Effect of Obstruction on Longitudinal Left Ventricular Shortening in Hypertrophic Cardiomyopathy
Ivan Barac, MD*,1,
Shrikanth Upadya, MD*,2,
Robert Pilchik, MD*,
Glenda Winson, RN*,
Michael Passick, RDCS*,
Farooq A. Chaudhry, MD* and
Mark V. Sherrid, MD*,*
* Division of Cardiology, St. Luke’s-Roosevelt Hospital Center, Columbia University, College of Physicians and Surgeons, New York, New York.
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Figure 1 Sampling Locations of PW and CW Doppler in the LV and LV Outflow Tract
The midsystolic drop of left ventricular (LV) ejection velocity is recorded with pulsed-wave (PW) Doppler in the apical 5-chamber view with the sample volume placed approximately 2.5 cm apical to the level of the tips of mitral leaflets (X). The continuous-wave (CW) Doppler (dashed line) traverses both the LV outflow tract and the medial LV cavity; velocities from both sites are recorded simultaneously.
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Figure 2 Timing of the Midsystolic Drop in LV CW Velocities Compared With Timing of ECG and LV TDI
Graphic depiction of continuous-wave (CW) Doppler of the superimposed left ventricular (LV) outflow tract and LV midsystolic drop velocities (top), electrocardiogram (ECG) (middle), and tissue Doppler imaging (TDI) traces of septal wall (bottom). PW = pulsed-wave.
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Figure 3 Midsystolic Drop in LV Velocity Seen on CW and PW Tracings
(Left) Continuous-wave (CW) Doppler through the left ventricular outflow tract (LVOT) in obstructive hypertrophic cardiomyopathy. The midsystolic drop (MSD) flow velocity curve (arrowheads) is seen superimposed on the higher LVOT ejection flow velocity signal. (Right) Pulsed-wave (PW) Doppler recording just apical of the entrance to the LVOT. Long arrow points to the nadir of LV MSD flow velocity.
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Figure 4 Septal TDI Tracing in Patient With Nonobstructive HCM Compared With Severe Obstructive HCM
(Top) Tissue Doppler imaging (TDI) tracing of a nonobstructed patient. (Bottom) TDI of a severely obstructed patient. Note the shortened duration of systolic septal contraction in the obstructed patient. The white arrows point to the beginning and the end of septal contraction, excluding the isovolumetric contraction. HCM = hypertrophic cardiomyopathy.
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Figure 5 Increase in the Duration of Left Ventricular Contraction After Gradient Abolition
Change in normalized duration of contraction (ratio of contraction time duration to ejection flow duration [CT/ET]) of the septal (top) and lateral (bottom) walls in 15 individual patients after gradient abolition with disopyramide.
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Figure 6 Pooled CW Doppler and Tissue Doppler Data of Controls and Patients With Nonobstructive HCM
(Top) Pooled data of normal controls. (Bottom) Pooled data from the nonobstructive patients. The septal and lateral tissue Doppler imaging (TDI) velocities are depicted above the zero velocity line, and the continuous-wave (CW) flow velocities are depicted below. Note that the TDI velocities and CW velocities are to different scales. HCM = hypertrophic cardiomyopathy; LVOT = left ventricular outflow tract.
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Figure 7 Pooled CW and TDI Data in Obstructive HCM Before and After Gradient Abolition With Disopyramide
The top graph shows the midsystolic drop of the left ventricular (LV) velocities (dotted line), the premature termination of tissue Doppler imaging (TDI) velocities, especially relative to flow, and dyssynchrony of the septal and lateral wall shortening. The bottom graph shows significant improvement in these abnormalities after gradient abolition. CW = continuous-wave; HCM = hypertrophic cardiomyopathy; LVOT = left ventricular outflow tract; MSD = midsystolic drop.
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