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To understand the effects of left ventricular outflow tract (LVOT) obstruction on clinical outcome.
To be aware of the treatment modalities available to deal with LVOT obstruction in hypertrophic cardiomyopathy.
To be aware of new developments in non-surgical septal reduction therapy.
Hypertrophic cardiomyopathy (HCM) is an inherited disease characterised by otherwise unexplained hypertrophy of the myocardium. It is transmitted in an autosomal dominant pattern with variable penetrance, with an estimated phenotypic prevalence of up to 1 in 500.1 HCM is a highly heterogeneous disease with varied patterns of hypertrophy. The prevalence of left ventricular outflow tract (LVOT) obstruction in HCM is 20%–30% at rest2 and up to 70% with provocation.3
Basal septal hypertrophy and systolic anterior motion (SAM) of the mitral valve (MV) are the key components to LVOT obstruction in HCM. The septal hypertrophy causes abnormal posteriorly directed flow through the left ventricle (LV).4 5 This flow circulates around the MV and back towards the LVOT, dragging the MV apparatus towards the septum. The MV is proposed to be abnormal as part of the HCM phenotype, with a variety of changes such as longer leaflets, abnormal papillary muscle architecture and anterior displacement of the apparatus. This anatomic predisposition means that the valve is more easily pushed towards the septum by the aberrant flow in the LV. Increased velocity through the LVOT also causes some drag effect pulling the MV towards the septum (the Venturi effect); however, SAM starts before velocities are notably elevated during systole, so this cannot be the sole cause of the anterior movement of the leaflets. The MV moves towards, and in severe cases contacts, the hypertrophied septum. Once mitral–septal contact occurs, the LVOT orifice is narrowed further and greater obstruction to flow develops, resulting in a higher pressure difference. This pressure difference forces the leaflet further against the septum, further narrowing the orifice, exacerbating the haemodynamic abnormalities. This establishes an amplifying feedback loop until systole is complete. The greater the length of time the Anterior mitral valve leaflet (AMVL) is in contact with the septum, the higher the pressure difference.4 Reduced preload can exacerbate dynamic LVOT obstruction in HCM; this is seen in dehydration and a postprandial state when blood is directed to the digestive system.
During SAM of the MV the anterior leaflet may be dragged anteriorly to such an extent that the valve tips fail to coapt. This leads to mitral regurgitation. As the AMVL is pulled anteriorly away from the posterior leaflet the angle of the open orifice directs the regurgitation posteriorly, central or anteriorly directed flow should raise concern over intrinsic MV disease.
Effect of LVOT obstruction on symptoms and clinical outcome
LVOT obstruction has multiple deleterious physiological effects, including reduction of forward cardiac output, mitral regurgitation of varying degrees, load-dependent diastolic dysfunction leading to an increase in LV end-diastolic pressure and coronary flow abnormalities.6 These factors contribute to symptoms of dyspnoea, chest pain, presyncope and syncope.7–9 LVOT obstruction is associated with a greater level of morbidity and mortality within a population of patients with HCM3 10 and now forms part of accepted risk stratification models for sudden cardiac death in HCM.11 Even those without significant symptoms seem to have a worse outcome with untreated LVOT obstruction.12 Removal of LVOT obstruction in symptomatic patients has been proposed to improve prognosis in some observational series; the survival in these cohorts was equivalent to a matched general population without HCM.13 14 These are small studies, and true long-term outcome following alcohol septal ablation (ASA) has not been fully determined. The lack of secure long-term survival data following ASA partly explains why ASA is reserved to treat symptoms only in current guidance. Not all patients with LVOT obstruction will report symptoms and invasive treatment is not indicated in these circumstances.15 16
Treatment of LVOT obstruction
General measures such as avoiding dehydration and weight loss should be discussed with patients. Medications that can exacerbate the LVOT gradient such as nitrates or phosphodiesterase inhibitors should be avoided. The first-line treatment of LVOT obstruction is the introduction of negatively inotropic medications.15 16 If this fails to satisfactorily control symptoms and LVOT gradients, then septal reduction should be considered. This may take the form of surgical myectomy or non-surgical septal reduction.
