Abstract 13991: Apical Akinetic Chambers Occur in Hypertrophic Cardiomyopathy Patients With the Most Severe Mid Left Ventricular Obstruction but Low or Absent Systolic Pressure Gradients
Background: The cause of apical akinetic chambers (AAC) in patients with HCM is uncertain. Some have hypothesized that AAC are caused by severe mid-LV obstruction (MVO) with afterload mismatch and ischemia, however, low or absent pressure gradients are recorded across the mid-LV narrowings. We hypothesized that this was due to near-complete or complete cessation of systolic flow (analogous to the fall in gradient with end-stage aortic stenosis).
Methods: Among 878 patients in a referred HCM population, 42 had mid-LV hypertrophy and complete systolic emptying (CSE) of the mid-LV. Of these, 16 were classified as AAC and 16 without AAC (8 with MVO and gradients > 30 mmHg and 8 just with CSE). Patients with inadequate echocardiograms and mitral-septal contact at rest were excluded. Besides analyzing Doppler gradients, we determined severity of obstruction on mid-LV short axis (SAX) views by measuring the duration and percentage of systole with narrowed systolic areas < 1cm2.
Results: The percentage of systole with SAX LV area < 1 cm2 was greater in patients with AAC (49 ± 14% vs. 35 ± 15%, p = 0.013); ≥ 40% of systole was associated with the presence of an AAC (OR 6.6; 95% CI 1.40-31.069; p = 0.032). Patients with AAC had longer length of LV wall apposition during systole on the apical 4 chamber view (2.87 ± 0.6 cm vs. 2.40 ± 0.7 cm, p < 0.05). Despite this dynamic anatomic evidence of mid-LV obstruction there was no systolic gradient in any of the AAC patients. A Doppler systolic signal void was present in 13 out of 16 (81%) AAC patients; ranging from 45-400 ms in duration. There was a correlation between the duration of the signal void and the percentage of systole with SAX LV area < 1cm2 (r = 0.589; p = 0.057). Paradoxical jet flow (PJF) was present in early diastole in 15 out of 16 (94%) AAC patients and was absent in the other patients. AAC patients had thinner apical wall thickness (0.75 ± 0.5 cm vs. 1.69 ± 0.6 cm, p < 0.0001) and thicker mid-LV wall thickness (1.66 ± 0.26 cm vs. 1.42 ± 0.35 cm; p = 0.034).
Conclusion: Severe dynamic anatomic mid-LV obstruction occurs in AAC patients even though there are no elevated systolic Doppler gradients. This is due to near-complete cessation of flow that is ≥ 40% of systole in duration across a severe mid-LV narrowing nearly 3 cm in length.
- © 2013 by American Heart Association, Inc.