Surgery for Obstructive Hypertrophic Cardiomyopathy

Surgery for relief of obstruction in hypertrophic cardiomyopathy is reserved for patients who have failed medical management. Such patients have persistent left ventricular outflow tract gradients and symptoms of dyspnea and chest pain, or are intolerant to medication.

Medical management and assessment of risk of sudden death: It has long been recognized that the majority of HCM patients are, in fact, not obstructed and are thus not surgical candidates, yet may have symptoms and be at risk for sudden cardiac death. Symptoms in non-obstructive patients are caused by LV diastolic dysfunction and myocardial ischemia in the absence of large vessel coronary stenoses. Ischemia is due to narrowing of the intramural small coronary arteries and arterioles in the face of severe hypertrophy.

Treatment of symptoms in non-obstructive HCM is parmacologic. Verapamil has been shown to reverse perfusion defects. Alternately beta-blockers may be given to prolong diastolic filling time. Dual chamber pacing has been applied in a rare subgroup with hyperdynamic LV function and complete systolic cavity obliteration/emptying.

A most important treatment focus for HCM patients, regardless of the presence of obstruction, has been an attempt to prevent sudden arrhythmic cardiac death. Though the annual risk of sudden death in unselected HCM patients is 1%, there are subgroups of patients with higher annual risk of dying suddenly. Risk factors can be identified that predispose young patients to sudden arrhythmic death. The presence of one or more of these risk factors may prompt referral for a prophylactic implantable cardioverter-defibrillator. A registry of patients implanted with ICDs showed appropriate potentially life-saving shocks delivered at an annual rate of 4.5% per year.

Obstructed patients have more prominent symptoms and the murmur often brings them to medical attention. Systolic anterior motion with mitral-septal contact is the most common cause of obstruction, though less common variants of mid-ventricular obstruction occur as well. Obstruction adds to the previously described HCM substrate the additional burdens of higher left ventricular systolic pressure, lower coronary perfusion pressure, contraction-load impairment of relaxation and mitral regurgitation. Maron and others have reported an increase in annualized death rate in obstructed patients. Most patients with obstruction will respond to medical therapy and only a minority will require intervention for refractory obstruction. Beta-blocker is tried first. Though these agents blunt exercise-related increase in gradient they do not reduce high resting gradients. Disopyramide is considered by many the single most efficacious agent in reducing obstruction; it had been shown to reduce gradient, improve symptoms and prolong exercise time. It is most often used in combination with beta-blockade. Negative inotropes decrease gradient by decreasing left ventricular ejection acceleration and the hydrodynamic force on the mitral leaflet. This delays mitral-septal contact and the duration that the amplifying feedback loop cycles in systole, reducing the final gradient. Verapamil is also used for obstruction; however, it is less predictable and may be associated with cardiac side effects because of vasodilation.

Those patients who fail medical management may be considered for surgical intervention. After surgical relief of obstruction the great majority of patients have striking, prolonged relief of symptoms and improvement in quality of life. The relatively safe and efficacious results from surgery form the standard against which newer interventions to relieve obstruction are judged.

We discuss the evolution of surgical procedures to relieve obstruction and review modern surgical approaches. Echocardiography has become central to understanding the complex phenomenon of obstruction, and for clinical diagnosis, operative planning and intra-operative management.

The pertinence of pathophysiology: A difficulty of operations for obstructive hypertrophic cardiomyopathy has perhaps been due to misunderstanding the pathophysiology of obstruction. Appreciation of the mechanism of obstruction in HCM has evolved with improvement in real time cardiac imaging, in particular, echocardiography.

Historical perspective

Initial notions: concept of outflow tract obstruction due to a muscular sphincter- myotomy and limited myectomy.
Brock’s first reports of muscular hypertrophy of the LV outflow tract (LVOT) led to the idea that incision myotomy might interrupt the septal muscle bundles of a sphincter-like contraction ring surrounding the outflow tract, and relieve obstruction. Brock’s notion was that LVOT obstruction was similar to dynamic right ventricular infundibular narrowing. Hence, in many early papers the condition was named muscular subaortic stenosis. Cleland and others began the surgical treatment of obstructive HCM with myotomy or limited excision myectomy through the transaortic approach in 1958. Reductions in gradient were observed in the majority of myotomy patients; but, in-hospital mortality was high and in some patients obstruction persisted. Morrow’s modification, the wider more extensive trough myectomy, consistently decreased obstruction and has become the standard operation. See Figure 1.

Trough Myectomy of Morrow
View larger version (40K):

Figure 1. The trough myectomy of Morrow

Flat, narrow, malleable retractors are placed over the mitral valve to protect leaflet and chordae. External pressure is placed on the right ventricle, and thus the septum, to push the septal bulge into view. A knife with a bent handle is used, to facilitate exposure of the septal bulge.

Recognition of systolic anterior motion and mitral-septal contact: the trough myectomy of Morrow.
The participation of the anterior mitral leaflet in dynamic obstruction was first seen at cineventriculography and at autopsy. After echocardiography it became clear that systolic anterior motion of the mitral valve (SAM) with mitral-septal contact was the cause of obstruction in most patients with obstruction. For many years SAM was thought to be due to the subaortic septal bulge narrowing the outflow tract with consequent high velocity flow resulting in a Venturi effect, a local underpressure. This low pressure was thought to suck the mitral valve anteriorly into the septum. With this model in mind, surgical resection focused on the subaortic septum to increase the size of the outflow tract to reduce Venturi forces. This sort of resection may be inadequate to abolish SAM because the magnitude and importance of the Venturi forces are much less than previously thought.

Operations tailored to reduce flow drag, the pushing force of flow: separating the inflow and outflow portions of the left ventricle:
Echocardiographic evidence indicates that drag, the pushing force of flow is the dominant hydrodynamic force on the mitral leaflets. In obstructive HCM the mitral leaflets are often large and are anteriorly positioned in the LV cavity. Jiang, Levine and co-workers observed anterior position of the papillary muscles in the left ventricular cavity. At surgery the hypertrophied papillary muscles are attached onto the anterior LV wall and are often fused to each other. Anterior position of the papillary muscles leads to an anteriorly positioned mitral coaptation plane. The mid-septal bulge protrudes posteriorly and laterally and aggravates the malposition of the valve relative to outflow. See Figure 2.

pushing force of flow
View larger version (60K):

Figure 2. The pushing force of flow

Top: Early systolic ejection flow relative to the mitral valve in the apical 5 chamber view. In obstructive HCM the mitral leaflet coaptation point is closer to the septum than normal. The protruding leaflets extend into the edge of the flowstream and are swept by the pushing force of flow towards the septum. Flow pushes the underside of the leaflets (arrow). Note that the midseptal bulge redirects flow so that it comes from a relatively lateral and posterior direction; on the 5 chamber view, flow comes from “right field” or “one o’clock” direction. This contributes to the high angle of attack relative to the protruding leaflets. Also note that the posterior leaflet is shielded and separated from outflow tract flow by the cowl of the anterior leaflet. Venturi flow in the outflow tract cannot be lifting the posterior leaflet because there is little or no area of this leaflet exposed to outflow tract flow. Venturi forces cannot be causing the anterior motion of the posterior leaflet. MV=mitral valve, OT=outflow tract, SB=septal bulge.

