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Effect of obstruction on longitudinal left ventricular shortening in hypertrophic cardiomyopathy
Ivan Barac1, Shrikanth Upadya, Robert Pilchik
1Division of Cardiology, St. Luke's-Roosevelt Hospital Center, Columbia University, College of Physicians and Surgeons, New York, New York 10019, USA.
Insights
The midsystolic drop (MSD) in hypertrophic cardiomyopathy (HCM) is caused by premature termination of left ventricular (LV) segmental shortening, indicating systolic dysfunction. This finding helps understand obstruction in HCM patients.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Echocardiography
Background:
- Dynamic left ventricular (LV) obstruction is a key factor in hypertrophic cardiomyopathy (HCM) symptoms and prognosis.
- Midsystolic drop (MSD) in velocity and flow is observed in HCM patients with gradients exceeding 60 mm Hg.
- The lowest LV ejection velocity (nadir) coincides with the peak obstruction gradient.
Purpose of the Study:
- To investigate the underlying cause of the midsystolic drop (MSD) in LV ejection velocities in obstructive hypertrophic cardiomyopathy (HCM).
- To determine if MSD is a manifestation of systolic dysfunction in HCM patients with severe obstruction.
Main Methods:
- Studied 36 patients with obstructive HCM and MSD, comparing them to 15 non-obstructed HCM patients and 25 healthy controls.
- Measured LV ejection velocity proximal and distal to obstruction, along with tissue Doppler velocities and time intervals.
- Assessed changes in MSD and contraction patterns after medical intervention to abolish obstruction.
Main Results:
- Obstructed HCM patients with MSD exhibited significantly shorter septal and lateral wall contraction durations and lengths compared to non-obstructed HCM patients.
- The LV ejection velocity nadir occurred during rapid deceleration of both walls, indicating premature termination of shortening.
- Medical abolition of obstruction resolved the MSD and normalized contraction duration and length.
Conclusions:
- The midsystolic drop (MSD) in obstructive hypertrophic cardiomyopathy (HCM) is caused by premature termination of LV segmental shortening.
- MSD is a direct manifestation of systolic dysfunction in the context of severe LV outflow tract obstruction in HCM.
Objectives:
We investigated the cause of the midsystolic drop (MSD) in left ventricular (LV) ejection velocities that are observed with hypertrophic cardiomyopathy (HCM) and severe obstruction.
Background:
Dynamic obstruction is an important determinant of symptoms and adverse outcome. The MSD in velocity and flow occurs in patients with gradients >60 mm Hg. The nadir velocity in the LV occurs simultaneously with peak gradient.
Methods:
We studied 36 patients with obstructive HCM and an MSD and compared them with 15 patients with HCM and no obstruction and with 25 age-matched normal control subjects. We measured LV ejection velocity proximal and distal to LV obstruction as well as tissue Doppler velocities and time intervals.
Results:
The duration of contraction of both the septum and lateral wall is shorter in obstructed patients with the MSD than in nonobstructed HCM patients: septal contraction 203 +/- 68 ms vs. 271 +/- 41 ms (p < 0.001). Parallel reduction in the length of shortening was noted: 1.2 +/- 0.6 cm vs. 1.9 +/- 0.4 cm (p < 0.001). The ejection velocity nadir follows the septal and lateral peak velocities by 100 ms and 60 ms, respectively. The velocity nadir occurs as both walls rapidly decelerate to their premature termination: septal deceleration 79 +/- 35 cm/s2 vs. 48 +/- 21 cm/s2 (p < 0.001). With medical abolition of obstruction the MSD disappears and the duration and length of contraction normalizes.
Conclusions:
These data indicate that the MSD is caused by premature termination of LV segmental shortening and is a manifestation of systolic dysfunction.
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