E ECHO DIDACTICS
Echocardiographic Assessment of Systolic Anterior Motion of the Mitral Valve Brad J. Hymel, MD, and Matthew M. Townsley, MD INDEX CASE
A 33-year-old woman with hypertrophic cardiomyopathy (HCM) presents for a septal myectomy. The preoperative transthoracic echocardiogram shows normal left ventricular (LV) function, severe hypertrophy of the interventricular septum, and systolic anterior motion (SAM) of the anterior mitral valve leaflet (AMVL) with moderate mitral regurgitation (MR). The resting peak gradient through the LV outflow tract (LVOT) is elevated at 67 mm·Hg.
DISCUSSION
SAM is defined as the anterior translation of 1 or both mitral valve (MV) leaflets into the LVOT during systole.1 The extent of this translation is variable and leads to differing degrees of SAM, ranging from no hindrance to blood flow to profound LVOT obstruction (LVOTO) and cardiovascular collapse. This variability results from the dynamic nature of SAM, because its presence and severity depend on the loading conditions and contractile state of the heart.2 Decreased LV end-diastolic volume and systemic vascular resistance, as well as increased LV contractility and chronotropy can all precipitate or exacerbate SAM. The clinical significance of SAM depends on the degree of LVOTO, which corresponds to the onset, extent, and duration of mitral-septal contact.2 The treatment of hemodynamically significant SAM focuses on alleviating LVOTO. While SAM is a common cause of LVOTO, there are also other potential etiologies (Table 1).
SAM in HCM-Pathophysiology
HCM is a genetic disorder of LV hypertrophy with no identifiable cause (i.e., aortic stenosis, chronic hypertension). The basal septal wall is often severely hypertrophied, leading to narrowing of the LVOT, whose borders include the septum and the AMVL. Systolic septal thickening occurring during LV contraction further diminishes the outflow tract dimension, resulting in elevated LVOT blood flow velocities. Hypertrophied, anteriorly displaced papillary muscles and elongated MV leaflets shift the mitral apparatus toward the enlarged septum. With this shift, the posterior MV leaflet (PMVL) now coapts closer to the base of the AMVL, From the Department of Anesthesiology, Division of Cardiothoracic Anesthesiology, University of Alabama at Birmingham, Birmingham, Alabama. Accepted for publication January 9, 2014. Funding: No Funding Required. The authors declare no conflicts of interest. Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s Web site (www.anesthesia-analgesia.org). Reprints will not be available from the authors. Address correspondence to Matthew M. Townsley, MD, Department of Anesthesiology, Division of Cardiothoracic Anesthesiology, University of Alabama at Birmingham, 619 South 19th St., JT 845, Birmingham, AL 35249. Address e-mail to [email protected]. Copyright © 2014 International Anesthesia Research Society DOI: 10.1213/ANE.0000000000000196
June 2014 • Volume 118 • Number 6
resulting in excess slack AMVL tissue protruding beyond the coaptation point. High-velocity flow can then lift the anteriorly displaced, slack MV leaflet into the LVOT in a phenomenon known as the Venturi effect, the initial proposed SAM mechanism.3 More recent evidence, however, proposes a drag force as the more predominant SAM mechanism. This suggests that the slack portion of the MV leaflet is swept into the LVOT and toward the septum by high-velocity LVOT flow. The narrowed mitral-aortic angle, created by septal hypertrophy and structural abnormalities of the mitral apparatus, aligns the MV leaflet in the direction of this flow, subjecting it to the drag force.1,3 During SAM, as the distal AMVL remains in the LVOT during systole, adequate mitral coaptation is inhibited, resulting in a posteriorly directed jet of MR. A channel created by the distal portions of both MV leaflets directs the regurgitant flow posteriorly through this opening.4 The MR occurs in mid-to-late systole after the onset of SAM and LVOTO. Hemodynamic management focuses on alleviating the LVOTO, because this will lead to resolution or improvement of the MR.
SAM in HCM-Echocardiographic Assessment
To assess for the presence of SAM in patients with HCM, the comprehensive transesophageal echocardiographic examination (TEE) begins with focused 2-dimensional (2D) imaging in either a midesophageal long-axis (ME LAX) or ME 5-chamber view. The nonstandard ME 5-chamber view, a variation of the more posteriorly directed ME 4-chamber view, is obtained by slight withdrawal or anteflexion of the probe from a ME 4-chamber view until the LVOT (“fifth chamber”) and aortic valve (AV) are seen in the center of the screen. The anterolateral portion of the MV is seen in this view. In either view, basal septal hypertrophy, often >2.0 cm (normal 0.6–0.9 cm, severe hypertrophy ≥1.7 cm), is assessed and measured (Fig. 1).5 Measurement is performed at end-diastole to exclude the effects of systolic thickening. When planning for septal myectomy, the distance from the aortic annulus to the point of maximum septal thickness is measured to guide the surgical approach.1,2 The LVOT diameter and distance from the mitral coaptation point to the septum (C-sept distance) are also measured, both at the onset of systole. A narrow LVOT (≤2.0 cm) and short C-sept distance (2.0 cm AMVL:PMVL ratio
Echocardiographic Assessment of Systolic Anterior Motion of the Mitral Valve Brad J. Hymel, MD, and Matthew M. Townsley, MD INDEX CASE
A 33-year-old woman with hypertrophic cardiomyopathy (HCM) presents for a septal myectomy. The preoperative transthoracic echocardiogram shows normal left ventricular (LV) function, severe hypertrophy of the interventricular septum, and systolic anterior motion (SAM) of the anterior mitral valve leaflet (AMVL) with moderate mitral regurgitation (MR). The resting peak gradient through the LV outflow tract (LVOT) is elevated at 67 mm·Hg.
