Echocardiography before and after Resect-Plicate-Release Surgical Myectomy for Obstructive Hypertrophic Cardiomyopathy


Anatomic features of obstructive hypertrophic cardiomyopathy are septal hypertrophy, elongated mitral leaflets, and anterior displacement of the papillary muscles. In addition to extended myectomy, the resect-plicate-release operation adds horizontal plication of the anterior mitral leaflet (AML) and release of the anterolateral papillary muscle (APM) in selected patients. The aim of this study was to test the hypotheses that (1) preoperative findings would be associated with procedures applied, (2) anatomic corrections would be observable postoperatively, and (3) there would be consistently good physiologic outcomes.


A retrospective study was conducted of patients with obstructive hypertrophic cardiomyopathy who had adequate echocardiograms before and 9.5 ± 12 months after the resect-plicate-release operation was performed from 2006 to 2012.


Seventy-seven patients underwent myectomy, 50 AML plication, and 50 APM release. Patients who underwent plication had longer AMLs (32 ± 4 vs 28 ± 4 mm; P < .004). Anterior extension of the APM was more common with papillary muscle release (86% vs 62%, P < .04). Twenty-seven (35%) had septal thickness ≤ 18 mm; mitral valve–sparing operations were possible because of plication in 19 patients (70%), papillary release in 21 (78%), and one or both in 96%. Patients who underwent plication had decreased AML length by 16%, residual leaflet length by 33%, and protrusion by 24%. After APM release, there was decreased distance from mitral coaptation to the posterior wall. Surgery abolished severe systolic anterior motion and resting gradients and reduced mitral regurgitation.


Echocardiographic AML length and directly observed slack provides a basis to recommend performance of plication and define its extent; plication decreases AML protrusion and stiffens the leaflet. Anterior APM recommends release, which drops the coaptation point posteriorly. Systematic relief of all aspects of obstructive pathophysiology results in consistent outcomes.

Surgical septal myectomy is considered among the most technically challenging surgical procedures for acquired heart disease. Variable anatomic features in hypertrophic cardiomyopathy (HCM), such as elongated mitral leaflets and anteriorly displaced papillary muscles, contribute to systolic anterior motion (SAM) pathophysiology and may render correction more challenging. Inconsistency in results at centers with less expertise may be the cause of limited adoption of myectomy for resistant cases. We hypothesized that an echocardiographically guided approach to myectomy that included corrective repair of the mitral valve and papillary muscles in selected patients would result in consistently good physiologic outcomes and that the anatomic corrections of the mitral valve would be of a magnitude observable with postoperative echocardiography.


Patient Selection

This was a retrospective study of patients who underwent surgery at St. Luke’s-Roosevelt Hospital Center (SLR) in New York City for relief of left ventricular (LV) outflow tract (LVOT) obstruction due to SAM and mitral-septal contact from 2006 to 2012. Patients were excluded from the study if they had undergone mitral valve replacement (MVR) for valvular calcification, if they had inadequate echocardiograms, if they had no postoperative studies because they lived at a distance, or if they had undergone surgery for mid LV obstruction. Pharmacotherapy and selection of patients for surgery were consistent with guidelines ; details of pharmacotherapy at our institution are described elsewhere. Patients in whom pharmacologic therapy failed who remained limited by heart failure symptoms and had persistent gradients > 50 mm Hg at rest or after physiologic provocation were referred for surgery. All patients provided written consent, approved by the institutional review board of SLR, for the use of their clinical data for research.

Preoperatively, transthoracic echocardiographic guidance for anterior leaflet plication was based on leaflet length > 30 mm, and guidance to address papillary muscle abnormalities depended on the detection of anteriorly displaced muscles bound to the anterior wall or anomalous muscles in the outflow tract. Intraoperative transesophageal echocardiography (TEE) was monitored by the anesthesiologist and remotely by HCM cardiologist. Decisions about plication and release were subject to change depending on intraoperative TEE and direct visual assessment by the surgeon.

Transthoracic Echocardiographic Measurements

Preoperative and postoperative echocardiography was performed at rest. Measurements were made blinded to operative reports. Variables measured included resting LVOT gradient, degree of mitral regurgitation (MR) (graded from 0 to 4+), short-axis LV dimensions (segmental thickness, cavity diameter), mitral leaflet lengths, and papillary muscle anatomic features. LVOT obstruction due to SAM was determined by the highest gradient acquired with continuous-wave Doppler in the apical three-chamber (or five-chamber) view. Provocative maneuvers for eliciting LVOT gradients included Valsalva and standing; treadmill exercise was performed in patients who could walk on the treadmill if the resting gradient was <80 mm Hg. Care was taken to avoid contamination of the Doppler gradient signal by the MR jet. The distance from the aortic annulus to the point of mitral-septal contact on the septum was noted on the preoperative imaging.

