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Transapical Approach to Myectomy for Midventricular Obstruction in Hypertrophic Cardiomyopathy
ADULT CARDIAC
Transapical Approach to Myectomy for Midventricular Obstruction in Hypertrophic Cardiomyopathy Meghana R. Kunkala, MD, Hartzell V. Schaff, MD, Rick A. Nishimura, MD, Martin D. Abel, MD, Paul Sorajja, MD, Joseph A. Dearani, MD, and Steve R. Ommen, MD Divisions of Cardiovascular Surgery and Cardiovascular Diseases, and the Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota
Background. Midventricular obstruction in hypertrophic cardiomyopathy (HCM) is less common than subaortic obstruction, and there are few data on outcomes after surgical treatment. Methods. We reviewed 56 consecutive patients (28 men) with HCM and midventricular obstruction who underwent myectomy between February 1997 and June 2012. Five patients had prior myectomy for subaortic obstruction. Mean age was 42 ± 17 years. Preoperatively, 51% of patients had dyspnea, and the remaining had palpitations (25%), angina (5%), or syncope (9%). Results. Midventricular obstruction was relieved by means of a transaortic myectomy in 5 patients, a transapical approach in 32 patients, and combined transaortic and transapical incisions in 19 patients. In 13 patients, an apical aneurysm or pouch was repaired at the time of midventricular myectomy. There were no early deaths. Intraoperative intraventricular gradients were reduced from 64 ± 32 mm Hg before myectomy to 6 ± 12 mm Hg
postoperatively (p £ 0.0001). Early complications included atrial arrhythmias in 5 patients and reoperation for bleeding in 4 patients. Fifty patients had follow-up beyond 30 days (median, 1.6 years; range, 33 days to 13 years). Survival at 1 and 5 years was 100% and 95%, and average New York Heart Association class improved from 2.9 ± 0.7 preoperatively to 1.3 ± 0.6 postoperatively (p [ 0.0001). There were no aneurysms related to the apical incision; 2 patients had late reoperation, 1 for resection of right atrial mass to prevent embolus. Conclusions. A transapical approach allows excellent exposure for midventricular myectomy and relief of intraventricular gradients and related symptoms. There were no complications unique to the apical incision, and 5-year survival was similar to expected survival (95% versus 97%).
n 1958, Teare [1] reviewed cases of “diffuse primary tumors of the heart” and described them instead to be patients with asymmetric hypertrophy of the heart, what we know now to be hypertrophic cardiomyopathy (HCM). Since then, clinical, hemodynamic, surgical, and pathologic observations have allowed characterization of multiple subgroups of patients with HCM, and molecular genetic studies have confirmed that HCM is a disease of the sarcomere inherited in an autosomal dominant fashion with an array of phenotypes [2]. Diagnosis of HCM is made by clinical features and echocardiography showing left ventricular hypertrophy in the absence of another cardiac or systemic disease [2]. In HCM, ventricular hypertrophy is variable. It may be asymmetric, involving mainly the proximal septum, or
there may be diffuse left ventricular hypertrophy. Other patterns of hypertrophy include midventricular and apical HCM [3]. With predominant midventricular hypertrophy, there may be an intraventricular pressure gradient owing to obstruction at the level of the papillary muscles, which in some patients may lead to apical myocardial infarction and small apical pouches or aneurysms. Midventricular obstruction was found in 9.4% of HCM patients in one large-scale prospective study from Japan [4]. Surgical treatment of midventricular obstruction has been reported infrequently, mainly in case reports [5–7]. The purpose of this study is to describe the transapical approach for relief of midventricular obstruction and present the hemodynamic and functional outcomes of the relief of midventricular obstruction.
I
(Ann Thorac Surg 2013;96:564–70) Ó 2013 by The Society of Thoracic Surgeons
Accepted for publication April 24, 2013. Presented at the Forty-ninth Annual Meeting of The Society of Thoracic Surgeons, Los Angeles, CA, Jan 26–30, 2013.
Patients and Methods
Address correspondence to Dr Schaff, Division of Cardiothoracic Surgery, Joseph 5-200, St. Mary’s Hospital, Mayo Clinic, 1216 Second St SW, Rochester, MN 55902; e-mail: [email protected].
After obtaining permission from the Mayo Clinic Institutional Review Board, we reviewed the records of 56 patients with HCM and midventricular obstruction who
Ó 2013 by The Society of Thoracic Surgeons Published by Elsevier Inc
0003-4975/$36.00 http://dx.doi.org/10.1016/j.athoracsur.2013.04.073
underwent myectomy between February 1997 and June 2012. During this interval 1,644 patients underwent myectomy for HCM-related obstruction. The study included data retrieval from the Mayo Clinic electronic health record, our cardiovascular surgical database, and follow-up questionnaires that include quality-of-life measures. The medications that were reviewed for the medication usage end point were b-blockers, calciumchannel blockers, diuretics, and angiotensin-converting enzyme inhibitors. All patients signed consent to be included in research studies. Probability values less than 0.05 were considered significant. This series includes only patients with true midventricular obstruction defined as a midcavitary gradient originating at the level of the papillary muscles and not related to systolic anterior motion of the mitral leaflets or anomalous insertion of papillary muscles. Further, we did not include patients with apical hypertrophy, which causes complete systolic obliteration of the left ventricular cavity. Preoperatively, all patients underwent a comprehensive transthoracic echocardiogram to measure the severity and location of the intraventricular gradient. Midventricular obstruction was separated from subaortic obstruction by the absence of true systolic anterior motion of the mitral leaflets and lack of asymmetric septal hypertrophy. In patients with hypertrophic cardiomyopathy, these atypical echocardiographic findings are characteristic of midventricular obstruction [8]. The intraventricular gradient was measured by the Doppler signal and estimated at maximal velocity of blood flow through the mid ventricle during contraction (the maximal instantaneous gradient). Intraoperatively, we measured severity of obstruction by simultaneous direct pressure measurements; needles were inserted into the aorta near the cannulation site and into the left ventricle through the right ventricle and
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septum [9]. These were connected to separate fluid-filled lines and manometers, and left ventricular and aortic pressure tracings were recorded simultaneously. Peakto-peak gradients were calculated by subtracting the peak systolic aortic pressure from the peak systolic left ventricular pressure (Fig 1). Before July 2001, operation for midventricular obstruction was performed infrequently because of difficulty gaining access to and exposing the midportion of the ventricle through the aortic valve; 5 patients in this series had isolated transaortic midventricular myectomy, and all cases were performed during this earlier period. Subsequently, we have used the transapical incision to expose the mid ventricle. A few technical points about the transapical approach deserve comment. After satisfactory cardioplegic arrest of the heart, the apex of the heart is delivered anteriorly. The ventriculotomy is begun over the apical dimple 1 to 2 cm lateral and parallel to the left anterior descending coronary artery; this avoids coronary compromise during closure of the ventriculotomy. Retractors are placed within the ventricle so the papillary muscles and chordae are protected and reflected laterally. The myectomy is initially focused on the ventricular septum where endocardial scar guides resection (Fig 2). If the anterolateral papillary muscle is hypertrophied and prominent, it can be shaved evenly to reduce further obstruction to blood flow at the mid ventricle. Muscular resection adjacent to the ventriculotomy is limited so that excessive thinning of the edges does not complicate closure. After completing myectomy, the mitral valve apparatus is inspected to ensure that there has been no injury. The ventriculotomy is repaired in two layers over felt strip reinforcement; the first suture layer is a running mattress suture, and the second is an over-and-over suture [10]. Fig 1. (A) Premyectomy intraoperative pressure recordings demonstrated an aortic pressure of 98/38 mm Hg and a left ventricular (LV) pressure of 173/8 mm Hg before provocation. After premature ventricular contraction (PVC), aortic pressure was 90/38 mm Hg and left ventricular pressure was 278/8 mm Hg, producing an intraventricular gradient of 188 mm Hg. (B) Postmyectomy intraoperative pressure recordings demonstrated an aortic pressure of 138/85 mm Hg and a left ventricular pressure of 139/13 mm Hg before provocation. After premature ventricular contraction, aortic pressure was 153/81 mm Hg and left ventricular pressure was 157/9 mm Hg, producing an intraventricular gradient of only 4 mm Hg.
