1. An unusual presentation of Systolic Anterior Motion (SAM) of Mitral valve leaflet leading to haemodynamic compromise- A case report Anirudda Pai, Aamer Ahmed Department of Anaesthesia, Glenfield Hospital, University Hospitals of Leicester NHS Trust
Background & aims: SAM is a phenomenon where there is a marked forward movement of anterior mitral leaflet touching the ventricular septum during systole causing severe subaortic ventricular obstruction. This often leads to unrecognised haemodynamic disturbances contributing to adverse postoperative outcomes. SAM is not familiar to many noncardiac anaesthetists. Only few cases have been reported in the non cardiac journals. The aim of this report is to provide a brief description of pathophysiology, diagnostic and therapeutic strategies of SAM.
Case report: 61 year old man was listed for elective CABG surgery having normal left ventricular function with borderline concentric hypertrophy. Chordal systolic motion with normally opening mitral valve was reported on echocardiography. After an uneventful anaesthetic induction two coronary vessels were grafted. Separation from cardiopulmonary bypass was routine with minimal inotropic support. Blood transfusion was not required, 1000 ml of colloid and 700 ml of recirculated blood from the pump were infused. Mean heart rate after separation from bypass was 80/min, MAP - 70 mmHg and CVP 11mmHg. With the surgical closure of the chest, ST segment changes were noted. At this time the heart rate was still 80-90/min, but MAP and CVP started to fall. Despite infusion of colloids, the SBP was around mmHg. But the ST-T changes continued to progress to -3.5mm.At this point the chest was reopened to reassess the integrity of the grafts under direct vision. The inotropic (dopamine) support was increased to 10mcg/kg/min, which did not improve the ST depression. Arterial pressure fell further and the heart rate increased to 100/min.Intraaortic balloon pump was inserted, noradrenaline infusion was also commenced. We decided to perform TOE to assess the presence of any regional wall motion abnormality. To our surprise the left ventricle was contracting vigorously without any wall motion changes. Severe anterior motion (SAM) of mitral valve leaflet was noted along with the chordae tendinae obstructing the left ventricular outflow tract during systole. More fluids were infused and noradrenaline support was increased. Dopamine was stopped. The ST depression reverted back to normal, with good control of heart rate and blood pressure. The intra aortic balloon was left in situ as a pre cautionary measure and removed after a few hours in the ITU. LA Ao LV
Antr mitral leaflet RV
Long axis TOE views. Above - normal ventricular systole; below -SAM (folded AML) LA Ao LV
Antr mitral leaflet RV
Discussion: SAM is well described in the literature and is an important echocardiographic feature of idiopathic hypertrophic subaortic stenosis. The incidence of chordal SAM1 is approximately 4% in patients who require echocardiography for other clinical reasons, but as an isolated finding in the normal population it is rare (1%).
SAM is not determined solely by anterior mitral leaflet length but rather on the interplay of a number of morphological variables. It has been classified as ‘typical SAM’ with flexible motion of anterior leafelt as central portion of the leaflet is mostly spared from fibrosis, and ‘atypical SAM’ with restricted valvular motion of the leaflet in cases of diffuse pattern of anterior leaflet thickening2. Angular motion ("buckling") of mitral chordal structures, rather than movement of the body of the anterior mitral leaflet into the left ventricular outflow tract may be the cause of SAM in patients with chordal SAM. Venturi effect has been postulated which may lift the mitral valve towards the septum due to rapid velocities in the outflow tract. Closer the mitral valve approaches the ventricular septum and the longer the leaflet is in contact with it, the higher is the pressure gradient and the degree of obstruction. This can occur in vigorously contracting volume depleted ventricles with completely obliterated systolic cavities which, in turn compounds the low output state further.
In the peri-operative setting SAM is mostly caused by a functional change in the ventricular geometry secondary to either relative or absolute reductions in the preload leading to an under filled hypercontractile ventricle. Often the extent of hypovolaemia caused by vasodilatation from most anaesthetic drugs and regional anaesthesia is underestimated which leads to inadequate fluid replacement and the inappropriate infusion of inotropic agents.
By performing transesophageal echocardiography (TOE) one can identify SAM, hypercontractile ventricles and acute mitral regurgitation. Although TOE is superior to transthoracic echocardiography (TTE) in identifying SAM, TTE can be used if the anterior chest wall can be exposed. It may be difficult for inexperienced people to diagnose SAM on echocardiography, in the perioperative setting visualising the empty hyperdynamic ventricles themselves should guide towards diagnosing SAM and need for infusion of more fluids than inotropic agents. Thus the acute treatment of SAM should be mainly focussed towards fluids, vasopressor drugs and control of tachycardia. In a well contracting heart inotropy leads only to tachycardia
References:
1. Pearson AC et al. Systolic anterior motion of the mitral chordae tendineae: prevalence and clinical and Doppler echocardiographic features; Am Heart J Apr;131(4):
2. Heinrich G. et al. Morphological Determinants of Echocardiographic Patterns of Mitral Valve Systolic Anterior Motion in Obstructive Hypertrophic Cardiomyopathy; Circulation 1993;87:
3. Julius M et al. Systolic Anterior Motion in the Absence of Asymmetric Septal Hypertrophy A Buckling Phenomenon of the Chordae Tendineae; Circulation 1981;63;