Background:
@EN Mid-ventricular obstruction (MVO) of the left ventricle has been reported to be associated with mid-ventricular hypertrophy, papillary muscle hypertrophy, severe apical hyperytrophy, elderly hypertension, and dobutamine stress
echocardiography
(DSE). The aim of this study is to determine the clinical and echocardiographic features of MVO.
@ES Method:
@EN MVO was defined as systolic hourglass narrowing of the left mid-ventricle in the apical long axis view with turbulent flow exceeding 1m/s. Fifteen patients were subjected to this retrospective analysis. Baseline patients characteristics were
mean
age 56(range. 26-74) years, male gender 10(66%). Associated diseases were hypertrophic cardiomyopathy 9, aortic stenosis 1, hypertension without left ventricular hypertrophy(LVH) 1, old myocardial infarction with apical aneurysm 2, stale angina
1,
and
idiopathic 1, DSE was performed in 7 of 15 subjected patients to evaluate the chest pain.
@ES Results:
@EN All patients had mild symptoms; chest tightness, palpitation, and weakness, without syncope nor hypotension. MVO was observed in 10 at rest, and 5 after provocation ; DSE 3, VPB 1, atropine 1. Observed peak velocity in the mid-ventricle
ranged
from
12 to 5.5m/s(mean ; 2.8±1.6m/s). Left ventricular outflow tract obstruction defined as the peak flow velocity exceeded 1.5m/s, was also present in 8, in 7 underwent to DSE, systolic blood pressure was changed from 144±15mmHg at rest to
175±28mmHg at
peak, heart rate from 73±12/min to 108±23/min, left ventricular end diastolic dimension from 42±5mm to 37±4mm, ejection fraction from 66±10% to 80±6%, and peak flow velocity at the mid-ventricle from 1.0±0.6m/s to 3.3±1.7m/s.
@ES Conclusion:
@EN MVO can be observed in patients without LVH and may account for clinical symptoms of chest discomfort. The mechanism of MVO, at least in part, can be explained with increased ventriculr contractility, increased rate, and small left
ventricular
cavity size.
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