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Fig 2. (A) Intraoperative photographs depict the location for the apical incision. (B) Through the ventriculotomy, endocardial scar on the anterolateral papillary muscle and septum are easily seen. (C) Septal myectomy is guided by endocardial scar.
Results Among the 56 patients who underwent myectomy for midventricular obstruction, the mean age was 42 17 years and 28 were men. Presenting symptoms were variable; 51% of patients had dyspnea, 25% had palpitations, 9% presented with syncope, and 5% presented with angina. Other presentations included thromboembolic stroke (2%), ventricular tachycardias (4%), and cardiac arrest (2%). Forty-two percent of patients (n ¼ 23) had an implantable cardiac defibrillator preoperatively. Five patients had undergone previous transaortic myectomy for dynamic left ventricular outflow tract obstruction and had residual or recurrent symptoms as a result of midventricular obstruction. Midventricular obstruction was resected by means of transaortic approach in 5 patients and transapical approach in 32 patients, and 19 patients underwent both approaches to achieve complete resection. Typically, endocardial scar in the midseptum and the anterolateral papillary muscle guided excision of the hypertrophied septum. Operation included myectomy from the midportion of the septum, shaving of hypertrophied papillary muscles, and excision of midventricular trabeculations and false chords to enlarge the chamber size (Fig 3). In 13 patients, an apical aneurysm or pouch was present before the myectomy (Fig 4). In these patients, endocardial scar in the pouch and adjacent myocardium was excised, and the pouch was repaired in the course of closure of the apical ventriculotomy (Fig 5). There were no early deaths. Intraventricular gradients were reduced from 64 32 mm Hg before myectomy to 6 12 mm Hg postoperatively (p 0.0001). Median hospital stay was 6 days (range, 4 to 15 days). Early complications included atrial arrhythmias, primarily
atrial fibrillation, which occurred in 5 patients (9%), and reoperation for bleeding that was necessary in 4 patients (8%); 1 patient was readmitted for right heart failure (2%). One patient had a sternal wound infection 3 weeks after operation, and 1 patient presented with pericarditis 6 months after operation. Follow-up beyond 30 days was available in 50 patients, and median follow-up was 1.6 years (range, 33 days to 13 years). Mean New York Heart Association class improved from 2.9 0.7 preoperatively to 1.3 0.6 postoperatively (p ¼ 0.0001; Fig 6). Medication use was significantly reduced postoperatively. Patients used an average of 1.6 cardiac medications preoperatively as compared with a postoperative average of 0.98 (p < 0.0001). Seventy-four percent of patients (n ¼ 41) had reductions in their medication dosages postoperatively. One-year survival was 100%. Five-year survival was 95% compared with an expected 97% with an age- and sex-matched Minnesota population. There were no late aneurysms related to the apical incision. Two patients had a late reoperation. One reoperation was for excision of a large right atrial mural thrombus. The other reoperation was for a left ventricular aneurysm in a patient who exhibited cardiomyopathy and recurrent ventricular arrhythmias; the patient had multiple attempts at catheter ablation of ventricular arrhythmias, and the lateral wall aneurysm was distant from the earlier apical ventriculotomy.
Comment Midventricular obstruction in HCM is less common than subaortic obstruction; it has a different pathophysiologic mechanism and, in untreated patients, may have a worse
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Fig 3. (A) Preoperative color Doppler echocardiogram at the beginning of systole shows no systolic anterior motion of the mitral leaflet and midventricular obstruction at the level of the papillary muscles (arrow). (B) Preoperative continuous-wave Doppler tracing shows obstruction at the mid ventricle. (C) Postmyectomy Doppler echocardiogram at systole shows relief of midventricular obstruction (arrow).
prognosis [4]. Unlike subaortic obstruction, which is caused by systolic anterior motion of the mitral valve leaflets, midventricular obstruction is attributable to systolic narrowing of the mid ventricle with apposition of the septum and papillary muscles. Thus, secondary mitral valve regurgitation is uncommon and is not a part of the pathophysiology of symptoms such as dyspnea. Minami and associates [4] studied the influence of midventricular obstruction on the natural history of patients with HCM in a follow-up of 490 patients for
Fig 4. A left ventriculogram demonstrates an apical pouch or aneurysm.
