FOCUS ISSUE: HYPERTROPHIC CARDIOMYOPATHY: STATE-OF-THE-ART PAPER
Reflections of Inflections in Hypertrophic Cardiomyopathy
Mark V. Sherrid, MD*,
Omar Wever-Pinzon, MD,
Ajay Shah, MD and
Farooq A. Chaudhry, MD
Echocardiography Laboratory and Hypertrophic Cardiomyopathy Program, Division of Cardiology, St. Luke's–Roosevelt Hospital Center, Columbia University, College of Physicians and Surgeons, New York, New York
Manuscript received February 16, 2009;
accepted March 18, 2009.
* Reprint requests and correspondence: Dr. Mark V. Sherrid, St. Luke's–Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons, 1000 10th Avenue, 3B-30, New York, New York 10019 (Email: msherrid{at}chpnet.org).
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Abstract
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The shape of Doppler velocity tracings in obstructive hypertrophic cardiomyopathy offers insights into its pathophysiology. Inflection points are the points on a curve where its shape changes from concave to convex, or vice versa. These dynamic systolic abnormalities are caused: 1) by the amplifying nature of the obstruction; and 2) by the adverse effect of the sudden imposition of afterload in midsystole. The midsystolic drop in left ventricular ejection velocities and the premature termination of longitudinal shortening are compelling evidence of the deleterious mechanical effect of obstruction on the ventricle. This dynamic systolic dysfunction, demonstrated on the Doppler curves, may contribute to heart failure symptoms and adverse outcome. In outflow obstruction, these abnormalities normalize after abolition of gradient. Therefore, their detection in an individual patient confirms obstruction as a therapeutic target.
Key Words: hypertrophic cardiomyopathy • left ventricular outflow obstruction • echocardiography • Doppler echocardiography • heart failure
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Abbreviations and Acronyms
| | HCM = hypertrophic cardiomyopathy | | LV = left ventricle/ventricular | | LVOT = left ventricular outflow tract | | SAM = systolic anterior motion of the mitral valve |
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In most patients with hypertrophic cardiomyopathy (HCM), obstruction is caused by systolic anterior motion of the mitral valve (SAM) and mitral-septal contact. These patients have a typical shape on continuous wave Doppler tracings through the orifice in the outflow tract and left ventricular (LV) body that shed light on the mechanics of obstruction (Fig. 1). In the rising portion of the continuous wave Doppler velocity tracing, an inflection point occurs early in systole where the tracing changes from convex-to-the-left to concave-to-the-left. This point is generally between a velocity of 1 and 2.5 m/s. The curve then continues convex-to-the-left until the peak velocity. This early systolic inflection point correlates temporally with the time of mitral-septal contact and beginning of the pressure gradient across the LV outflow tract (1–3).
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Figure 1 CW Doppler Echocardiographic Tracing Through the Obstructing Orifice in the LVOT of a Patient With a Gradient of 64 mm Hg
The inflection point is shown with a long arrow and the concave-to-the-left contour is shown with arrowheads. The contour after the inflection point is concave-to-the-left because of the progressive decrease in the size of the orifice formed as the mitral valve is pushed by the rising pressure gradient into the septum. CW = continuous wave; LVOT = left ventricular outflow tract.
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The concave-to-the-left pattern that follows the inflection point is a familiar pattern: it is that of increasing acceleration. This pattern contrasts with that seen in aortic stenosis where as velocity increases, acceleration decreases. In HCM, as velocity increases, acceleration increases too (Fig. 2). Acceleration increases because of the progressive decrease in the size of the orifice formed as the mitral valve is pushed by the rising pressure gradient into the septum (3–6). In contrast, in aortic stenosis the orifice remains relatively fixed in systole. In HCM, obstruction begets more obstruction. The orifice narrows because of the rising pressure difference, and the pressure difference rises because of the decreasing orifice size—an amplifying feedback loop. What of the inflection point? LV ejection is unobstructed in early systole—at the inflection point mitral-septal contact and obstruction begin (4,6).
