Stenting in Unusual Settings:
Stenting of the Septal Perforator Coronary Artery

The interventricular septum (IVS), which is a common wall for the right and left ventricles, makes up about one-third of the total left ventricular mass and plays an important role in both right and left ventricular function.1 The major part of the IVS is supplied by septal perforator (SP) branches of the left anterior descending coronary artery (LAD). This report describes the first application of intracoronary stenting to the septal perforator coronary artery in a patient with a totally occluded LAD and a patent venous graft to the distal LAD. Case Report. A 42-year-old male admitted to our clinic with unstable angina pectoris. He had undergone coronary artery bypass graft surgery 5 years prior and received a sequential saphenous vein graft from the aorta to the first diagonal and LAD coronary arteries. When he came to us 2 months ago with the complaint of class IV angina, he was found to have a totally occluded LAD after the first SP, significant stenosis of the ostium of the first SP itself, a normal dominant left circumflex artery, a 70% stenosis in the body of a non-dominant small-caliber right coronary artery (RCA) and a high-grade thrombotic lesion in the proximal one-third of the vein graft. The anterolateral and apical walls of the left ventricle were aneurysmal. The culprit lesion was considered to be the one in the vein graft; the patient subsequently underwent stenting of the vein graft under intravenous tirofiban infusion. A Wallstent (Boston Scientific/Vascular, Natick, Massachusetts) was successfully placed with no complications and the patient was discharged 3 days later. After a period of 2 months resting the patient tried to resume his working activities, but experienced angina with the slightest effort and returned to the hospital with unstable angina pectoris. He described no rest angina at this time. He was known to be hypertensive and a heavy smoker, with a strong family history for premature coronary artery disease. He had a negative troponin-T assay upon presentation and was hospitalized with the diagnosis of unstable angina pectoris. On his third admission day, the patient was taken to the catheterization laboratory. The stented vein graft was patent, with no restenosis within the stented segment. The native coronary lesions were unchanged from the previous angiogram. The first SP artery, which was rather large (2.5–3.0 mm), had a significant and long lesion involving its ostium that extended back into the body of the LAD (Figure 1). After 10,000 units of intravenous heparin, the left coronary artery was engaged with an 8 French JL4 Guider guiding catheter (Schneider AG, Switzerland) using the transfemoral approach. A 0.014´´ ACS ExtraSport guidewire (Guidant Corporation, Santa Clara, California) was easily advanced across the stenosis into the distal SP artery. The lesion was first dilated with a 2.5 x 20 mm balloon up to 10 atmospheres (atm) of pressure, which yielded about 30–40% residual stenosis and a linear dissection (Figure 2). Considering that the lesion was ostial with a great tendency for recoil and subsequent restenosis, we decided to place a stent at this location. We crossed the lesion easily with a 3.0 x 19 mm premounted Jostent (Jomed AB, Helsingborg, Sweden), which was deployed at 10 atm of pressure and post-dilated to 14 atm with no complications. Since the LAD distal to the origin of the SP was totally occluded, we placed the stent in such a way that the proximal portion of the stent lay in the proximal LAD and the whole ostial lesion was covered. Stenting reduced the residual stenosis to almost 0% (Figure 3). The patient was followed for 2 days post-procedure with no complications or recurrence of angina and discharged thereafter on atenolol, ramipril, simvastatin and acetylsalicylic acid. When he was seen a month later at the outpatient department, he described a major relief of angina with only a residual class I angina on heavy exertion. Discussion. The interventricular septum, which is a common wall for the right and left ventricles, makes up about one-third of the total left ventricular mass and plays an important role in both right and left ventricular function.1 The major part of the IVS is supplied by SP branches of the LAD artery. These arteries enter the heart at almost right angles and course intramyocardially throughout the septum. The first SP branch of the LAD may sometimes be a large vessel, approaching the diameter of a diagonal artery or even larger. In a review of 100 normal coronary arteriograms, Stoney et al. noted large first septal perforators in 30%.2 The first SP supplies branches of the His bundle and contributes to the supply of the atrioventricular node about 50% of the time.3 Moreover, in disease states, septal arteries may provide collaterals between the right and left coronary arteries. Obstructive disease of large SP arteries may cause angina, ischemia or infarction of the IVS, conduction abnormalities or arrhythmias.4 Atherosclerotic disease of the SP arteries often accompanies disease in the LAD,5 but a discrete lesion in a large SP may create clinical symptomatology itself and deserve revascularization.6 Bypass surgery has a limited role in SP revascularization because SP arteries originate beneath the epicardial coronary arteries and traverse within the myocardium and are almost inaccessible surgically.2,6 On the other hand, coronary angioplasty appears to be a rather practical therapeutic option in this relatively difficult location, permitting complete revascularization even in patients with previous bypass.5 There have been various case reports and two rather large retrospective series describing balloon angioplasty of the septal perforators.2–4,7,8 Vemuri et al.5 and Topaz et al.8 have reported angiographic success rates of SP angioplasty to be 95–100% (a number similar to that of epicardial major coronary arteries). Topaz et al.8 reported 1 acute closure out of 11 cases of SP angioplasty, which was successfully treated by repeat PTCA. There have been no other complications reported with balloon angioplasty of the septal arteries and the procedure was associated with marked improvement in angina in the series by Vemuri et al.,5 who reported no myocardial infarction, death or target lesion revascularization during long-term follow-up in 21 cases. On the other hand, Topaz et al.8 detected angiographic restenosis in 27% of dilated SP lesions and all were successfully redilated by balloon angioplasty. Septal perforators are generally small-caliber vessels which originate from the LAD at almost right angles; SP lesions are usually branch-ostial in location. Branch-ostial lesions tend to yield high residual stenosis due to significant elastic recoil and a subsequent high restenosis rate when treated by balloon angioplasty alone.9,10 Rotational atherectomy in conjunction with adjunctive low-pressure balloon angioplasty has been successfully utilized in 4 cases with septal artery stenoses.6 By preventing elastic recoil, stenting may result in a larger post-procedural lumen diameter and thus probably a lower restenosis rate than balloon angioplasty alone in this branch-ostial location.11 To our knowledge, there has been no report of SP artery stenting to date. The small vessel size, intramyocardial course, branch-ostial location and the right angle take-off of the SP make stenting in this position particularly difficult to perform. Moreover, in cases of acute closure, emergency bypass surgery is almost impossible. We had no difficulty in crossing the lesion and deploying the stent, producing a satisfactory result. Although ostial, the lesion was long, extending back into the body of the LAD; therefore, we had to utilize a 19 mm stent to cover it thoroughly. Technological improvements in the equipment used in the catheterization laboratory (e.g., low-profile balloons and stents, extra-support guidewires, etc.) make almost every coronary segment accessible to coronary intervention provided the vessel caliber is large enough. The major point of concern in SP stenting is the ostial location of the lesion and the risk of jeopardizing a disease-free and patent LAD while trying to revascularize the SP. In our case, there was no such problem because the LAD was totally occluded just distal to the origin of the large SP we had stented. We therefore had no risk of occluding the LAD while stenting the SP, and we placed the stent in such a way that the proximal one-third was positioned in the LAD itself. Thus, our patient represented an ideal case for SP stenting. The 1-month clinical follow-up shows the efficacy of the procedure in relieving angina and suggests no restenosis within this period.

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