10 years. In univariate analysis, patients with midventricular obstruction had a significantly greater likelihood of HCM-related death compared with patients without midventricular obstruction (log-rank p < 0.017); this difference persisted in multivariate analysis. Also the probability of the combined end point of sudden death and potentially lethal arrhythmic events was greater in patients with midventricular obstruction than in those with subaortic obstruction [4]. Minami and coworkers hypothesized that this may be caused by a higher incidence of apical aneurysm formation in patients with midventricular obstruction with the scarred rim of the aneurysm predisposing to serious ventricular arrhythmias [4]. The present series differs from the natural history study of Minami and colleagues [4] in that 80% (n ¼ 45) of our surgical patients had New York Heart Association class III or greater limitations compared with only 13% in the previously mentioned review. The incidence of apical aneurysms was generally similar (23% versus 28.3%), and the slightly lower incidence in our series may be because we included patients with both subaortic and midventricular obstruction in this group and they did not. In this study of patients having myectomy for midventricular obstruction, 5-year survival was similar to an age- and sex-matched Minnesota population (95% versus 97%). This is also comparable to patients who have undergone myectomy for subaortic obstruction (5-year survival, 96%) [11]. In regard to intervention in patients with dynamic outflow tract obstruction, surgery is generally reserved for patients who have limiting symptoms refractory to medical treatment [2, 12]. The decision for myectomy in patients with midventricular obstruction is more difficult because, in many cases, there is uncertainty whether
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Fig 5. Intraoperative photographs demonstrate (A) an apical pouch from an external view and (B) the internal view; note the endocardial scar within the pouch. ADULT CARDIAC
symptoms of dyspnea and angina are related to the midcavitary gradient or diastolic dysfunction related to left ventricular hypertrophy. There are cases reported in which high-velocity late-peaking systolic jets are seen on Doppler echocardiography secondary to a hypercontractile left ventricle and do not reflect true obstruction [13]. In our surgical patients, the decision to operate was based on the presence of persistent symptoms combined with echocardiographic signs of obstruction in the mid ventricle. Importantly, patients’ symptoms were improved with relief of the obstruction, indicating that midcavitary gradients can be of pathophysiologic significance and are not benign Doppler echocardiographic findings. Preoperatively, the key echocardiographic feature in establishing the diagnosis is a midcavitary gradient in the absence of systolic anterior motion of the mitral valve. Also, there is an open apical chamber, and the obstruction is at the midcavity and does not produce complete systolic obliteration of the cavity. But there is a wide spectrum of phenotypes, and some patients will have both subaortic obstruction (with systolic anterior motion of the mitral leaflets) as well as midventricular
obstruction. As is true for subaortic myectomy for obstructive HCM, a complete myectomy is important to relieve midventricular muscular obstruction. In our experience, midventricular obstruction is most easily exposed through a transapical incision, and the contact lesion that is uniformly present guides excision of the septum. Intraoperative measurement of gradients is helpful in determining complete relief of obstruction and is especially helpful in patients with combined subaortic and midventricular obstruction. Septal alcohol ablation (infarction) is a proposed alternative for patients with HCM-related obstruction. This has been performed in patients with midventricular obstruction [14], but no large series with substantial follow-up have been reported. Septal ablation for obstructive HCM is arguably less effective than surgical myectomy [15, 16], and we would assume that the same is true for HCM patients with midventricular obstruction. Alcohol ablation is not without its own morbidity and mortality, but the procedure might be considered as an alternative approach in patients with midventricular obstruction and suitable anatomy of the perforating branches of the left anterior descending coronary artery. Transient postoperative atrial fibrillation is not uncommon in patients with HCM undergoing subaortic or midventricular myectomy. Importantly, we have not seen early or late ventricular arrhythmias in this group of patients with the apical ventriculotomy. This may or may not be influenced by continued used of b-blockers or other antiarrhythmic drugs. In conclusion, the presence of midventricular gradients in patients with HCM can produce symptoms, and relief of obstruction improves the functional status of patients. We have found that the transapical incision provides the best exposure of the hypertrophied septum and papillary muscles, and any associated apical pouches can be repaired concomitantly with this approach.
References
Fig 6. Functional status of patients (New York Heart Association [NYHA] class, % of patients) preoperatively and postoperatively.
1. Teare D. Asymmetrical hypertrophy of the heart in young adults. Br Heart J 1958;20:1–8. 2. Maron BJ. Hypertrophic cardiomyopathy: a systematic review. JAMA 2002;287:1308–20. 3. Wigle ED, Rakowski H, Kimball BP, Williams WG. Hypertrophic cardiomyopathy. Clinical spectrum and treatment. Circulation 1995;92:1680–92.
4. Minami Y, Kajimoto K, Terajima Y, et al. Clinical implications of midventricular obstruction in patients with hypertrophic cardiomyopathy. J Am Coll Cardiol 2011;57: 2346–55. 5. Fan K, Chau E, Chiu CS. Hypertrophic cardiomyopathy with mid ventricular obstruction, apical infarction and aneurysm formation. Heart 2005;91:e42. 6. Seggewiss H, Faber L. Percutaneous septal ablation for hypertrophic cardiomyopathy and mid-ventricular obstruction. Eur J Echocardiogr 2000;1:277–80. 7. Osawa H, Fujimatsu T, Takai F, Suzuki H. Hypertrophic cardiomyopathy with apical aneurysm: left ventricular reconstruction and cryoablation for ventricular tachycardia. Gen Thorac Cardiovasc Surg 2011;59:354–8. 8. Falicov RE, Karunaratne HB, Cahill N, Lamberti JJ Jr. Hypertrophic cardiomyopathy with midventricular obstruction associated with mitral stenosis: partial relief of the obstruction by papillary muscle and trabecular resection. Cathet Cardiovasc Diagn 1977;3:247–58. 9. Ashikhmina EA, Schaff HV, Ommen SR, Dearani JA, Nishimura RA, Abel MD. Intraoperative direct measurement of left ventricular outflow tract gradients to guide surgical myectomy for hypertrophic cardiomyopathy. J Thorac Cardiovasc Surg 2011;142:53–9. 10. Said SM, Schaff HV, Abel MD, Dearani JA. Transapical approach for apical myectomy and relief of midventricular
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obstruction in hypertrophic cardiomyopathy. J Card Surg 2012;27:443–8. Ommen SR, Maron BJ, Olivotto I, et al. Long-term effects of surgical septal myectomy on survival in patients with obstructive hypertrophic cardiomyopathy. J Am Coll Cardiol 2005;46:470–6. Gersh BJ, Maron BJ, Bonow RO, et al. 2011 ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2011;124:2761–96. Jaber WA, Nishimura RA, Ommen SR. Not all systolic velocities indicate obstruction in hypertrophic cardiomyopathy: a simultaneous Doppler catheterization study. J Am Soc Echocardiogr 2007;20:1009.e5–7. Seggewiss H. Percutaneous transluminal septal myocardial ablation: a new treatment for hypertrophic obstructive cardiomyopathy [editorial]. Eur Heart J 2000;21:704–7. Sorajja P, Ommen SR, Holmes DR Jr, et al. Survival after alcohol septal ablation for obstructive hypertrophic cardiomyopathy. Circulation 2012;126:2374–80. Valeti US, Nishimura RA, Holmes DR, et al. Comparison of surgical septal myectomy and alcohol septal ablation with cardiac magnetic resonance imaging in patients with hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 2007;49: 350–7.
