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Dobutamine induced cardiogenic shock due to systolic anterior motion after mitral valve repair.

An adult male with severe eccentric mitral regurgitation caused by posterior leaflet prolapse underwent mitral valve repair by creation of new chordae at the posterior mitral leaflet. Mild basal septal hypertrophy (diastolic interventricular septal thickness 15 mm) was noted. After the repair, transoesophageal echocardiography confirmed no significant residual mitral regurgitation and he was stable without inotropic support. Four hours later his systolic blood pressure suddenly decreased from 80 to 40 mmHg. We thought that his left ventricular geometry might have been affected by repair and we started intravenous dobutamine at 5/[micro]g/kg/min. The patient's systolic blood pressure rose to 100 mmHg temporarily, but decreased thereafter with progressive haemodynamic instability and a decrease in systolic blood pressure to 30 to 40 mmHg. The dobutamine was then increased up to 10 [micro]g/kg/min and norepinephrine of 0.01 [micro]g/kg/min was added. At that time a loud systolic murmur was heard at the cardiac apex and an emergent transthoracic echocardiogram showed severe systolic anterior motion of mitral valve (SAM) and dynamic obstruction of the left ventricular outflow tract (LVOT) with a mean pressure gradient of 64 mmHg (Figure 1). We stopped intravenous dobutamine and norepinephrine immediately and infused large amounts of fluid to increase his left ventricular preload. His systolic murmur disappeared rapidly and the SAM and LVOT obstruction resolved.

To explain why SAM occurs after mitral valve repair, Varghese et al (1) described the two mechanisms; the 'venturi effect' and the 'drag effect'. Although the exact incidence of catecholamine induced LVOT obstruction after mitral valve repair has not yet been reported, these effects could be worsened when anatomical abnormalities, such as degenerative changes on the anterior cusp of the mitral valve and basal septal hypertrophy, are combined (2). In these cases otherwise insignificant basal septal hypertrophy may cause LVOT obstruction with the usual dobutamine dosage (3).

This case emphasises that early after mitral valve repair, SAM could be a cause of cardiogenic shock, especially when an anatomical predisposing factor like mild basal septal hypertrophy is combined with postoperative dobutamine, as pointed out by Auer et aP. In these cases haemodynamic management should focus on adequate preload and echocardiography should be used early if haemodynamic instability develops, especially if inotropes are being considered.

Caption: Figure 1: Postoperative echocardiography showed systolic anterior motion of mitral valve (upper) with severe left ventricular outflow tract obstruction (lower).


(1.) Varghese R, Anyanwu AC, Itagaki S, Milla E Castillo J, Adams DH. Management of systolic anterior motion after mitral valve repair: an algorithm. J ThoracCardiovasc Surg 2012: 143:$2-7.

(2.) Charls LM. SAM-systolic anterior motion of the anterior mitral valve leaflet post-surgical mitral valve repair. Heart Lung 2003; 32:402-406.

(3.) Yalcin E Muderrisoglu H, Korkmaz ME, Ozin B, Baltali M, Yigit E The effect of dobutamine stress on left ventricular outflow tract gradients in hypertensive patients with basal septal hypertrophy. Angiology 2004; 55:295-301.

(4.) Auer J, Berent R, Weber T, Lamm G, Eber B. Catecholamine therapy inducing dynamic left ventricular outflow tract obstruction. Int J Cardiol 2005; 101:325-328.

Y. B. Jeon

K. Y. Park

J. K. Moon

C. H. Park

C. H. Choi

J. I. Lee

Incheon, South Korea
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Author:Jeon, Y.B.; Park, K.Y.; Moon, J.K.; Park, C.H.; Choi, C.H.; Lee, J.I.
Publication:Anaesthesia and Intensive Care
Article Type:Clinical report
Date:Jul 1, 2013
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