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William H. Spencer III, MD
Baylor College of Medicine, Houston,
Texas and Medical University of
South Carolina, Charleston, SC, USA
First performed and reported by Dr. Ulrich Sigwart, alcohol septal ablation for hypertrophic obstructive cardiomyopathy (HOCM) has now been performed in several thousand patients worldwide (1). The technique is a percutaneous coronary intervention utilizing currently available technology (1-4). After coronary arteriograms are performed, a short (9-10 mm) over-the-wire coronary balloon is placed in one or more septal perforators with the aid of soft, flexible coronary guide wires. After the coronary balloon is inflated and its position is verified, an arteriogram is carried out through the balloon lumen to verify its presence in the desired septal perforator and to ensure that no leakage of radio-opaque contrast to the left anterior descending coronary artery or the coronary venous system has occurred. The exact area of the septum to be infarcted can be identified by myocardial contrast echocardiography (5-6). The pressure gradient across the left ventricular outflow tract (LVOT) is constantly measured by either Doppler echocardiography or another arterial catheter placed in the left ventricle from the left groin. Following verification of the proper position of the balloon, 1-3 ccs of absolute, desiccated ethanol are infused slowly into the septum via the central lumen of the balloon catheter. Cardiac pacing support is required during and after the procedure. Relatively few periprocedural complications have been reported. After 2 - 3 days of hospitalization, patients are discharged home for quiet rest for at least two weeks.
Patient selection for alcohol septal ablation in HOCM is very important (7-8). All patients should be very symptomatic and refractory to medical and/or pacing therapy. All subjects should understand the necessity for and the significance of the procedure. By echocardiography, the patient should have asymmetric septal hypertrophy with an inter-ventricular septal thickness of 1.6 cm or greater and have a septal to posterior wall ratio of 1.3 to 1.0 or greater. Systolic anterior motion of the anterior leaflet of the mitral valve producing left ventricular outflow tract obstruction must be demonstrated during the qualifying echocardiogram. Certain minimal outflow tract gradients are necessary to justify the procedure, that is, at least a 30 mmHg gradient or greater by Doppler echo at rest. Because of the well-known variability of the LVOT gradients in these patients (9), provocation of the gradient at the time of the echo Doppler study may be necessary. Provocation of the gradient may be carried out by a number of means: by the Valsalva maneuver, amyl nitrite inhalation, post PVC potentiation, exercise, and the use of sympathomimetic amines such as dobutamine. Provoked gradients that qualify for the procedure are 60 mmHg or more. Because it is possible to artificially produce an outflow tract gradient with high doses of sympathomimetic amines, low doses of these medications must be used and the patients must be screened thoroughly to ensure that they have the anatomic substrate of hypertrophic obstructive cardiomyopathy prior to administration of the provoking medications. In summary, patient selection for alcohol septal ablation in HOCM now requires that all patients be very symptomatic and have demonstrable pathophysiology of HOCM with significant LVOT obstruction.
Successful alcohol septal ablation in HOCM results in an immediate decline in the LVOT gradient in the catheterization laboratory associated with diminution of systolic anterior motion of the mitral valve and lessening of mitral regurgitation (1-4). Myocardial infarctions with 750-2500 units of peak creatinine phosphokinase release measuring 6-10% of the total left ventricular mass have been reported (3,10). Short and long-term follow-up have revealed significant and dramatic improvements in New York Heart Association class for heart failure (from III to I long-term), marked diminution in chest pain and significant improvement in the quality of life (1-4,10). Objective improvement in exercise performance has been demonstrated by a significant increase in total treadmill time and maximal oxygen consumption with exercise post-procedure (1-4). On long-term follow-up, patients who qualified for the procedure with provokable gradients have benefited showing both gradient reduction and symptomatic and objective improvement in the same manner as patients who qualified with high resting gradients (11). Long-term follow-up has shown a progressive decrease in the LVOT gradient over several years associated with a progressive decrease in basal septal thickness and an associated increase in the area of the left ventricular outflow tract (12-14). Improvement in left ventricular diastolic function combined with preserved systolic function has been demonstrated on follow-up (15). Improvements in the left ventricular ejection pattern, left atrial function and size, and an increase in left ventricular end diastolic volume again combined with preserved systolic function have been reported (15-17). Regression of left ventricular hypertrophy in the remainder of the uninfarcted ventricle combined with a significant decrease in the cardiac cytokine, tumor necrosis factor alpha, a decrease in overall myocyte size and a diminution in total myocardial collagen content have been reported on long-term follow-up (18-19). Histologically, a myocardial infarction with discrete margins lacking the marked inflammatory element associated with naturally occurring infarctions has been demonstrated (10). Complications of the procedure have included a remarkably low mortality (less than 1%) for a recently introduced procedure (1-4,13,20,21). Following a relatively high incidence of complete heart block post-procedure requiring permanent pacemakers, the latest incidence of complete heart block with the procedure ranges from 7-10%. Numerous other complications have been reported in a very low incidence. No increase in the incidence of sudden cardiac death in this high-risk population has been reported following alcohol septal ablation.