Beta-blockers are generally used first, despite a lack of clear evidence for efficacy. Propranolol has been shown to have some effect on LVOT gradients.17–19 If beta-blockers are contraindicated or not tolerated, verapamil can be trialled. If symptoms and LVOT gradients persist, then disopyramide can be added. Disopyramide can be effective at reducing LVOT gradients20 21; the treating team needs to monitor for prolongation of QTc interval along with other anticholinergic side effects.
Surgical relief of LVOT obstruction
Surgical myectomy involves removal of myocardium from the basal septum in a limited (Morrow) or extended (Messmer) manner.22 When performed in high-volume centres, the outcomes are excellent with substantial reduction in LVOT gradients in >90%, mortality of <1% and long-term survival comparable to that of the general population.23–25 Outcome from surgical relief of LVOT obstruction is related to volume, and the mortality rate among 6386 patients undergoing myectomy in multiple centres across the USA in 2003–2011 was 5.2%.26
Most operations performed internationally involved myectomy only,25 27 but the approach has the benefit of being able to treat multiple cardiac lesions concomitantly. MV abnormalities are relatively common in HCM, and identification of defects such as direct papillary muscle insertion into MV leaflets, fusion of papillary muscles to the septum, and abnormal chordae attaching to the septum or accessory papillary muscles should prompt a surgical referral.28 29 Patients with intrinsic degenerative MV disease should also be considered for surgical correction rather than a non-surgical approach.
Right ventricular (RV) apical pacing
RV apical pacing can be used in addition to medical therapy when other septal reduction treatments are contraindicated.15 In those with an indication for Implantable Cardioverter Defibrillator (ICD) or a pre-existing dual-chamber device, a short Atrio-Ventricular (A-V) delay can be programmed. Response should be assessed both by echocardiography and clinical assessment for improvement of symptoms. One study suggested older patients (>65) are more likely to benefit from this treatment modality.30
Non-surgical septal reduction therapy
The aim of non-surgical septal reduction therapy (NSRT) is to damage myocardium in the left ventricular basal septum to reduce size and systolic excursion into the LVOT. A successful intervention will reduce interaction with the MV and reduce SAM and therefore LVOT gradients. The predominant approach to this form of treatment currently is ASA. The first procedure was performed by Ulrich Sigwart in 1994 following the observation that balloon occlusion of coronary arteries induced wall motion abnormalities.31 This only had a temporary effect so a more permanent solution was adopted with the injection of intracoronary alcohol to create iatrogenic cell death.32 Those same principles of ASA remain today.
Appropriate patient selection is imperative to the performance of effective and safe ASA. It is generally accepted that patients must have New York Heart Association (NYHA class III dyspnoea to warrant ASA.15 16 There must be a demonstrable LVOT gradient to correct in order for ASA to be effective. The American College of Cardiology Foundation/American Heart Association and European Society of Cardiology (ESC) guidelines state a resting or provoked gradient of ≥50 mm Hg is required for a patient to derive benefit from treatment.15 16 The basal septum should be ≥17 mm (box 1).
Indications for non-surgical septal reduction therapy
Left ventricular outflow tract gradient >50 mm Hg at rest or with provocation
Severe dyspnoea or chest pain (usually NYHA III) refractory to medical therapy
Sufficient septal size to perform procedure safely (usually >17 mm)15
No concurrent cardiac pathology requiring surgical correction
ESC guidelines state the choice of invasive therapy should be decided upon by an experienced multidisciplinary team.15 All patients who do not respond to medical therapy should therefore be discussed at heart team meetings and treatment planned according to local expertise. ASA is generally favoured over surgical myectomy when there is a high predicted operative mortality. Although no restrictions are placed on age of patient, it is generally recommended that it is inappropriate to perform ASA in children.16 A deliberate assessment should be performed to exclude alternative causes of LVOT obstruction such as subaortic ring or abnormal papillary muscle architecture. MV abnormalities are relatively common in HCM.33 When intrinsic MV disease is present, the chosen septal reduction method should be myectomy with valve repair or replacement. MV repair is performed in 11%–20% of myectomy procedures.34 ASA can be used if mitral regurgitation is posteriorly directed and related to SAM, and this often improves after NSRT. Concomitant significant coronary artery disease may prompt a surgical approach as bypass grafting can be performed at operation.
