- Email: [email protected]
Percutaneous transluminal septal myocardial ablation: A new catheter-based therapy for patients with hypertrophic obstructive cardiomyopathy
Percutaneous Transluminal Septal Myocardial Ablation: A New Catheter-Based Therapy for Patients with Hypertrophic Obstructive Cardiomyopathy H. M. Omar Farouque, MB BS (Hons), FRACP, Stephen G. Worthley, MB BS, FRACP, PhD, R. Andrew P. Skyrme-Jones, MBChB, MRCP, PhD, Sarah A. Hope, MBChB, MRCP and Ian T. Meredith, MB BS (Hons), FRACP, PhD Centre for Heart and Chest Research, Monash Medical Centre and Monash University, Melbourne, Australia
Hypertrophic obstructive cardiomyopathy is a complex disorder with serious clinical implications. Percutaneous transluminal septal myocardial ablation is a promising new addition to existing therapies for this condition. It is a catheter-based approach that involves instilling alcohol into the septal branches of the left anterior descending artery to induce a ‘controlled’ septal myocardial infarct. The result is a decrease in thickness of the hypertrophied interventricular septum and a reduction of the left ventricular outflow tract gradient. To date, the results from several series have been promising, with improvements in haemodynamic and clinical parameters without prohibitive complication rates. In this article, the indications, technique and outcomes of this procedure are reviewed. (Heart, Lung and Circulation 2001; 10: 63–67) Key words: catheterisation, hypertrophic cardiomyopathy, septal alcohol ablation.
H
ypertrophic cardiomyopathy (HCM) is a genetically determined condition with an autosomal dominant mode of inheritance and an estimated prevalence of one in 500.1 Although many patients may be asymptomatic, the clinical manifestations of this disorder include dyspnoea, angina, syncope or near syncope, and sudden death. In pathological terms, HCM is characterised by inappropriate left or right ventricular hypertrophy that is typically asymmetrical, with the histological hallmarks of myocyte hypertrophy and disarray.2 Of the various forms of asymmetrical involvement, ventricular septal hypertrophy accounts for the majority of cases. In this setting, hypertrophy of the upper part of the interventricular septum may lead to narrowing and obstruction of the left ventricular outflow tract (LVOT). There is also a dynamic component to LVOT obstruction caused by systolic anterior motion of the mitral valve.
Correspondence: Ian T. Meredith, Cardiovascular Research Centre, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia. Email: [email protected]
Other features that contribute to symptom development include the presence of diastolic or systolic dysfunction, myocardial ischaemia due to impaired vasodilator reserve, mitral regurgitation and arrhythmia. Several therapeutic options have been used for the relief of symptoms in obstructive HCM. In general, these treatments serve to reduce the degree of LVOT obstruction thereby improving left ventricular filling pressures, myocardial perfusion and symptoms. The use of negatively inotropic drugs such as beta-blockers, verapamil and disopyramide are the mainstays of pharmacological therapy.2 In patients with drug-refractory symptoms and significant LVOT obstruction (resting gradient ≥50 mmHg), surgical ventricular septal myotomy– myectomy has been recommended. In experienced hands the results of this procedure are excellent, with low operative complication rates and good long-term symptom relief.3 In recent years, two less invasive therapeutic strategies have been introduced for drug-refractory obstructive HCM. The first of these is dual-chamber (DDD) pacing; however, the early promise of this method
64
H.M. Omar Farouque et al. Septal alcohol ablation
has not been realised.4 The second strategy is known as percutaneous transluminal septal myocardial ablation (PTSMA), and it will be the focus of this article.
