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Case Report

Percutaneous Transseptal Myocardial Ablation with Wire (PTSAW): A New Technique

Vijay Trehan MD, DM, Saibal Mukhopadhyay MD, DM, Umamahesh C Rangasetty MD, DM
April 2004
ABSTRACT. Alcohol septal ablation has recently been described as a safe alternative to surgical myectomy for treatment of symptomatic patients with hypertrophic obstructive cardiomyopathy. We describe a case where percutaneous myectomy was performed by mechanically occluding the septal artery using thrombogenic floppy tips of used PTCA wires instead of alcohol, as the anatomy of the septal artery was not suitable for alcohol ablation. J INVAS CARDIOL 2004;16:204–206 Key words: hypertrophic obstructive cardiomyopathy, left ventricular outflow tract obstruction, floppy tips of percutaneous transluminal coronary angioplasty guidewire Alcohol septal ablation has recently been described as a catheter-based treatment for drug refractory symptomatic patients of hypertrophic obstructive cardiomyopathy (HOCM). The procedure is in effect a chemical myectomy and studies have shown it to be as effective as surgical myectomy in reducing left ventricular outflow tract (LVOT) obstruction. Since the intent of the procedure is to produce local septal infarction, thus reducing the septal mass, we describe a case where instead of chemical myectomy, we produced septal infarction by mechanically occluding the septal artery using thrombogenic floppy tips of used percutaneous transluminal coronary angioplasty (PTCA) guidewires. Case report. A 38-year-old male patient with a known case of HOCM for 2 years who was receiving optimal treatment with a combination of beta blocker and calcium channel blocker, presented with increasing dyspnea (New York Heart Association Class III) which he had been experiencing for six months and which was associated with episodes of presyncope during violent coughing or while straining during defecation. His electrocardiogram revealed evidence of left ventricular hypertrophy with strain pattern. Two-dimensional echocardiography showed hypertrophy of the anterolateral free wall (25 mm) and the basal anterior septum (22 mm). M-mode echocardiography revealed systolic anterior motion of the anterior mitral leaflet. Pulsed wave Doppler at mitral inflow showed Grade I diastolic dysfunction. Color flow Doppler revealed turbulence in the LVOT and continuous wave Doppler across the LVOT revealed a peak instantaneous gradient (PIG) of 187 mmHg, with the Doppler spectrum showing a late-peaking dagger-shaped appearance (Figure 1A). Color flow also revealed an eccentric posterior wall-hugging mitral regurgitation jet reaching up to mid left atrium level. The valves were normal. There was no regional wall motion abnormality and ejection fraction was 60%. The patient was taken up for coronary angiography to delineate the anatomy of the septal perforator supplying the hypertrophied septum with the aim of ablating the septum. Coronary angiography revealed normal coronary arteries with a large first septal perforator dividing into two major branches (Figure 2). After hooking the left coronary artery with a JL4 7 French guiding catheter, a 0.014-inch floppy tip PTCA wire was passed into the septal artery. A 1.5 x 20 mm over-the-wire Ranger balloon (Boston scientific Scimed, Inc., Maple Grove, Minn.) was passed into the septal artery and inflated (Figure 3). While occluding the septal artery, 2-D echocardiography was performed simultaneously. It showed severe hypokinesia of the basal septum with a decrease in LVOT gradient from 187 mmHg to 80 mmHg, while the mid and apical septum showed normal contractility. For further confirmation of the target septal artery, myocardial contrast echocardiography was performed using Levovist. Though it showed a match between the area of contrast opacification and the area of peak LVOT gradient generation, contrast was also seen filling the mid and apical septum. It was thus assumed that although the mid and apical septum had adequate supply through separate septal perforators, it was also receiving collaterals from the target septal artery. We decided that if absolute alcohol was used, it would percolate through the collaterals and damage the mid and apical septum. Since the arterial anatomy was not suitable for alcohol ablation, we gave the option of surgical myectomy to the patient. The patient was reluctant to undergo surgery and persuaded us to try some alternative method of transcutaneous ablation. Hence we thought of inducing infarction of the basal septum