Bottom: Two apical 5 chamber echocardiographic views of one patient with obstructive HCM are shown; resting gradient = 54 mm Hg. Top: 2-D shows the protruding mitral leaflet on the first frame in systole that showed mitral coaptation. Arrowhead points to mitral valve. MV=mitral valve, OT=outflow tract, SB=septal bulge. On the next sequential frame there was fully developed SAM. Bottom: shows the same view, of the first systolic frame with color flow. Color flow is seen lateral to the leaflet tips (arrow). Color flow velocity is quite low. On the next frame there was aliased high velocity flow. These images show the event graphically drawn in left panel. Early in systole flow pushes the underside of the mitral leaflets and pushes them into the septum.

The mid-septal bulge redirects outflow direction so that it comes from a lateral and posterior direction. The abnormally directed outflow gets behind and lateral to the enlarged mitral valve, catches it, and pushes it into the septum. There is crucial overlap between the inflow and outflow portions of the left ventricle.

As SAM progresses in early systole the angle between outflow and the protruding mitral leaflet increases. A greater surface area of the leaflets are now exposed to drag which amplifies the force on the leaflets - drag increases with increasing angle relative to flow. An example of this is a widely opened door in a drafty corridor: the door starts by moving slowly and then accelerates as it presents a greater surface area to the wind and finally it slams shut.

SAM begins before systolic ejection in two thirds of patients, before high velocity occurs. SAM onset is a low velocity phenomenon. It begins at a velocity no different from velocities measured in normals. Hence, the Venturi force cannot be the main force that initiates SAM. A summary of evidence for the current altered understanding of the hydrodynamic cause for SAM is presented in figure 3.

SAM and myectomies
Figure 3.

Evidence in the debate between Venturi (lift) and drag (pushing) force as the dynamic cause for SAM.

SAM has been described as anteriorly directed mitral valve prolapse. This analogy has merit; in both conditions the mitral valve is often large and is pushed by flow from its normal systolic position, resulting in mitral regurgitation.

Three features are necessary for SAM, mitral-septal contact and obstruction: anterior position of mitral coaptation; an angle of flow onto the mitral valve such that flow gets behind the mitral valve (angle of attack) and chordal slack. All efforts are focused on abolishing SAM because once mitral-septal contact occurs, especially if it occurs early in systole, failure is assured. This is because obstruction begets more obstruction. Once the mitral valve touches the septum and a narrowed orifice occurs, the pressure difference across the orifice becomes the new hydrodynamic force across the mitral leaflet. This pressure difference pushes the leaflet further into the septum, narrowing the orifice further and an amplifying feedback loop is established that cycles for much of ejection. The longer in systole that it cycles, the higher the gradient. Overall, obstruction in HCM may be understood as a flow drag triggered, time-dependent, amplifying feedback loop.

Surgical approach

An inadequate operation focused on widening the outflow tract and lowering Venturi forces is shown in the second panel of figure 4.

Surgical Seperation
View larger version (32K):

Fig 4. Sugical separation of left ventricular inflow from outflow in obstructive HCM: Extended myectomy and papillary muscle mobilization

Top: Line drawing of outflow relative to the mitral valve in early systole. Note the anterior position of the mitral valve coaptation. The prominent mid-septal bulge redirects outflow so that it comes from a relatively posterior direction, catching the anteriorly positioned mitral valve and pushing it into the septum.
Second: After subaortic septal resection. The subaortic septum has been resected, but only down to the tips of the mitral leaflets. Flow is still redirected by the remaining septal bulge so that it comes from a posterior direction. It still catches the mitral valve; SAM persists, as does obstruction.
Third: The septal bulge below the mitral leaflet tips has been resected, an extended myectomy. Now, flow tracks more anteriorly and medially, away from the mitral leaflets.
Bottom: Mobilization and partial excision of the papillary muscles is added to extended myectomy. The mitral coaptation plane is now more posterior, explicitly out of the flow stream.

With this resection the residual mid-septal bulge still redirects flow posteriorly: SAM persists because flow still gets behind the mitral valve. Thus, resection of the subaortic bar plays very little role in relieving the obstruction and may cause a higher risk of creating a ventricular septal defect because the septum here tends to be relatively thin. With the heart arrested, and the ventricles collapsed, the weight of the right ventricle on the septum gives the appearance of a septal bulge, just under the annulus of the aortic valve. Unfortunately, this easily accessible septum is not the area that creates the obstructive physiology. It is only when the deeper portion of the septal bulge is resected that flow is redirected medially and anteriorly away from the mitral valve, abolishing SAM. With this in mind, a modification of the Morrow myectomy termed extended myectomy, mobilization and partial excision of the papillary muscles has been performed in Aachen since the 80’s and at New York University Medical Center since 1998. The way this modification helps relieve SAM pathophysiology is important.

In extended myectomy the septal bulge is resected further, to the base of the papillary muscles. The strategy of this operation can be paraphrased as “take out as much of the septal bulge as one safely can”. The shape of the myectomy differs from Morrow’s resection. The classic resection usually results in the thinnest portion of the septum below the aortic valve and extends just below the mitral valve tips. The extended myectomy extends well below the mitral valve tips, and leaves a more even distribution of the septal thickness, and spares 3-5 mm below the aortic valve to avoid VSD and aortic regurgitation. Such a resection places a premium on resection of the mid-septal bulge, allows flow to track anteriorly and medially away from the mitral valve, minimizing drag on the mitral leaflets. See figure 4, third panel.

Technique: The patient is placed on cardiopulmonary bypass with a single 2 stage venous cannula and a coronary sinus cannula for retrograde cardioplegia. The left ventricle is vented with a 28F catheter from the right superior pulmonary vein-left atrial junction. The cross clamp is applied and antegrade and retrograde cardioplegia are delivered. We routinely measure septal temperature to assure adequate cooling of the marked hypertrophy.