Rationale and Patient Selection Percutaneous transluminal septal myocardial ablation is a non-surgical catheter-based treatment for obstructive HCM. It involves the induction of a localised myocardial infarct in the hypertrophied proximal interventricular septum by injecting absolute alcohol into a septal branch of the left anterior descending artery. The decrease in septal mass in the infarcted area leads to a reduction in LVOT obstruction. Ulrich Sigwart at the Royal Brompton Hospital, London, first introduced PTSMA into clinical practice in 1994.5 However, the basis for this procedure dates back to earlier observations that the LVOT gradient could be reduced with temporary balloon occlusion of the first septal artery.5 Although the indications for PTSMA for obstructive HCM may be expanded in the future, at this stage it is prudent to consider only patients with drug-refractory symptoms (New York Heart Association functional class III or IV) and a significant peak resting LVOT gradient (≥50 mmHg) for this procedure.6 Specific contraindications for PTSMA include septal thickness <18 mm, intrinsic mitral valve disease, and advanced coronary disease necessitating coronary bypass grafting.7
Technical Considerations All patients being considered for PTSMA require diagnostic left heart catheterisation and coronary angiography to ascertain the magnitude of the LVOT gradient, to exclude advanced coronary disease and ensure that septal coronary anatomy is suitable for intervention. Additional baseline investigations include transthoracic echocardiography, an electrocardiogram and cardiac enzymes. Vascular access is obtained with cannulation of the right femoral vein and right and left femoral arteries. A temporary pacing catheter is positioned in the right ventricle, as complete heart block is a common occurrence with septal artery occlusion. A double-lumen ‘pigtail’ catheter is passed into the left ventricle allowing simultaneous ventricular and aortic pressure measurement. A guiding catheter is then used to cannulate the left main coronary artery. After the patient is systemically heparinized, a 0.014-inch angioplasty guidewire is passed into the first septal artery and a short, slightly oversized over-the-wire balloon (9–15 × 2.0–2.5 mm) is completely advanced into the main trunk of this vessel. The balloon is then gently inflated to occlude the vessel and angiographic contrast is injected through its central
Heart, Lung and Circulation 2001; 10
lumen to define the area supplied by the septal branch and to ensure no reflux into the left anterior descending artery occurs. Intraprocedural myocardial contrast echocardiography (MCE) is recommended as it provides additional information on the myocardial perfusion bed of the septal branch and assists in the selection of an appropriate target vessel.8,9 During balloon inflation, an echocardiographic contrast agent is selectively injected into the septal branch while performing transthoracic or transoesophageal echocardiography to visualise the interventricular septum. One should see opacification of the basal septum implicated in LVOT obstruction. If more extensive opacification of the interventricular septum is observed, alcohol should not be injected into the septal branch, as an unnecessarily large area of infarction will result. The use of MCE during PTSMA has been associated with smaller induced infarction, reduced requirement for permanent pacing, and a greater proportion of patients achieving a significant decrease in the LVOT gradient compared to PTSMA without MCE.9 Once the correct septal branch has been identified, 2–5 mL of absolute ethanol is instilled through the lumen of the inflated balloon catheter at a rate of 1 mL per min. To prevent reflux of alcohol into the left anterior descending artery the balloon is left inflated for a total duration of 10–15 min. All patients experience transient chest pain of moderate severity during alcohol injection, therefore effective sedation and analgesia is required. Once the balloon is deflated and withdrawn, the LVOT gradient is remeasured and coronary angiography performed to confirm occlusion of the septal branch. If a significant residual resting LVOT gradient remains, intervention to an adjacent septal branch could be considered using the same technique. Close monitoring is then undertaken in the coronary care unit for 2–4 days. The procedural sequence is depicted in Fig. 1.