by mechanically occluding the target septal artery with coils. We explained the procedure to the patient saying that it might be successful and he consented for the procedure. But instead of using conventional metallic coils, we decided to use highly flexible thrombogenic floppy tips of used PTCA guide wires that had been sterilized with ethylene oxide. We have already reported the efficacy of these wires in occluding a congenital coronary artery fistula in a patient whose anatomy was not suitable for delivering conventional metallic coils.1 In this case, the 1.5 x 20 mm Ranger balloon with an internal diameter of 0.014 inches was already lying within the target septal artery. We decided to push cut floppy tips of angioplasty wires (diameter 0.014 in.) through it. Delivering conventional metallic coils would have required a separate delivery catheter to be placed in the septal artery with a minimum internal diameter of 0.025 inches, and placing the delivery catheter in the septal artery would have required manipulations with the risk of traumatizing the normal left anterior descending coronary artery. Furthermore, placement of metallic coils would have increased the cost of the procedure, which is an important issue in a developing country like India. The septal artery supplying the hypertrophied septum had two major branches: an upper and a lower branch (Figure 2). The floppy tip guidewire was first passed into the lower branch over which the 1.5 x 20 mm over-the-wire Ranger Balloon (Boston Scientific Scimed, Inc.) was passed. Keeping the balloon inflated, radiopaque floppy tips of used PTCA wires which were cut into small pieces of around 1 cm each, were successively passed through the Ranger balloon into the target artery using the hard end of an exchange length PTCA wire (Figure 4). Finally after passing 6 pieces of cut floppy wires, TIMI-1 flow was achieved in the artery. After 1 hour, an angiogram revealed no flow through that artery with all 6 wires lying in situ (Figure 5). Loss of flow through one of the branches decreased the LVOT gradient from 187 mmHg to 140 mmHg. The floppy tip wire was then passed into the upper branch over which the same 1.5 x 20 mm over-the-wire balloon was passed (Figure 6). After inflating the balloon, 4 cut pieces of floppy wires were successively pushed into the target artery (Figure 7), following which there was TIMI-1 flow in the artery. After 1 hour, an angiogram revealed complete occlusion of this artery with no antegrade flow (Figure 8). Measurement of the gradient across LVOT by 2-D echocardiography showed a decrease in gradient from 187 mmHg to 64 mmHg (Figure 1B). The patient tolerated the procedure well, was haemodynamically stable, and had only mild chest pain during the procedure. The patient was shifted to the CCU and kept under constant ECG monitoring. Serial estimation of CPK-MB was conducted at 1, 6, 12 and 18 hours. During 48 hours of monitoring in the CCU, the patient did not show any evidence of heart block or ventricular arrhythmias. CPK-MB at 12 hours was elevated. The patient was shifted to the general ward and discharged after one week. Echocardiography at the time of discharge revealed akinesia of the basal septum with a peak gradient across LVOT of 64 mmHg. So the patient was discharged on a combination of beta-blocker and calcium channel blocker with advice to come for follow up. The patient who has recently completed one year of follow up, has become totally asymptomatic with decrease in LVOT gradient to 20 mmHg. Usually after inducing septal infarction, a progressive reduction in gradient is seen for up to 12 months due to ongoing fibrosis, leading to thinning of the septum and an increase in LVOT diameter. Discussion. Despite revolutionary advances in the field of cardiology in the last decade, HOCM has been a difficult condition to treat until recently. In patients with significant basal gradient (> 50 mmHg) and NYHA class III or IV symptoms refractory to medical therapy, ventricular septal myotomy myectomy (Morrow’s operation) is considered by many as the gold standard of treatment,2 but is associated with a mortality of up to 5%,3,4 even in experienced centers. Introduced by Sigwart in 1995,5 the occlusion of the septal artery by injecting alcohol has been shown to be highly effective in reducing LVOT gradient and improving symptoms,5–8 with long-term studies showing no recurrence of obstruction with time.9–11 The early and intermediate results of myotomy-myectomy and alcohol septal ablation are comparable.3,4 Technically, however, the procedure