The surgical approach for the relief of HCM obstruction may be divided into three considerations:

Extended septal myectomy: After the aortotomy is done, stay sutures of 4-0 polypropyline are placed along the proximal edge of the aortotomy for retraction. We do not place any retraction sutures on the leaflets themselves since this may lead to damage. Rather, small, flat bladed leaflet retractors are used to displace the leaflets towards the aortic wall and out of the way. As described by Messmer, a trefoil hook retractor with a long handle is then introduced deeply into the ventricular cavity and imbedded into the farthest portion of the septal bulge with an orientation between the right coronary ostium and the right and left coronary commissure. See figure 5.

trefoil hook
View larger version (32K):

Figure 5. Trefoil hook to grasp the apical portion of the septal bulge

Stabilizing the position of the septal bulge with a trefoil hook retractor makes myectomy results more predictable and lessens the chance of ventricular septal defect.
The trefoil hook retractor with a long handle is introduced deeply into the ventricular cavity and imbedded into the farthest portion of the septal bulge with an orientation between the right coronary ostium and the right and left coronary commissure . When drawn forward, a larger bulge in the septal muscle is created which lends itself to resection. The trefoil hook serves two purposes. It defines in the anterior-posterior direction the point towards which the #15 scalpel blade is pushed and it stabilizes the muscle to be resected and prevents it from being pushed out and away from the blade and surgeon. Two parallel incisions are made into the bulge with the knife directed towards the prongs of the hook; the first is below the right coronary ostium and the second below the left and right coronary commissure.

When drawn forward, a more prominent bulge in the septal muscle is created which lends itself to resection. The trefoil hook serves double duty: First, it defines the point towards which the #15 scalpel blade is pushed. Second, it stabilizes the muscle to be resected and prevents it from being pushed out and away from the surgeon. Two parallel incisions are made into the bulge with the knife directed towards the prongs of the hook; the first is below the right coronary ostium and the second below the left and right coronary commissure. The two incisions are then connected by an incision between the two made roughly 3 mm below the aortic annulus and the muscle mass is removed by extending the trough gradually into the LV lumen. We find it most important to remove as much as possible in the first attempt.

After the first muscle mass is removed, additional resection is performed after careful digital palpation of the septum from within the ventricular cavity. The myectomy trough is extended to the base of papillary muscles. A rim of muscle just under the aortic valve is left, to minimize the risk of a ventricular septal defect, aortic valvular insufficiency, and heart block. This area is not involved in the pathogenesis of SAM. The area of the AV node is also spared to avoid heart block.

Mobilization and partial excision of the papillary muscles: This approach severs the abnormal connections that bind the papillary muscles to the anterior wall which allows the mitral valve to assume its more normal posterior position, explicitly out of the outflow tract and its drag forces. Extended septal myectomy is necessary to gain exposure to the base of the papillary muscles that are otherwise obscured by the septal bulge. After the septum is resected, it is now possible to see the abnormal connections that bind the papillary muscles to the anterior wall. The leaflet retractors that were earlier positioned just under the aortic valve are now pushed deeper into the ventricular cavity and the anterior papillary muscle is gently grasped with long, broad toothed forceps and pushed medially. A #15 blade is again used to divide the abnormal attachments between the papillary muscle and the anterolateral ventricular wall and a portion of the junction of the papillary muscle and lateral wall is also resected either with the #15 blade or with long Potts scissors. The same is done for the posterior papillary muscle. Often the papillary muscles are so thick that grasping them is difficult and retraction medially impossible. We have found it simple in these instances to resect this area with a long, double action bone rongeur. In these patients, the muscles involved are so thick, that with a medium sized rongeur, it is unlikely one will resect too much. Similarly, all connections that bind the papillary muscles together are resected.

When this resection is completed, the papillary muscles, with their diameters reduced, are separated from the wall and from each other (figure 4, fourth panel). This allows the papillary muscles to assume a more posterior position in the left ventricle. This resection does not appear to compromise papillary muscle function in respect to mitral valve closure. We believe that this complete mobilization is a most essential step in the relief of SAM.

Anterior Mitral Leaflet Plication: After the two procedures described above, attention is then directed to the anterior leaflet of the mitral valve. The mitral valve is often enlarged both in area and length in obstructive HCM especially in its relationship to the small left ventricular cavity. In selected patients with large floppy valves we plicate the anterior mitral leaflet with a modification of the technique of that described by McIntosh and Cooley and their co-workers. Plication of the native anterior mitral leaflet decreases the size of the leaflet and attendant drag forces and reduces chordal and leaflet slack. See figure 6.

longitudinal plication
View larger version (32K):

Figure 6. Longitudinal plication of the anterior mitral leaflet

Left: Anterior leaflet plication viewed from the aortotomy. Interrupted sutures are placed in the anterior leaflet starting at the distal portion of the leaflet, near its attachment with the chordae, with additional sutures placed longitudinally towards the annulus depending on changes in mobility. Reproduced from McIntosh CL et al, Circulation 1992;86:II60-7.

Right: Another depiction of longitudinal anterior leaflet plication. Here sutures are placed more centrally in the leaflet, still in a longitudinal orientation.

Plication is applied using the criteria of McIntosh when patients are judged to be at increased risk for a suboptimal hemodynamic result due to residual SAM because of increased mobility, size or length of the anterior mitral leaflet.

We prefer to perform plication by placing three to four fine mattress sutures of 5-0 polypropylene in a horizontal rather than longitudinal orientation using the fibrotic area on the leaflet for the location of the horizontal line. See figure 7.

longitudinal plication
View larger version (32K):

Figure 7. Horizontal plication of the anterior mitral leaflet to reduce leaflet length and leaflet/chordal slack.

The fibrotic area on the anterior leaflet that is the contact point between the leaflet and the septum is identified. Plication is performed by placing three to four fine mattress sutures of 5-0 polypropylene in a horizontal rather than longitudinal orientation though the fibrotic area of the leaflet. The width of the mattress sutures is dictated by the degree of redundancy of the leaflet and mobility when assessed by the nerve hook. This modification more directly reduces leaflet-chordal slack and excess length than a suture line in the longitudinal orientation. Abbreviations: Ao=aortic root, AML=anterior mitral leaflet; LMO=left main coronary ostium; NCL=non-coronary aortic leaflet.

The width of the mattress sutures is dictated by the degree of redundancy of the leaflet and mobility when assessed by the nerve hook. This modification more directly reduces leaflet-chordal slack and excess length than a suture line in the longitudinal orientation. We have performed this technique in four of our last eleven patients. There has been no incidence of significant mitral insufficiency and we feel this adjunctive procedure has significantly contributed to preventing SAM and post-operative outflow tract gradient.

In the series from Aachen experience with extended myectomy and mobilization and partial excision of the papillary muscles in 58 patients there were no perioperative deaths. Nor did any patient have postoperative SAM, gradient, significant mitral regurgitation or ventricular septal defect.