DISCUSSION DR EZZELDIN MOSTAFA (Cairo, Egypt): I have a comment and three questions for you. My comment is that you have stressed here on a very crucial point, which is the combined technique. We have published a paper on 27 patients for the combined technique, transaortic, transatrial, transmitral, with or without anterior mitral valve detachment. But for these lesions I guess most of them are not coming from the mid ventricle as I have noticed here. They are coming from the apical. But your success rate is good. My questions to you are, firstly, what did you do for the bilateral obstruction? How many cases in your series? I guess 1,600 is a very good number. Can you give us your experience in bilateral obstruction? I mean combined left ventricular obstruction and right ventricular obstruction. The second point is about how can you deal with the recurrent cases of obstructions? What is your preferred technique in these patients? The third is about the arrhythmias. I guess your study is more or less some sort of short-term one, because actually these patients should be subjected to whatsoever the sudden death and also, you know, as long as their left ventricle and their subendocardial ischemias are a constant feature of these patients. What is your long-term study about the incidence of arrhythmia, which you have denied totally in your study? Thank you. DR KUNKALA: Thank you for your questions. First, this series does not include patients with only apical hypertrophy; this cohort of patients is only those with true midventricular obstruction.
DR MOSTAFA: And you do the left from the transapical, also? DR KUNKALA: No, right ventricular obstruction is corrected through a limited right ventriculotomy with or without patch closure. In response to your second question about the recurrent cases, in this cohort there were 5 patients that were referred to us with recurrent obstruction. In those patients there was an incomplete myectomy at original operation, because they were thought to have only a subaortic obstruction and were approached through a standard aortotomy; thus, the midventricular obstruction was not fully relieved. At the second operation, these patients were approached transapically. We were able to confirm complete relief of obstruction with the aid of intraoperative gradient measuring. And finally, regarding your comment about arrhythmias, ventricular arrhythmias are possible complications of ventriculotomies, but we have not observed serious ventricular arrhythmias in patients having apical ventriculotomy. DR MOSTAFA: Thank you. DR TARA KARAMLOU (San Francisco, CA): I have two questions and a comment. How did you close the ventriculotomy in the patients, and how did you deal with the patients who presented with ventricular aneurysm? The point I would make is that a median follow-up of 13 months is probably too short to make real conjectures about development of late complications. So how did you deal with closing the ventriculotomy in those two subsets?
DR MOSTAFA: You didn’t mention this. DR KUNKALA: I apologize, but yes we did exclude those patients with apical hypertrophy. Regarding your question about bilateral obstruction, in these 56 patients there was only 1 patient that had both right ventricular and left ventricular obstruction, and there was a rightventricular outflow tract patch that was created for that 1 patient.
DR KUNKALA: To close the ventriculotomy, we used two strips of felt to buttress the incision and closed using horizontal mattress sutures. In those patients who present with an apical pouch, we make the ventriculotomy in the pouch and then resect the pouch, and the ventriculotomy is closed in much the same way as in those patients without an apical pouch. Regarding your second comment, follow-up of these patients is relatively short,
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but we have experience over 15 years with patients who have had apical ventriculotomy for apical myectomy, and we have not observed complications of aneurysm formation or arrhythmias.
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DR DANIEL SWISTEL (New York, NY): First, I would like to congratulate you and your colleagues at the Mayo Clinic. You certainly set the gold standard for surgical management of hypertrophic cardiomyopathy. I just have a couple of comments. We have found over the last 5 years a heightened awareness for hypertrophic cardiomyopathy, and this has certainly increased the number of cases referred for surgery. We have also seen a dramatic increase in the number of cases referred with midventricular obstruction, and I know the Cleveland Clinic has very similar statistics when you follow their numbers for standard subaortic obstruction versus midventricular obstruction. We at St. Luke’s Hospital have recently done possibly 6 or 8 midventricular cases, all transaortic, and I think that as our experience grows to over 100 or 200 or 500 surgical cases, you certainly become more adept at transaortic extended myectomies. The reason I bring this up is because in our caseload, we have found, more often than not, midventricular obstruction is secondary to abnormal papillary muscle anatomy rather than septal hypertrophy, and I was wondering if you had any thoughts or comments? I’m skeptical that one would be able to do an adequate midventricular resection transapically in these cases where there is more papillary muscle abnormality than simple septal hypertrophy. DR KUNKALA: Abnormal papillary muscle insertion into the mitral valve is best dealt with through the aorta. We have not had difficulty with other papillary muscle abnormalities, and in 23% of these patients, we shaved the hypertrophied papillary muscle to further reduce midventricular obstruction. DR SWISTEL: I was just commenting on the variations in anatomy. My point is that if you are lucky enough to have a patient with severe septal hypertrophy, then doing a transapical resection of the septum is one thing, but in our experience, we, more often than not, have seen not necessarily papillary muscle hypertrophy but abnormal anatomy often including accessory papillary muscles. The Mayo Clinic has published extensively on these findings, as have we. It is easier, I think, to
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approach those patients, which happen to be the ones that we have seen more frequently, transaortically than transapically. It is a leap of faith, in some instances, and certainly requires a great deal of expertise to resect these cases transaortically. Being able to recognize the anatomic variants and visualizing them properly is key to the successful resolution of what is often a refractory gradient in these cases. DR RICHARD GATES (Orange, CA): The most startling part of the report seemed to be the New York Heart Association class dropping from III to close to I. But I noticed in the abstract that 49% of your patients could exert themselves without any symptoms and only 5% had angina. So how does that jive with New York Heart Association class III preoperative criteria? DR KUNKALA: We assigned an NYHA (New York Heart Association) functional limitation to all symptoms, not just dyspnea. DR GATES: Well, most patients in New York Heart Association category III are quite symptomatic and ill. The definition of NYHA class III is dyspnea on exertion or angina with minimal exertion (ie, 20 steps). DR KUNKALA: Correct. DR GATES: But if 49% of your patients can exert themselves without any dyspnea and only 5% have angina, that means at least 44% of your patients are NYHA class I (by definition). So to have an average preoperative NYHA class of III seems statistically impossible, so I am asking how do you explain this? DR KUNKALA: As noted previously, we assigned an NYHA functional limitation to all symptoms, not just dyspnea. DR GATES: Okay. So I see that you meant to say in your abstract “most troubling presenting symptom was dyspnea in 51%” rather than what you wrote, which was “preoperatively 51% of patients had dyspnea.” DR KUNKALA: Yes, sir. DR GATES: Okay. That makes sense.
