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Percutaneous Alcohol Septal Ablation Following Surgical Myectomy
J INVASIVE CARDIOL 2010;22:E147–E149
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The management strategy for hypertrophic obstructive cardiomyopathy (HOCM) generally begins with medical therapy. When this fails to control symptoms, consideration is given to attempt to mechanically eliminate the obstruction of blood flowing out of the left ventricle that results from a thickened and bulging interventricular septum. The literature is abundant with data about the safety and efficacy of both surgical myectomy and the newer and now more widely utilized percutaneous alcohol septal ablation procedure. Controversy still exists as to which of these procedures should in fact be offered first to patients who qualify for both.1 Many cases of successful surgical myectomy performed on patients with recurrent or residual symptoms following percutaneous septal ablation have been published.2,3 However, there remains a paucity of information available to the clinician faced with a patient with recurrent or residual symptoms after undergoing surgical myectomy. We were faced with 2 such patients who presented to our institution after presumed successful myectomy who had recurrence of both symptoms and a gradient across the left ventricular outflow tract (LVOT). Both patients were offered percutaneous ablation after failure of medical therapy, with excellent results.
Case Report. A 52-year-old female was diagnosed with HOCM in 2004. Her interventricular septum measured 1.5 cm. She proceeded to undergo surgical myectomy 1 year later after failing maximal medical therapy with beta-blockers. Intraoperatively her post-myectomy pressure gradient between the left ventricle and aorta was 0 mmHg. She derived significant but incomplete improvement in dyspnea and exercise intolerance. Three years after her surgery she presented to us complaining of worsening exertional dyspnea and palpitations. Auscultation of her precordium uncovered a harsh (grade 3) systolic ejection murmur at the left lower sternal border that intensified with the Valsalva maneuver. Transthoracic echocardiography (TTE) revealed septal hypertrophy (1.6 cm), systolic anterior motion of the mitral valve, LVOT obstruction and a peak LVOT gradient of 85 mmHg. In light of recurrence of her symptoms despite maximally tolerated doses of beta-blockers, she elected to undergo percutaneous alcohol septal ablation.
Coronary angiography revealed angiographically normal epicardial arteries. A LVOT resting gradient of 50 mmHg was identified at the onset of the procedure. Two septal perforators were identified and 3 mL of 100% alcohol were infused into each artery in 1 mL aliquots. There was a 0 mmHg gradient at rest at the conclusion of the procedure. The procedure was well tolerated, although she did develop intraprocedural complete heart block, a well-reported complication of percutaneous ablation. The heart block persisted and necessitated placement of a permanent pacemaker 2 days after the ablation.Her post-ablation creatine kinase (CK) peaked at 1,760 units/L and CK-MB fraction (CKMB) at 196 ng/mL. Nine months after the ablation, the patient was seen again in follow up and was free of symptoms except for mild fatigue. TTE revealed a peak resting gradient of only 14 mmHg and a septum measuring 1.3 cm.
Our second patient was a 22-year-old female diagnosed with severe HOCM in 2007 after being evaluated for a murmur during her fourth pregnancy. Her interventricular septum measured 2.4 cm. She underwent elective prophylactic dual-chamber ICD implantation after experiencing several episodes of syncope. Following the birth of her child, she suffered progressively worsening dyspnea with minimal exertion, and after failing maximal beta-blocker therapy, she was offered both percutaneous septal ablation and surgical myectomy as possible treatment strategies. The patient elected to undergo surgical myectomy. The intraoperative LVOT peak gradient was 10 mmHg at the completion of the procedure. She initially reported complete resolution of her symptoms, however, unfortunately, 4 months after surgery she developed a recurrence of her symptoms including syncope, severe exertional dyspnea and lightheadedness. Examination revealed a harsh (grade 3) systolic ejection murmur over the left upper sternal border that increased in intensity with the Valsalva maneuver. TTE unveiled a resting LVOT peak gradient of 65 mmHg and an interventricular septum measuring 1.7 cm (Figure 1). In light of symptoms that were intolerable to her, she elected to undergo percutaneous alcohol septal ablation.
Selective coronary angiography was performed and showed angiographically normal coronary arteries except for severe mid-systolic compression of the left anterior descending artery. The aortic outflow tract resting gradient was 50 mmHg. Two septal perforators were identified and 3 mL of 100% alcohol were infused into the first septal artery and 2 mL into the second septal artery in 1 mL aliquots. There was a 0 mmHg gradient at rest at the conclusion of the procedure and a 10 mmHg gradient with catheter provocation. The procedure was well tolerated and there were no apparent complications. Her post-ablation CK peaked at 2,191 units/L and CK-MB at 389 ng/mL. She was seen 9 months later in follow up and reported complete resolution of her dyspnea and fatigue. TTE at that time unveiled a resting LVOT peak gradient of 10 mmHg and an interventricular septum now measuring 1.2 cm (Figure 2).
