Journal of the American College of Cardiology
Volume 37, Issue 1, January 2001 DOI: 10.1016/S0735-1097(00)01045-7
PDF Article
Clinical study: hypertrophic cardiomyopathy

Echocardiographic insights into the mechanisms of relief of left ventricular outflow tract obstruction after nonsurgical septal reduction therapy in patients with hypertrophic obstructive cardiomyopathy

Ramiro Flores-Ramirez, Nasser M Lakkis, Katherine J Middleton, Donna Killip, William H Spencer III and Sherif F Nagueh

Author + information

vol. 37 no. 1 208-214
DOI: 
https://doi.org/10.1016/S0735-1097(00)01045-7
Published By: 
Journal of the American College of Cardiology
Print ISSN: 
0735-1097
Online ISSN: 
1558-3597
History: 
  • Received March 3, 2000
  • Revision received July 24, 2000
  • Accepted September 11, 2000
  • Published online January 1, 2001.
Copyright & Usage: 
American College of Cardiology

Author Information

  1. Ramiro Flores-Ramirez, MDa,
  2. Nasser M Lakkis, MD, FACCa,
  3. Katherine J Middleton, RCTa,
  4. Donna Killip, RNa,
  5. William H Spencer III, MD, FACCa and
  6. Sherif F Nagueh, MD, FACCa,* (sherifn{at}bcm.tmc.edu)
  1. a
  1. ↵*Reprint requests and correspondence: Dr. Sherif F. Nagueh, Cardiology Section, 6550 Fannin Street, SM-1246, Houston, Texas 77030

Abstract

OBJECTIVES

We sought to evaluate the mechanisms by which nonsurgical septal reduction therapy (NSRT) reduces left ventricular outflow tract (LVOT) obstruction in patients with hypertrophic obstructive cardiomyopathy (HOCM) both acutely and on a long-term basis.

BACKGROUND

NSRT reduces LVOT obstruction in patients with HOCM and leads to symptomatic improvement. The mechanisms involved, however, are not well studied.

METHODS

An initial group of 30 HOCM patients (age 46 ± 17, 16 women) who underwent NSRT had echocardiographic studies performed at baseline and six months after the procedure. Measurements included LVOT diameter, end-diastolic distance between the anterior mitral leaflet and interventricular septum, septal base function and the angle between LV systolic flow and the protruding mitral leaflets. In addition, pulse Doppler recordings at a point 2.5 cm apical to the mitral valve were acquired and analyzed for peak and mean ejection velocity, peak acceleration rate and the ratio of acceleration time to ejection time (AT/ET).

RESULTS

Significant changes were observed after the procedure, with widening in the LVOT, thinning and akinesis of the septal base, decrease in the angle between LV systolic flow and the protruding mitral leaflets, a decrease in peak acceleration rate and an increase in AT/ET. All of these variables had significant relations with the decrease in LVOT obstruction (r = 0.5 to 0.79, p < 0.01). These correlations were then evaluated in a test group of 15 patients who underwent echocardiographic examinations at baseline, acutely in the catheterization laboratory with ethanol injection and at six weeks post NSRT. Acute changes in peak acceleration rate (r = 0.65) and AT/ET (r = 0.73) related significantly (p < 0.01) to the decrease in LVOT obstruction with ethanol. At six weeks, changes similar to those noted in the initial group were observed in LVOT geometry, the angle between LV systolic flow and the protruding mitral leaflets, peak acceleration rate and AT/ET. In both populations combined, these parameters accounted for 72% to 77% of the variance in gradient reduction.

CONCLUSIONS

Changes in LV ejection dynamics and septal base function account in part for the acute relief of LVOT gradient after NSRT. The long-term relief of obstruction is dependent on remodeling of LVOT as well as the changes in LV ejection.