Transapical Approach to Myectomy for Midventricular Obstruction in Hypertrophic Cardiomyopathy Meghana R. Kunkala, MD, Hartzell V. Schaff, MD, Rick A. Nishimura, MD, Martin D. Abel, MD, Paul Sorajja, MD, Joseph A. Dearani, MD, and Steve R. Ommen, MD Divisions of Cardiovascular Surgery and Cardiovascular Diseases, and the Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota
Background. Midventricular obstruction in hypertrophic cardiomyopathy (HCM) is less common than subaortic obstruction, and there are few data on outcomes after surgical treatment. Methods. We reviewed 56 consecutive patients (28 men) with HCM and midventricular obstruction who underwent myectomy between February 1997 and June 2012. Five patients had prior myectomy for subaortic obstruction. Mean age was 42 ± 17 years. Preoperatively, 51% of patients had dyspnea, and the remaining had palpitations (25%), angina (5%), or syncope (9%). Results. Midventricular obstruction was relieved by means of a transaortic myectomy in 5 patients, a transapical approach in 32 patients, and combined transaortic and transapical incisions in 19 patients. In 13 patients, an apical aneurysm or pouch was repaired at the time of midventricular myectomy. There were no early deaths. Intraoperative intraventricular gradients were reduced from 64 ± 32 mm Hg before myectomy to 6 ± 12 mm Hg
postoperatively (p £ 0.0001). Early complications included atrial arrhythmias in 5 patients and reoperation for bleeding in 4 patients. Fifty patients had follow-up beyond 30 days (median, 1.6 years; range, 33 days to 13 years). Survival at 1 and 5 years was 100% and 95%, and average New York Heart Association class improved from 2.9 ± 0.7 preoperatively to 1.3 ± 0.6 postoperatively (p [ 0.0001). There were no aneurysms related to the apical incision; 2 patients had late reoperation, 1 for resection of right atrial mass to prevent embolus. Conclusions. A transapical approach allows excellent exposure for midventricular myectomy and relief of intraventricular gradients and related symptoms. There were no complications unique to the apical incision, and 5-year survival was similar to expected survival (95% versus 97%).
n 1958, Teare [1] reviewed cases of “diffuse primary tumors of the heart” and described them instead to be patients with asymmetric hypertrophy of the heart, what we know now to be hypertrophic cardiomyopathy (HCM). Since then, clinical, hemodynamic, surgical, and pathologic observations have allowed characterization of multiple subgroups of patients with HCM, and molecular genetic studies have confirmed that HCM is a disease of the sarcomere inherited in an autosomal dominant fashion with an array of phenotypes [2]. Diagnosis of HCM is made by clinical features and echocardiography showing left ventricular hypertrophy in the absence of another cardiac or systemic disease [2]. In HCM, ventricular hypertrophy is variable. It may be asymmetric, involving mainly the proximal septum, or
there may be diffuse left ventricular hypertrophy. Other patterns of hypertrophy include midventricular and apical HCM [3]. With predominant midventricular hypertrophy, there may be an intraventricular pressure gradient owing to obstruction at the level of the papillary muscles, which in some patients may lead to apical myocardial infarction and small apical pouches or aneurysms. Midventricular obstruction was found in 9.4% of HCM patients in one large-scale prospective study from Japan [4]. Surgical treatment of midventricular obstruction has been reported infrequently, mainly in case reports [5–7]. The purpose of this study is to describe the transapical approach for relief of midventricular obstruction and present the hemodynamic and functional outcomes of the relief of midventricular obstruction.
I
(Ann Thorac Surg 2013;96:564–70) Ó 2013 by The Society of Thoracic Surgeons
Accepted for publication April 24, 2013. Presented at the Forty-ninth Annual Meeting of The Society of Thoracic Surgeons, Los Angeles, CA, Jan 26–30, 2013.
Patients and Methods
Address correspondence to Dr Schaff, Division of Cardiothoracic Surgery, Joseph 5-200, St. Mary’s Hospital, Mayo Clinic, 1216 Second St SW, Rochester, MN 55902; e-mail: [email protected].
After obtaining permission from the Mayo Clinic Institutional Review Board, we reviewed the records of 56 patients with HCM and midventricular obstruction who
Ó 2013 by The Society of Thoracic Surgeons Published by Elsevier Inc
0003-4975/$36.00 http://dx.doi.org/10.1016/j.athoracsur.2013.04.073
underwent myectomy between February 1997 and June 2012. During this interval 1,644 patients underwent myectomy for HCM-related obstruction. The study included data retrieval from the Mayo Clinic electronic health record, our cardiovascular surgical database, and follow-up questionnaires that include quality-of-life measures. The medications that were reviewed for the medication usage end point were b-blockers, calciumchannel blockers, diuretics, and angiotensin-converting enzyme inhibitors. All patients signed consent to be included in research studies. Probability values less than 0.05 were considered significant. This series includes only patients with true midventricular obstruction defined as a midcavitary gradient originating at the level of the papillary muscles and not related to systolic anterior motion of the mitral leaflets or anomalous insertion of papillary muscles. Further, we did not include patients with apical hypertrophy, which causes complete systolic obliteration of the left ventricular cavity. Preoperatively, all patients underwent a comprehensive transthoracic echocardiogram to measure the severity and location of the intraventricular gradient. Midventricular obstruction was separated from subaortic obstruction by the absence of true systolic anterior motion of the mitral leaflets and lack of asymmetric septal hypertrophy. In patients with hypertrophic cardiomyopathy, these atypical echocardiographic findings are characteristic of midventricular obstruction [8]. The intraventricular gradient was measured by the Doppler signal and estimated at maximal velocity of blood flow through the mid ventricle during contraction (the maximal instantaneous gradient). Intraoperatively, we measured severity of obstruction by simultaneous direct pressure measurements; needles were inserted into the aorta near the cannulation site and into the left ventricle through the right ventricle and
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septum [9]. These were connected to separate fluid-filled lines and manometers, and left ventricular and aortic pressure tracings were recorded simultaneously. Peakto-peak gradients were calculated by subtracting the peak systolic aortic pressure from the peak systolic left ventricular pressure (Fig 1). Before July 2001, operation for midventricular obstruction was performed infrequently because of difficulty gaining access to and exposing the midportion of the ventricle through the aortic valve; 5 patients in this series had isolated transaortic midventricular myectomy, and all cases were performed during this earlier period. Subsequently, we have used the transapical incision to expose the mid ventricle. A few technical points about the transapical approach deserve comment. After satisfactory cardioplegic arrest of the heart, the apex of the heart is delivered anteriorly. The ventriculotomy is begun over the apical dimple 1 to 2 cm lateral and parallel to the left anterior descending coronary artery; this avoids coronary compromise during closure of the ventriculotomy. Retractors are placed within the ventricle so the papillary muscles and chordae are protected and reflected laterally. The myectomy is initially focused on the ventricular septum where endocardial scar guides resection (Fig 2). If the anterolateral papillary muscle is hypertrophied and prominent, it can be shaved evenly to reduce further obstruction to blood flow at the mid ventricle. Muscular resection adjacent to the ventriculotomy is limited so that excessive thinning of the edges does not complicate closure. After completing myectomy, the mitral valve apparatus is inspected to ensure that there has been no injury. The ventriculotomy is repaired in two layers over felt strip reinforcement; the first suture layer is a running mattress suture, and the second is an over-and-over suture [10]. Fig 1. (A) Premyectomy intraoperative pressure recordings demonstrated an aortic pressure of 98/38 mm Hg and a left ventricular (LV) pressure of 173/8 mm Hg before provocation. After premature ventricular contraction (PVC), aortic pressure was 90/38 mm Hg and left ventricular pressure was 278/8 mm Hg, producing an intraventricular gradient of 188 mm Hg. (B) Postmyectomy intraoperative pressure recordings demonstrated an aortic pressure of 138/85 mm Hg and a left ventricular pressure of 139/13 mm Hg before provocation. After premature ventricular contraction, aortic pressure was 153/81 mm Hg and left ventricular pressure was 157/9 mm Hg, producing an intraventricular gradient of only 4 mm Hg.