Papillary muscle mobilization is analogous to the sliding leaflet modification of mitral anuloplasty procedures: both modifications result in a posterior mitral coaptation plane that prevents SAM. Indeed the sliding leaflet mitral valve repair added to myectomy has been reported in rare cases of obstructive HCM. Placement of an annuloplasty ring could prove problematic since rings may displace the mitral valve anteriorly.

Mitral Valve Replacement: Cooley and others have reported on mitral valve replacement to abolish SAM. While this is hemodynamically successful, the patient is burdened with a prosthetic valve and its life-long risks of valve failure, embolism, infection and warfarin-induced hemorrhage. In these series there was a significant cumulative incidence of prosthetic thrombosis and valve failure though few of these patients had the benefit of the newer mechanical mitral valves. Sparing the native mitral valve is the preferred route.

In some patients however, mitral valve replacement is sometimes necessary. Structural abnormalities of the mitral valve may be identified with echocardiography, like prolapse or valvular calcification with immobility, that would cause significant mitral regurgitation post-operatively and thus require mitral replacement. A central or anteriorly directed mitral regurgitation jet is a clue to the presence of structural mitral regurgitation. In the absence of structural mitral regurgitation, septal myectomy with abolition of SAM markedly decreases mitral regurgitation.

Surgical indications and results: Patients with symptoms refractory to medication, and obstruction either at rest or with provocation, are generally referred for surgery, which is considered the gold standard for intervention because of its long successful track record. In publications of results of myectomy from 1987 to 1999, mortality within one month of operation ranged from 0 to 6%. Survival of patients operated in the last 10 years have improved. In a series with 519 patients reported by Schulte and co-workers early mortality was 1.9% in patients operated on within 10 years of publication; other centers report no early mortality. Survival at 5 years has ranged from 85-93% and survival at 10 years from 70-88%. In the large series reported by Schulte, 10 year cumulative survival was 88%. Survival, both short and long-term is better in patients who just have myectomy as compared to those who also require CABG or valve replacement. Postoperative resting gradient ranged from 4.5 - 16 mm Hg, excellent relief of obstruction, with parallel improvement in symptoms and NYHA classification. Need for permanent pacemaker for heart block was low, ranging from 0 – 10%. Ventricular septal defect ranged from 0-2%. After relief of obstruction the great majority of patients have prolonged relief of symptoms and improvement in quality of life. The relatively efficacious results from surgery form the standard against which newer interventions to relieve obstruction are judged.

Non-surgical Interventions to Relieve Obstruction. In recent years two alternatives to surgery have been advanced. The main benefit of these interventions over surgery is avoidance of sternotomy and cardiopulmonary bypass. The first, DDD pacing with short AV delay to assure complete ventricular paced activation has been shown to reduce resting gradients by approximately 50%. However, patients are left with residual gradients of 30-48 mmHg on average, generally higher than that found after successful surgery. There have been two randomized crossover trials of DDD pacing that have confirmed the beneficial effect on gradient, but could show no quantifiable improvement in exercise capacity. Only in the subgroup of patients >65 years did a higher proportion accrue a benefit of both reduction in symptoms and increase in exercise capacity. Both studies showed that in addition to gradient reduction, pacing had a placebo effect as well. Thus, pacing cannot be considered a primary treatment for obstructive HCM. Nevertheless, DDD pacing is still applied in patients refractory to medication who are elderly, have contraindications, or do not want surgery. A minority have individual, and currently, unpredictable substantial clinical benefit. An additional benefit of pacing is the opportunity (especially in the elderly) to give more negatively inotropic medication to patients now protected against bradycardia.

Alcohol ablation of the septum, a percutaneous catheter-based method to decrease septal thickness by therapeutic infarction was introduced in 1995. After a small balloon catheter is placed into a proximal septal artery, it is inflated and a small amount of echocardiographic contrast is injected into the target septal perforator to assure that the septal site of mitral-septal contact is supplied by the selected vessel. As many as 7% of initially selected vessels are abandoned because contrast is seen in non-septal structures such as the papillary muscles, LV free wall or right ventricle. After occlusion of a septal perforator by a small balloon to prevent back leakage, 1-4 cc of absolute alcohol in injected into the distal perforator. The balloon is left inflated for 5 – 10 minutes to prevent back leakage of alcohol. Patients experience chest pain and modest myocardial infarction with CPK elevations.

Cohort studies have shown sustained reduction in left ventricular outflow gradients, improvement in symptoms and exercise capacity. Myocardial contrast echo has resulted in more effective gradient reduction and a lower permanent pacemaker rate. There have been 2 comparisons of septal ablation and surgical myectomy. Both of these studies were non-randomized comparisons. One study matched age and gradient in an attempt to make groups comparable. Gradient reduction and symptom relief was similar with the 2 treatment modalities. Requirement for permanent pacemaker was higher in the ablation group, 22 vs. 2%. In the other study patients were selected for alcohol ablation if they were older or had other co-morbid conditions. Follow-up pressure gradients were lower in the surgically treated patients and need for permanent pacing was again greater in the ablated group.

Mechanism of ablation benefit: Flores-Ramirez found that the immediate post-procedure reduction in gradient is caused by an immediate reduction in left ventricular ejection acceleration, caused the direct negative inotropic effect of the septal infarct and perhaps by left ventricular dysynergy from RBBB. Immediately after alcohol ablation peak LV ejection acceleration decreased 39%; reduced acceleration was still present six months later, 33%. This is very similar to the 36% reduction in acceleration seen after medication that abolishes gradient. The mechanism of early gradient reduction after ablation is similar to that of medication: reduced LV ejection acceleration.

Six weeks and 6 months later, decreased acceleration persists, but now in addition, septal thinning and increase in the LV outflow tract diameter is seen, very similar to surgical results; flow is directed anteriorly and medially away from the mitral valve. Anatomic and dynamic effects are synergistic in reducing SAM.

Complications of ablation include death in 0-4%, LAD dissection, leakage of alcohol back into the LAD with LAD occlusion and large infarction, and complete heart block in 9-38%. There is concern about the possible late development of an arrhythmogenic scar at the site of the infarction in patients already prone to arrhythmia. In this regard there has been relatively short follow-up of ablated patients (3-5 years) compared with surgically treated patients; and, there have been few pathologic examinations of the site of alcohol ablated septa. In light of the short follow-up intervals and uncertain long term results compared with surgery, alcohol ablation should be done under protocol. Expertise not only with percutaneous catheter techniques but also with the pathophysiology and medical management of patients with hypertrophic cardiomyopathy is requisite.

From encouraging results it appears likely that alcohol ablation will have a role in the management of selected patients with refractory symptoms and refractory gradients. There are drawbacks and benefits of both procedures.

From the above discussions there are three therapeutic approaches that have reduced SAM and gradient: decreasing left ventricular ejection acceleration, redirecting ejection flow anteriorly and medially away from the valve to decrease angle of attack of flow onto the valve, and reducing chordal slack.