Hypertrophic obstructive cardiomyopathy (HOCM) is a complex disease with a great diversity of presentation. The clinical course varies markedly, from asymptomatic to heart failure and sudden death. Molecular studies of the genetic alterations in this disease have provided some insight into the heterogeneity of its clinical features (1). Beta-blockers, the calcium channel blocker verapamil and disopyramide have traditionally been administered to symptomatic patients. In some, medical therapy ultimately proves insufficient to control symptoms and other therapeutic strategies are needed. In the few patients in whom medical therapy fails, septal myectomy is usually offered. At experienced centers, surgery produces a dramatic elimination of the outflow tract gradient in ≥90% of the patients along with reduction of symptoms and improvement in exercise tolerance (2–8). Its mechanism appears to be predominantly through enlarging the left ventricular outflow tract (LVOT), which in turn decreases the forces causing obstruction, usually with a sustained effect (9,10). Recently, the injection of alcohol into the first major septal coronary artery has been advanced as a means of reducing septal thickness and LVOT gradient in HOCM patients (11–14). Similar mechanisms may be operable after nonsurgical septal reduction therapy (NSRT). We hypothesized that NSRT leads to acute changes in septal base function, and later on, LV remodeling (including LVOT), which may result in reducing the obstruction in HOCM patients. The purpose of this study, therefore, was to examine these mechanisms both acutely and on a longer term basis.

Methods

The initial patient population consisted of 30 consecutive subjects (age 46 ± 17 years, 16 women) with severe, symptomatic HOCM despite maximal medical therapy who underwent NSRT at our institution. All patients were in sinus rhythm and had asymmetric septal hypertrophy and a baseline LVOT gradient ≥40 mm Hg at rest. Twenty-nine patients were receiving beta-blockers, 12 were on verapamil, and 10 were on disopyramide. On follow-up only 10 were still receiving beta-blockers (at a lower dose compared with baseline). Baylor College of Medicine’s Institutional Review Board approved the study protocol, and all patients provided written, informed consent prior to participation. The echocardiographic evaluations were performed at baseline and six months after NSRT.

Echocardiographic studies

Echocardiograms were performed on either an Acuson or a Hewlett-Packard ultrasound imaging system. Patients were imaged while in a left lateral position in the echocardiography laboratory and while in a supine position in the catheterization laboratory. Standard parasternal and apical views were acquired first. Color Doppler was applied in these views to assess the severity of mitral regurgitation (MR) and to help determine the location of intraventricular gradients. Color-guided continuous-wave Doppler was performed in the apical views to determine the peak LVOT gradient, with care taken to avoid contamination with the MR jet. In the apical long-axis view, the sample volume was positioned at a point 2.5 cm apical to the mitral coaptation locale and 1 cm from the interventricular septum. This site was chosen in order to record LV systolic flow far from the area of septal leaflet contact and therefore avoid recording of the flow acceleration developing in relation to LVOT obstruction (15).

Echocardiographic analysis

Investigators blinded to the patient’s identity and clinical status performed the analysis. In the parasternal long-axis views, septal base thickness and excursion, systolic LVOT diameter and the end-diastolic distance between the anterior mitral valve leaflet (AML) and the septum were measured. The mean interobserver differences for LVOT diameter and AML septal distance measurements were 0.2 ± 0.1 and 0.15 ± 0.1 cm, respectively. In the short-axis views, septal base function was assessed as: (end-systolic thickness − end-diastolic thickness)/end-diastolic thickness (mean interobserver difference = 5% ± 3%; mean intraobserver difference = 3% ± 2%). Mitral regurgitation was assessed utilizing the size of the regurgitant jet in relation to the left atrial (LA) area (16). A semiquantitative score was applied where 0 = no or trivial MR, 1 = mild MR, 2 = moderate MR and 3 = severe MR (intra- and interobserver 100% agreement). The direction of the color-flow stream was determined in the parasternal long-axis view as the angle between the line bisecting color flow and LV basal posterior wall (10). In the apical five-chamber view, LV flow direction was determined by a line bisecting systolic flow as noted by color Doppler, and the angle of this line with the protruding mitral leaflets was then measured (mean interobserver difference = 6 ± 3 degrees; mean intraobserver difference = 3 ± 2 degrees) (17). The Doppler tracings at the point 2.5 cm apical to the mitral coaptation locale were analyzed for peak and mean velocity, peak acceleration rate, acceleration time and ejection time. The ratio between the acceleration and ejection times (AT/ET) was also determined. Peak LVOT gradient was calculated as: gradient (mm Hg) = 4v2m/s) (18). Left ventricular volumes and ejection fraction were calculated as recommended by the American Society of Echocardiography (19).