Efficacy To date, the results of PTSMA have been very encouraging. A reduction in resting and provoked LVOT gradient is seen in approximately 90% of patients after PTSMA10 (Fig. 2). In many patients, further reductions have been noted in the ensuing 3–6 months. The magnitude of this reduction from published studies is significant, with a mean preintervention resting gradient of 62 mmHg and an immediate postintervention gradient of 16 mmHg.8,9,11–15 This effect appears to be durable in the short to medium term (mean follow-up duration of 3–30 months).15,16 Post-procedural echocardiographic analyses have revealed beneficial changes, including a reduction in septal and posterior wall thickness,9 an
H.M. Omar Farouque et al. Septal alcohol ablation
Heart, Lung and Circulation 2001; 10
65
Figure 1. (a) Angiogram of the left coronary arterial system taken in the antero–posterior cranial projection before alcohol septal ablation. The position of the catheters, pacing wire and transoesophageal echocardiographic (TOE) probe are indicated. (b) An angioplasty guidewire is positioned in the first septal branch of the left anterior descending artery (LAD). (c) Radiographic contrast injection into the first septal artery during balloon occlusion showing the distal territory of this vessel with absence of contrast reflux into the left anterior descending artery. (d) Final result after alcohol injection showing occlusion of the first septal branch. increase in LVOT area,17 and a reduction in systolic anterior motion of the mitral valve and mitral regurgitation.11 These structural changes are accompanied by persistent clinical benefits based on symptom assessment, with an improvement of one to two NYHA functional classes. 8,9,11,13–15 Several studies have also reported improved exercise capacity as determined by greater
treadmill exercise duration8,9,11,12,14 and peak oxygen consumption.12,14
Complications Significant complications may arise following PTSMA. The pooled procedure-related mortality rate from six
66
H.M. Omar Farouque et al. Septal alcohol ablation
Heart, Lung and Circulation 2001; 10
Figure 2. Resting left ventricular and ascending aortic pressures (a) before and (b) immediately after alcohol septal ablation in the same patient shown in Figure 1. The preprocedural peak-to-peak left ventricular outflow tract gradient of more than 100 mmHg is abolished by alcohol injection. published studies from different centres around the world is 1.7%, with a range of 0–4%.8,9,11–14 These figures are comparable to the postoperative mortality rates for isolated septal myotomy–myectomy performed in experienced surgical centres. The most common complication is the occurrence of complete heart block, which may occur in as many as 70% of patients.9 It is usually a transitory phenomenon with most cases resolving within 48 to 72 h. The overall rate of permanent DDD pacemaker implantation due to persisting complete heart block is approximately 19%,8,9,11–14 but the use of intraprocedural MCE has reduced the need for permanent pacing to around 7%.9 The other common conduction abnormality is the occurrence of a bundle branch block, which tends to be persistent and typically involves the right bundle
branch. The overall rate of sustained ventricular tachycardia or ventricular fibrillation in the early postprocedural phase was 2.5%.8,9,11–14 The tachy-arrhythmia was successfully terminated in all but one instance. Another potentially serious complication is reflux of alcohol from the septal perforator into the left anterior descending artery with resulting anterior myocardial infarction. Published reports suggest that this may occur in 2.5% of procedures, although detailed attention to technique should eliminate this risk.8,9,11–14 There have been concerns about the potential for longterm complications after PTSMA. The issue of creating a substrate in the form of a myocardial infarct for future arrhythmia in the ventricle of a patient already predisposed to malignant dysrhythmias has been raised.
H.M. Omar Farouque et al. Septal alcohol ablation
Heart, Lung and Circulation 2001; 10
Although the data are reassuring in this regard, the longest reported follow-up period at the time of writing is a mean of only 30 months.16 It has also been suggested that postinfarct remodelling may occur after PTSMA, leading to progressive global left ventricular dilatation. To date, there is no convincing evidence that this is the case. Notably, the larger studies have reported slight reductions in the left ventricular ejection fraction, although overall contractility was still within normal limits.8,9,11,14
Conclusions Percutaneous transluminal septal myocardial ablation is a promising new technique for the treatment of obstructive HCM. It is associated with improvement in symptoms and haemodynamic parameters without prohibitive complication rates. As with other therapeutic strategies, it is unclear whether it alters prognosis in this condition. Based on current knowledge, it cannot as yet be recommended for asymptomatic or mildly symptomatic patients with this condition. Larger patient numbers and long-term follow-up data are required to enable valid conclusions to be drawn about the enduring safety and efficacy of this procedure. To achieve these aims in the minimum time, authorities have called for the establishment of a multicentre registry.18 Until these data are available, PTSMA should be considered as a valuable therapeutic option and a potential alternative to surgical myotomy–myectomy for the small subset of patients with obstructive HCM and drugrefractory symptoms.
