoil, increases the luminal diameter of the vessel, and may reduce the likelihood for restenosis,³ but stenting septal perforators is technically difficult. These vessels are usually small in caliber, course within the myocardium, and have a sharp right angle take-off from the LAD.^1,3 Moreover, septal branch disease usually involves the ostium, and stenting their branch-ostial location could jeopardize a patent LAD.^1,3 In fact, the majority of patients who have undergone septal branch stenting have a totally occluded LAD, which is bypassed.^2,3 Given the limitations of treating large septal perforators with both angioplasty alone and stenting, rotational atherectomy has even been investigated in this setting.^1,14 There is even a case series of 4 patients who underwent septal branch angioplasty after successful rotational atherectomy.¹ The residual stenoses in all of these patients were less than 20%, and no complications were reported.¹

It is also unclear if septal branch revascularization in the setting of MI is clinically indicated. After transient acute occlusion of the septal branch in 19 dogs, early reperfusion of the septal perforator failed to reduce the extent of necrosis across the IVS.¹⁵ However, dogs have more collateral supply of the IVS than humans. Nevertheless, unlike MI involving occlusion of major epicardial coronary arteries, there is a paucity of data that early reperfusion of the septal coronary artery minimizes the size of infarction. A recent case report demonstrated that stenting an occluded septal branch in the setting of MI alleviated intractable angina,⁴ but controversy about stenting septal branches certainly exists.

To our knowledge, this is the first reported case of aspiration thrombectomy being used to successfully treat a septal MI due to a thrombotic occlusion of a large septal branch. Not only did thrombectomy resolve our patient’s chest pain and normalize her ST-segments, her troponin and creatinine kinase peaked at 0.06 mg/dl and 103 mg/dl, respectively, and her septal wall motion was preserved prior to discharge from the hospital. Manual aspiration thombectomy in the setting of acute MI results in enhanced myocardial reperfusion and less myocardial necrosis and is also associated with a lower risk of distal embolization and no reflow as compared with either angioplasty or stenting alone.¹⁶ In the present case, we did not perform angioplasty or stenting of the septal perforator given the risk of compromising the LAD, the resolution of her angina, the normalization of her electrocardiogram, the restoration of TIMI III flow, and the reasonable angiographic result achieved with aspiration thrombectomy alone.

Conclusion. It is extremely unusual for septal infarction to occur as a result of an occluded septal branch in the absence of thrombosis in the LAD. Approximately 30% of patients have a large septal branch, and these vessels can have obstructive disease and cause significant clinical ischemia. While angioplasty and stenting of septal perforator coronary arteries are both feasible and relatively safe options, their utility is limited due to the small size of the vessel, the acutely angulated take-off from the LAD, the ostial location of the stenosis and the high rate of restenosis. To our knowledge, this is the first case of a thrombotic occlusion of a large septal branch presenting as ST-segment elevation in V1-V2, which was treated successfully with aspiration thrombectomy. Further studies addressing the role for aspiration thrombectomy in this setting are certainly warranted.

Editor’s Note:

This excellent challenging case highlights the feasibility of septal perforator intervention using an aspiration thrombectomy catheter similar to what is done in other coronary arteries. This case also emphasizes that in some cases where following aspiration thrombectomy, if there is no residual obstructive lesion, then PTCA or stenting may not be warranted.

— Samin K. Sharma, MD, Mount Sinai Medical Center, New York, New York

References

1. Cohen ID, Khosla S, Levin TN, Feldman T. Rotational atherectomy for left anterior descending artery septal perforator stenosis. Catheter Cardiovasc Interv 1999;46:79–82. 2. Regar E, Kozuma K, Ligthart J, et al. Coronary stent implantation in a septal perforator artery: Case report and review of the literature. Jpn Circ J 2000;64:802–804. 3. Ozdemir M, Timurkaynak T, Cemri M, et al. Stenting of the septal perforator coronary artery. J Invasive Cardiol 2001;13:694–697. 4. Trehan V, Mukhopadhyay S, Rangasetty UC, et al. Stenting of a septal perforator for post-myocardial infarction angina. Indian Heart J 2003;55:368–369. 5. Topaz O, Cacchione J, Nair R. Septal perforator artery angioplasty: The advantage of application of an ultralow-profile balloon system — A case history. Angiology 1993;44:69–72. 6. Stoney WS, Vernon RP, Alford WC Jr, et al. Revascularization of the septal artery. Ann Thorac Surg 1976;21:2–6. 7. Azuma T, Maeda K, Akagi H, Yamamoto T. [Rest angina induced by coronary artery spasm at the first septal artery: A case report]. J Cardiol 1994;24:161–165. 8. Vemuri DN, Kochar GS, Maniet AR, Banka VS. Angioplasty of the septal perforators: Acute outcome and long-term clinical efficacy. Am Heart J 1993;125:682–686. 9. Topaz O, DiSciascio G, Vetrovec GW, et al. Application of coronary angioplasty to the septal perforator arteries. Cathet Cardiovasc Diagn 1991;22:7–13. 10. Comazzi JL, Jang GC, Marsa RJ, et al. Percutaneous transluminal angioplasty of a large septal artery. Cathet Cardiovasc Diagn 1983;9:181–186. 11. Trivedi A, Voci G, Banka VS. Coronary angioplasty of septal perforator. Am Heart J 1988;115:466–468. 12. Piscione F, Beatt K, de Feyter PJ, Serruys PW. Sequential dilatation of septal and left anterior descending artery: Single guiding catheter and double guidewire technique. Cathet Cardiovasc Diagn 1987;13:33–38. 13. Marti V, Auge JM, Garcia J, et al. [Percutaneous coronary transluminal angioplasty in a heart transplant recipient]. Rev Esp Cardiol 1993;46:257–259. 14. Jain D, Richardt G, Katus HA. Rotational atherectomy of a stent-jailed septal perforator: A good verdict for the prisoner. J Invasive Cardiol 2001;13:702–704. 15. Wilson JL, Netherland DE, Ingram LA, et al. Myocardial infarction following acute occlusion and reperfusion of the septal coronary artery. Basic Res Cardiol 1985;80:670–676. 16. Silva-Orrego P, Colombo P, Bigi R, et al. Thrombus aspiration before primary angioplasty improves myocardial reperfusion in acute myocardial infarction: The DEAR-MI (Dethrombosis to Enhance Acute Reperfusion in Myocardial Infarction) study. J Am Coll Cardiol 2006;48:1552–1559.

———————————————————— From the Division of Cardiology, Johns Hopkins University, Baltimore, Maryland. The authors report no conflicts of interest regarding the content herein. Manuscript submitted March 16, 2010, provisional acceptance given April 8, 2010, final version accepted April 14, 2010. Address for correspondence: Todd A. Dorfman, MD, Division of Cardiovascular Disease, Johns Hopkins Hospital, 600 N. Wolfe St, Carnegie 568, Baltimore, MD  21287-073. E-mail: tdorfma1@jhmi.edu