Mitral Valve Measurements

On the parasternal long-axis view at the moment of systolic coaptation, we measured distances between the mitral valve coaptation point and the anteroseptum and the posterior wall. On the apical three-chamber view, anterior mitral leaflet (AML) length was measured in diastole, and protrusion height was measured at coaptation from the most protruding mitral leaflet tip to the mitral annular plane ( Figure 1 ). On this view, residual length was the uncoapted portion of the mitral valve (usually the AML) that protrudes distally beyond the coaptation point. The coaptation zone was the length of the coapted leaflets. Postoperative severe SAM was noted when the mitral valve either touched or nearly touched the interventricular septum. Mild SAM was noted when there was mild deflection toward the septum but still 1 cm of separation from contact.

Figure 1

Schematic three-chamber transthoracic measurements of the mitral valve apparatus in diastole ( left ) and systole ( right ). AL , Anterior leaflet mitral valve; PH , protrusion height; PL , posterior leaflet mitral valve; RL , residual leaflet length, which extends past coaptation. Modified with permission from Alhaj et al .

Papillary Muscle Location and Measurements

Short-axis scans were performed from the mid left ventricle to the outflow tract. Traditional long-axis and off-axis views of the mid left ventricle and outflow tract were performed as well. The particular location of the anterolateral papillary was noted on the mid LV parasternal short-axis views; it was considered in its normal posterior position when arising below, or on, the line bisecting the LV cavity into two equal halves. It was considered anterior when more than half of it originated from the anterior wall above this line. On the parasternal short-axis view, we assessed the transverse diameter of major muscle heads and the distances between the papillary muscle plane (a line that transversely connects the two major muscles) and the anterior and the posterior walls.

Operative Technique

Surgical decision making, technique, and clinical outcomes for the resect-plicate-release (RPR) operation in selected patients are reported elsewhere ; some patients in the present detailed echocardiographic study were described in these clinical reports. The septal myectomy is extended axially well past the point of mitral-septal contact as measured preoperatively from the aortic annulus. In many patients, a friction patch on the septum marks the spot of mitral-septal contact ( Figure 2 ). After the extended myectomy, papillary muscle release is performed to induce a posterior drop of the anterolateral papillary muscle. These include release of the origin of the anterolateral papillary muscle in the mid left ventricle, on the basis of anterior position of its base, detected preoperatively on short-axis echocardiography and shown in Figures 3 and 4 A . Additionally, the surgeon releases abnormal muscular attachments from the anterolateral papillary muscle to the anterolateral free LV wall, at a level closer to the mitral leaflets. These are detected directly by the surgeon during the operation ( Figure 4 B). Then, mitral valve leaflet redundancy and slack are evaluated using a nerve hook. Horizontal plication of the AML was performed with three or four 5-0 polypropylene sutures placed through the most pliable area of the leaflet near its midportion in a horizontal mattress fashion, usually shortening the AML by 2 to 5 mm ( Figure 5 ). It is believed important to stay distant from the aortomitral curtain and aortic annulus to maximize the stiffening effect on the anterior leaflet; the desired effect is to prevent the systolic bowing-out of the leaflet. The extent of shortening was prospectively estimated by preoperative echocardiography and refined by direct surgical inspection.

Figure 2

RPR repair in obstructive HCM: outflow relative to the mitral valve in early systole. Note the anterior position of the mitral valve coaptation, the long anterior leaflet and the residual leaflet that extends past coaptation into the left ventricle. The prominent midseptal bulge redirects outflow so that it comes from a relatively posterior direction, catching the anteriorly positioned mitral valve and pushing it into the septum. (B) After extended myectomy. Flow tracks more anteriorly and medially, away from the mitral leaflets. Modified from Sherrid et al .

Figure 3

Short-axis parasternal views in four patients with obstructive hypertrophic cardiomyopathy. Two patients (A,B) had anterior extension of their anterolateral papillary muscles, shown with red arrows , and underwent papillary muscle release. The yellow arrows point to the normally positioned portions of the lateral papillary muscle. Note also the normally positioned posteromedial papillary muscle. Two patients (C,D) had normal posterior position of the anterolateral papillary muscle, shown with yellow arrows . At this level, papillary muscle release is predicted by anterior extension of the lateral papillary muscle on the short-axis view, which is readily appreciated with echocardiography.

