Stress Induction of Subaortic Stenosis and Mitral Regurgitation
A 67-year-old woman presented with a 2-year history of increasing exertional dyspnea without angina or syncope. There was a maternal family history of hypertrophic obstructive cardiomyopathy. On examination, she had a jerky pulse and an ejection systolic murmur, which increased in intensity on exercise. Echocardiography showed hypertrophic cardiomyopathy. Doppler ultrasound recorded an estimated outflow gradient of 20 mm Hg at rest, which rose to >100 mm Hg during dobutamine stress.
Magnetic resonance cine imaging (field strength, 0.5 T; echo time, 6 ms) performed at rest and during dobutamine stress (Figure⇓) showed that during stress only, marked systolic signal loss developed in the aortic root, indicating turbulent jet formation from a restriction between the hypertrophied ventricular septum and the anterior mitral valve leaflet. This was associated, also only on stress, with the turbulent jet of mitral regurgitation back into the left atrium.
Stress induction of both subaortic stenosis and mitral incompetence in this case can be explained by the fluid dynamic phenomenon known as the Venturi effect. During stress, increased velocity of flow through the narrow outflow region, which is bounded posteriorly by a mobile valve leaflet, is associated with a local decrease of pressure. This pressure drop tends to draw the anterior mitral leaflet even closer to the septum (and away from the posterior leaflet), increasing outflow velocity to a point at which rising flow resistance or valve tension breaks the cycle. The cycle could repeat itself in an oscillating mode, depending on the resonant properties of the stream and adjacent tissues.
This can be compared with the sounding of a clarinet. Gentle blowing into the slit between flexible reed and stem meets little resistance and makes no sound. More forceful blowing meets with higher resistance as the Venturi/occlusive cycle comes into play and becomes coupled with oscillations in the air column of the sounding instrument.
In the case of the patient illustrated here, a certain level of stress appears to have precipitated acute deterioration of heart function by left ventricular outflow obstruction combined with mitral regurgitation. Investigation only at rest would have been incomplete.
Philip Kilner is funded by the British Heart Foundation.
The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Luke's Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.
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