DISCUSSION
SAM is defined as the anterior translation of 1 or both mitral valve (MV) leaflets into the LVOT during systole.1 The extent of this translation is variable and leads to differing degrees of SAM, ranging from no hindrance to blood flow to profound LVOT obstruction (LVOTO) and cardiovascular collapse. This variability results from the dynamic nature of SAM, because its presence and severity depend on the loading conditions and contractile state of the heart.2 Decreased LV end-diastolic volume and systemic vascular resistance, as well as increased LV contractility and chronotropy can all precipitate or exacerbate SAM. The clinical significance of SAM depends on the degree of LVOTO, which corresponds to the onset, extent, and duration of mitral-septal contact.2 The treatment of hemodynamically significant SAM focuses on alleviating LVOTO. While SAM is a common cause of LVOTO, there are also other potential etiologies (Table 1).
SAM in HCM-Pathophysiology
HCM is a genetic disorder of LV hypertrophy with no identifiable cause (i.e., aortic stenosis, chronic hypertension). The basal septal wall is often severely hypertrophied, leading to narrowing of the LVOT, whose borders include the septum and the AMVL. Systolic septal thickening occurring during LV contraction further diminishes the outflow tract dimension, resulting in elevated LVOT blood flow velocities. Hypertrophied, anteriorly displaced papillary muscles and elongated MV leaflets shift the mitral apparatus toward the enlarged septum. With this shift, the posterior MV leaflet (PMVL) now coapts closer to the base of the AMVL, From the Department of Anesthesiology, Division of Cardiothoracic Anesthesiology, University of Alabama at Birmingham, Birmingham, Alabama. Accepted for publication January 9, 2014. Funding: No Funding Required. The authors declare no conflicts of interest. Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s Web site (www.anesthesia-analgesia.org). Reprints will not be available from the authors. Address correspondence to Matthew M. Townsley, MD, Department of Anesthesiology, Division of Cardiothoracic Anesthesiology, University of Alabama at Birmingham, 619 South 19th St., JT 845, Birmingham, AL 35249. Address e-mail to [email protected]. Copyright © 2014 International Anesthesia Research Society DOI: 10.1213/ANE.0000000000000196
June 2014 • Volume 118 • Number 6
resulting in excess slack AMVL tissue protruding beyond the coaptation point. High-velocity flow can then lift the anteriorly displaced, slack MV leaflet into the LVOT in a phenomenon known as the Venturi effect, the initial proposed SAM mechanism.3 More recent evidence, however, proposes a drag force as the more predominant SAM mechanism. This suggests that the slack portion of the MV leaflet is swept into the LVOT and toward the septum by high-velocity LVOT flow. The narrowed mitral-aortic angle, created by septal hypertrophy and structural abnormalities of the mitral apparatus, aligns the MV leaflet in the direction of this flow, subjecting it to the drag force.1,3 During SAM, as the distal AMVL remains in the LVOT during systole, adequate mitral coaptation is inhibited, resulting in a posteriorly directed jet of MR. A channel created by the distal portions of both MV leaflets directs the regurgitant flow posteriorly through this opening.4 The MR occurs in mid-to-late systole after the onset of SAM and LVOTO. Hemodynamic management focuses on alleviating the LVOTO, because this will lead to resolution or improvement of the MR.
SAM in HCM-Echocardiographic Assessment
To assess for the presence of SAM in patients with HCM, the comprehensive transesophageal echocardiographic examination (TEE) begins with focused 2-dimensional (2D) imaging in either a midesophageal long-axis (ME LAX) or ME 5-chamber view. The nonstandard ME 5-chamber view, a variation of the more posteriorly directed ME 4-chamber view, is obtained by slight withdrawal or anteflexion of the probe from a ME 4-chamber view until the LVOT (“fifth chamber”) and aortic valve (AV) are seen in the center of the screen. The anterolateral portion of the MV is seen in this view. In either view, basal septal hypertrophy, often >2.0 cm (normal 0.6–0.9 cm, severe hypertrophy ≥1.7 cm), is assessed and measured (Fig. 1).5 Measurement is performed at end-diastole to exclude the effects of systolic thickening. When planning for septal myectomy, the distance from the aortic annulus to the point of maximum septal thickness is measured to guide the surgical approach.1,2 The LVOT diameter and distance from the mitral coaptation point to the septum (C-sept distance) are also measured, both at the onset of systole. A narrow LVOT (≤2.0 cm) and short C-sept distance (2.0 cm AMVL:PMVL ratio