Discussion. At this time, clinicians faced with a patient with recurrent or residual symptoms after undergoing surgical myectomy find themselves in a dilemma. They lack the necessary data or published real-life examples to assist them with clinical decision making and are unable to quote successful case scenarios to their patients. Additionally, the proposed treatment algorithms of the American College of Cardiology and the European Society of Cardiology stop short of recommending what to do in patients after failure of a myectomy to lead to lasting symptomatic relief.4
A review of the literature unveils several experiences utilizing surgical myectomy following failed percutaneous ablation, but the reverse is very sparsely documented. The first case report involves a 54-year-old male published by Juliano et al in 2005.5 However, their patient was very different from ours in that he had undergone simultaneous mitral valve annuloplasty for mitral regurgitation at the time of surgical myectomy and had known severe pulmonary hypertension. In addition, despite a reported subsequent improvement in symptoms, his resting and provocable gradients during the procedure following septal ablation were still elevated at 35 and 80 mmHg, respectively. A more recent paper reports a 46-year-old male who underwent successful alcohol septal ablation after myectomy, but in this case, the intraoperative LVOT gradient rose to 70 mmHg during re-warming and the procedure was aborted.6 Therefore, the physicians involved knew the myectomy had failed prior to the patient leaving the operating room, which addresses a unique subset of myectomy patients that is very different from the two scenarios we described.
Finally, a recent German database review identified 11 patients with significant, symptomatic LVOT obstruction after myectomy who underwent percutaneous ablation resulting in 9 of 11 patients reporting significant and stable improvement in symptoms.7 The remaining 2 patients had progression of New York Heart Association Class III symptoms. It has been well-established that while centers highly experienced in surgical myectomy report very high success rates, these results cannot be generalized to all institutions. Here, the myectomies had been performed in various institutions inside and outside Germany, although detailed data concerning these operations were not available.
Our first patient had incomplete resolution of symptoms following surgical myectomy despite an intraoperative LVOT residual peak gradient of only 7 mmHg and underwent successful percutaneous septal ablation more than 3 years later. Our second patient had initial complete resolution of symptoms following surgical myectomy with an intraoperative LVOT residual peak gradient of 10 mmHg and underwent successful percutaneous septal ablation 8 months later for recurrent symptoms. Both surgical myectomies were performed by a very experienced surgeon specifically trained in this procedure. While repeat surgery is an option, we believe our experience demonstrates that percutaneous alcohol septal ablation is an acceptable option that should be offered to patients who have recurrent or incomplete relief of symptoms following presumed successful surgical myectomy. There are no clear data to guide us as to which patients would benefit more from repeat surgery versus percutaneous ablation. We intuitively believe that a trial of established medical therapy (beta-blockers, calcium channel-blockers or disopyramide) should be offered prior to embarking on a second procedure, although in reality, there is no evidence that this necessarily leads to better long-term outcomes. Larger series are needed to confirm the efficacy and long-term outcomes of the above approach and to determine which subset of patients, if any, would either derive more benefit from a second procedure or be at higher risk of possible complications.
References
1. Maron BJ, Maron MS, Wigle ED, Braunwald E. The 50-year history, controversy, and clinical implications of left ventricular outflow tract obstruction in hypertrophic cardiomyopathy. From idiopathic hypertrophic subaortic stenosis to hypertrophic cardiomyopathy. J Am Coll Cardiol 2009;54:191–200. 2. Arrazaghi AA, Butany JW, Williams WG, et al. Myectomy for hypertrophic obstructive cardiomyopathy after failed alcohol septal ablation: Clinicopathological correlations. Can J Cardiol 2001;17:197–202. 3. Dörge H, Schmitto JD, Liakopoulos OJ, et al. Extended myectomy for hypertrophic obstructive cardiomyopathy after failure or contraindication of septal ablation or with combined surgical procedures. Thorac Cardiovasc Surg 2004;52:344–348. 4. Maron BJ, McKenna WJ, Danielson GK, et al. American College of Cardiology/European Society of Cardiology Clinical Expert Consensus Document on Hypertrophic Cardiomyopathy. J Am Coll Cardiol 2003;42:1687–1713. 5. Juliano N, Wong SC, Naidu, SS. Alcohol septal ablation for failed surgical myectomy. J Invasive Cardiol 2005:27:569–571. 6. Joyal D, Arab D, Chen-Johnston C, Leya F. Alcohol septal ablation after failed surgical myectomy. Catheter Cardiovasc Interv 2007:69:999–1002. 7. Faber L, Welge D, Hering D, et al. Percutaneous septal ablation after unsuccessful surgical myectomy for patients with hypertrophic obstructive cardiomyopathy. Clin Res Cardiol 2008:97:899–904.
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From the Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, Indiana. The authors report no conflicts of interest regarding the content herein. Manuscript submitted December 3, 2009, provisional acceptance given December 14, 2009, final version accepted January 7, 2010. Address for correspondence: Ziad Jaradat, MD, Krannert Institute of Cardiology, Indiana University School of Medicine, 1800 N. Senate Avenue, Indianapolis IN 46202. E-mail zjaradat@iupui.edu
