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Left ventricular cavity obliteration: Mechanism of the intracavitary gradient and differentiation from hypertrophic
Charles Pollick1, Hezzy Shmueli1, Nicolas Maalouf1
1Smidt Heart Institute, Cedars Sinai Medical Center, Los Angeles, California, USA.
Insights
The intracavitary gradient (ICG) in left ventricular cavity obliteration (LVCO) is linked to the extent and duration of LVCO. Differentiating ICG spectral profiles helps distinguish LVCO from hypertrophic obstructive cardiomyopathy (HOCM) and aortic stenosis (AS).
Area of Science:
- Cardiology
- Cardiovascular Imaging
- Hemodynamics
Background:
- The cause of pressure gradients in hypertrophic obstructive cardiomyopathy (HOCM) is debated, with both left ventricular cavity obliteration (LVCO) and systolic anterior motion (SAM) of the mitral valve implicated.
- While distinct in origin, LVCO and SAM-associated gradients share characteristics like a
Purpose of the Study:
- To clarify the cause and characteristics of intracavitary gradients (ICG) in patients with LVCO without HOCM.
- To differentiate ICG spectral profiles in LVCO from those in HOCM and severe aortic stenosis (AS).
Main Methods:
- Assessed the extent and duration of LVCO in patients without HOCM.
- Compared spectral profiles of ICG in LVCO patients with those of HOCM and severe AS patients.
Main Results:
- Higher ICG correlates with greater LV wall apposition extent and duration, and smaller left ventricular cavity size.
- Peak/mean gradient ratios differentiate spectral profiles: ≤2 for AS, 2-3 for HOCM, and >3 for LVCO (>90% accuracy).
- Most LVCO patients without HOCM or severe LVH have ICG < 36 mm Hg.
Conclusions:
- The magnitude of ICG is quantitatively associated with LVCO extent and duration.
- Spectral profiles, specifically the peak/mean gradient ratio, effectively differentiate severe AS, HOCM, and LVCO.
Background:
Controversy surrounds the cause of the pressure gradient in patients with hypertrophic obstructive cardiomyopathy (HOCM). Left ventricular cavity obliteration (LVCO) was first described as the cause of the gradient but subsequently systolic anterior motion (SAM) of the mitral valve has been established as the cause. Nevertheless, the two gradients, though different in origin and significance, share similar characteristics. They both have a similar "dagger" profile, are obtained from the cardiac apex, are associated with a hyperdynamic left ventricle, and the gradients are worsened by Valsalva. The distinction has clinical relevance, because treating the intracavitary gradient (ICG) of LVCO as if it were a SAM-associated gradient associated with HOCM would be inappropriate and possibly harmful.
Materials And Methods:
To clarify the cause and characteristics of the ICG in patients with LVCO in patients without HOCM, we assessed the extent and duration of cavity obliteration, and for differentiation, we compared the spectral profiles with patients with HOCM and severe aortic stenosis (AS).
Results:
Higher ICG is associated with a greater extent and more prolonged apposition of LV walls, and smaller left ventricular cavity size. The spectral profile of patients with AS, HOCM, and LVCO is differentiated by the peak/mean gradient ratios of 2 or less, 2-3, and 3 or greater, respectively, in >90% of patients. Most patients with LVCO without HOCM or severe LVH have an ICG < 36 mm Hg.
Conclusion:
The magnitude of ICG is quantitatively associated with the extent and duration of LVCO. Spectral profiles of severe AS, HOCM, and LVCO can be differentiated by the peak/mean gradient ratio.
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