ASA: The procedure
A temporary pacing wire should be sited at the RV apex in those that do not already have a cardiac rhythm management device. Septal pacing must be avoided as early activation of the septum can increase LVOT obstruction. Arterial access is secured and a guide catheter manoeuvred to the coronary arteries. A guidewire is advanced to the septal artery of choice. This may be a sub-branch of a septal artery as septal vessels often supply both the right and left septal myocardium. An over-the-wire balloon is then advanced into the septal artery. Once inflated this then creates a secure, hollow channel from the operator to the target myocardium.
Myocardial contrast echocardiography is used to demonstrate the area of myocardium supplied by the vessel. Contrast is injected into the chosen septal artery with continuous echocardiographic screening.35 36 An obvious opacification of the area of the septum involved in the contact point for SAM will be seen if the artery is the correct choice (figure 1). Multiple projections are required to ensure the correct distribution. If contrast is seen elsewhere, an alternative artery will need to be explored (figure 1).
A small amount of angiographic contrast (0.5 mL) is then injected into the septal artery beyond balloon occlusion to ensure no spillback in to the parent artery or collateral connection to other septal or major epicardial vessels. Once the target artery has been satisfactorily identified, a small volume (1–3 mL) of absolute alcohol is injected slowly in small increments. Analgesia should be given as injection of alcohol can cause some discomfort. Balloon occlusion should be maintained for at least 5 min. A final angiographic image is taken to show the septal branch no-reflow and rule out any unwanted coronary artery damage.
The patient is kept under coronary care supervision for 24–48 hours with the emporary pacing wire (TPW) in situ. If no complete heart block is present at that time, it can be removed. Hospital stay is usually 4–5 days if no complication is observed (although some centres advocate up to 1 week), and this is predominantly to observe for late complete heart block.37
Periprocedural complications of ASA
The most prominent complication associated with ASA is the need for permanent pacemaker (PPM). The risk in large multicentre observations remains around 10%–12%.38–43 Higher doses of alcohol are associated with a higher risk of heart block and subsequent PPM requirement. There is a reduction in PPM implantation with increased operator volume.39 44 A significant proportion of patients with HCM require cardiac rhythm management devices prior to ASA. In the largest case series reported, the Euro-ASA registry, 3.7% already had a PPM and 4.1% had an ICD.43 Patients with long-term pacing seem to have a similar outcome as those without pacing following ASA.41 45
Other periprocedural complications have a significantly lower frequency. Ventricular arrhythmia was seen in 0.6%39 and 1.3%.43 Coronary artery damage is rare, and dissection was reported in 0.9%.39 Ventricular septal defect as a result of ASA is very rare, with only one reported case in the literature.39 Death is a result of the procedure, with rates of 6 in 874,39 2 of 17714 (both in cardiogenic shock prior to ASA), 3 of 45942 and 0 in 465 reported.13
Results following ASA
Patients with HCM with resting LVOT obstruction have a higher mortality than matched patients with non-obstructive HCM.2 The rate of mortality at 30 days in the Euro-ASA study was low (1.2%), and the 7057 patient years of follow-up identified an all-cause mortality rate of just 2.42% per 100 patient years.43 Recent series have suggested that removing LVOT obstruction may improve medium-term survival.13 14 46 47
Symptom and gradient resolution
The Euro-ASA registry represents the largest multicentre series to date (n=1275) and reported an improvement of NYHA status from 2.9±0.5 to 1.6±0.7, and 11% had persisting NYHA class III dyspnoea. LVOT gradient improved from 67±36 to 16±21 mm Hg.43 The North American multicentre series (n=874) reported 78% of patients in NYHA class III prior to ASA, and this improved to 3.9%.39 LVOT gradient improved from 70 to 35 mm Hg, and this is a higher residual gradient than the Euro-ASA registry. Most smaller studies also report a higher residual gradient and persisting symptoms.44 48 49 The Scandinavian multicentre study included 279 patients with similar results, with NYHA III/IV breathlessness reduced from 94% to 21%, and outflow tract gradients falling from 58 to 12 mm Hg.