5. 6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
References 1. Maron BJ, Gardin JM, Flack JM, Gidding SS, Kurosaki TT, Bild DE. Prevalence of hypertrophic cardiomyopathy in a general population of young adults. Echocardiographic analysis of 4111 subjects in the CARDIA Study. Coronary Artery Risk Development in (Young) Adults. Circulation 1995; 92: 785–9. 2. Wigle ED, Rakowski H, Kimball BP, Williams WG. Hypertrophic cardiomyopathy: clinical spectrum and treatment. Circulation 1995; 92: 1680–92. 3. McCully RB, Nishimura RA, Tajik AJ, Schaff HV, Danielson GK. Extent of clinical improvement after surgical treatment of hypertrophic obstructive cardiomyopathy. Circulation 1996; 94: 467–71. 4. Maron BJ, Nishimura RA, McKenna WJ et al. Assessment of permanent dual-chamber pacing as a treatment for drugrefractory symptomatic patients with obstructive hypertrophic
16.
17.
18.
67
cardiomyopathy: a randomized double-blind crossover study (M-PATHY). Circulation 1999; 99: 2927–33. Sigwart U. Non-surgical myocardial reduction for hypertrophic obstructive cardiomyopathy. Lancet 1995; 346: 211–14. Maron BJ. New interventions for obstructive hypertrophic cardiomyopathy: promise and prudence. Eur. Heart J. 1999; 20: 1292–4. 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. Lakkis NM, Nagueh SF, Kleiman NS et al. Echocardiographyguided ethanol septal reduction for hypertrophic obstructive cardiomyopathy. Circulation 1998; 98: 1750–55. Faber L, Seggewiss H, Gleichmann U. Percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: results with respect to intraprocedural myocardial contrast echocardiography. Circulation 1998; 98: 2415–21. Seggewiss H. Percutaneous transluminal septal myocardial ablation: a new treatment for hypertrophic obstructive cardiomyopathy. Eur. Heart J. 2000; 21: 704–7. Gietzen FH, Leuner CJ, Raute-Kreinsen U et al. Acute and longterm results after transcoronary ablation of septal hypertrophy: catheter interventional treatment for hypertrophic obstructive cardiomyopathy. Eur. Heart J. 1999; 20: 1342–54. Kim J-J, Lee CW, Park S-W et al. Improvement in exercise capacity and exercise blood pressure response after transcoronary alcohol ablation therapy of septal hypertrophy in hypertrophic cardiomyopathy. Am. J. Cardiol. 1999; 83: 1220–23. Knight C, Kurbaan AS, Seggewiss H et al. Nonsurgical septal reduction for hypertrophic cardiomyopathy: outcome in the first series of patients. Circulation 1998; 95: 2075–81. Ruzyllo W, Chojnowska L, Demkow M et al. Left ventricular outflow tract gradient decrease with non-surgical myocardial reduction improves exercise capacity in patients with hypertrophic obstructive cardiomyopathy. Eur. Heart J. 2000; 21: 770–77. Seggewiss H, Gleichmann U, Faber L, Fassbender D, Schmidt HK, Strick S. Percutaneous transluminal septal myocardial ablation in hypertrophic cardiomyopathy: acute results and 3-month follow-up in 25 patients. J. Am. Coll. Cardiol. 1998; 31: 252–8. Faber L, Meissner A, Ziemssen P, Seggewiss H. Percutaneous transluminal septal myocardial ablation for obstructive hypertrophic cardiomyopathy: long term follow up of the first series of 25 patients. Heart 2000; 83: 326–31. Kuhn H, Gietzen FH, Schafers M et al. Changes in the left ventricular outflow tract after transcoronary ablation of septal hypertrophy (TASH) for hypertrophic obstructive cardiomyopathy as assessed by transoesophageal echocardiography and by measuring myocardial glucose utilization and perfusion. Eur. Heart J. 1999; 20: 1808–17. Spencer WH III, Roberts R. Alcohol septal ablation in hypertrophic obstructive cardiomyopathy: the need for a registry. Circulation 2000; 102: 600–601.
