Prosthetic mitral valve tamponade alternans

Abstract

We wish to report an important clinical observation that combined several forms of imaging followed by pharmacological intervention that saved a patient froma potentially unnecessary surgical intervention. This was in a 65-year-old lady with previous Ultracor single tilting disc mitral valve replacement in 1996, systemic hypertension, chronic atrial fibrillation and epilepsy; who complained of worsening breathlessness. Clinically, she had physical signs of right heart failure. Trans-thoracic echocardiogram (TTE) showed mild left ventricular systolic impairment, dilated left atrium, significantly dilated right ventricle, moderate right ventricular systolic impairment, moderate rise of the systolic pulmonary artery pressure (55 mmHg), and a well-seated mechanical mitral valve prosthesis with no para-valvular leak. However, the Ultracor single-tilting-disc mechanical MV prosthesis was not opening on alternate cardiac cycles, Fig. 1. We did not agree with those who suspected a catastrophic malfunctioning of mechanical MV prosthesis and proposed a re-do operation. We noted that the function of the MV prosthesis was normal on alternate beats. We postulated that the intermittentmalfunction indicated a dynamic intermittent problem most likely related to the impact of the high right sided pressure on the diastolic pressure of the left ventricle which is preventing themechanicalMVprosthesis fromopeningeveryother beat. This is similar, though intermittent, to tamponade. We called that tamponade alternans of the MV prosthesis. We went on to confirm our hypothesis and performed fluoroscopy and an invasive simultaneous left and right heart catheter study [1]. Fluoroscopy confirmed the intermittent opening of the Ultracor singletilting-disc mechanical MV prosthesis every other beat (Fig. 2). The invasive studies showed severe pulsus alternans. The beats with the lower cardiac output were preceded by equalisation of right and left ventricular diastolic pressures (Fig. 2). The beats with the higher left ventricular output were preceded by a left ventricular end diastolic pressure higher than the right ventricular end diastolic pressure. The pulmonary artery pressure was 50/23 mm Hg with a mean of 38 mm Hg. The pulmonary capillary wedge pressure was high at 34/28 mm Hg. We had thus confirmed our hypothesis that the pulmonary hypertension is pushing the inter-ventricular septum paradoxically to the left (Fig. 2), and raising the left ventricular diastolic pressure to a level higher than the left atrial pressure as shown by changes in the diastolic left ventricular pressure curves (Fig. 2). This is preventing the opening of themitral valve. However, by the following cardiac cycle, the