EDITORIAL
Percutaneous septal
ablation: a new treatment for hypertrophic obstructive cardiomyopathy Uypertrophic obstructive cardiomyopathy (HOCM) is defined as a
U primary myocardial hypertrophy with dynamic left ventricular outflow tract obstruction. It is also characterised by a variant degree of diastolic dysftmction. In addition to asymmetrical hypertrophy of the ventricular myocardium, primarily of the interventricular septw ;-/-orphological changes ofthe papillary muscles and mitral valves are-i ooften observed. HOCM is the most frequent cause of exertional syncope or sudden cardiac death in younger patients.' Until the early 1990s, surgical myectomy was the standard treatment for patients with HOCM and drug refractory symptoms. In the past years the potential therapeutic options have dramatically changed by the introduction of DDD-pacemaker implantation and percutaneous septal ablation (PTSMA) by alcohol-induced septal branch occlusion.2 In this issue, Ten Berg and colleagues3 report on their initial experience of PTSMA in 24 patients with HOCM. This editorial sets their results in context with previous reports and compares PTSMA with the results of surgical myectomy.
PTSMA, like surgical myectomy, aims directly at reducing the hypertrophied interventricular septum with consecutive expansion of the left ventricular outflow tract and a reduction in the left ventricular outflow tract gradient. This is achieved through a circumscribed infarction of the area supplied by the occluded septal branch. In the short history of PTSMA, several modifications to the original technique have been described.2'4'6 With a few exceptions, the operators prefer the echocardiography-guided anatomic approach for identfying the target septal branch, which we introduced in 1996, as do most cardiac surgeons. Isolated haemodynamic estimation of the target septal branch showed that temporary balloon occlusion ofthe first larger septal branch resulted in a >50% reduction in resting outflow tract gradient in only three out often patients, and had no effect in four patients.6 Furthermore, about 20-25% ofthe patients in whom haemodynamic identification of the target septal branch was performed need a second PTSMA; the increase of the induced septal scar is primarily due to an incorrectly placed or sized alcohol depot. In the meantime, we7 and others have reported that opacification of any other cardiac structure can be recognised and potential risk of complications due to alcohol injection (rupture of papillary muscle, lateral or posterior wall infarction) can be avoided. Inclusion criteria for PTSMA include symptomatic patients .NYHA III/CCS III despite drug therapy or with serious side effects ofmedication. Patients with less severe symptoms were only treated if they had particularly high outflow tract gradients (.50 mmHg at rest or 100 mmHg under stress) and documented high-risk factors for sudden cardiac death, or objective reduction of exercise capacity. However, it should be taken into Netherlands Heart Journal, Volume 9, Number 8, November 2001
315
Editorial
consideration that at present there are few data to suggest that a resting gradient >30 mmHg has an impact on the risk for sudden death.8 Patients with exercise-induced syncope and recurrent episodes ofatrial fibrillation with negative impact on clinical symptoms and potential embolic events are candidates for a more active treatment. In patients with mitral regurgitation, pre-interventional echocardiography should be used to clarify whether it is due to systolic anterior motion (SAM) associated outflow tract obstruction or to morphological changes ofthe mitral valve and papillary muscle, which should be treated by surgery.
rA
,i!'
1_1
"'
316
In the meantime, about 1000 patients are known to have been treated worldwide. All groups report a gradient reduction in about 90% of the patients.4'5'9"10-13 The results ofTen Berg and co-workers are comparable, taking into account their learning curve. The introduction of echocardiographic guidance led to an improvement in haemodynamic results despite a reduction in infarcted septal area (estimated by maximal CKrise), number of occluded septal arteries, and need for re-interventions. Thereby, enlargement of the septal scar, with the associated potential negative consequences for left ventricular systolic and diastolic function, can be avoided. ; eThe most significant complications observed to date are hospital deaths, at a rate of up to 4%.13 Our own experience, including our learning curve, showed hospital mortality of 1%. This low mortality is comparable with experienced surgical centres. Hospital mortality predominantly occurred m elderly patients and - as in the series often Berg et al. - during the postinterventional period, which underlines the importance of careful hospital monitoring. Particular attention should be paid to a case report of a death occurring ten days after the intervention as the result of an unexpected trifascicular block, underlining the need for close rhythmological monitoring for several days following the intervention. The most frequent complications are peri- and post-interventional trifascicular blocks at a rate of 60%. In the majority of cases these blocks are only transitory. After the introduction ofechocardiographic guidance, the number of permanent pacemaker implantations due to trifascicular block was reduced from 20-40%4,",'l to
Percutaneous septal
ablation: a new treatment for hypertrophic obstructive cardiomyopathy Uypertrophic obstructive cardiomyopathy (HOCM) is defined as a
U primary myocardial hypertrophy with dynamic left ventricular outflow tract obstruction. It is also characterised by a variant degree of diastolic dysftmction. In addition to asymmetrical hypertrophy of the ventricular myocardium, primarily of the interventricular septw ;-/-orphological changes ofthe papillary muscles and mitral valves are-i ooften observed. HOCM is the most frequent cause of exertional syncope or sudden cardiac death in younger patients.' Until the early 1990s, surgical myectomy was the standard treatment for patients with HOCM and drug refractory symptoms. In the past years the potential therapeutic options have dramatically changed by the introduction of DDD-pacemaker implantation and percutaneous septal ablation (PTSMA) by alcohol-induced septal branch occlusion.2 In this issue, Ten Berg and colleagues3 report on their initial experience of PTSMA in 24 patients with HOCM. This editorial sets their results in context with previous reports and compares PTSMA with the results of surgical myectomy.