Mid-Ventricular obstruction: Mid-ventricular obstruction due to systolic apposition of left ventricular walls is uncommon. It can occur as an isolated cause of obstruction, but can also coexist with SAM. Mid-cavity obstruction is a potential cause of morbidity or mortality after successful surgical relief of SAM. Mid-cavity obstruction may trap blood in the LV apex, which may only escape in diastole. Infrequently high systolic apical cavity pressures may lead to apical infarction in the absence of epicardial coronary disease, apical aneurysm, apical thrombus and potential for emboli and arrhythmia. Initially, symptomatic mid-cavity obstruction is managed with negative inotropic medication, often to good effect. However, when symptoms and obstruction persist, surgical relief of obstruction is indicated. The transaortic approach is made more difficult by the greater distance of the obstruction from the aortotomy, but has been successful in relieving obstruction and is the preferred route. Other approaches have been reported.

It is vital to identify, before surgery, obstruction due to anomalous insertion of the papillary muscle directly into the base of the anterior mitral leaflet without intervening chordae. This uncommon but not rare anomaly, when missed before surgery, can lead to persistent post-operative obstruction and death.

Apical hypertrophic cardiomyopathy can lead to systolic cavity obliteration and increased Doppler velocities in the apex. However, the ventricle is essentially empty when these high velocities are created and apical HCM is managed medically.

Echocardiography before surgery: Transthoracic echo (TTE) is now the most frequent source of diagnosis. Doppler echocardiography provides reliable and reproducible quantification of the pressure gradient. Presence or absence of regional wall motion abnormalities are assessed, as well as ejection fraction. The mitral valve is assessed for structural abnormalities that require valve replacement as described above.

In our patients, we use TTE to plan the length of surgical resection. In the apical long axis view we routinely measure the distance from the aortic root to that portion of the left ventricular septum well past the mid-septal bulge. This defines the minimum extent of the length of resection. On occasion, transthoracic imaging is inadequate due to technical reasons. When this occurs, pre-operative transesophageal echocardiogram (TEE) before the day of surgery may be indicated.

Intraoperative echocardiography is useful to assure adequate repair after cardiopulmonary bypass and myectomy. Initially, an epicardial probe was used. Transesophageal echocardiography offers excellent imaging and has the advantage of having the probe out of the operative field and has generally supplanted epicardial imaging. Persistent early SAM, with resting outflow gradient >50 mm Hg, or more than moderate mitral regurgitation should prompt immediate revision. Using these criteria Marwick and co-workers reported that 20% of patients were placed back on heart-lung bypass and revised using TEE to guide the location of additional resection. After the patient is taken off bypass most centers give intravenous inotropes to exclude provocable obstruction. Others provoke with premature ventricular beats.

There has been progress in our understanding of the nature of obstruction in HCM. The concept of a muscular sphincter gave way to the model of SAM caused by Venturi, and now to SAM caused by flow drag. Innovations will be successful if they are tailored to address the true nature of dynamic obstruction.