Test population

The relations identified in the initial group of patients were validated in 15 consecutive patients (age 46 ± 15 years, six women). All 15 patients were on beta-blockers and/or verapamil at baseline. Cardiac medications were stopped for three days before NSRT. At six weeks, only five patients with some recurrence in LVOT gradient were still on beta-blockers, though at a lower dose. Data were acquired at baseline, immediately after NSRT in the catheterization laboratory and six weeks afterward.

Statistical analysis

Paired ttests were used to evaluate the changes after NSRT in the initial population. Repeated measures of ANOVA with Bonferroni correction were applied to compare the Doppler and LV geometric changes at the three different time intervals of data acquisition in the test population. Regression analysis was utilized to relate the changes in LVOT gradient to the two-dimensional and Doppler measurements. Significance was set at a p value ≤0.05.

Results

Initial population

All but one of the 30 patients experienced a significant reduction in LVOT gradient. Septal reduction therapy was not possible in the patient with an unchanged gradient because of unsuitable coronary anatomy. Six months after NSRT, septal basal thickness was significantly less (p < 0.01), as was its systolic function, with this myocardial segment developing features of scar tissue (i.e., thinning and akinesis) but with no paradoxical septal motion noted in this cohort. The systolic excursion of the septum towards the mitral valve decreased from a median of 0.6 cm at baseline to 0 cm (range = 0 to 0.2 cm) at six months. Several changes were also observed in the LVOT. The LVOT widened as the basal interventricular septum became thinner (Fig. 1), which led to an increase in the end-diastolic distance between the AML and the basal septum (Table 1). Importantly, several significant relations were present between LVOT gradient reduction and these geometric changes (Fig. 2). Regarding mitral leaflet motion, systolic anterior motion (SAM) of the mitral valve was present, with mitral-septal contact extending for ≥30% of systole’s duration at baseline. After NSRT, the systolic distance between the mitral valve and septum was >1 cm in 23 patients and <1 cm in six patients, with none having mitral-septal contact.

Figure 1
Figure 1

Parasternal long-axis view (LAX) of left ventricular outflow tract at baseline and six months after nonsurgical septal reduction therapy (NSRT). Note the thinning of the septal base and the widening of the outflow tract.

Figure 2
Figure 2

Relation of the change in left ventricular outflow tract gradient to that in left ventricular outflow tract (LVOT) diameter (left)and end-diastolic mitral septal distance (right)as observed in the initial population. AML = anterior mitral leaflet.

View this table:
Table 1

LV Changes After NSRT in the Initial Populationlegend

Accompanying the remodeling of the LVOT, the angle between the direction of ventricular systolic blood flow and LV posterior wall (58 ± 11 to 30 ± 10 degrees, p < 0.01), as well as between the flow direction and the coapted mitral leaflets, decreased (Table 1, p < 0.01) and accounted for 41% of the variance observed in gradient reduction (Fig. 3). Of note, changes in LV ejection also appeared to play a role in gradient reduction. After NSRT, the peak acceleration rate at the point proximal to LVOT obstruction was significantly less and there was an increase in the AT/ET ratio. Both of these parameters also related significantly to the gradient reduction at six months (Fig. 4).

Figure 3
Figure 3

Relation of the change in left ventricular outflow tract (LVOT) gradient to that in the angle between left ventricular systolic flow and mitral leaflets as observed in the initial population. AML = anterior mitral leaflet.

Figure 4
Figure 4

Relation of the change in left ventricular outflow tract gradient (LVOT) to that in peak acceleration rate (left)and acceleration time/ejection time (AT/ET) (right)in the initial population.

Test population (Table 2)

View this table:
Table 2

LV Changes After NSRT in the Test Populationlegend

In the catheterization laboratory, immediately after intracoronary ethanol injection, peak LVOT gradient was significantly lower. Changes were observed in peak acceleration rate and AT/ET (Fig. 5), as well as in septal base function. These parameters were significantly related to the reduction in LVOT gradient (Fig. 6). Systolic septal excursion toward the mitral valve was reduced from 0.5 ± 0.3 cm at baseline to 0.3 ± 0.15 cm in the catheterization lab (p < 0.05). Although SAM was still observed in the acute studies, the duration of the mitral-septal contact was <30% of systole. No changes were noted in the LVOT diameter or in the angle between AML and blood flow. MR improvement paralleled the improvement in LVOT obstruction (r = 0.81, p < 0.01).