PTSMA, like surgical myectomy, aims directly at reducing the hypertrophied interventricular septum with consecutive expansion of the left ventricular outflow tract and a reduction in the left ventricular outflow tract gradient. This is achieved through a circumscribed infarction of the area supplied by the occluded septal branch. In the short history of PTSMA, several modifications to the original technique have been described.2'4'6 With a few exceptions, the operators prefer the echocardiography-guided anatomic approach for identfying the target septal branch, which we introduced in 1996, as do most cardiac surgeons. Isolated haemodynamic estimation of the target septal branch showed that temporary balloon occlusion ofthe first larger septal branch resulted in a >50% reduction in resting outflow tract gradient in only three out often patients, and had no effect in four patients.6 Furthermore, about 20-25% ofthe patients in whom haemodynamic identification of the target septal branch was performed need a second PTSMA; the increase of the induced septal scar is primarily due to an incorrectly placed or sized alcohol depot. In the meantime, we7 and others have reported that opacification of any other cardiac structure can be recognised and potential risk of complications due to alcohol injection (rupture of papillary muscle, lateral or posterior wall infarction) can be avoided. Inclusion criteria for PTSMA include symptomatic patients .NYHA III/CCS III despite drug therapy or with serious side effects ofmedication. Patients with less severe symptoms were only treated if they had particularly high outflow tract gradients (.50 mmHg at rest or 100 mmHg under stress) and documented high-risk factors for sudden cardiac death, or objective reduction of exercise capacity. However, it should be taken into Netherlands Heart Journal, Volume 9, Number 8, November 2001
315
Editorial
consideration that at present there are few data to suggest that a resting gradient >30 mmHg has an impact on the risk for sudden death.8 Patients with exercise-induced syncope and recurrent episodes ofatrial fibrillation with negative impact on clinical symptoms and potential embolic events are candidates for a more active treatment. In patients with mitral regurgitation, pre-interventional echocardiography should be used to clarify whether it is due to systolic anterior motion (SAM) associated outflow tract obstruction or to morphological changes ofthe mitral valve and papillary muscle, which should be treated by surgery.
rA
,i!'
1_1
"'
316
In the meantime, about 1000 patients are known to have been treated worldwide. All groups report a gradient reduction in about 90% of the patients.4'5'9"10-13 The results ofTen Berg and co-workers are comparable, taking into account their learning curve. The introduction of echocardiographic guidance led to an improvement in haemodynamic results despite a reduction in infarcted septal area (estimated by maximal CKrise), number of occluded septal arteries, and need for re-interventions. Thereby, enlargement of the septal scar, with the associated potential negative consequences for left ventricular systolic and diastolic function, can be avoided. ; eThe most significant complications observed to date are hospital deaths, at a rate of up to 4%.13 Our own experience, including our learning curve, showed hospital mortality of 1%. This low mortality is comparable with experienced surgical centres. Hospital mortality predominantly occurred m elderly patients and - as in the series often Berg et al. - during the postinterventional period, which underlines the importance of careful hospital monitoring. Particular attention should be paid to a case report of a death occurring ten days after the intervention as the result of an unexpected trifascicular block, underlining the need for close rhythmological monitoring for several days following the intervention. The most frequent complications are peri- and post-interventional trifascicular blocks at a rate of 60%. In the majority of cases these blocks are only transitory. After the introduction ofechocardiographic guidance, the number of permanent pacemaker implantations due to trifascicular block was reduced from 20-40%4,",'l to