Messmer BJ. Extended myectomy for hypertrophic obstructive cardiomyopathy. Ann Thorac Surg 1994;58:575-7.
Morrow AG. Hypertrophic subaortic stenosis. Operative methods utilized to relieve left ventricular outflow obstruction. J Thorac Cardiovasc Surg 1978;76:423-30.
McIntosh C, Maron B. Current operative treatment of obstructive hypertrophic cardiomyopathy. Circ 1988;78:487-495.
Maron BJ, Merrill WH, Freier PA, Kent KM, Epstein SE, Morrow AG. Long-term clinical course and symptomatic status of patients after operation for hypertrophic subaortic stenosis. Circ 1978;57:1205-13.
Williams WG, Wigle ED, Rakowski H, Smallhorn J, LeBlanc J, Trusler GA. Results of surgery for hypertrophic obstructive cardiomyopathy. Circ 1987;76:V104-8.
Ten Berg JM, Suttorp MJ, Knaepen PJ, Ernst SM, Vermeulen FE, Jaarsma W. Hypertrophic obstructive cardiomyopathy: initial results and long-term follow-up after Morrow septal myectomy. Circ 1994;90:1781-5.
Kirklin J, Barratt-Boyes B. Hypertrophic obstructive cardiomyopathy. In: Cardiac Surgery. 2nd edition. NY: Churchill-Livingston 1992: 1239-62, 1220.
McCully RB, Nishimura RA, Tajik AJ, Schaff HV, Danielson GK. Extent of clinical improvement after surgical treatment of hypertrophic obstructive cardiomyopathy. Circ 1996;94:467-71.
Schulte HD, Bircks WH, Loesse B, Godehardt EAJ, Schwartzkopff B. Prognosis of patients with hypertrophic obstructive cardiomyopathy after transaortic myectomy. J Thorac Cardiovasc Surg 1993;106:709-17.
Schulte HD, Borisov K, Gams E, Gramsch-Zabel H, Losse B, Scwhartzkopff B. Management of symptomatic hypertrophic obstructive cardiomyopathy – long term results after surgical therapy. Thorac Cardiovasc Surg 1999;47:213-8.
Schulte HD, Bircks W, Losse B. Techniques and complications of transaortic subvalvular myectomy in patients with hypertrophic obstructive cardiomyopathy (HOCM). Z Kardiol 1987;76 Suppl 3:145-51.
Schulte HD, Bircks W, Korfer R, Kuhn H. Surgical aspects of typical subaortic and atypical midventricular hypertrophic cardiomyopathy (HOCM). Thorac Cardiovasc Surg 1981;29:375-380.
Cohn LH, Trehan H, Collins JJ Jr. Long-term follow-up of patients undergoing myotomy/myectomy for obstructive hypertrophic cardiomyopathy. Am J Cardiol 1992;70:657-60.
Robbins RC, Stinson EB. Long-term results of left ventricular myotomy and myectomy for obstructive hypertrophic cardiomyopathy. J Thorac Cardiovasc Surg 1996;111:586-94.
Heric B, Lytle BW, Miller DP, Rosenkranz ER, Lever HM, Cosgrove DM. Surgical management of hypertrophic obstructive cardiomyopathy: early and late results. J Thorac Cardiovasc Surg 1995;110:195-208.
Schoendube FA, Klues HG, Reith S, Flachskampf FA, Hanrath P, Messmer BJ. Long-term clinical and echocardiographic follow-up after surgical correction of hypertrophic obstructive cardiomyopathy with extended myectomy and reconstruction of the subvalvular mitral apparatus. Circ 1995;92:II-122-7.
Kofflard MJ, VanHerwerden LA, Waldstein DJ, et al. Initial results of combined anterior mitral leaflet extension and myectomy in patients with obstructive hypertrophic cardiomyopathy. J Am Coll Cardiol 1996;28:197-202.
McIntosh CL, Maron BJ, Cannon RO, Klues H. Initial results of combined anterior mitral valve plication and ventricular septal myotomy-myectomy for relief of left ventricular outflow obstruction in patients with hypertrophic cardiomyopathy. Circ 1992;86:II-60-7.
Roberts CS, McIntosh CL, Brown PS, Cannon RO III, Gertz SD, Clark RE. Reoperation for persistent outflow obstruction in hypertrophic cardiomyopathy. Ann Thorac Surg 1991;51:455-60.
Cooper MM, McIntosh CL, Tucker E, Clark R. Operation for hypertrophic subaortic stenosis in the aged. Ann Thorac Surg 1987;44:370-378.
Siegman I, Maron BJ, Permut L, McIntosh C, Clark R. Results of operation for coexistent obstructive hypertrophic cardiomyopathy and coronary artery disease. J Am Coll Cardiol 1989;13:1527-33.
Wigle ED. Schwartz L, Woo A, Rakowski H. To ablate or operate? That is the question! J Am Coll Cardiol 2001;38:1708-10.
Brock R. Functional obstruction of the left ventricle (acquired aortic subvalvular stenosis). Guy’s Hospital Report 1957;106:221-238.
Bigelow WG, Trimble AS, Auger P, Marquis Y, Wigle ED. The ventriculomyotomy operation for muscular subaortic stenosis. J Thorac Cardiovasc Surg 1966;52:514.
Kirklin JW, Ellis FH Jr. Surgical relief of diffuse subvalvular aortic stenosis. Circ 1961;24:739-42.
Cleland WP. The surgical management of obstructive cardiomyopathy. J Cardiov Surg 1963;4:489-491.
Morrow AG, Brockenbrough EC. Surgical treatment of idiopathic hypertrophic subaortic stenosis. Technic and hemodynamic results of subaortic ventriculomyotomy. Ann Surg 1961;154:181.
Morrow AG, Fogarty TJ, Hannah H III, Braunwald E. Operative treatment in idiopathic hypertrophic subaortic stenosis. Techniques and results of postoperative clinical and hemodynamic assessments. Circ 1968;37:589-96.
Fix P, Moberg A, Soderberg H, Karnell J. Muscular subvalvular aortic stenosis. Abnormal anterior mitral leaflet possibly the primary factor. Acta Radiologica Diagnosis 1964;2:177-193.
Adelman AG, McCoughlin MJ, Marquis Y, Auger P, Wigle ED. Left ventricular cineangiographic observations in muscular subaortic stenosis. Am J Cardiol 1969;24:689-697.
Shah PM, Graniak R, Kramer DH. Ultrasound localization of left ventricular outflow tract obstruction in hypertrophic cardiomyopathy. Circ 1969;40:3-11.
Popp RL, Harrison DC. Ultrasound in the diagnosis and evaluation of therapy of idiopathic hypertrophic subaortic stenosis. Circ 1969;40:905-914.
Jiang L, Levine RA, King ME, Weyman AE. An integrated mechanism for systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy based on echocardiographic observations. Am Heart J 1987;113:633-44.
Sherrid MV, Chu Ck, DeLia E, Mogtader A, Dwyer Jr. EM. An echocardiographic study of the fluid mechanics of obstruction in hypertrophic cardiomyopathy. J Am Coll Cardiol 1993;22:816-25.
Cape EG, Simons D, Jimoh A, Weyman AE, Yognathan AP, Levine RA. Chordal geometry determines the shape and extent of systolic anterior motion: in vitro studies. J Am Coll Cardiol 1989;13:1438-48.
Levine RA, Vlahakes GJ, Lefebvre X, et al. Papillary muscle displacement causes systolic anterior motion of the mitral valve. Circ 1995;91:1189-95.
Sherrid MV, Gunsburg DZ, Moldenhauer S, Pearle G. Systolic anterior motion begins at low left ventricular outflow tract velocity in obstructive hypertrophic cardiomyopathy. J Am Coll Cardiol 2000;36:1344-54.
Schwammenthal E, Levine RA. Dynamic subaortic obstruction: a disease of the mitral valve suitable for surgical repair? J Am Coll Cardiol 1996;28:203-6.
Lefebre XP, Yoganathan AP, Levine RA. Insights from in vitro flow visualization into the mechanism of systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy under steady flow conditions. J Biomed Eng 1992;114:406-13.
Reis R, Bolton MR, King JF, Pugh DM, Dunn MI, Mason DT. Anterior-superior displacement of papillary muscles producing obstruction and mitral regurgitation in idiopathic hypertrophic subaortic stenosis. Circ 1974;50:II-181-8.
Henry WL, Clark CE, Griffith JM, Epstein SE. Mechanism of left ventricular outflow obstruction in patients with obstructive asymmetric septal hypertrophy (idiopathic hypertrophic subaortic stenosis). Am J Cardiol 1975;35:337-45.
Shah PM, Taylor RD, Wong M. Abnormal mitral valve coaptation in hypertrophic obstructive cardiomyopathy: proposed role in systolic anterior motion in mitral valve. Am J Cardiol 1981;48:258-62.
Klues HG, Maron BJ, Dollar AL, Roberts WC. Diversity of structural mitral valve alterations in hypertrophic cardiomyopathy. Circ 1992;85:1651-60.
Grigg LE, Wigle ED, Williams WG, Transesophageal echocardiography in obstructive hypertrophic cardiomyopathy. Clarification of pathophysiology and importance of intraoperative decision making. J Am Coll Cardiol 1992;20:42-52.
Nakatani S, Schwammenthal E, Lever HM, Levine RA, Lytle BW, Thomas JD. New insights into the reduction of mitral valve systolic anterior motion after ventricular septal myectomy in hypertrophic obstructive cardiomyopathy. Am Heart J 1996;131:294-300.
Sherrid, MV, Gunsburg DZ, Pearle G. Mid-systolic drop in left ventricular ejection velocity in obstructive hypertrophic cardiomyopathy – the lobster claw abnormality. J Am Soc Echocardiogr 1997;10:707-12.
Sherrid MV, Pearle G, Gunsburg DZ. Mechanism of benefit of negative inotropes in obstructive hypertrophic cardiomyopathy. Circ 1998;97:41-47.
Cooley DA. Surgical techniques for hypertrophic left ventricular obstructive myopathy including mitral valve plication. J Cardiac Surg 1991;6:29-33.
