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Interact CardioVasc Thorac Surg 2005;4:486-487. doi:10.1510/icvts.2005.111039 © 2005 European Association of Cardio-Thoracic Surgery
Severe mitral systolic anterior motion complicating aortic valve replacementDepartment of Cardiothoracic Surgery, Papworth Hospital, Papworth Everard, Cambridgeshire CB3 8RE, UK Received 19 April 2005; received in revised form 28 June 2005; accepted 4 July 2005
*Corresponding author. Tel.: +44 01480 830541.
This case illustrates a severe dynamic left ventricular outflow obstruction after aortic valve replacement (AVR). This phenomenon is little recognised but probably occurs more frequently than appreciated, and should be considered when managing patients with severe haemodynamic instability after AVR. The possible mechanisms and treatment are discussed.
Key Words: Aortic valve replacement; Mitral valve; Echocardiography
Dynamic left ventricular outflow tract (LVOT) obstruction is a well-recognised problem in hypertrophic cardiomyopathy (by septal muscle) and following mitral valve repair (by systolic anterior motion of the anterior leaflet). We present a case of LVOT obstruction complicating aortic valve replacement (AVR), and discuss the mechanisms and treatment of this probably under-recognised phenomenon.
An 82-year-old woman was referred for AVR. She was fit and active, complaining only of dizziness. Transthoracic echocardiography demonstrated a calcified, immobile aortic valve with a gradient of 100 mmHg. The left ventricle was mildly hypertrophied with good systolic function. The coronary arteries were normal at angiography. Her logistic EuroSCORE predicted-mortality for AVR was 8.44%. At AVR her heavily calcified, stenotic aortic valve was replaced with a 21 mm bovine pericardial-mounted xenograft, using normothermic bypass and antegrade cold blood cardioplegia. The operation was uneventful. She was extubated three hours later. There were episodes of dramatic hypotension during the first post-operative day, which resolved with fluid administration. She was transferred to the ward on day 2. Later that day she suffered a witnessed aystolic arrest. She was rapidly resuscitated, with full recovery of consciousness. She was found to be in complete atrioventricular block, and had a permanent pacemaker implanted. She was re-admitted to ITU. During the following 24 h she exhibited profound haemodynamic instability, with normotensive periods alternating with profound hypotension. These oscillations occurred 2–3 times per hour. Treatment was with inotropes, but this worsened the situation. A trans-oesophageal echocardiogram was performed.
During the hypotensive episodes this showed obstruction of the LVOT during systole, by anterior motion of the anterior leaflet of the mitral valve (Video 1).
Initial management was non-surgical. To open out the LVOT, the heart was filled to supra-normal end-diastolic dimensions, and a phenylephrine infusion started to increase afterload to further ‘splint’ open the LVOT. A labetolol infusion was started to reduce contractility and thus reduce the muscular component of the obstruction. There was some improvement but the hypotensive episodes continued to occur, and the patient was returned to the operating theatre. Bypass was commenced and the mitral valve approached via right atrial and septal incisions. It appeared structurally normal. An edge-to-edge (Alfieri) repair was performed to tether the anterior leaflet and prevent its systolic anterior motion. On separation from bypass, this had been achieved, but at the expense of creating mitral stenosis (judged by spontaneous echo contrast in the left atrium and hypotension). Bypass was re-commenced and the mitral valve replaced with a 25 mm pericardial prosthesis. It was then possible to wean the patient from bypass easily, with no further LVOT obstruction. The patient went on to make a slow but steady recovery and was discharged home three weeks later.
We believe that the dynamic LVOT obstruction was caused by the aortic valve replacement, and that this may be an under-recognised cause for haemodynamic instability following aortic valve replacement. The end systolic pressure in the LVOT is high in the presence of a downstream obstruction (a stenotic aortic valve), holding the walls apart. Following relief of this obstruction, end-systolic pressure in the LVOT falls, exacerbating any tendency for obstruction. Local anatomical (depth of the anterior mitral valve leaflet, septal hypertrophy) and physiological factors (filling state, contractility and systemic vascular resistance) determine whether obstruction then occurs. Fortunately, in the great majority of cases it does not. Treatment is initially to manipulate the physiology, to reduce the tendency to obstruction. This involves filling to increase end-diastolic LV dimensions, reduction in contractility and afterload increase with vasoconstrictors. Of note, the usual actions taken to support a failing heart after cardiac surgery (inotropes, intra-aortic balloon counter-pulsation) will be dangerous. This case underlines the importance of pre-operative echocardiographic assessment. The largest prospective study of this phenomenon is by Bartunek et al. [1] They studied 100 patients undergoing aortic valve replacement for stenosis. They found evidence of LVOT gradients in 14% of patients, with the situation exacerbated by vasodilation or beta agonists. The mechanism was a combination of a muscular cavity and systolic anterior motion of the mitral valve. They found that the phenomenon was associated with small, hyperdynamic, and asymmetrically hypertrophied ventricles. In none of their patients did the situation require surgical treatment. Other studies have reported similar findings [2–4]. The mechanism is usually muscular obstruction. Obstruction by abnormal motion of the anterior mitral valve leaflet is rarely reported as the causative mechanism [5]. The presence of echo gradient is associated with an increased incidence of early post-operative hypotension, and increased mortality [3,4,6]. In all studies, offloading with vasodilators, or intra-aortic balloon pump [7] worsened the haemodynamic situation. This condition should be considered when, after AVR, patients exhibit haemodynamic instability which does not respond to, or worsens after the usual supportive measures.
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Abstract
1. Introduction