Hypertrophic obstructive cardiomyopathy is a complex disorder with serious clinical implications. Percutaneous transluminal septal myocardial ablation is a promising new addition to existing therapies for this condition. It is a catheter-based approach that involves instilling alcohol into the septal branches of the left anterior descending artery to induce a ‘controlled’ septal myocardial infarct. The result is a decrease in thickness of the hypertrophied interventricular septum and a reduction of the left ventricular outflow tract gradient. To date, the results from several series have been promising, with improvements in haemodynamic and clinical parameters without prohibitive complication rates. In this article, the indications, technique and outcomes of this procedure are reviewed. (Heart, Lung and Circulation 2001; 10: 63–67) Key words: catheterisation, hypertrophic cardiomyopathy, septal alcohol ablation.
H
ypertrophic cardiomyopathy (HCM) is a genetically determined condition with an autosomal dominant mode of inheritance and an estimated prevalence of one in 500.1 Although many patients may be asymptomatic, the clinical manifestations of this disorder include dyspnoea, angina, syncope or near syncope, and sudden death. In pathological terms, HCM is characterised by inappropriate left or right ventricular hypertrophy that is typically asymmetrical, with the histological hallmarks of myocyte hypertrophy and disarray.2 Of the various forms of asymmetrical involvement, ventricular septal hypertrophy accounts for the majority of cases. In this setting, hypertrophy of the upper part of the interventricular septum may lead to narrowing and obstruction of the left ventricular outflow tract (LVOT). There is also a dynamic component to LVOT obstruction caused by systolic anterior motion of the mitral valve.
Correspondence: Ian T. Meredith, Cardiovascular Research Centre, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia. Email: [email protected]
Other features that contribute to symptom development include the presence of diastolic or systolic dysfunction, myocardial ischaemia due to impaired vasodilator reserve, mitral regurgitation and arrhythmia. Several therapeutic options have been used for the relief of symptoms in obstructive HCM. In general, these treatments serve to reduce the degree of LVOT obstruction thereby improving left ventricular filling pressures, myocardial perfusion and symptoms. The use of negatively inotropic drugs such as beta-blockers, verapamil and disopyramide are the mainstays of pharmacological therapy.2 In patients with drug-refractory symptoms and significant LVOT obstruction (resting gradient ≥50 mmHg), surgical ventricular septal myotomy– myectomy has been recommended. In experienced hands the results of this procedure are excellent, with low operative complication rates and good long-term symptom relief.3 In recent years, two less invasive therapeutic strategies have been introduced for drug-refractory obstructive HCM. The first of these is dual-chamber (DDD) pacing; however, the early promise of this method
64
H.M. Omar Farouque et al. Septal alcohol ablation
has not been realised.4 The second strategy is known as percutaneous transluminal septal myocardial ablation (PTSMA), and it will be the focus of this article.
