Obstructive hypertrophic cardiomyopathy (HCM) presents complex anatomic and physiologic challenges that require precise surgical planning and execution. In this expert-level surgical overview, we examine transaortic and apical septal myectomy techniques used to relieve left ventricular outflow tract and mid-ventricular obstruction while optimizing long-term outcomes.
With decades of experience and thousands of procedures performed, this approach demonstrates excellent survival, low operative mortality, minimal residual gradient, and durable symptomatic improvement.
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Surgical treatment for obstructive hypertrophic cardiomyopathy. Obstructive hypertrophic cardiomyopathy affects approximately 1 in 500 people. Obstruction can be at the base of the ventricular septum, in the midventricular septum, or close to the apex. At Mayo Clinic, we separate these into zones 12, and 3. The most important concept with transaortic septal myectomy is to ensure that the myectomy trough is opposite the anterior leaflet of the mitral valve, cords, and papillary muscles in order to completely abolish systolic anterior motion. Additional resection along the posterior lateral free wall is typically performed. Hypertrophic papillary muscles can also be shaved on their sides to augment the sides of the midventricular cavity. It is important to measure pressures with needles in the left ventricle and the ascending aorta before and after myectomy. It is our practice to also apply maneuvers such as the premature ventricular contraction. And in the setting of a low gradient at rest under the conditions of anesthesia, we would plan to provoke pharmacologically with isoppril. Duplicating pressure measurements at the end of the procedure ensure that the gradient has completely been eliminated. The degree of muscular resection is proportionate to the degree of hypertrophy of the ventricular septum and posterior lateral free wall. Late survival following transaortic myectomy for basal and midventricular obstruction is excellent, with survival equal to an age-matched population at 10 years following surgery. Mayo Clinic has a long history of myectomy surgery for obstructive hypertrophic cardiomyopathy. We are approaching 5000 surgical myectomies for this disease. Early mortality for isolated myectomy is less than 1%, with a high probability of no significant residual gradient and minimal mitral regurgitation. The need for permanent pacing is low at less than 2%. Mitral valve replacement is rarely indicated except in cases of rheumatic mitral valve disease, most commonly for mitral stenosis. Both quality of life and late survival show substantial improvement following the procedure. There is a subgroup of patients with hypertrophic cardiomyopathy where hypertrophy is confined to the apex, and there is no evidence of obstruction. These patients are typically felt to have diastolic dysfunction and are often referred for cardiac transplantation. Atrial fibrillation can be quite common due to physiology of the restrictive cardiomyopathy. Our goal with evaluation in the hypertrophic cardiomyopathy clinic in combination with our imaging colleagues in surgery is to determine whether symptoms are related to a small left ventricular cavity as opposed to diastolic dysfunction. This differentiation is important since there is a role for conventional surgery to enlarge the left ventricular cavity when it is determined that the stroke volume is below normal. A combination of echocardiogram and MRI imaging is performed. The classic finding on MRI is a slit-like cavity shape of the left ventricle as opposed to the conical shape. These images depict a small left ventricular cavity with a low stroke volume. When low stroke volume has been determined by imaging studies, our approach has been apical myectomy with excision of septal and freewall hypertrophy to enlarge the left ventricular cavity. Our experience with this procedure approaches 500 patients. These images demonstrate the location of the incision in the areas of the mid ventricular resection that include shaving of the papillary muscles. In the early experience with this procedure, it was common to perform pressure volume loops in the cardiac catheterization laboratory. This figure demonstrates increase in stroke volume and a reduction in the left ventricular end diastolic pressure following trans apical myectomy for a small left ventricular cavity. Since many of these patients were initially referred for transplantation for the presumed diagnosis of restricted cardiomyopathy, we reviewed the late results following surgery versus survival on the transplant wait list. Late survival following surgery was quite favorable relative to cumulative mortality on the waitlist for heart transplantation.