At Baylor College of Medicine and The Medical University of South Carolina we have attempted nonsurgical septal reduction therapy (NSRT) for hypertrophic obstructive cardiomyopathy (HOCM) 241 times in 219 patients. Therapy was not performed in four patients mostly because of associated coronary arteriosclerosis. Selection criteria remained the same and include classic HOCM with asymmetric septal hypertrophic, systolic anterior motion of the mitral valve and a resting gradient of > 30 mmHg or provoked gradient of > 60 mmHg. All patients were severely symptomatic and refractory to medical and/or pacing therapy. By producing a significant reduction in the outflow tract gradient, therapy has been successful in 213 patients (97%). Second procedures have been performed in 20 patients. All patients treated have seen a marked reduction in their left ventricular outflow tract gradient from 56 mmHg to 7 mmHg to 1 mmHg to 1 mmHg to 0 mmHg at baseline 1,2,3 and 4 years respectively. Patients qualifying for the procedure based on provokable gradients have had similar objective and subjective improvement. Significant improvement in the functional class for heart failure, angina and syncope has been achieved (2.7 + 0.5 to 0.2 + 0.4 (3 yrs) in NYHA for dyspnea). It now appears that the level of total CK release and the acute reduction of a LV outflow tract gradient in the catheterization laboratory are major determinants of long-term success. The average post-procedure maximum CK release has been 1592 units resulting in a thallium perfusion defect of approximately 6% of the left ventricular LV mass. At long-term follow-up, 88% of patients were asymptomatic, 10% were improved, but still symptomatic and 2% were unimproved. Objectively, the mean exercise time (Bruce) increased from 330 seconds at baseline to 420 seconds at two years. Major complications in the overall total of 219 patients have included four deaths (two short-term, two long-term) five ventricular fibrillations and six coronary dissections. The incidence of complete heart block requiring permanent pacemaker therapy has been 7% in the last 100 patients who presented without pacemakers.
In conclusion, it appears that alcohol septal ablation for HOCM is a promising new therapy, which can be carried out successfully with a low incidence of complications and certainly less expense than left ventricular septal myotomy myomectomy.
1. Sigwart U. Non-surgical myocardial reduction for hypertrophic obstructive cardiomyopathy. Lancet 1995;346:211-14.
2. Fassbender D, Gleichmann U, Sigwart U. Non-surgical septal reduction for hypertrophic obstructive cardiomyopathy: Outcome in the first series of patients. Circulation 1997;95:2075-81.
3. Lakkis NM, Nagueh SF, Kleiman NS, Killip DM, He Z-X, Verani M, Roberts R, Spencer III WH. Echocardiography guided ethanol septal reduction for hypertrophic obstructive cardiomyopathy. Circulation 1998;98:1750-55.
4. Seggewise H, Gleichmann U, Faber L, Fassbender D, Schmidt HK, Strick S. Percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: acute results and 3-month follow-up in 25 patients. J Am Coll Cardiol 1998:252-8.
5. Nagueh SF, Lakkis NM, He ZX, Middleton KJ, Killip D, Zoghbi WA, Quinones MA, Roberts R, Verani MS, Kleiman NS, Spencer III WH. Role of myocardial contrast echocardiography during nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 1998;32:225-9.
6. Faber L, Ziemssen P, Seggewiss H. Targeting percutaneous transluminal septal ablation for hypertrophic obstructive cardiomyopathy by intraprocedural echocardiographic monitoring. J Am Soc Echocardiogr 2000;13(12):1074-9.
7. Fananapazir L, McAreavey D. Therapeutic options in patients with obstructive hypertrophic cardiomyopathy and severe drug-refractory symptoms. J Am Coll Cardiol 1998;31:259-64.
8. Maron BJ. Role of alcohol in septal ablation in treatment of obstructive hypertrophic cardiomyopathy. Lancet 2000;355:425-26.
9. Kizilbah AM, Heinle SK, Grayburn PA. Spontaneous variability of left ventricular outflow tract gradient in hypertrophic obstructive cardiomyopathy. Circulation 1998;97:461-66.
10. Kuhn H, Gietzen FH, Leuner C, Schafers M, Schober O, Strunk-Muller C, Obergassel L, Freick M, Gockel B, Lieder F, Raute-Kreisen U. Transcoronary ablation of septal hypertrophy (TASH): a new treatment option for hypertrophic obstructive cardiomyopathy. Z Kardiol 2000;89 Suppl 4:IV41-54.
11. Lakkis N, Plana JC, Nagueh S, Killip D, Roberts R, Spencer WH. Efficacy of non-surgical septal reduction therapy in symptomatic patients with obstructive hypertrophic cardiomyopathy and provocable gradients. Am J Cardiol. In Press.
12. Airoldi F, Di Mario C, Catanoso A, Dharmadhikari A, Tzifos V, Anzuini A, Carlino M, Briguori C, Montorfano M, Vaghetti M, Tolaro S, Colombo A. Progressive decrease of outflow gradient and septum thickness after percutaneous alcoholization of the interventricular septum in hypertrophic obstructive cardiomyopathy. Ital Heart J 2000;1(3):200-6.
13. Lakkis NM, Nagueh SF, Killip D, Spencer III WH. Non-surgical septal reduction therapy for hypertrophic obstructive cardiomyopathy: one-year follow-up. J Am Coll Cardiol 2000;36:852-55.
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2nd Virtual Congress of Cardiology
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