CLINICAL STUDY
Nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy: one-year follow-up
Nasser M. Lakkis, MD, FACCa,
Sherif F. Nagueh, MD, FACCa,
J. Kay Dunn, PhDa,
Donna Killip, RNa and
William H. Spencer, III, MD, FACCa
a Baylor College of Medicine, Department of Medicine, Section of Cardiology, Houston, Texas, USA
Manuscript received November 10, 1998;
revised manuscript received February 1, 2000,
accepted April 14, 2000.
Reprint requests and correspondence: Dr. William H. Spencer, III, The Baylor Heart Clinic, 6550 Fannin, SM 1901, Houston, Texas 77030
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Abstract
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OBJECTIVE
The objective of this study is to evaluate the one-year outcome of the first 50 patients who underwent nonsurgical septal reduction for symptomatic hypertrophic obstructive cardiomyopathy at our institution.
BACKGROUND
Left ventricular outflow tract obstruction is an important determinant of clinical symptoms in patients with hypertrophic obstructive cardiomyopathy. Nonsurgical septal reduction is a new therapy that has been shown to result in left ventricular outflow tract gradient reduction and resolution of symptoms immediately after the procedure and on midterm follow-up.
METHODS
Fifty patients with hypertrophic obstructive cardiomyopathy who underwent nonsurgical septal reduction at our institution and completed 1-year follow-up are described. Complete history, physical examination, two-dimensional echocardiography with Doppler and exercise treadmill testing have been analyzed.
RESULTS
The mean age of the study group was 53 ± 17 years. All patients had refractory symptoms before enrollment. Ninety-four percent had class III or IV New York Heart Association class symptoms at baseline compared to none at 1 year (p < 0.001). The exercise duration increased by 136 s at 1 year (p < 0.021). Only 20% of patients were either receiving beta-blockers or calcium-channel blockers on follow-up. The resting left ventricular outflow tract gradient decreased from 74 ± 23 mm Hg to 6 ± 18 mm Hg (p < 0.01) and from 84 ± 28 mm Hg to 30 ± 33 mm Hg (p < 0.01) in patients with dobutamine-provoked gradient at one year. These changes are associated with decreased septal thickness and preserved systolic function.
CONCLUSION
Nonsurgical septal reduction therapy is an effective therapy for symptomatic patients with hypertrophic obstructive cardiomyopathy with persistence of the favorable outcome up to one year after the procedure.
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Abbreviations and Acronyms
| | HOCM | = hypertrophic obstructive cardiomyopathy | | LVOT | = left ventricular outflow tract | | NSRT | = nonsurgical septal reduction therapy | | SAM | = systolic anterior motion |
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Left ventricular outflow tract (LVOT) obstruction is an important determinant of clinical outcome in patients with hypertrophic obstructive cardiomyopathy (HOCM). It has been reported that therapies which reduce the intracavitary pressure gradient improve symptoms, myocardial perfusion and reduce the left ventricular filling pressures (1,2). LVOT obstruction is usually caused by contraction of the hypertrophied proximal interventricular septum and by systolic anterior motion (SAM) of the mitral valve. Obstruction may be evident under basal conditions or may develop only after provocation.
Nonsurgical septal reduction therapy (NSRT) is a new alternative therapy that has been reported to readily reduce the LVOT gradient and to improve symptoms in HOCM patients refractory to medications (37). These beneficial effects continue up to 3 months (5). To our knowledge, this study is the first to report the one-year follow-up on the first 50 HOCM patients who underwent NSRT in the U.S.
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Methods
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The investigational protocol was approved by the institutional review board of The Methodist Hospital and Baylor College of Medicine, and all patients gave a written consent form before participation.
Fifty HOCM patients enrolled between November 1996 and August 1998 completed one-year follow-up. All patients had drug refractory dyspnea with asymmetric septal hypertrophy and SAM of the mitral valve, with resting echo/Doppler gradient of >40 mm Hg or a dobutamine-provoked gradient of >60 mm Hg using 5 to 20 µg/kg/min of dobutamine.
A complete history and physical examination were performed before NSRT along with two-dimensional echocardiograms with Doppler and dobutamine provocation if indicated. Treadmill exercise testing using the standard Bruce protocol was done in patients who were able to or agreed to exercise.
Procedure.