Rationale and Patient Selection Percutaneous transluminal septal myocardial ablation is a non-surgical catheter-based treatment for obstructive HCM. It involves the induction of a localised myocardial infarct in the hypertrophied proximal interventricular septum by injecting absolute alcohol into a septal branch of the left anterior descending artery. The decrease in septal mass in the infarcted area leads to a reduction in LVOT obstruction. Ulrich Sigwart at the Royal Brompton Hospital, London, first introduced PTSMA into clinical practice in 1994.5 However, the basis for this procedure dates back to earlier observations that the LVOT gradient could be reduced with temporary balloon occlusion of the first septal artery.5 Although the indications for PTSMA for obstructive HCM may be expanded in the future, at this stage it is prudent to consider only patients with drug-refractory symptoms (New York Heart Association functional class III or IV) and a significant peak resting LVOT gradient (≥50 mmHg) for this procedure.6 Specific contraindications for PTSMA include septal thickness <18 mm, intrinsic mitral valve disease, and advanced coronary disease necessitating coronary bypass grafting.7
Technical Considerations All patients being considered for PTSMA require diagnostic left heart catheterisation and coronary angiography to ascertain the magnitude of the LVOT gradient, to exclude advanced coronary disease and ensure that septal coronary anatomy is suitable for intervention. Additional baseline investigations include transthoracic echocardiography, an electrocardiogram and cardiac enzymes. Vascular access is obtained with cannulation of the right femoral vein and right and left femoral arteries. A temporary pacing catheter is positioned in the right ventricle, as complete heart block is a common occurrence with septal artery occlusion. A double-lumen ‘pigtail’ catheter is passed into the left ventricle allowing simultaneous ventricular and aortic pressure measurement. A guiding catheter is then used to cannulate the left main coronary artery. After the patient is systemically heparinized, a 0.014-inch angioplasty guidewire is passed into the first septal artery and a short, slightly oversized over-the-wire balloon (9–15 × 2.0–2.5 mm) is completely advanced into the main trunk of this vessel. The balloon is then gently inflated to occlude the vessel and angiographic contrast is injected through its central
Heart, Lung and Circulation 2001; 10
lumen to define the area supplied by the septal branch and to ensure no reflux into the left anterior descending artery occurs. Intraprocedural myocardial contrast echocardiography (MCE) is recommended as it provides additional information on the myocardial perfusion bed of the septal branch and assists in the selection of an appropriate target vessel.8,9 During balloon inflation, an echocardiographic contrast agent is selectively injected into the septal branch while performing transthoracic or transoesophageal echocardiography to visualise the interventricular septum. One should see opacification of the basal septum implicated in LVOT obstruction. If more extensive opacification of the interventricular septum is observed, alcohol should not be injected into the septal branch, as an unnecessarily large area of infarction will result. The use of MCE during PTSMA has been associated with smaller induced infarction, reduced requirement for permanent pacing, and a greater proportion of patients achieving a significant decrease in the LVOT gradient compared to PTSMA without MCE.9 Once the correct septal branch has been identified, 2–5 mL of absolute ethanol is instilled through the lumen of the inflated balloon catheter at a rate of 1 mL per min. To prevent reflux of alcohol into the left anterior descending artery the balloon is left inflated for a total duration of 10–15 min. All patients experience transient chest pain of moderate severity during alcohol injection, therefore effective sedation and analgesia is required. Once the balloon is deflated and withdrawn, the LVOT gradient is remeasured and coronary angiography performed to confirm occlusion of the septal branch. If a significant residual resting LVOT gradient remains, intervention to an adjacent septal branch could be considered using the same technique. Close monitoring is then undertaken in the coronary care unit for 2–4 days. The procedural sequence is depicted in Fig. 1.