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Figure 2 Contrasting the CW Doppler Through the Orifice of Patients With Aortic Stenosis and Obstructive HCM
In aortic stenosis the orifice remains relatively fixed in systole. In hypertrophic cardiomyopathy (HCM) obstruction begets more obstruction, and the orifice narrows through systole. The left ventricular ejection is unobstructed in early systole, and the curve is convex-to-the-left. At the inflection point (long arrow), mitral-septal contact and obstruction begin. The orifice narrows because of the rising pressure difference; the pressure difference rises because of the decreasing orifice size—an amplifying feedback loop. Hence, the contour shows an increasing acceleration pattern: it is concave-to-the-left (arrowheads). CW = continuous wave. Adapted, with permission, from Sherrid et al. (1).
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The amplifying nature of outflow obstruction has significance for the therapy of symptomatic gradients. The longer in systole that the gradient acts, and the longer the duration of mitral-septal contact, the higher the gradient. Successful therapy abolishes or delays SAM (6). The amplifying nature of outflow obstruction also may explain the dramatic changes in gradient that occur with loading conditions, and may explain the sometimes explosive emergence of severe outflow obstruction in the elderly.
In obstructive HCM with gradients >60 mm Hg, another inflection point occurs simultaneously, but apical of the mitral valve in the body of the LV cavity. At the entrance of the outflow tract, a midsystolic drop in LV ejection velocities and flow occur because of the obstruction. The abrupt drop in velocity averages 60% from its peak. It has been called the "lobster claw abnormality" because of its characteristic appearance (1,3) (Fig. 3). The inflection point, the beginning of the drop in LV ejection velocities occurs just after the moment of mitral-septal contact. The nadir of the drop times exactly with the peak of the gradient in the left ventricular outflow tract (LVOT) because the drop is caused by afterload—mismatch (7). The LV is unable to maintain instantaneous ejection against the sudden rise in afterload. Dobutamine exacerbates the drop in ejection velocities and flow (3). Because of continuity considerations, the midsystolic drop in velocity can only be explained by a progressive decrease in orifice size, because velocities in the jet rise while velocities in the LV fall. Midsystolic closure of the aortic valve seen on M-mode echocardiography is caused by the drop in LV ejection velocity and flow (8) (Fig. 4). The midsystolic drop in velocity and flow is caused by premature and abrupt termination of LV longitudinal shortening (2,9). Moreover, both the premature truncation of shortening and the drop in ejection flow are reversed by abolition of the gradient (2). Breithardt et al. (9) have recorded an inflection point in the velocity of systolic shortening on tissue Doppler tracings from the apex of patients with obstructive HCM (9) (Fig. 5).
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Figure 3 Doppler Echocardiographic Tracings in a Patient With SAM of the Mitral Valve, Mitral-Septal Contact, and an LVOT Gradient of Over 100 mm Hg
(A) Pulsed wave (PW) tracing with the cursor at the entrance of the LVOT, upstream from the mitral valve. The midsystolic drop in left ventricular ejection velocities begins at the inflection point (arrows). It is caused by afterload-mismatch (7). The left ventricle is unable to maintain instantaneous ejection against the sudden rise in afterload. (B) CW tracing through both the orifice and also through the entrance of the LVOT that is apical of the mitral valve. After the inflection point (white arrow), the contour of the jet velocity becomes concave-to-the-left. The superimposed midsystolic drop that occurs at the entrance of the LVOT is shown with the yellow arrow. The midsystolic drop also begins at the same point (white arrow). SAM = systolic anterior motion of the mitral valve; other abbreviations as in Figure 1.
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Figure 4 4 Tracings From a Patient With LVOT Systolic Gradient of 120 mm Hg Due to SAM and Mitral-Septal Contact
Tracings were obtained during the same examination. (A) M-mode echocardiogram shows midsystolic closure of the aortic valve leaflets. The arrow points to midsystolic closure. (B) The midsystolic drop in left ventricular ejection velocities are shown on pulsed Doppler tracing obtained from the apex. The pulsed cursor is in the body of the left ventricle, at the entrance of the left ventricular outflow tract (LVOT). Velocity drops from 0.8 to 0.5 m/s. The arrow indicates the nadir of the midsystolic drop. (C) Tissue Doppler echocardiogram of the interventricular septum as measured from the apex of the left ventricle. Premature termination of systolic septal shortening is shown (arrow). Scale in cm/s. (D) Continuous wave LVOT jet velocities are shown from the left ventricular apex. LVOT gradient is 120 mm Hg. Scale in m/s. Symmetry of events in early and midsystole is shown. The midsystolic closure of aortic valve correlates with the midsystolic drop in the left ventricular ejection velocities at the entrance of the outflow tract, with premature termination of the septal shortening, and with the peak of the gradient, afterload. SAM = systolic anterior motion of the mitral valve.