Figure 5
Figure 5

Pulse Doppler recordings of left ventricular systolic flow at a point 2.5 cm apical to the mitral valve. The left panel shows the baseline data with immediate changes after ethanol injection in the middle panel and the six-week results on the right. Notice the increase in acceleration time relative to ejection time. NSRT = nonsurgical septal reduction therapy.

Figure 6
Figure 6

Relation of the change in left ventricular outflow tract (LVOT) gradient acutely in the catheterization laboratory to that in peak acceleration rate (left)and acceleration time/ejection time (AC/ET) (right)in the test population.

After six weeks, LVOT diameter and the distance between AML and the septum were significantly higher in comparison to baseline (Fig. 7). Both the angle between AML and blood flow as well as basal septal thickness and septal systolic excursion (0.2 cm, p < 0.05 vs. baseline) were significantly lower. In nine patients the systolic distance between the mitral leaflet and the septum was >1 cm, but in six cases, mitral-septal contact was still present (in four patients <30% and in two patients ≥30% of systole). In general, the acute changes in LV ejection dynamics (peak acceleration rate and AT/ET) were preserved at six weeks (Table 2).

Figure 7
Figure 7

Relation of the change in left ventricular outflow tract gradient to that in left ventricular outflow tract (LVOT) diameter (left)and end-diastolic mitral septal distance (right)six weeks after NSRT as observed in the test population. AML = anterior mitral leaflet.

Interestingly, five patients had some recurrence of LVOT gradient elevation at six weeks despite an initial acute reduction of ≥50%. This elevation occurred despite a decrease in septal basal thickness and in septal systolic function. Also, all five patients demonstrated no change in the angle between AML and blood flow or the angle between blood flow and LV posterior wall, and their peak acceleration rate and AT/ET approached baseline values. Furthermore, LVOT diameter in these five patients had a minimal increase (1.82 ± 0.08 vs. 1.88 ± 0.13, p = 0.07). These five patients had a mean volume of 1.3 ± 1 ml of ethanol injection versus 2.8 ± 1 ml in the other 10 (p = 0.08). Both the mean value of the peak CK (750 ± 300 vs. 1,560 ± 550, p = 0.07) and the septal area opacified during intracoronary contrast injection (3.3 ± 1.9 vs. 6.5 ± 1.5 cm2, p = 0.06) were lower.

At the end of the study, the initial and test populations were combined in order to examine the impact of changes in LVOT geometry, the angle between AML and blood flow, and ventricular ejection on the long-term reduction in LVOT gradient. Significant results that were similar in each separate group of patients were observed in the total population. Multiple regression models (Table 3)demonstrated that, in general, changes in LVOT geometry, the angle between AML and blood flow, septal function and LV ejection dynamics accounted for 72% to 77% of the variance in the magnitude of gradient reduction. Likewise, in the 45 patients combined, MR severity decreased in parallel to the improvement in LVOT obstruction (r = 0.83, p < 0.01).

View this table:
Table 3

Relation of LVOT Gradient Reduction to Changes in Outflow Geometry and LV Ejectionlegend

Discussion

The present study demonstrates that changes in LV ejection dynamics and septal base function account in part for the acute relief of LVOT gradient after NSRT. The long-term relief of LVOT obstruction, however, appears to be dependent on remodeling of LVOT together with changes in LV flow and ejection.

Mechanism of the acute relief of LVOT obstruction with NSRT

As the present study shows, NSRT induces an acute decrease in septal thickening and peak acceleration rate of LV ejection with no geometric changes. These observations indicate that changes in ejection and septal thickening alone play an important role in relieving obstruction. Furthermore, because the change in septal excursion is small (0.2 cm), the decrease in flow acceleration appears to be the more important factor in reducing obstruction acutely.