Complete details of the procedure have been reported previously (6). In brief, on the day of the procedure, a baseline ECG was performed. Blood was collected for CK enzyme and MB isoforms both before and up to 36 h after the procedure. A temporary pacemaker was placed in the apex of the right ventricle in all except for 12 patients who already had a permanent dual-chamber pacemaker in place for symptomatic HOCM and were referred to us for pacing-therapy failure. All patients with >50% stenosis in the left anterior descending artery were excluded from the study. The septal branches supplying the septal bulge were identified. Contrast echocardiography using Albunex (Mallinkrodt; St. Louis, Missouri) diluted in an equal volume of saline solution was injected to further delineate the area to be infarcted (8). Two to 5 mL of ethanol was injected in each septal branch. The volume of ethanol was determined according to the size of the vessel. Other septal branches were done if the gradient was not reduced to <20 mm Hg at rest, granted that other septal branches supplying the septal bulge could be identified. Patients were observed in the coronary care unit for at least 24 h. The pacemaker lead was removed if the patients did not manifest evidence of high-degree atrioventricular block; otherwise, it was kept in place until a permanent pacemaker was implanted or the patients rhythm returned back to baseline. The mean length of hospital stay was 3.1 ± 1.8 days. Seven of 50 patients have come back for a redo procedure. The exact characteristics of these patients are detailed in the "Results" section.
Statistical analysis.
Continuous variables are presented as mean ± SD. For continuous variables, changes from preprocedure to postprocedure were evaluated by paired Student t test. Functional class changes and change in severity of mitral regurgitation were evaluated using the Wilcoxon signed rank test. A p value 0.05 was considered statistically significant.
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Results
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Baseline characteristics.
The mean age of the study patients who have completed their one-year follow-up was 53 ± 17 years (range, 32 to 83 years). Half of the patients were women. All patients were receiving two or more medications for HOCM. Medications included a beta-blocker (n = 37), a calcium-channel blocker (n = 28) or antiarrhythmic drugs (n = 14).
The number of arteries injected was 1.7 ± 0.3 arteries per patient. The mean volume of ethanol injected was 2.7 ± 1 mL per artery. The mean rise in CK was 1,951 ± 780 U. All patients experienced burning chest pain during alcohol injection despite premedication with meperidine and midazolam.
Effect of NSRT on symptoms and exercise tolerance.
Ninety percent of patients had class III or IV New York Heart Association class symptoms on enrollment in the study compared to none (p < 0.001) at one year (Fig. 1). Four patients continue to have class II symptoms, and six patients had class I symptoms at one year. Objectively, the exercise duration on the treadmill increased from 271 ± 160 s to 407 ± 211 s at one year (p = 0.024). Five patients could not undergo treadmill testing before NSRT because of severe dyspnea on presentation.
Seven patients (three with pacemakers and four without pacemakers) underwent a redo procedure during follow-up for recurrent symptoms and significant LVOT gradient (dobutamine-provoked in three patients and four patients with a resting gradient >40 mm Hg). Six patients underwent a successful redo procedure and the remaining one patient did not undergo a redo procedure owing to the small caliber of the remaining septal branches. This patient underwent a successful myomectomy operation. There was no difference in the baseline septal thickness, the volume of ethanol injected per vessel or the total number of vessels injected among these patients and those who did not require a redo procedure.
Effect of NSRT on LVOT gradient.
NSRT resulted in a significant reduction of the LVOT gradient in all patients whether they had a resting gradient or a dobutamine-provoked gradient. The mean resting gradient decreased from 74 ± 23 mm Hg to 6 ± 18 mm Hg at one year (p < 0.001) in patients who were initially enrolled with significant resting gradient. Similarly, the dobutamine-provoked gradient decreased from 84 ± 28 mm Hg to 30 ± 33 mm Hg at one year (p < 0.001). Figure 2 shows the change in resting and dobutamine-provoked LVOT gradients in all patients at one year.
Echocardiographic findings after NSRT at one year.
No change was noted in the left ventricular ejection fraction at one year (74 ± 7% vs. 73 ± 7%, p = NS). The septal thickness was reduced from 2.1 ± 0.7 cm to 1.5 ± 0.6 cm (p = 0.001). No difference was noted in the posterior wall thickness (1.3 ± 0.2 cm vs. 1.3 ± 0.2 cm, p = NS).
Mitral regurgitation was assessed by color Doppler to evaluate the size of the regurgitant jet in the left atrium on a grade of 0 for no regurgitation, 1 for mild, 2 for moderate, and 3 for severe. Overall, the severity was mild to moderate at baseline in all studied patients and decreased to trivial regurgitation at one year after NSRT (p < 0.01).