Efficacy To date, the results of PTSMA have been very encouraging. A reduction in resting and provoked LVOT gradient is seen in approximately 90% of patients after PTSMA10 (Fig. 2). In many patients, further reductions have been noted in the ensuing 3–6 months. The magnitude of this reduction from published studies is significant, with a mean preintervention resting gradient of 62 mmHg and an immediate postintervention gradient of 16 mmHg.8,9,11–15 This effect appears to be durable in the short to medium term (mean follow-up duration of 3–30 months).15,16 Post-procedural echocardiographic analyses have revealed beneficial changes, including a reduction in septal and posterior wall thickness,9 an
H.M. Omar Farouque et al. Septal alcohol ablation
Heart, Lung and Circulation 2001; 10
65
Figure 1. (a) Angiogram of the left coronary arterial system taken in the antero–posterior cranial projection before alcohol septal ablation. The position of the catheters, pacing wire and transoesophageal echocardiographic (TOE) probe are indicated. (b) An angioplasty guidewire is positioned in the first septal branch of the left anterior descending artery (LAD). (c) Radiographic contrast injection into the first septal artery during balloon occlusion showing the distal territory of this vessel with absence of contrast reflux into the left anterior descending artery. (d) Final result after alcohol injection showing occlusion of the first septal branch. increase in LVOT area,17 and a reduction in systolic anterior motion of the mitral valve and mitral regurgitation.11 These structural changes are accompanied by persistent clinical benefits based on symptom assessment, with an improvement of one to two NYHA functional classes. 8,9,11,13–15 Several studies have also reported improved exercise capacity as determined by greater
treadmill exercise duration8,9,11,12,14 and peak oxygen consumption.12,14
Complications Significant complications may arise following PTSMA. The pooled procedure-related mortality rate from six
66
H.M. Omar Farouque et al. Septal alcohol ablation
Heart, Lung and Circulation 2001; 10
Figure 2. Resting left ventricular and ascending aortic pressures (a) before and (b) immediately after alcohol septal ablation in the same patient shown in Figure 1. The preprocedural peak-to-peak left ventricular outflow tract gradient of more than 100 mmHg is abolished by alcohol injection. published studies from different centres around the world is 1.7%, with a range of 0–4%.8,9,11–14 These figures are comparable to the postoperative mortality rates for isolated septal myotomy–myectomy performed in experienced surgical centres. The most common complication is the occurrence of complete heart block, which may occur in as many as 70% of patients.9 It is usually a transitory phenomenon with most cases resolving within 48 to 72 h. The overall rate of permanent DDD pacemaker implantation due to persisting complete heart block is approximately 19%,8,9,11–14 but the use of intraprocedural MCE has reduced the need for permanent pacing to around 7%.9 The other common conduction abnormality is the occurrence of a bundle branch block, which tends to be persistent and typically involves the right bundle
branch. The overall rate of sustained ventricular tachycardia or ventricular fibrillation in the early postprocedural phase was 2.5%.8,9,11–14 The tachy-arrhythmia was successfully terminated in all but one instance. Another potentially serious complication is reflux of alcohol from the septal perforator into the left anterior descending artery with resulting anterior myocardial infarction. Published reports suggest that this may occur in 2.5% of procedures, although detailed attention to technique should eliminate this risk.8,9,11–14 There have been concerns about the potential for longterm complications after PTSMA. The issue of creating a substrate in the form of a myocardial infarct for future arrhythmia in the ventricle of a patient already predisposed to malignant dysrhythmias has been raised.
H.M. Omar Farouque et al. Septal alcohol ablation
Heart, Lung and Circulation 2001; 10
Although the data are reassuring in this regard, the longest reported follow-up period at the time of writing is a mean of only 30 months.16 It has also been suggested that postinfarct remodelling may occur after PTSMA, leading to progressive global left ventricular dilatation. To date, there is no convincing evidence that this is the case. Notably, the larger studies have reported slight reductions in the left ventricular ejection fraction, although overall contractility was still within normal limits.8,9,11,14
Conclusions Percutaneous transluminal septal myocardial ablation is a promising new technique for the treatment of obstructive HCM. It is associated with improvement in symptoms and haemodynamic parameters without prohibitive complication rates. As with other therapeutic strategies, it is unclear whether it alters prognosis in this condition. Based on current knowledge, it cannot as yet be recommended for asymptomatic or mildly symptomatic patients with this condition. Larger patient numbers and long-term follow-up data are required to enable valid conclusions to be drawn about the enduring safety and efficacy of this procedure. To achieve these aims in the minimum time, authorities have called for the establishment of a multicentre registry.18 Until these data are available, PTSMA should be considered as a valuable therapeutic option and a potential alternative to surgical myotomy–myectomy for the small subset of patients with obstructive HCM and drugrefractory symptoms.
