Abnormal left ventricular diastolic filling in chronic thromboembolic pulmonary hypertension: true diastolic dysfunction or left ventricular underfilling?
OBJECTIVE
The purpose of this study was to investigate the cause of abnormal left ventricular (LV) Doppler diastolic filling characteristics in chronic thromboembolic pulmonary hypertension (CTEPH).


BACKGROUND
In CTEPH, LV diastolic function often appears abnormal. It is unclear whether this "impaired relaxation" (E<A) filling pattern is caused by septal hypertrophy, right ventricular (RV) enlargement and LV chamber distortion, or low LV preload and underfilling.


METHODS
We studied 61 patients with an E<A transmitral pattern and CTEPH who underwent pulmonary thromboendarterectomy (PTE). We compared the results of pre- and postoperative transthoracic echocardiography and right heart catheterization measurements.


RESULTS
After PTE, mitral E velocity increased (from 54 +/- 16 cm/s to 81 +/- 20 cm/s, p < 0.001), whereas A velocity decreased (77 +/- 22 cm/s to 71 +/- 20 cm/s, p < 0.001). E/A ratio normalized (0.72 +/- 0.16 cm/s to 1.22 +/- 0.40 cm/s, p < 0.001). Pulmonary venous systolic and diastolic velocities both increased (57 +/- 13 cm/s to 68 +/- 16 cm/s and 39 +/- 15 cm/s to 70 +/- 21 cm/s, respectively, p < 0.001 for both). Diastolic velocity of the septal mitral annulus (E(m)) did not change after PTE (8.0 +/- 3.1 cm/s to 8.1 +/- 2.0 cm/s, p = ns), whereas the velocity of the lateral mitral annulus increased (9.3 +/- 3.2 cm/s to 11.8 +/- 3.1 cm/s, p < 0.001). Mean pulmonary capillary wedge pressure increased from 9.3 +/- 3.2 mm Hg to 10.6 +/- 3.8 mm Hg (p = 0.035). Despite these marked changes in LV inflow, M-mode measurements of LV septal and posterior wall thickness were normal before PTE and did not change after surgery (septal: 10 +/- 2 mm vs. 10 +/- 1 mm; posterior: 10 +/- 2 mm vs. 10 +/- 1 mm; p = NS for both comparisons).


CONCLUSIONS
The results of this study strongly suggest that the impaired relaxation pattern observed in patients with CTEPH is not solely the result of geometric effects of RV enlargement and LV chamber distortion but is caused in large part by low LV preload and relative underfilling.
Gurudevan
Swaminatha V
SV
Division of Cardiology, University of California Irvine School of Medicine, Irvine, California, USA.
Malouf
Philip J
PJ
Auger
William R
WR
Waltman
Thomas J
TJ
Madani
Michael
M
Raisinghani
Ajit B
AB
DeMaria
Anthony N
AN
Blanchard
Daniel G
DG
D000328:Adult; D000368:Aged; D002908:Chronic Disease; D003971:Diastole / Q000502:physiology; D004691:Endarterectomy / Q000379:methods; D005260:Female; D006801:Humans; D006976:Hypertension, Pulmonary / Q000175:diagnosis / Q000503:physiopathology* / Q000601:surgery; D008297:Male; D008875:Middle Aged; D011655:Pulmonary Embolism / Q000175:diagnosis / Q000503:physiopathology* / Q000601:surgery; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis / Q000503:physiopathology* / Q000601:surgery; D016277:Ventricular Function, Left / Q000502:physiology