Other effects of NSRT.
One patient died during coronary artery bypass grafting after she was rushed into the operating room for left anterior descending artery dissection that could not be treated in the catheterization laboratory. Another patient died suddenly 10 days after the procedure. The autopsy results showed a right coronary artery thrombosis. Another patient experienced a witnessed sudden cardiac death 22 weeks after the procedure, was resuscitated and had a defibrillator implanted without neurologic or cardiac sequelae.
None of the patients developed a ventricular septal defect, worsening or new mitral or aortic insufficiency. Forty-five patients had isolated premature ventricular contractions during alcohol injection. Five patients had nonsustained ventricular tachycardia on ECG monitoring within 24 h of NSRT. Eleven patients developed complete heart block within three days of the procedure requiring DDD pacemaker implantation. Eight patients continue to be pacemaker dependent at one year. All patients had ECG changes after NSRT. Of those who did not have pacemakers or developed complete heart block, 20 had new right bundle branch block, 14 patients had right bundle branch block with left anterior fascicular block and 6 patients had left bundle branch block.
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Discussion
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Current therapies for HOCM compared to NSRT.
Relief of LVOT obstruction in HOCM leads to positive clinical and hemodynamic effects (9,10). Obstruction can be relieved by either medications, surgery or dual-chamber pacing (11). Medications are tolerated by some patients and their positive clinical and hemodynamic effects may be maintained (12). Surgical myotomy-myomectomy is effective in relieving the LVOT gradient, but it requires open heart surgery and surgical studies have reported a small incidence of postoperative atrial fibrillation, aortic insufficiency, complete heart block, remyectomy, ventricular septal defect and death (13,14). Dual-chamber pacing studies have demonstrated a modest gradient reduction associated with subjective symptomatic improvement. The mechanism of benefit is unclear, but may be related to both an acute decrease in the LVOT gradient and induced by alteration in septal activation and a long-term effect due to ventricular remodeling (1517). Recently, NSRT has been introduced as an alternative modality to treat patients with incapacitating symptoms due to HOCM. All the reported studies so far have documented a significant improvement in symptoms along with a significant reduction in LVOT gradient immediately after the procedure and up to 3 months afterwards (36). In this article, we report the results of the 1-year follow-up that were completed in August 1999 on the first 50 patients who underwent NSRT at our institution. Most of the patients enrolled in the study have shown a significant resolution of their heart failure symptoms on follow-up.
Comparative efficacy of NSRT to myomectomy and DDD pacing.
Ten Berg et al. (18) have reported persistent symptoms of angina in 14% and dyspnea in 20% of their 38 patients who underwent surgery for HOCM. McCully et al. (19) reported 50% improvement in symptoms in 90% of their patients and persistent symptoms in 10%. Mohr et al. (20) reported on the long-term outcome of 115 patients who underwent surgery for refractory symptoms due to HOCM. In their series, 76% of their patients were relieved from dyspnea, and 83% had resolution of their anginal symptoms. NSRT results compare favorably to the reductions achieved after surgical myotomy-myomectomy, avoiding the associated morbidity (1820).
NSRT is also effective in relieving the LVOT gradient in both patients with resting and dobutamine-provoked gradient. These results are far superior to those reported after dual-chamber pacing. In a recent study, Nishimura et al. (21) reported the results of a double-blind crossover study showing that the average decrease in the LVOT gradient during pacing was approximately 25% and varied substantially among patients. In addition, objective measures of exercise capacity did not differ significantly in the same study. Using echocardiographic methods, we were able to demonstrate that the symptomatic improvement after NSRT was associated with a decrease in septal thickness, without changing the left ventricular ejection fraction, indicating no worsening in systolic function (8).
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Conclusions
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These findings reaffirm that NSRT is an efficacious procedure with comparatively low risk in selected patients with HOCM who have incapacitating symptoms despite maximal medical therapy. It is safe and rational, and can be performed at medical centers with competent interventional and echocardiographic services. Repeat procedures can be performed at a low risk on patients with persistent symptoms or significant LVOT gradients on follow-up.
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Footnotes
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Supported in part by grants from the T.L.L. Temple Foundation, Lufkin, Texas; The Dunn Foundation, Houston, Texas; and The Methodist Hospital, Houston, Texas.