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Fig 2. (A) Intraoperative photographs depict the location for the apical incision. (B) Through the ventriculotomy, endocardial scar on the anterolateral papillary muscle and septum are easily seen. (C) Septal myectomy is guided by endocardial scar.
Results Among the 56 patients who underwent myectomy for midventricular obstruction, the mean age was 42 17 years and 28 were men. Presenting symptoms were variable; 51% of patients had dyspnea, 25% had palpitations, 9% presented with syncope, and 5% presented with angina. Other presentations included thromboembolic stroke (2%), ventricular tachycardias (4%), and cardiac arrest (2%). Forty-two percent of patients (n ¼ 23) had an implantable cardiac defibrillator preoperatively. Five patients had undergone previous transaortic myectomy for dynamic left ventricular outflow tract obstruction and had residual or recurrent symptoms as a result of midventricular obstruction. Midventricular obstruction was resected by means of transaortic approach in 5 patients and transapical approach in 32 patients, and 19 patients underwent both approaches to achieve complete resection. Typically, endocardial scar in the midseptum and the anterolateral papillary muscle guided excision of the hypertrophied septum. Operation included myectomy from the midportion of the septum, shaving of hypertrophied papillary muscles, and excision of midventricular trabeculations and false chords to enlarge the chamber size (Fig 3). In 13 patients, an apical aneurysm or pouch was present before the myectomy (Fig 4). In these patients, endocardial scar in the pouch and adjacent myocardium was excised, and the pouch was repaired in the course of closure of the apical ventriculotomy (Fig 5). There were no early deaths. Intraventricular gradients were reduced from 64 32 mm Hg before myectomy to 6 12 mm Hg postoperatively (p 0.0001). Median hospital stay was 6 days (range, 4 to 15 days). Early complications included atrial arrhythmias, primarily
atrial fibrillation, which occurred in 5 patients (9%), and reoperation for bleeding that was necessary in 4 patients (8%); 1 patient was readmitted for right heart failure (2%). One patient had a sternal wound infection 3 weeks after operation, and 1 patient presented with pericarditis 6 months after operation. Follow-up beyond 30 days was available in 50 patients, and median follow-up was 1.6 years (range, 33 days to 13 years). Mean New York Heart Association class improved from 2.9 0.7 preoperatively to 1.3 0.6 postoperatively (p ¼ 0.0001; Fig 6). Medication use was significantly reduced postoperatively. Patients used an average of 1.6 cardiac medications preoperatively as compared with a postoperative average of 0.98 (p < 0.0001). Seventy-four percent of patients (n ¼ 41) had reductions in their medication dosages postoperatively. One-year survival was 100%. Five-year survival was 95% compared with an expected 97% with an age- and sex-matched Minnesota population. There were no late aneurysms related to the apical incision. Two patients had a late reoperation. One reoperation was for excision of a large right atrial mural thrombus. The other reoperation was for a left ventricular aneurysm in a patient who exhibited cardiomyopathy and recurrent ventricular arrhythmias; the patient had multiple attempts at catheter ablation of ventricular arrhythmias, and the lateral wall aneurysm was distant from the earlier apical ventriculotomy.
Comment Midventricular obstruction in HCM is less common than subaortic obstruction; it has a different pathophysiologic mechanism and, in untreated patients, may have a worse
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Fig 3. (A) Preoperative color Doppler echocardiogram at the beginning of systole shows no systolic anterior motion of the mitral leaflet and midventricular obstruction at the level of the papillary muscles (arrow). (B) Preoperative continuous-wave Doppler tracing shows obstruction at the mid ventricle. (C) Postmyectomy Doppler echocardiogram at systole shows relief of midventricular obstruction (arrow).
prognosis [4]. Unlike subaortic obstruction, which is caused by systolic anterior motion of the mitral valve leaflets, midventricular obstruction is attributable to systolic narrowing of the mid ventricle with apposition of the septum and papillary muscles. Thus, secondary mitral valve regurgitation is uncommon and is not a part of the pathophysiology of symptoms such as dyspnea. Minami and associates [4] studied the influence of midventricular obstruction on the natural history of patients with HCM in a follow-up of 490 patients for
Fig 4. A left ventriculogram demonstrates an apical pouch or aneurysm.