Grossi EA, Steinberg BM, LeBoutillier M, Ribacove g, Spencer FC, Galloway AC, Colvin SB. Decreasing incidence of systolic anterior motion after mitral valve reconstruction. Circ 1994;90:II-195-7.
Joyce F, Lever H, Cosgrove D. Treatment of hypertrophic cardiomyopathy by mitral valve repair and septal myectomy. Ann Thoracic Surg 1994;54:1025-7.
Matsui Y, Shiiya N, Murashita T, Sasaki S, Yasuda K. Mitral valve repair and septal myectomy for hypertrophic obstructive cardiomyopathy. J Cardiovasc Surg 2000;41:53-56.
Cooley DA, Leachman RD, Wukasch DC. Mitral valve replacement for idiopathic hypertrophic cardiomyopathy. J Cardiovasc Surg 1976;17:380-87.
Krajcer Z, Leachman RD, Cooley DA, Ostojic M, Coronado R. Mitral valve replacement and septal myomectomy in hypertrophic cardiomyopathy. Ten-year follow-up in 80 patients. Circ 1988;78:I35-43.
Walker WS, Reid KG, Cameron EW, Walbaum PR, Kitchin AH. Comparison of ventricular septal surgery and mitral valve replacement for hypertrophic obstructive cardiomyopathy. Ann Thorac Surg 1989;48:528-34; discussion 535.
McIntosh CL, Greenberg GJ, Maron BJ, Leon MB, Cannon RO, Clark RE. Clinical and hemodynamic results following mitral valve placement in patients with obstructive hypertrophic cardiomyopathy. Ann Thorac Surg 1989;47:236-46.
Roberts WC. Operative treatment of hypertrophic obstructive cardiomyopathy. The case against mitral valve replacement. Am J Cardiol 1973;32:377.
Yu E, Omran A, Wigle ED, Williams WG, Siu S, Rakowski H. Mitral regurgitation in hypertrophic obstructive cardiomyopathy: Relationship to obstruction and relief with myectomy. J Am Coll Cardiol 2000;36:2219-25.
Spirito P, Seidman CE, McKenna WJ, Maron BJ. The management of hypertrophic cardiomyopathy. N Engl J Med 1997;336:775-785.
Wigle ED, Rakowski H, Kimball BP, Williams WG. Hypertrophic cardiomyopathy. Clinical spectrum and treatment. Circ 1995;92:1680-92.
Maron BJ, Casey SA, Poliac LC, Gohman TE, Almquist AK, Aeppli DM. Clinical course of hypertrophic cardiomyopathy in a regional United States cohort. JAMA 1999;281:650-5.
Maron BJ. Hypertrophic cardiomyopathy: a systematic review. JAMA 2002;287:1308-1320.
Matsumura Y, Elliott PM, Virdee MS, Sorajja P, Doi Y, McKenna WJ. Left ventricular diastolic function assessed using Doppler tissue imaging in patients with hypertrophic cardiomyopathy: relation to symptoms and exercise capacity. Heart 2002;87:247-51.
Lele SS, Thomson HL, Seo H, Belenkie I, McKenna WJ, Frenneaux MP. Exercise capacity in hypertrophic cardiomyopathy: Role of stroke volume limitation, heart rate and diastolic filling characteristics. Circ 1995;92:2886-2894.
Cannon RO, Rosing DR, Maron BJ, et al. Myocardial ischemia in patients with hypertrophic cardiomyopathy: Contribution of inadequate vasodilator reserve and elevated left ventricular filling pressures. Circ 1985;71:234-243.
Dilsiziam V, Bonow RO, Epstein SE, Fananapazir L. Myocardial ischemia detected by thallium scintigraphy is frequently related to cardiac arrest and syncope in young patients with hypertrophic cardiomyopathy. J Am Coll Cardial 1993;22:796-80.
Udelson JE, Bonow RO, O’Gara PT, Maron BJ, Van Lingen A, Bacharach SL, Epstein SE. Verapamil prevents silent myocardial perfusion abnormalities during exercise in asymptomatic patients with hypertrophic cardiomyopathy. Circulation 1995;79:1052-60.
Kass DA, Chen CH, Talbot MW, Rochitte CE, Lima JA, Berger RD, Calkins H. Ventricular pacing with premature excitation for treatment of hypertensive-cardiac hypertrophy with cavity-obliteration. Circ 1999;100:807-12.
Elliott PM, Gimeno Blanes JR, Mahon NG, Poloniecki JD, McKenna WJ. Relation between severity of left-ventricular hypertrophy and prognosis in patients with hypertrophic cardiomyopathy. Lancet 2001;357:420-4.
Maron BJ, Shen WK, Link MS, Epstein AE, Almquist AK, Daubert JP, Bardy GH, Favale S, Rea RF, Boriani G, Estes NA 3rd, Spirito P. Efficacy of implantable cardioverter-defibrillators for the prevention of sudden death in patients with hypertrophic cardiomyopathy. N Engl J Med 2000;342:365-73.
Wigle D, Sasson Z, Henderson MA, Ruddy TD, Fulop J, Rakowski H, Williams WG. Hypertrophic cardiomyopathy. The importance of the site and the extent of hypertrophy. A review. Progress in Cardiovascular Diseases 1985;28:1-83.
Harrison DC, Braunwald E, Glick G, et al. Effects of beta adrenergic blockade on the circulation with particular reference to observations in patients with hypertrophic subaortic stenosis. Circ 1964;29:84-98.
Pollick C. Disopyramide in hypertrophic cardiomyopathy. Noninvasive assessment after oral administration. Am J Cardiol 1988; 62:1252-1255.
Sherrid M, DeLia E, Dwyer E. Oral disopyramide therapy for obstructive hypertrophic cardiomyopathy. Am J Cardiol 1988;62:1085-1088.
Rosing DR, Kent KM, Maron BJ, Epstein SE. Verapamil therapy: A new approach to the pharmacologic treatment of hypertrophic cardiomyopathy: II: Effects on exercise capacity and symptomatic status. Circ 1979; 60:1208-1213.
Epstein SE, Rosing DR. Verapamil: its potential for causing serious complications in patients with hypertrophic cardiomyopathy. Circ 1979;60:437-441.
Jeanrenaud X, Goy JJ, Kappenberger L. Effects of dual-chamber pacing in hypertrophic obstructive cardiomyopathy. Lancet. 1992 May 30;339(8805):1318-23.
Fananapazir L, Cannon RO, Tripodi D, Panza JA. Impact of dual-chamber permanent pacing in patient with obstructive hypertrophic cardiomyopathy with symptoms refractory to verapamil and b-adrenergic blocker therapy. Circ 1992;85:2149-2161.
Kappenberger L, Linde C, Daubert C, McKenna W, Meisel E, Sadoul N, Chojnowska L, Guize L, Gras D, Jeanrenaud X, Ryden L. Pacing in hypertrophic obstructive cardiomyopathy. A randomized crossover study. PIC Study Group. Eur Heart J 1997;18:1249-56.
Gadler F, Linde C, Ryden L. Rapid return of left ventricular outflow tract obstruction and symptoms following cessation of long-term atrioventricular synchronous pacing for obstructive hypertrophic cardiomyopathy. Am J Cardiol. 1999;83:553-7.
Maron BJ, Nishimura RA, McKenna WJ, Rakowski H, Josephson ME, Kieval RS. Assessment of permanent dual-chamber pacing as a treatment for drug-refractory symptomatic patients with obstructive hypertrophic cardiomyopathy. A randomized, double-blind, crossover study (M-PATHY). Circulation 1999;99:2927-33.
Linde C, Gadler F, Kappenberger L, Ryden L. Placebo effect of pacemaker implantation in obstructive hypertrophic cardiomyopathy. PIC Study Group. Pacing In Cardiomyopathy. Am J Cardiol 1999;83:903-7.
Knight C, Kurbaan AS, Seggewiss H, Henein M, Gunning M, Harrington D, Fassbender D, Gleichmann U, Sigwart U. Nonsurgical septal reduction for hypertrophic obstructive cardiomyopathy: outcome in the first series of patients. Circ 1997;95:2075-2081.
Faber L, Ziemssen P, Seggewiss H. Targeting percutaneous transluminal septal ablation for hypertrophic obstructive cardiomyopathy by intraprocedural echocardiographic monitoring. J Am Soc Echocardiogr 2000;13:1074-9.
Nagueh SF, Lakkis NM, He Z-X, Middleton KJ et al. Role of myocardial contrast echocardiography during nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy. JACC 1998;32:225-9.
Lakkis NM, Nagueh SF, Kleiman NS, Killip D et al. Echocardiography-guided ethanol septal
reduction for hypertrophic obstructive cardiomyopathy. Circ 1998;98:1750-1755.
Gietzen FH, Leuner J, Raute-Kreinsen U, Dellmann A, Hegselmann J, Strunk-Mueller C, Kuhn HJ. Acute and long-term results after transcoronary ablation of septal hypertrophy: catheter interventioanl treatment for hypertrophic obstructive cardiomyopathy. Eur Heart J 1999;20:1342-1354.
Seggewiss H, Gleichmann U, Faber L, Fassbender D, Schmidt HK, Strick S. Percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: acute results and 3-month follow-up in 25 patients. .JACC 1998;31:252-8.
Faber L, Meissner A, Ziemssen P, Seggewiss H. Percutaneous transluminal septal myocardial ablation for hypertrophic obstructive cardiomyopathy: long term follow up of the first series of 25 patients. Heart 2000;83:326-31.
Nagueh SF, Ommen SR, Lakkis NM, Killip D, Zoghbi WA Schaff HV, Danielson GK, Quinones MA, Tajik AJ, Spencer WH. Comparison of ethanol septal reduction therapy with surgical myectomy for the treatment of hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 2001;38:1701-6.
Qin JX, Shiota T, Lever HM, Kapadia SR Sitges M, Rubin DN, Bauer F, Greenberg NL, Agler DA, Drinko JK, Martin M, Tuzcu EM, Smedira NG, Lytle B, Thomas JD. Outcome of patients with hypertrophic obstructive cardiomyopathy after percutaneous transluminal septal myocardial ablation and septal myectomy surgery. J Am Coll Cardiol 2001;38:1994-2000.