These studies report the outcomes in those who receive transcoronary alcohol. It is worth noting that 5%–15% of patients forwarded for ASA do not receive alcohol due to restrictions of coronary anatomy.44 50 51
Comparison to myectomy
No randomised trials comparing ASA and myectomy have been performed. It is unlikely one will ever definitively answer which method is superior due to difficulties with patient recruitment, differing morphologies requiring tailored treatment and differing skill levels of operators between centres.52 Meta-analyses of cohort studies have identified no significant difference between resolution of symptoms, sudden cardiac death or long-term all-cause mortality.53 These studies can only provide medium-term data, as ASA has not been available long enough to assess the true long-term outcome. There was a superior gradient reduction postmyectomy and a higher requirement for pacing post-ASA.54–56 Perioperative mortality is greater following myectomy.26
Timing of assessment of ASA outcome and need for repeat procedure
The remodelling of the septum associated with ASA is not immediate. There is hypokinesia of the basal septum following alcohol injection, but the reduction in septal size can take some months. The reduction in LVOT gradient is often not seen during inpatient stay and a full assessment should take place 3–6 months after the procedure.57 A repeat procedure can be considered in those with a persisting gradient, and this was used in 7% of the largest reported cohort to date.43 Surgical myectomy can be performed after unsuccessful ASA,58 and ASA is more rarely performed after unsuccessful myectomy.
Limitations of ASA
Identification of septal artery targets
We get little information regarding myocardium supplied from invasive angiography alone. The process of myocardial contrast injection is essential but still follows an initial selection from angiographic images. The optimum vessel may not be appreciated if it is small or originates from a vessel other than the left anterior descending (LAD).
Some arteries cannot be injected as we are unable to safely occlude the vessel. Accessing the artery with coronary wires can be difficult if many turns need to be negotiated. We cannot introduce contrast or alcohol if the balloon shaft kinks on bends; this kinking will occlude the shaft and prevent injection.
Difficulty controlling infarct size and location
It is difficult to assess the volume of myocardium supplied by a chosen vessel. There is unpredictable tissue dwell time and absorption. The variable run-off of septal arteries is complicated by differential resistance in the distal perfusion beds; most septal arteries have a bifurcation with sub-branches to the right and left ventricular septum. The right-sided branch can drain directly into the RV cavity and therefore has a low pressure run-off; conversely the left-sided branch enters densely packed, hypertrophied myocardium with high resistance. Any fluid injected will therefore preferentially run towards the right side of the septum. The RV septum is a common site for undesirable infarction59 (figure 2). Right bundle branch block is reported in up to 60% of patients following ASA and may represent an underestimate.55 60–62 The right bundle cannot be the primary target in ASA and is unnecessary collateral damage. The volume of alcohol to be delivered can also be restricted by conduction system disturbance.43
These factors contribute to difficulty in controlling the effects of alcohol injection. Some series have reported a loose correlation of alcohol to cardiac enzyme release (as a marker of infarct size),49 and others show no meaningful correlation.44
The demands of precision
In the ideal procedure we seek to impact a very small target zone and need very precise localisation.