10 years. In univariate analysis, patients with midventricular obstruction had a significantly greater likelihood of HCM-related death compared with patients without midventricular obstruction (log-rank p < 0.017); this difference persisted in multivariate analysis. Also the probability of the combined end point of sudden death and potentially lethal arrhythmic events was greater in patients with midventricular obstruction than in those with subaortic obstruction [4]. Minami and coworkers hypothesized that this may be caused by a higher incidence of apical aneurysm formation in patients with midventricular obstruction with the scarred rim of the aneurysm predisposing to serious ventricular arrhythmias [4]. The present series differs from the natural history study of Minami and colleagues [4] in that 80% (n ¼ 45) of our surgical patients had New York Heart Association class III or greater limitations compared with only 13% in the previously mentioned review. The incidence of apical aneurysms was generally similar (23% versus 28.3%), and the slightly lower incidence in our series may be because we included patients with both subaortic and midventricular obstruction in this group and they did not. In this study of patients having myectomy for midventricular obstruction, 5-year survival was similar to an age- and sex-matched Minnesota population (95% versus 97%). This is also comparable to patients who have undergone myectomy for subaortic obstruction (5-year survival, 96%) [11]. In regard to intervention in patients with dynamic outflow tract obstruction, surgery is generally reserved for patients who have limiting symptoms refractory to medical treatment [2, 12]. The decision for myectomy in patients with midventricular obstruction is more difficult because, in many cases, there is uncertainty whether
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Fig 5. Intraoperative photographs demonstrate (A) an apical pouch from an external view and (B) the internal view; note the endocardial scar within the pouch. ADULT CARDIAC
symptoms of dyspnea and angina are related to the midcavitary gradient or diastolic dysfunction related to left ventricular hypertrophy. There are cases reported in which high-velocity late-peaking systolic jets are seen on Doppler echocardiography secondary to a hypercontractile left ventricle and do not reflect true obstruction [13]. In our surgical patients, the decision to operate was based on the presence of persistent symptoms combined with echocardiographic signs of obstruction in the mid ventricle. Importantly, patients’ symptoms were improved with relief of the obstruction, indicating that midcavitary gradients can be of pathophysiologic significance and are not benign Doppler echocardiographic findings. Preoperatively, the key echocardiographic feature in establishing the diagnosis is a midcavitary gradient in the absence of systolic anterior motion of the mitral valve. Also, there is an open apical chamber, and the obstruction is at the midcavity and does not produce complete systolic obliteration of the cavity. But there is a wide spectrum of phenotypes, and some patients will have both subaortic obstruction (with systolic anterior motion of the mitral leaflets) as well as midventricular
obstruction. As is true for subaortic myectomy for obstructive HCM, a complete myectomy is important to relieve midventricular muscular obstruction. In our experience, midventricular obstruction is most easily exposed through a transapical incision, and the contact lesion that is uniformly present guides excision of the septum. Intraoperative measurement of gradients is helpful in determining complete relief of obstruction and is especially helpful in patients with combined subaortic and midventricular obstruction. Septal alcohol ablation (infarction) is a proposed alternative for patients with HCM-related obstruction. This has been performed in patients with midventricular obstruction [14], but no large series with substantial follow-up have been reported. Septal ablation for obstructive HCM is arguably less effective than surgical myectomy [15, 16], and we would assume that the same is true for HCM patients with midventricular obstruction. Alcohol ablation is not without its own morbidity and mortality, but the procedure might be considered as an alternative approach in patients with midventricular obstruction and suitable anatomy of the perforating branches of the left anterior descending coronary artery. Transient postoperative atrial fibrillation is not uncommon in patients with HCM undergoing subaortic or midventricular myectomy. Importantly, we have not seen early or late ventricular arrhythmias in this group of patients with the apical ventriculotomy. This may or may not be influenced by continued used of b-blockers or other antiarrhythmic drugs. In conclusion, the presence of midventricular gradients in patients with HCM can produce symptoms, and relief of obstruction improves the functional status of patients. We have found that the transapical incision provides the best exposure of the hypertrophied septum and papillary muscles, and any associated apical pouches can be repaired concomitantly with this approach.
References
Fig 6. Functional status of patients (New York Heart Association [NYHA] class, % of patients) preoperatively and postoperatively.
1. Teare D. Asymmetrical hypertrophy of the heart in young adults. Br Heart J 1958;20:1–8. 2. Maron BJ. Hypertrophic cardiomyopathy: a systematic review. JAMA 2002;287:1308–20. 3. Wigle ED, Rakowski H, Kimball BP, Williams WG. Hypertrophic cardiomyopathy. Clinical spectrum and treatment. Circulation 1995;92:1680–92.
4. Minami Y, Kajimoto K, Terajima Y, et al. Clinical implications of midventricular obstruction in patients with hypertrophic cardiomyopathy. J Am Coll Cardiol 2011;57: 2346–55. 5. Fan K, Chau E, Chiu CS. Hypertrophic cardiomyopathy with mid ventricular obstruction, apical infarction and aneurysm formation. Heart 2005;91:e42. 6. Seggewiss H, Faber L. Percutaneous septal ablation for hypertrophic cardiomyopathy and mid-ventricular obstruction. Eur J Echocardiogr 2000;1:277–80. 7. Osawa H, Fujimatsu T, Takai F, Suzuki H. Hypertrophic cardiomyopathy with apical aneurysm: left ventricular reconstruction and cryoablation for ventricular tachycardia. Gen Thorac Cardiovasc Surg 2011;59:354–8. 8. Falicov RE, Karunaratne HB, Cahill N, Lamberti JJ Jr. Hypertrophic cardiomyopathy with midventricular obstruction associated with mitral stenosis: partial relief of the obstruction by papillary muscle and trabecular resection. Cathet Cardiovasc Diagn 1977;3:247–58. 9. Ashikhmina EA, Schaff HV, Ommen SR, Dearani JA, Nishimura RA, Abel MD. Intraoperative direct measurement of left ventricular outflow tract gradients to guide surgical myectomy for hypertrophic cardiomyopathy. J Thorac Cardiovasc Surg 2011;142:53–9. 10. Said SM, Schaff HV, Abel MD, Dearani JA. Transapical approach for apical myectomy and relief of midventricular
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obstruction in hypertrophic cardiomyopathy. J Card Surg 2012;27:443–8. Ommen SR, Maron BJ, Olivotto I, et al. Long-term effects of surgical septal myectomy on survival in patients with obstructive hypertrophic cardiomyopathy. J Am Coll Cardiol 2005;46:470–6. Gersh BJ, Maron BJ, Bonow RO, et al. 2011 ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2011;124:2761–96. Jaber WA, Nishimura RA, Ommen SR. Not all systolic velocities indicate obstruction in hypertrophic cardiomyopathy: a simultaneous Doppler catheterization study. J Am Soc Echocardiogr 2007;20:1009.e5–7. Seggewiss H. Percutaneous transluminal septal myocardial ablation: a new treatment for hypertrophic obstructive cardiomyopathy [editorial]. Eur Heart J 2000;21:704–7. Sorajja P, Ommen SR, Holmes DR Jr, et al. Survival after alcohol septal ablation for obstructive hypertrophic cardiomyopathy. Circulation 2012;126:2374–80. Valeti US, Nishimura RA, Holmes DR, et al. Comparison of surgical septal myectomy and alcohol septal ablation with cardiac magnetic resonance imaging in patients with hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 2007;49: 350–7.