5. 6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
References 1. Maron BJ, Gardin JM, Flack JM, Gidding SS, Kurosaki TT, Bild DE. Prevalence of hypertrophic cardiomyopathy in a general population of young adults. Echocardiographic analysis of 4111 subjects in the CARDIA Study. Coronary Artery Risk Development in (Young) Adults. Circulation 1995; 92: 785–9. 2. Wigle ED, Rakowski H, Kimball BP, Williams WG. Hypertrophic cardiomyopathy: clinical spectrum and treatment. Circulation 1995; 92: 1680–92. 3. McCully RB, Nishimura RA, Tajik AJ, Schaff HV, Danielson GK. Extent of clinical improvement after surgical treatment of hypertrophic obstructive cardiomyopathy. Circulation 1996; 94: 467–71. 4. Maron BJ, Nishimura RA, McKenna WJ et al. Assessment of permanent dual-chamber pacing as a treatment for drugrefractory symptomatic patients with obstructive hypertrophic
16.
17.
18.
67
cardiomyopathy: a randomized double-blind crossover study (M-PATHY). Circulation 1999; 99: 2927–33. Sigwart U. Non-surgical myocardial reduction for hypertrophic obstructive cardiomyopathy. Lancet 1995; 346: 211–14. Maron BJ. New interventions for obstructive hypertrophic cardiomyopathy: promise and prudence. Eur. Heart J. 1999; 20: 1292–4. 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. Lakkis NM, Nagueh SF, Kleiman NS et al. Echocardiographyguided ethanol septal reduction for hypertrophic obstructive cardiomyopathy. Circulation 1998; 98: 1750–55. Faber L, Seggewiss H, Gleichmann U. Percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: results with respect to intraprocedural myocardial contrast echocardiography. Circulation 1998; 98: 2415–21. Seggewiss H. Percutaneous transluminal septal myocardial ablation: a new treatment for hypertrophic obstructive cardiomyopathy. Eur. Heart J. 2000; 21: 704–7. Gietzen FH, Leuner CJ, Raute-Kreinsen U et al. Acute and longterm results after transcoronary ablation of septal hypertrophy: catheter interventional treatment for hypertrophic obstructive cardiomyopathy. Eur. Heart J. 1999; 20: 1342–54. Kim J-J, Lee CW, Park S-W et al. Improvement in exercise capacity and exercise blood pressure response after transcoronary alcohol ablation therapy of septal hypertrophy in hypertrophic cardiomyopathy. Am. J. Cardiol. 1999; 83: 1220–23. Knight C, Kurbaan AS, Seggewiss H et al. Nonsurgical septal reduction for hypertrophic cardiomyopathy: outcome in the first series of patients. Circulation 1998; 95: 2075–81. Ruzyllo W, Chojnowska L, Demkow M et al. Left ventricular outflow tract gradient decrease with non-surgical myocardial reduction improves exercise capacity in patients with hypertrophic obstructive cardiomyopathy. Eur. Heart J. 2000; 21: 770–77. Seggewiss H, Gleichmann U, Faber L, Fassbender D, Schmidt HK, Strick S. Percutaneous transluminal septal myocardial ablation in hypertrophic cardiomyopathy: acute results and 3-month follow-up in 25 patients. J. Am. Coll. Cardiol. 1998; 31: 252–8. Faber L, Meissner A, Ziemssen P, Seggewiss H. Percutaneous transluminal septal myocardial ablation for obstructive hypertrophic cardiomyopathy: long term follow up of the first series of 25 patients. Heart 2000; 83: 326–31. Kuhn H, Gietzen FH, Schafers M et al. Changes in the left ventricular outflow tract after transcoronary ablation of septal hypertrophy (TASH) for hypertrophic obstructive cardiomyopathy as assessed by transoesophageal echocardiography and by measuring myocardial glucose utilization and perfusion. Eur. Heart J. 1999; 20: 1808–17. Spencer WH III, Roberts R. Alcohol septal ablation in hypertrophic obstructive cardiomyopathy: the need for a registry. Circulation 2000; 102: 600–601.