Figure 4

(A,B) Two levels of abnormal anterolateral papillary muscle (APM) attachments. (A) ( Left ) A schematic echocardiographic mid LV view. The origin or base of the APM is anteriorly displaced. The surgical release of this portion of the papillary muscle from the anterior wall is shown as a continuation of the mid LV portion of the myectomy by the white dotted line and the blue arrow . (B) ( Right ) A surgeon’s view after the myectomy through the outflow tract, a view that is closer to the mitral valve leaflets, and at a higher level than that depicted in (A) . The APM is hypertrophied and more anterior than normal. (B) Shows with red arrows abnormal attachments of the APM to the anterolateral wall that draw it anteriorly into the outflow tract. These are separated from the free wall with sharp dissection to allow the papillary muscle to drop posteriorly in the LV cavity. In the present work, these accessory attachments to the anterolateral wall were noted by the surgeon but were imperfectly visualized with echocardiography. Judgments are modified by the directly observed surgical anatomy; the surgeon may release previously undetected adherent bands between the papillary muscle and lateral wall if they are deemed to contribute to SAM. Ao , Ascending aorta; L , left; M , mitral valve anterior leaflet margin; PPM , posteromedial papillary muscle; R , right; S , septal myectomy.

Figure 5

Anterior leaflet plication performed in a patient with a very elongated slack anterior leaflet. Horizontal plication of the AML is performed with three or four 5-0 polypropylene sutures placed through the most pliable area of the leaflet near its midportion in a horizontal mattress fashion, usually shortening the AML by 2 to 5 mm. It is believed to be important to stay distant from the aortomitral curtain and aortic annulus to maximize the stiffening effect on the anterior leaflet; the desired effect is to prevent the systolic bowing-out of the leaflet. Reproduced with permission from Sherrid et al . Ao , Aortic root; LCO , left coronary os.

Statistical Analysis

Continuous data are presented as mean ± SEM. Paired and unpaired Student’s t tests were used to compare continuous variables. Significance was based on two-tailed tests. P values < .05 were considered to indicate statistical significance. Categorical variables were compared using χ 2 or Fisher exact tests as appropriate.


From 1998 to August 2013, 162 patients underwent surgery for obstructive HCM at SLR. In the time period of this echocardiographic analysis, between 2006 and 2012, 117 patients underwent surgery for symptomatic LV obstruction. We excluded 14 patients who underwent MVR for extensive calcification, two with mid LV obstruction, 14 in whom postoperative follow-up echocardiographic studies were inadequate, and 10 in whom imaging was not performed because patients lived at distance. Thus, 77 patients remained for echocardiographic analysis. Table 1 shows clinical characteristics of the patients. Fifty patients underwent horizontal anterior leaflet plication; 50 underwent papillary muscle release, of whom 37 underwent papillary muscle resection (32 partial resections and five complete resections); and 18 underwent papillary muscle thinning. Additional concomitant operations included 15 coronary artery bypass graft procedures, seven maze procedures, six aortic valve replacements for mild to moderate aortic disease, and two ascending aortic replacements for aneurysm.

Table 1

Baseline clinical characteristics ( n = 76)

Mean age (y) 52
Men 43 (56%)
Family history of HCM 32 (42%)
NYHA class
I 0 (0%)
II 1 (1.3%)
III 72 (93.5%)
IV 3 (3.9%)
Coronary artery disease 10 (13%)
Hypertension 32 (42%)
Hypercholesterolemia 17 (22%)
Diabetes mellitus 3 (4%)
Ventricular arrhythmias 6 (8%)
COPD 3 (4%)
Smoking 6 (8%)
Prior pharmacologic therapy
β-blockers 73 (95%)
Disopyramide 39 (51%)
Calcium channel blockers 5 (6%)

COPD , Chronic obstructive pulmonary disease; NYHA , New York Heart Association.

Echocardiograms were performed 125 ± 283 days before and 285 ± 370 days after surgery. Echocardiographic results before and after RPR surgery are shown in Table 2 . Representative pre- and postoperative echocardiograms are shown in ( Figures 6 and 7 and Videos 1 to 4 ; available at ).