DISCUSSION DR EZZELDIN MOSTAFA (Cairo, Egypt): I have a comment and three questions for you. My comment is that you have stressed here on a very crucial point, which is the combined technique. We have published a paper on 27 patients for the combined technique, transaortic, transatrial, transmitral, with or without anterior mitral valve detachment. But for these lesions I guess most of them are not coming from the mid ventricle as I have noticed here. They are coming from the apical. But your success rate is good. My questions to you are, firstly, what did you do for the bilateral obstruction? How many cases in your series? I guess 1,600 is a very good number. Can you give us your experience in bilateral obstruction? I mean combined left ventricular obstruction and right ventricular obstruction. The second point is about how can you deal with the recurrent cases of obstructions? What is your preferred technique in these patients? The third is about the arrhythmias. I guess your study is more or less some sort of short-term one, because actually these patients should be subjected to whatsoever the sudden death and also, you know, as long as their left ventricle and their subendocardial ischemias are a constant feature of these patients. What is your long-term study about the incidence of arrhythmia, which you have denied totally in your study? Thank you. DR KUNKALA: Thank you for your questions. First, this series does not include patients with only apical hypertrophy; this cohort of patients is only those with true midventricular obstruction.
DR MOSTAFA: And you do the left from the transapical, also? DR KUNKALA: No, right ventricular obstruction is corrected through a limited right ventriculotomy with or without patch closure. In response to your second question about the recurrent cases, in this cohort there were 5 patients that were referred to us with recurrent obstruction. In those patients there was an incomplete myectomy at original operation, because they were thought to have only a subaortic obstruction and were approached through a standard aortotomy; thus, the midventricular obstruction was not fully relieved. At the second operation, these patients were approached transapically. We were able to confirm complete relief of obstruction with the aid of intraoperative gradient measuring. And finally, regarding your comment about arrhythmias, ventricular arrhythmias are possible complications of ventriculotomies, but we have not observed serious ventricular arrhythmias in patients having apical ventriculotomy. DR MOSTAFA: Thank you. DR TARA KARAMLOU (San Francisco, CA): I have two questions and a comment. How did you close the ventriculotomy in the patients, and how did you deal with the patients who presented with ventricular aneurysm? The point I would make is that a median follow-up of 13 months is probably too short to make real conjectures about development of late complications. So how did you deal with closing the ventriculotomy in those two subsets?
DR MOSTAFA: You didn’t mention this. DR KUNKALA: I apologize, but yes we did exclude those patients with apical hypertrophy. Regarding your question about bilateral obstruction, in these 56 patients there was only 1 patient that had both right ventricular and left ventricular obstruction, and there was a rightventricular outflow tract patch that was created for that 1 patient.
DR KUNKALA: To close the ventriculotomy, we used two strips of felt to buttress the incision and closed using horizontal mattress sutures. In those patients who present with an apical pouch, we make the ventriculotomy in the pouch and then resect the pouch, and the ventriculotomy is closed in much the same way as in those patients without an apical pouch. Regarding your second comment, follow-up of these patients is relatively short,
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but we have experience over 15 years with patients who have had apical ventriculotomy for apical myectomy, and we have not observed complications of aneurysm formation or arrhythmias.
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DR DANIEL SWISTEL (New York, NY): First, I would like to congratulate you and your colleagues at the Mayo Clinic. You certainly set the gold standard for surgical management of hypertrophic cardiomyopathy. I just have a couple of comments. We have found over the last 5 years a heightened awareness for hypertrophic cardiomyopathy, and this has certainly increased the number of cases referred for surgery. We have also seen a dramatic increase in the number of cases referred with midventricular obstruction, and I know the Cleveland Clinic has very similar statistics when you follow their numbers for standard subaortic obstruction versus midventricular obstruction. We at St. Luke’s Hospital have recently done possibly 6 or 8 midventricular cases, all transaortic, and I think that as our experience grows to over 100 or 200 or 500 surgical cases, you certainly become more adept at transaortic extended myectomies. The reason I bring this up is because in our caseload, we have found, more often than not, midventricular obstruction is secondary to abnormal papillary muscle anatomy rather than septal hypertrophy, and I was wondering if you had any thoughts or comments? I’m skeptical that one would be able to do an adequate midventricular resection transapically in these cases where there is more papillary muscle abnormality than simple septal hypertrophy. DR KUNKALA: Abnormal papillary muscle insertion into the mitral valve is best dealt with through the aorta. We have not had difficulty with other papillary muscle abnormalities, and in 23% of these patients, we shaved the hypertrophied papillary muscle to further reduce midventricular obstruction. DR SWISTEL: I was just commenting on the variations in anatomy. My point is that if you are lucky enough to have a patient with severe septal hypertrophy, then doing a transapical resection of the septum is one thing, but in our experience, we, more often than not, have seen not necessarily papillary muscle hypertrophy but abnormal anatomy often including accessory papillary muscles. The Mayo Clinic has published extensively on these findings, as have we. It is easier, I think, to
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approach those patients, which happen to be the ones that we have seen more frequently, transaortically than transapically. It is a leap of faith, in some instances, and certainly requires a great deal of expertise to resect these cases transaortically. Being able to recognize the anatomic variants and visualizing them properly is key to the successful resolution of what is often a refractory gradient in these cases. DR RICHARD GATES (Orange, CA): The most startling part of the report seemed to be the New York Heart Association class dropping from III to close to I. But I noticed in the abstract that 49% of your patients could exert themselves without any symptoms and only 5% had angina. So how does that jive with New York Heart Association class III preoperative criteria? DR KUNKALA: We assigned an NYHA (New York Heart Association) functional limitation to all symptoms, not just dyspnea. DR GATES: Well, most patients in New York Heart Association category III are quite symptomatic and ill. The definition of NYHA class III is dyspnea on exertion or angina with minimal exertion (ie, 20 steps). DR KUNKALA: Correct. DR GATES: But if 49% of your patients can exert themselves without any dyspnea and only 5% have angina, that means at least 44% of your patients are NYHA class I (by definition). So to have an average preoperative NYHA class of III seems statistically impossible, so I am asking how do you explain this? DR KUNKALA: As noted previously, we assigned an NYHA functional limitation to all symptoms, not just dyspnea. DR GATES: Okay. So I see that you meant to say in your abstract “most troubling presenting symptom was dyspnea in 51%” rather than what you wrote, which was “preoperatively 51% of patients had dyspnea.” DR KUNKALA: Yes, sir. DR GATES: Okay. That makes sense.