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Biphasic left ventricular outflow and its mechanism in hypertrophic obstructive cardiomyopathy
Heidi M Conklin1, Xiaoyan Huang, Crispin H Davies
1Division of Cardiology, Oregon Health and Science University, Portland 97239, USA.
Insights
Biphasic systolic velocity in the left ventricular outflow tract (LVOT) in hypertrophic obstructive cardiomyopathy (HOCM) is linked to altered flow dynamics and mitral-septal separation. This finding may stem from "afterload mismatch" in HOCM patients.
Area of Science:
- Cardiology
- Cardiovascular Physiology
Background:
- Biphasic systolic velocity in the left ventricular (LV) outflow tract (LVOT) is observed in hypertrophic obstructive cardiomyopathy (HOCM).
- The underlying mechanisms and clinical significance of this phenomenon are not well understood.
Purpose of the Study:
- To investigate the cause and implications of biphasic LVOT velocity in HOCM.
- To correlate LVOT flow dynamics with the presence of biphasic velocity and mitral-septal separation.
Main Methods:
- Matched case-control study comparing 25 HOCM patients with 30 controls.
- Estimation of LVOT systolic flow rate using a derived function relating aortic and LVOT flow.
- Grouping HOCM patients based on the presence or absence of biphasic LVOT velocity.
Main Results:
- Biphasic LVOT velocity significantly correlated with biphasic estimated LVOT outflow (P =.002).
- LVOT pressure gradient showed an inverse relationship with LV outflow rate at peak gradient (r = -.64, P <.001).
- Dobutamine administration exacerbated the LVOT gradient and reduced outflow, while mitral-septal separation occurred in HOCM patients with biphasic velocity despite a gradient.
Conclusions:
- Biphasic LVOT flow in HOCM is associated with "afterload mismatch."
- Late systolic flow increase relates to mitral-septal separation.
- Resolution of systolic anterior motion despite a persistent gradient suggests non-pressure-related forces are involved.
Background:
Biphasic systolic velocity in the left ventricular (LV) outflow tract (LVOT) occurs in hypertrophic obstructive cardiomyopathy (HOCM). The cause and importance of this observation remain poorly understood.
Methods:
A total of 25 patients with HOCM were matched to 30 control subjects. A function derived from the relation of flow in the proximal descending aorta to that in the LVOT was used to estimate the LVOT systolic flow rate in HOCM. Patients with HOCM were grouped by absence (group I) or presence (group II) of biphasic LVOT velocity.
Results:
Biphasic LVOT velocity was associated with biphasic estimated LVOT outflow (P =.002). The LVOT pressure gradient was inversely related to LV outflow rate at the time of the peak gradient (r = -.64, P <.001). Dobutamine increased the gradient and reduced LVOT outflow at the time of the peak gradient. In group II, mitral-septal separation occurred despite a LVOT gradient (36 mm Hg).
Conclusion:
Biphasic LVOT flow in HOCM occurs and may be caused by "afterload mismatch." The late systolic increase in flow is related to mitral-septal separation. Resolution of systolic anterior motion occurs despite a persistent LVOT pressure gradient, implying a role for forces other than pressure differences.
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