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Figure 5 The ECG, Invasively Measured LVOT Pressure Gradient, and the TDI Velocity Trace From the Basal Septum
Note the simultaneous development of the left ventricular outflow tract (LVOT) gradient (open arrow) and the midsystolic septal deceleration notch (solid arrow). ECG = electrocardiogram; LV = left ventricular; TDI = tissue Doppler imaging. Reprinted, with permission, from Breithardt et al. (9).
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The midsystolic drop in velocities and the premature termination of shortening are compelling evidence of the deleterious mechanical effect of obstruction on the LV. They are a manifestation of systolic dysfunction, and may contribute to an inability to increase stroke volume after exercise and to decreased exercise tolerance (10), and contribute to adverse outcome particularly from heart failure (11).
In mid-LV hypertrophy and midcavity obstruction, blood may be trapped in the apex. An apical akinetic chamber may result, caused by high pressures in the chamber that leads to supply-demand mismatch, and ischemia in the absence of epicardial coronary disease (12–16). Such patients may suffer from severe heart failure symptoms, ventricular arrhythmias, apical thrombi, and premature death.
Blood trapping in the apex leads to its own unique Doppler echocardiographic tracings and curves. When blood is trapped by a narrowed neck, it may not emerge at all until diastole, when it flows into the body of the LV. This is termed paradoxical jet flow and is a sign of a concealed apical chamber (12–15). Such flow is termed "paradoxic" because it courses towards the mitral valve in diastole. At the neck of the apical chamber, when obstruction occurs, there is an early systolic inflection and drop in ejection velocity, again caused by the sudden imposition of afterload (Fig. 6). The tissue Doppler anatomical M-mode tracing in such a patient shows a red-blue-red pattern caused by initial shortening towards the transducer, followed by blue lengthening, followed by late systolic shortening. This inflection is shown in Figure 7.
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Figure 6 Mid-Systolic Drop in Ejection Velocities in Mid-Left Ventricular Obstruction
Pulsed wave (PW) spectral Doppler with cursor located in the apical akinetic chamber at the neck of the mid-left ventricular obstruction showing prominent midsystolic drop in ejection velocity (thin arrow). There is an initial rise in velocities during the unobstructed phase (thick arrow), followed by the marked decrease in midsystolic velocities and a second peak in early diastole. The drop in velocities corresponds to the attenuation of the flow signal of the systolic jet in the obstructing neck during mid- and late systole (49). HR = heart rate.
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Figure 7 Color Tissue Doppler Tracings in an HCM Patient With Mid-LV Obstruction and an Apical Akinetic Chamber in the Absence of Epicardial Coronary Disease
(A) Anatomic M-mode display of the apical 2-chamber view. Left ventricular (LV) segmental shortening velocities towards the base are shown. Time is on the horizontal axis. On the vertical axis are velocities (top to bottom) from the inferior wall, apex, and anterior wall. The red-blue-red pattern is caused by initial shortening towards the transducer coded in red, followed by blue lengthening, followed by red late systolic shortening. The white arrows point to the blue dyskinetic motion occurring in midsystole in the midinferior and anterior walls. (B) The tissue Doppler velocities in this patient's midinferior wall are shown. The sampling location is shown with the yellow arrow at left. The inflection is shown on the right, with the white arrow. HCM = hypertrophic cardiomyopathy.
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In complete systolic emptying of the nonobstructed hyperdynamic, hypertrophied LV, a different velocity curve is identified (17). Here, as the LV decreases in size, the remaining volume is propelled out of the outflow tract with increasing acceleration because the LV diastolic cross section is progressively narrowing. But there are 2 differences compared with the SAM mitral-septal contact patients. First, the acceleration curve is smooth—there is no inflection point—because there is no obstruction and no amplifying feedback loop. Second, after peak velocity, the LV cavity is empty. There are no red cells left, so the velocity trace simply returns to zero. In contrast, in SAM mitral-septal contact patients, volume continues to be ejected against the high-pressure gradient (8,18,19).