New thinking in non-surgical septal reduction
Lessons learnt from traditional ASA series
Dose of alcohol versus outcome and risk of PPM
Recent trends have been to inject 1–2 mL alcohol based on registry studies, and a rare randomised controlled trial in HCM compared a 1 mL versus 3 mL dose. No significant difference in outcome was observed between the high-dose and low-dose injections.49 The recent Euro-ASA registry suggested a higher dose of alcohol has a greater effect on LVOT gradients; a dose of <1.5 mL fails to make a significant impact on LVOT gradient in 20% of patients, whereas a dose of >3 mL fails to impact gradient in 10% of patients. Higher doses of alcohol are inevitably associated with an increased risk of PPM.43 44 It is worth considering other predictors of heart block when deciding dose of alcohol to be injected, and these include pre-existing first-degree AV block, left bundle branch block (LBBB), lack of use of myocardial contrast echocardiography, injection of alcohol by bolus rather than infusion, injection of more than 1 septal artery and female sex.63
Predictors of outcome and patient selection
All-cause mortality following ASA has been linked to preprocedural systolic dysfunction, increased septal thickness, NYHA class and higher age.13 14 39 43 All-cause mortality is also independently associated with a residual LVOT gradient after ASA.43
Predictors of successful resolution of LVOT gradient with ASA are reported to include lower baseline LVOT gradient, modest basal septal hypertrophy (<18 mm) and older age (>65).64
Survival and risk of ventricular arrhythmia post-ASA
The early fears regarding proarrhythmic risk from the iatrogenic scar created by ASA do not appear to have been substantiated. There is conflicting evidence, but most large case series report no increased risk of sudden cardiac death (SCD), ventricular arrhythmias or appropriate ICD therapy,13 14 43 46 47 65–67 while some smaller series numbers claim an increased risk of ventricular arrhythmia.68 69 ten Cate et al reported a higher incidence of mortality and ICD therapy in their series of 91 patients undergoing ASA; it is worth noting, however, that inpatient mortality was higher (there were two on-table deaths due to tamponade and intractable ventricular fibrillation (VF)). Procedural technique was also different with faster speed of injection of alcohol and higher doses than reported in most series (mean 3.5 mL, with an average of 4.5 mL in the first 25 patients).68
There is a learning curve associated with performing ASA.70 Given the low numbers of patients undergoing the procedure, expert centres with high-volume operators should be responsible for ASA. Currently only 3 of 17 centres performing ASA in the UK are registering more than five procedures per year.71 Ninety-two per cent of 245 institutions in the USA performed less than seven procedures per year in the period 2003–2011.26 European and American guidelines suggest operators should be performing >10 ASA procedures per year15 and have a total procedural volume of >20 or work in a centre with a total volume of >50.16 The development of regional centres of excellence should be encouraged to ensure adequate operator volumes to optimise outcomes.
Improving infarct location with ASA
Those with significant persisting gradients after ASA often have inaccurate infarct location.59 72 Infarction that is too apical, predominantly in the RV septum or too inferior in the septum will not have any meaningful effect on LVOT haemodynamics (figure 2).
Transthoracic echocardiography (TTE) is routinely used to localise myocardial contrast following arterial injection. There are significant difficulties in using TTE. The images must be taken on-table, with the patient in a supine position. There are further logistical difficulties in the catheterisation lab. These factors can result in substandard image quality.
Intracardiac echocardiography (ICE) allows excellent images of the SAM–septal contact point, but its use has been hampered by difficulties in visualising myocardial contrast accurately.73 74 Power Doppler imaging shows promise in visualising the target area following myocardial contrast injection75 and warrants further exploration. Despite these efforts to improve periprocedural echocardiographic guidance, the imaging of choice in most units is still TTE.
CT angiography to guide ASA
Invasive angiography provides us with information on the course and lumen of the coronary arteries only. We rely on the use of myocardial contrast echocardiography (MCE) to describe the interaction with the myocardium. CT angiography offers information on the path of the arteries but also the myocardium they supply. Preliminary work exploring feasibility of the use of CT to guide ASA was encouraging.76–78 Single-centre experience of CT angiography prior to ASA been reported for 21 consecutive patients.79
The target myocardium at the SAM–septal contact area is identified using a short section of systolic imaging. This myocardium is examined in diastole to identify a segment of its arterial branch supply. The vessel is tracked back to its artery of origin (figure 3). This target artery is analysed and marked in CT software to create a coronary angiogram ‘map’. The coronary map is rotated through horizontal and vertical planes to allow optimal visualisation (figure 4). The projections are noted and used as the ‘working views’ in the catheterisation laboratory.
