[Mental stress echocardiography for patients with mitral valve prolapse].
Our clinical experience suggests that anxiety may provoke the augmentation of the degree of mitral valve prolapse (MVP) and change the mitral inflow velocity pattern in patients with MVP. To evaluate this systematically, we recorded 2-dimensional (2-D) and pulsed wave Doppler echocardiograms during acute mental stress in eight patients with MVP and eight age-matched normal subjects. Acute mental stress was administered by applying arithmetical task or reminding each patient of their most uncomfortable memories. Heart rate and blood pressure were significantly increased during mental stress and returned to the control level within a few minutes after its release in both groups. 2-D and Doppler echocardiograms were constantly recorded before, during and after acute mental stress. MVP was prominently augmented during mental stress in three of the eight patients. During mental stress, the mitral inflow velocity decreased in the rapid filling phase (R) and increased in the atrial filling phase (A), resulting in significant increase of the A/R in seven of the eight patients with MVP, especially in the patients associated with an increase of MVP. In normal subjects, mitral valve prolapse did not develop and the A/R was minimally increased or remained almost the same during mental stress. In conclusion, mental stress echocardiography seems to be a useful provocation test for the assessment of MVP and it is further expected to propose a lot of potential applications as a new method of stress echocardiography.
Tei
C
C
Department of Rehabilitation and Physical Medicine, Faculty of Medicine, Kagoshima University.
Park
J C
JC
Horikiri
Y
Y
Tanaka
N
N
Mizukami
N
N
Toyama
Y
Y
D000328:Adult; D000368:Aged; D015150:Echocardiography, Doppler; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D008945:Mitral Valve Prolapse / Q000503:physiopathology / Q000523:psychology*; D013315:Stress, Psychological / Q000503:physiopathology*