is still in its infancy. The amount of alcohol injected as well as the rate of injection varied in different studies,4,5 10–12 and no criteria has yet been developed on this aspect. Excess alcohol injection carries the risk of inducing permanent infrahisian block requiring pacemaker therapy12 and excessive thinning of the ventricular septum, sometimes causing ventricular septal defect. Sometimes the septal artery, through extensive capillary network, supplies other areas of the myocardium. Even if these areas have dual blood supply (as in this case), alcohol percolating into these areas causes myocardial damage, thus making this procedure inappropriate in such cases. In patients whose septal artery anatomy is not suitable for alcohol ablation, our method of mechanically occluding the septal artery using cut floppy tips of used PTCA wires can be considered as a safe and cost-effective procedure in lieu of surgery. Recently, to avoid the limitations of alcohol ablation, a case report13 involving mechanical occlusion of the septal artery in a patient with HOCM was published, in which a stent graft was placed in the left anterior descending artery (LAD) across the origin of the target septal artery, thus exposing the normal LAD to the risk of in-stent thrombosis and restenosis. In light of the limitations of alcohol injection or covered stent placement as previously discussed, our method may be considered as an alternative safe strategy for septal ablation. Furthermore, in comparison to placing conventional metallic coils, our method of using floppy tips of PTCA wires offers the following advantages: 1) ready availability in the catheterization laboratory; 2) no requirement for special delivery catheters; 3) ease of deployment; and 4) cost-effectiveness. In summary, the technique we employed can be considered as an alternative to chemical myectomy with alcohol in patients whose anatomy is not suitable for alcohol ablation. Due to the drawbacks of alcohol ablation discussed here, we believe that our technique can be considered as an alternative to alcohol ablation, even in patients with septal artery anatomy suitable for alcohol ablation.
1. Trehan VK, Arora R, Mukhopadhyay S, et al. Percutaneous closure of coronary pulmonary arterial fistula using catheterization laboratory trash. Cathet Cardiovasc Interven 2003;59:49–51. 2. Spirito P, Seidman CE, McKenna WJ, et al. The management of hypertrophic cardiomyopathy. N Eng J Med 1997; 336:775–785. 3. Nagueh SF, Omnen SR, Lakkis NM, et al. Comparison of ethanol septal reduction therapy with surgical myectomy for the treatment of hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 2001;38:1701–1706. 4. Xin J, Shiota T, Lever HM, et al. Outcome of patients with hypertrophic obstructive cardiomyopathy after percutaneous transluminal septal myocardial ablation and septal myectomy surgery. J Am Coll Cardiol 2001;38:1994–2000. 5. Sigwart U. Non surgical myocardial reduction of hypertrophic obstructive cardiomyopathy. Lancet 1995; 346:211–214. 6. Knight C, Kurbaan AS, Seggewiss H, et al. Non-surgical septal reduction for hypertrophic obstructive cardiomyopathy: Outcome in first series of patients. Circulation 1997;95:2075–2081. 7. Seggewiss H, Gleichmann U, Faber L, et al. Percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: acute results and 3 months follow up in 25 patients. J Am Coll Cardiol 1998; 31: 252–258. 8. Spencer WH and Roberts R. Alcohol septal ablation in hypertrophic obstructive cardiomyopathy. Circulation 2000; 102:600–601. 9. Geitzen FH, Leiuer CJ, Raute Kriensen U, et al. Acute and long-term results after transcoronary ablation of septal hypertrophy (TASH) for hypertrophic cardiomyopathy. Eur Heart J 1999;20:1342–1354. 10. Faber L, Meissner A, Ziemssen P, Seggeweiss H. Percutaneous transluminal septal myocardial ablation for hypertrophic obstructive cardiomyopathy. Long-term follow-up of the first series of 25 patients. Heart 2000;84:326–331. 11. Oomman A, Ramachandran P, Subramanian K, et al. Percutaneous transluminal septal myocardial ablation in drug-resistant hypertrophic obstructive cardiomyopathy. 18-month follow up results. J Invas Cardiol 2001;13:326–330. 12. Boekstegers P, Steinbigler P, Molnar A, et al. Pressure-guided non surgical myocardial reduction induced by small septal infarctions in hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 2001;38:846–853. 13. Vanderheyden M, Willaert W, Claessens P. Non-alcoholic percutaneous transluminal septal ablation for hypertrophic cardiomyopathy with obstruction. Am J Cardiol 2002;89:361–362.