A septal artery can be seen on CT to supply both the RV and LV septum in 85% of cases; these are very different environments with implications for variable ‘run-off’ for any injected fluid. Traditional teaching for alcohol ablation is to site a coronary balloon at the ostium of the septal artery and inject beyond, allowing fluid to travel to either the right or left ventricular septum.80 81 This results in echocardiographic contrast highlighting the RV (figure 2). The vessel is dismissed as serving an incorrect area of myocardium. Engaging the sub-branch of the septal vessel that supplies the LV myocardium results in target myocardium being highlighted. An artery that previously was dismissed now becomes an ideal target. The importance of considering sub-branches was first discussed in 199836; the use of CT allows a full anatomical plan to propose which branches should be engaged prior to entering the catheter lab.
The parent vessel for the appropriate septal artery is not always the LAD.80 These patients may be dismissed as not having an appropriate artery by operators who may not consider other parent arteries. The approach to identifying the correct artery is reversed in CT. A target septal artery originating from the circumflex was seen in 5% and from the diagonal in 2% using CT.
Adopting CT guidance for ASA has improved the success at first procedure from 59% to 85% (p=0.02). The rate of RBBB has reduced from 62% to 13%, and this suggests more accurate infarction in the left ventricular side of the septum rather than the right. This is supported by Cardiac Magnetic Resonance studies.
CT planning requires further investigation, larger series and adoption in multiple centres to validate its role in planning ASA. This is still an emerging technique.
Alternative methods of NSRT
Although alternative methods of NSRT have been proposed, the numbers treated so far are small, and they are not yet considered to be of similar utility to ASA. The following methods are largely performed in research settings or in patients unsuitable for traditional methods of septal reduction.
Endocardial radiofrequency ablation of the interventricular septum
ASA relies on coronary anatomy to provide access to target myocardium, and this is a limitation. Up to 15% of patients have no septal vessel suitable for injection.50 51 82 Endocardial radiofrequency (RF) ablation can bypass this reliance by damaging the basal septum from the LV endocardial surface rather than via coronary arteries.83–88
Lawrenz et al85 reported the first series of 19 adults, 8 of whom had ineffective ASA due to inappropriate coronary anatomy. Ablation was performed from the RV cavity in 10 patients and LV cavity in 9. Follow-up imaging showed a small reduction in septal width, 22.6–21.4 mm. This is in contrast to ASA where a more marked change in septal width in diastole is seen. Despite a modest effect on septal width, a reduction of resting gradients of 77–27 mm Hg and provoked gradients of 158–64 mm Hg was observed. NYHA status reduced from a mean of 3.0–1.7.85 Similar results have been seen in other adult series in smaller numbers and also in paediatric populations.86 87
Most patients are offered RF ablation when alternatives have been exhausted; this usually means they are not candidates for surgery due to high risk of complication. Carrying out RF ablation at an advanced stage of disease is associated with increased risk. Of the total of 79 patients reported in these series, two deaths were reported, one due to paradoxical increase in LVOT gradients post procedure and one resulting from retroperitoneal haemorrhage associated with femoral artery access. Paradoxical increase in LVOT gradient was observed in the paediatric population due to tissue oedema. To reduce the effect of tissue oedema, empirical periprocedural dexamethasone has been employed; its efficacy is not known due to small number of patients.89
Although the principle of using RF is constant throughout these series, the approach to identifying the target for energy delivery differs somewhat. The use of electroanatomic mapping systems was consistent in all reports and offers the prospect of detailing and avoiding specialised conduction tissue to reduce the need for PPM. The use of ICE and CARTO electrical merging systems has been proposed to identify the target myocardium at the SAM–septal contact point with increased accuracy (figure 5).89 RF energy can then be delivered specifically to the SAM–septal contact point with increased accuracy of cell death (figure 6).