LVOT obstruction is related to the apposition of mitral valve leaflets with the interventricular septum (20), which occurs as both the basal septum and mitral leaflet(s) move toward one another. Because the acute interruption of basal septum blood flow results in its hypo- or akinesis, it is not surprising that the relief of outflow tract obstruction was in part related to the extent of septal dysfunction. Interestingly, mitral valve motion was apparently not restricted, as the mitral valve had the same excursion in diastole and continued to move toward the septum during systole. These findings indicate that NSRT has no immediate effect on the mitral valve apparatus. In addition, there appear to be global changes in LV ejection that take place acutely. The peak acceleration rate at a point proximal to LVOT obstruction was significantly lower. This alteration led to later onset of the dynamic narrowing of the LVOT. Accordingly, less time was available for the progressive increase in outflow gradient (15). The electromechanical changes after NSRT with the development of bundle branch block (right bundle branch block alone in 60% and with left anterior hemiblock in 20%) and further inhomogeneity in LV contraction (21)may be reasons for the lower acceleration rate and the later onset of the peak ejection velocity. Interestingly, pacemaker therapy in HOCM patients—with ensuing inhomogeneity in LV contraction—was recently reported to produce a rightward shift in the end-systolic pressure–volume relation (22), lending further credence to the hypothesis relating conduction abnormalities to the reduction in the acceleration rate. Alternatively, it is also possible that acute septal ischemia or infarction lead to slower acceleration of LV ejection as the septal contribution to LV systolic function diminishes.

Mechanism of the long-term relief of LVOT obstruction with NSRT

Our study shows the important contribution of LVOT widening to the relief of obstruction after NSRT. LVOT widening develops secondary to infarction necrosis and replacement fibrosis of the septal base. This LVOT remodeling is already apparent by six weeks and in some patients further widening develops at later follow-up. Of note, this mechanism is similar to the acute results induced by surgical myectomy, which has been shown to be associated with relief of obstruction and symptomatic improvement (2–10). There are additional reasons for the relief of LVOT obstruction by NSRT. Mitral valve leaflets have been observed to be redundant (20,23,24)and anteriorly displaced (25)in patients with HOCM. Consequently, they readily protrude into the LVOT stream, making them amenable to the action of the drag forces. These forces have direct relations with the LV ejection velocity and the exposed surface area of the protruding leaflets such that the drag forces push the mitral leaflets against the septum and contribute to LVOT obstruction. Following NSRT, the angle between ventricular flow and mitral valve leaflets decreases as the leaflets become more parallel with the direction of blood flow. This happens as flow is directed anteriorly and septally. The ejection velocity proximal to the mitral valve also decreases after the procedure. In all likelihood, therefore, the drag forces decrease with successful NSRT. Likewise, similar observations were made after surgical reduction of the interventricular septum (10). Furthermore, changes in LV ejection dynamics still appear to play a role in the reduction of outflow tract gradient, but with a somewhat lower contribution in comparison to the geometric changes.

The recurrence of some outflow tract obstruction in five of the 15 test group patients in association with smaller amounts of ethanol injection and smaller infarcts suggests that not only a critical site but also a certain threshold extent of septal infarction is needed for the success of this procedure. However, this remains a hypothesis for further investigation.

Acknowledgements

We thank the reviewer for the helpful and stimulating comments. The authors gratefully acknowledge the assistance of Maria E. Frias.

Footnotes

  • ☆ This work was supported in part by grants from the T.L.L. Temple Foundation, Lufkin, Texas; the Dunn Foundation; and The Methodist Hospital Foundation, Houston, Texas. Dr. Flores-Ramirez was supported by grants from both the Hospital Universitario “Jose E. Gonzalez” U.A.N.L. and the Sociedad Mexicana de Cardiologia. Dr. Nagueh is supported by a Scientist Development Grant (0030235N) from the AHA National Center, Dallas, Texas.

Abbreviations
AML
anterior mitral leaflet
AT
acceleration time
ET
ejection time
HOCM
hypertrophic obstructive cardiomyopathy
LA
left atrial
LVOT
left ventricular outflow tract
MR
mitral regurgitation
NSRT
nonsurgical septal reduction therapy
SAM
systolic anterior motion
  • Received March 3, 2000.
  • Revision received July 24, 2000.
  • Accepted September 11, 2000.

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