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Clinical Implications
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In obstructive HCM, increased LV systolic pressures require increased LV systolic work despite lower diastolic aortic and coronary perfusion pressures (20). The Doppler phenomena described here explain some of the more puzzling clinical aspects of obstruction. Amplification of obstruction is demonstrated by the concave-to-the-left tracing of the systolic Doppler jet velocity. Obstructionbegets obstruction (4). This explains how changes inloading or contractility may lead to a gradient rise from 0 to 120 mm Hg in a few minutes. It also explains how gradient may be abolished after successful pharmacologic therapy or removal of vasodilators (4,6). Thus, all therapeutic efforts are focused on preventing or delaying mitral-septal contact—the trigger point of obstruction—because after mitral-septal contact amplification begins (21–26).
Exercise intolerance in HCM correlates best with an inability to increase stroke volume after exertion (10,27,28). Attention recently has focused on the role of diastolic dysfunction in limiting rise in cardiac output (29,30). However, systolic shortening and instantaneous stroke volume are reduced by obstruction (1–3,9). This systolic impairment worsens after inotropic stimulation (3,9). Afterload-dependence of stroke volume has also been observed in other clinical scenarios: after handgrip in LV dysfunction, in dilated cardiomyopathy, and in hypertensive heart disease (31–33). In aortic valve disease, this has been termed afterload mismatch (7). What causes the exquisite vulnerability to afterload seen in obstructive HCM? Research using magnetic resonance spectroscopy has disclosed that the myocytes of HCM patients utilize adenosine triphosphate inefficiently, leading to impaired contractile reserve and thought to act as an impetus to hypertrophy. A prolonged or a sudden increase in demand may lead to an "energy crisis" and left ventricular systolic dysfunction (34–36). Thus, in HCM patients diastolic dysfunction may not be the sole determinant of the inability to increase stroke volume: patients with obstruction may labor from dynamic systolic dysfunction as well, while others may be hobbled by both (37–39). Moreover, relief of systolic load not only improves instantaneous stroke volume (2,3) but also improves diastolic relaxation through relief of load-dependent impaired relaxation (40–44). Relief of systolic contraction load by relief of obstruction is currently the best therapy for diastolic dysfunction in obstructed patients.
In patients with gradients >60 mm Hg, premature deceleration and termination of systolic shortening occur with each beat of the heart. Forced sudden termination of contraction may cause cumulative deceleration injury to the LV myocardium. The tensile strength of myocardium has been assessed in vitro (45). We hypothesize that its structural resilience to repeated abrupt deceleration may be sorely tested in obstructive HCM (2,9) and that this may contribute to progressive heart failure symptoms and higher mortality from heart failure associated with obstruction (11,15,18).
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Relief of Obstruction and the Midsystolic Drop
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In a patient with LVOT gradient and symptoms, detection of a midsystolic drop in LV ejection velocities provides clear evidence that the LV is laboring from the obstruction. When detected, it may be regarded with cautious optimism, since it reaffirms a therapeutic target: removing LVOT obstruction always normalizes the midsystolic drop (2). Reversal of dynamic systolic dysfunction may contribute to the improved hemodynamics, symptoms, and survival that are observed after relief of obstruction (1,2,39–42,44,46–48).
A more difficult clinical scenario is presented by the more extreme case of systolic dysfunction occurring in patients with mid-LV obstruction and an apical akinetic chamber (12,13,15,49). Afterload mismatch (shown graphically by the drop in pulsed Doppler velocities just before the neck) also may be due to impaired energenics in conjunction with supply-demand ischemia (12,13,16). Contractility is overcome to such an extent that systolic shortening abnormalities progress to akinesia or dyskinesia. In some cases apical akinesia represents scar (14). In others, reversing obstruction would be beneficial, but when such patients become refractory to pharmacologic treatment, choices become difficult and limited. Surgery has been successfully performed for midventricular HCM; however, there are technical considerations that make this challenging: the greater distance to the obstruction from the aortotomy, the sheer bulk of the hypertrophy, and the length of the obstructing neck (24,49–52).
There is a certain harsh logic concealed in the curves of HCM. No doubt there is additional information hidden therein.
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