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References
|
|---|
1. Wigle ED, Sasson Z, Henderson MA, et al. Hypertrophic cardiomyopathy: the importance of the site and the extent of hypertrophy: a review. Prog Cardiovasc Dis. 1985;28:183[CrossRef][Medline]
2. Maron BJ, Gardin JM, Flack JM, et al. Prevalence of hypertrophic cardiomyopathy in a general population of young adults: echocardiographic analysis of 4111 subjects in the CARDIA study. Circulation. 1995;95:785789
3. Sigwart U. Nonsurgical myocardial reduction for hypertrophic obstructive cardiomyopathy. Lancet. 1995;346:211214[CrossRef][Medline]
4. Knight C, Kurbaan AS, Seggewiss H, et al. Non-surgical septal reduction for hypertrophic obstructive cardiomyopathy: outcome in the first series of patients. Circulation. 1997;95:20752081[Abstract/Free Full Text]
5. Seggewiss H, Gleichmann U, Faber L, et al. Catheter treatment of hypertrophic obstructive cardiomyopathy: acute and mid-term results. J Am Coll Cardiol. 1998;31:252258[Abstract/Free Full Text]
6. Lakkis N, Nagueh S, Killip D, et al. Echocardiographic-guided ethanol septal reduction for hypertrophic obstructive cardiomyopathy. Circulation. 1998;98:17501755[Abstract/Free Full Text]
7. Lakkis N, Kleiman N, Killip D, Spencer WJ III. Hypertrophic obstructive cardiomyopathy: alternative therapeutic options. Clin Cardiol. 1997;20:417418[Medline]
8. Nagueh S, Lakkis N, He ZX, et al. J Am Coll Cardiol. 1998;32:225229[Abstract/Free Full Text]
9. Wigle ED. Hypertrophic cardiomyopathy: a 1987 view-point. Circulation. 1987;75:311322[Free Full Text]
10. Spirito P, Seidman C, McKenna W, et al. The management of hypertrophic cardiomyopathy. N Engl J Med. 1997;336:775785[Free Full Text]
11. Fananapazir L, McAreavey D. Therapeutic options in patients with obstructive hypertrophic cardiomyopathy and severe drug-refractory symptoms. J Am Coll Cardiol. 1998;31:259264[Free Full Text]
12. Frank MJ, Abdullah AM, Canedo MI, et al. Long-term medical management of hypertrophic obstructive cardiomyopathy. Am J Cardiol. 1978;42:9931001[CrossRef][Medline]
13. Robbins RC, Stinson EB, Daily PO. Long-term results of left ventricular myotomy and myectomy for obstructive hypertrophic cardiomyopathy. J Thorac Cardiovasc Surg. 1996;111:586594[Abstract/Free Full Text]
14. Krajcer Z, Leachman R, Cooley D, et al. Septal myotomy-myomectomy versus mitral valve replacement in hypertrophic cardiomyopathy: ten year follow-up in 185 patients. Circulation. 1989;80:I-57I-64
15. Fananapazir L, Canon RO III, Tripodi D, Panza JA. Impact of dual-chamber permanent pacing in patients with obstructive hypertrophic cardiomyopathy with symptoms refractory to verapamil and beta-adrenergic blocker therapy. Circulation. 1992;85:21492161[Abstract/Free Full Text]
16. Jeanrenaud X, Goy JJ, Kappenberger L. Effects of dual-chamber pacing in hypertrophic cardiomyopathy. Lancet. 1992;339:13181323[CrossRef][Medline]
17. Kappenberger L, Linde C, Daubert C, et al. Pacing in hypertrophic obstructive cardiomyopathy (PIC): a randomized crossover study. Eur Heart J. 1997;18:12491256[Abstract/Free Full Text]
18. Ten Berg J, Suttorp MJ, Knaepen P, et al. Hypertrophic obstructive cardiomyopathy: initial results and long-term follow-up after morrow septal myectomy. Circulation. 1994;90:17811785[Abstract/Free Full Text]
19. McCully RB, Nishimura RA, Tajik AJ, et al. Extent of clinical improvement after surgical treatment for hypertrophic obstructive cardiomyopathy. Circulation. 1996;94:467471[Abstract/Free Full Text]
20. Mohr R, Schaff H, Danielson GK, et al. The outcome of surgical treatment for hypertrophic obstructive cardiomyopathy: experience over 15 years. J Thorac Cardiovasc Surg. 1989;97:666674[Abstract]
21. Nishimura RA, Trusty JM, Hayes DL. Dual-chamber pacing for hypertrophic obstructive cardiomyopathy: a randomized, double-blind, crossover study. J Am Coll Cardiol. 1997;29:435441[Abstract]
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|
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|
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|
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