Table 2

Comparison between echocardiographic parameters before and after RPR surgery

Parameter Before RPR surgery After RPR surgery P
Resting LVOT gradient (mm Hg) ( n = 76) 56 ± 36 1 ± 1 <.01
Provoked LVOT gradient (mm Hg) ( n = 76) 107 ± 43 10 ± 14 <.01
Septal thickness (mm) ( n = 76) 21 ± 5 13 ± 3 <.01
MR (0–4) ( n = 76) 1.8 ± 1.2 1.2 ± 0.9 <.01
End-diastolic diameter (mm) ( n = 76) 39 ± 8 42 ± 7 <.05
AML length (mm) ( n = 76) 30 ± 4 27 ± 4 <.01
Indexed to BSA 16 ± 2 14 ± 2 <.01
Horizontal plication ( n = 49) 32 ± 4 27 ± 4 <.01
Indexed to BSA 17 ± 2 14 ± 2 <.01
No horizontal plication ( n = 27) 28 ± 4 28 ± 4 .76
Indexed to BSA 15 ± 2 15 ± 2 .79
Protrusion height (mm) ( n = 76) 24 ± 05 20 ± 5 <.01
Horizontal plication ( n = 49) 25 ± 6 19 ± 4 <.01
No horizontal plication ( n = 27) 23 ± 4 20 ± 5 .067
Residual length (mm) ( n = 76) 6 ± 3 4 ± 2 <.01
Horizontal plication ( n = 49) 6 ± 3 4 ± 3 <.01
No horizontal plication ( n = 27) 6 ± 3 5 ± 2 .18
Coaptation zone (mm) ( n = 76) 9 ± 3 8 ± 3 .10
Horizontal plication ( n = 49) 10 ± 3 9 ± 3 .16
No horizontal plication ( n = 27) 9 ± 2 8 ± 4 .42
Mitral coapt to septal distance) (mm) ( n = 76) 18 ± 4 24 ± 5 <.01
Papillary muscle release ( n = 49 ) 18 ± 5 24 ± 5 <.01
Papillary muscle resection ( n = 35) 18 ± 4 23 ± 4 <.01
Papillary muscle thinned ( n = 18) 17 ± 4 23 ± 4 <.01
Any pap muscle surgery ( n = 63) 18 ± 4 24 ± 5 <.01
No papillary surgery ( n = 12) 20 ± 3 24 ± 5 .016
Mitral coapt to post wall distance) (mm) ( n = 76) 16 ± 3 14 ± 3 <.01
Papillary muscle release ( n = 49) 16 ± 3 14 ± 3 <.01
Papillary muscle resection ( n = 35) 16 ± 3 14 ± 3 <.01
Papillary muscle thinned ( n = 18) 17 ± 3 16 ± 3 <.01
Any papillary muscle surgery ( n = 63) 16 ± 3 14 ± 3 <.01
No papillary surgery ( n = 12) 15 ± 4 15 ± 4 .34
Walls to papillary muscles transverse plane distance (mm) ( n = 76)
Anterior wall to plane—any papillary surgery ( n = 63) 25 ± 6 26 ± 6 .39
Posterior wall to plane—any papillary surgery ( n = 63) 15 ± 4 15 ± 4 .75
Anterior wall to plane—no papillary surgery ( n = 12) 23 ± 7 24 ± 7 .63
Posterior wall to plane—no papillary surgery ( n = 12) 15 ± 4 14 ± 4 .25
Anterolateral papillary muscle width—papillary thinning surgery (mm) 14 ± 3 13 ± 3 .86
Posteromedial papillary muscle width—papillary thinning surgery (mm) 13 ± 3 13 ± 2 .69
Doppler measurements (mm/sec) ( n = 76)
Early diastolic mitral inflow velocity (E wave) 80 ± 22 82 ± 24 .79
Late diastolic mitral inflow velocity (A wave) 77 ± 26 75 ± 25 .52
Tissue Doppler systolic velocity (S′ lateral) 8.7 ± 3 8.9 ± 3 .92
Tissue Doppler systolic velocity (S′ septal) 7.6 ± 3 6.8 ± 2 <.05
Tissue Doppler early diastolic velocity (e′ lateral) 8.2 ± 3 9.2 ± 4 .25
Tissue Doppler early diastolic velocity (e′ septal) 6.3 ± 2.6 6.2 ± 2.4 .054

P < .004, comparison of AML before surgery, between the plicated and nonplicated groups.

Apr 21, 2018 | Posted by in CARDIOLOGY | Comments Off on Echocardiography before and after Resect-Plicate-Release Surgical Myectomy for Obstructive Hypertrophic Cardiomyopathy

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