Reduction of septal thickening in systole is proposed to be responsible for the reduced gradient. This akinesia of the basal septum prevents narrowing of the LVOT in systole and alters flow dynamics so less blood is directed posterior to the MV, therefore reducing push and drag forces. This results in less SAM of the MV and therefore less obstruction. The flexibility of RF ablation appeals to physicians dealing with hypertrophic obstructive cardiomyopathy (HOCM), and early results are comparable to results of early ASA series.90 With a clear learning curve for operators performing ASA,91 this indicates significant promise for this procedure.
Alternative transcoronary methods of NSRT
The injection of cyanoacrylate ‘glue’ into a vessel supplying the target myocardium has been performed in a series of 27 patients.92 The immediate polymerisation of the glue occludes the septal artery and creates a localised infarct. A third of these patients required injection into more than one septal artery. LVOT gradients reduced from 78 to 21 mm Hg, and 15% had a significant persisting gradient. No patient required PPM.
The success of coil embolisation of non-coronary arteries led to the concept being adapted to septal reduction.93 One feasibility study reported outcomes in 20 patients. LVOT gradients reduced from 80 mm Hg to 36 mm Hg, and 18/20 found some improvement in symptoms.94 One person died during admission from a confirmed ventricular septal defect postprocedure. No patient required implantation of a pacemaker.94
The injection of microspheres to occlude septal arteries has also been explored. Early experience with polyvinyl alcohol foam particles was reported in 2004 with encouraging initial results. Gradients reduced from 83+/−32 mm Hg to 31+/−35 mm Hg with improvement in NYHA from 3.3 to 1.3. There were minimal complications in these 18 patients.95 There has been only low-level sporadic interest in this method since then.96–98
Limitations of ischaemia alone
The extensive network of septal arcades and collateral supply may restrict the use of ischaemia alone as a method of delivering sufficient myocardial infarction.99 100 As one artery is occluded the myocardium can recruit some vascular supply from the arcade or nearby collateral supply. Using these methods is appealing in those with septal collateralisation to distant vessels to avoid alcohol escape and unwanted infarction. The delivery of alcohol or RF energy causes direct myocardial injury and may provide a more definitive result in the long term.
LVOT obstruction is associated with greater morbidity and mortality in HCM. In appropriately selected patients NSRT provides symptomatic relief for the majority of patients and might offer some prognostic benefit in the medium term. ASA is the most frequently used method of NSRT, and the major risk of ASA is the need for pacemaker in 10%–12%. ASA cannot be performed in 5%–15% of patients and does not resolve LVOT gradient and symptoms in all. Studies to improve ASA outcomes centre on improving infarct location with better periprocedural imaging, better patient selection and correct dosing of alcohol. Alternative transcoronary methods of delivering infarct such as glue and microsphere injection have been explored in low numbers but remain experimental techniques. RF ablation provides an option for delivering myocardial damage that is independent of coronary anatomy and is emerging as an attractive therapeutic option.
Left ventricular outflow tract (LVOT) obstruction increases morbidity and mortality in hypertrophic cardiomyopathy.
Removal of LVOT obstruction improves symptoms and might improve prognosis.
Alcohol septal ablation provides symptomatic relief for 80%–90% patients when performed effectively.
Those with persisting gradients often have inaccurate iatrogenic infarction; better periprocedural imaging can improve infarct location and clinical outcome.
Some patients cannot receive transcoronary alcohol due to anatomical limitations: radiofrequency ablation of the septum shows promise in treating these patients.
There does not appear to be an increased risk of sudden cardiac death associated with alcohol septal ablation.
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Contributors RMC and RHS were equal authors in the compilation and review of the article.
Competing interests None declared.
Provenance and peer review Commissioned; externally peer reviewed.