Flores-Ramirez R, Lakkis NM, Middleton KJ, Killip D, Spencer WH 3rd, Nagueh SF. Echocardiographic insights into the mechanisms of relief of left ventricular outflow tract obstruction after nonsurgical septal reduction therapy in patients with hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 2001;37:208-14.
Henein MY, O’Sullivan CA, Ramzy IS, Sigwart U, Gibson DG. Electromechanical left ventricular behavior after nonsurgical septal reduction in patients with hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 1999;34:1117-22.
Arrazaghi AA, Butany JW, Williams WG, Wigle DE, Rakowski H. Myectomy for hypertrophic obstructive cardiomyopathy after failed alcohol septal ablation: clinicopathological correlations. Can J Cardiol 2001;17:197-202.
Falikov RE, Resnekov L, Bharati S, Lev M. Mid-ventricular obstruction: A variant of obstructive cardiopathy. Am J Cardiol 1976;37:432-437.
Zoghbi WA , Haichin RN, Qui-ones MA. Mid-cavity obstruction in apical hypertrophy: Doppler evidence of diastolic intraventricular gradient with higher apical pressure. Am Heart J 1988;116:1469-1474.
Nakamura T, Matsubara K, Furukawa K, Azuma A, Sugihara H, Katsume H, Nakagawa M. Diastolic paradoxic jet flow in patients with hypertrophic cardiomyopathy: Evidence of concealed apical asynergy with cavity obliteration. J Am Coll Cardiol 1992;19:516-524.
Matsuda H, Nomura F, Kadoba K, Taniguchi K, Imagawa H, Kagisaki K, Sano T. Transatrial and transmitral approach for left ventricular myectomy and mitral valve plication for diffuse-type hypertrophic obstructive cardiomyopathy: A novel approach. J Thorac Cardiovasc Surg 1996;112:195-196.
Seggewiss H, Faber L. Percutaneous septal ablation for hypertrophic cardiomyopathy and mid-ventricular obstruction. Eur J Echocardiogr 2000;1:277-80.
Klues HG, Roberts WC, Maron BJ. Anomalous insertion of papillary muscle directly into anterior mitral valve lealet in hypertrophic cardiomyopathy. Significance in producing left ventricular outflow obstruction. Circ 1991;84:1188-97.
Maron BJ, Nishimura RA, Danielson GK. Pitfalls in clinical recognition and a novel operative approach for hypertrophic cardiomyopathy with severe outflow obstruction due to anomalous papillary muscle. Circ 1998;98:2505-8.
Maron BJ. Utility of intraoperative echocardiography in planning surgical strategy in hypertrophic cardiomyopathy, in Baroldi G, Camerini F, Goodwin JF (eds): Advances in Cardiomyopathies. Berlin, Springer-Verlag 1990:136-50.
Marwick TH, Stewart WJ, Lever HM, Lytle BW, Rosenkranz ER, Duffy CI, Salcedo EE . Benefits of intraoperative echocardiography in the surgical management of hypertrophic cardiomyopathy. J Am Coll Cardiol 1992;20:1066-72.
Franke A, Schöndube FA, Kühl HP, Klues HG, Erena C, Messmer BJ, Flachskampf FA, Hanrath P. Quantitative assessment of the operative results after extended myectomy and surgical reconstruction of the subvalvular mitral apparatus in hypertrophic obstructive cardiomyopathy using dynamic three-dimensional transesophageal echocardiography. J Am Coll Cardiol 1998;31:1641-9.