Abstract
Acute inferior myocardial infarction can be complicated by conduction disorders and/or by extension to the right ventricle (RV). Both situations can resolve with an early percutaneous revascularization.
We report a case of a 73-year-old woman, with arterial hypertension, dyslipidemia, and studied by cardiology for atypical chest pain, with several negative ischemia detection tests. She was brought to the Emergency Department due to oppressive chest pain irradiated to the left upper extremity. An electrocardiogram was performed, highlighting a complete atrioventricular block with suprahisian escape and ST segment elevation in inferior leads. Tendency to arterial hypotension and multiple episodes of asymptomatic non-sustained monomorphic ventricular tachycardias as well as self-limiting Torsade de Pointes were registered. The transthoracic echocardiogram (TTE) showed an akinesia circumscribed to the basal segment of the inferior left ventricle wall, a non-dilated RV with akinesia of its anterior wall and a new onset functional and asymmetric severe tricuspid regurgitation (TR) by tethering of the anterior leaflet. It was not possible to estimate the RV-RA gradient by obtaining a dense triangular doppler continuous wave jet contour with early peak. Vena contracta was 7 mm long.
An urgent coronary angiography was performed in which the presence of an acute thrombotic occlusion of the proximal segment of the right coronary artery was confirmed. A drug-eluting stent was implanted, with good result. With all this, it was possible to stabilize the patient"s electrical and hemodynamic situation. A TTE was repeated one week after, in which mild to moderate tricuspid regurgitation was observed, coinciding with improvement of the RV systolic function and better mobility of the anterior tricuspid leaflet.
Anatomically, the tricuspid valve consists of anterior, septal, and posterior leaflets. Each leaflet is connected via chordae tendineae to the anterior, posterior, and septal papillary muscles of the right ventricle, respectively. The cause of functional TR appears to be tricuspid annular dilatation and tethering of the tricuspid valve leaflets (because of LV failure, pulmonary hypertension, left-to-right shunt, or RV infarction). Primary disorders of the tricuspid valve causing TR are less common. RV myocardial infarction may involve the wall supporting the papillary muscle with resulting tension on the chordae causing TR. The 2D TTE demonstrates incomplete and often asymmetric closure of the tricuspid leaflets with apical displacement of the coaptation point. This phenomenon is similar to that seen with LV myocardial infarction with resulting loss of support of mitral papillary muscle and ischemic mitral regurgitation.
We report a case of acute inferior myocardial infarction involving the RV that caused a transient dysfunction of the papillary muscle of the anterior tricuspid leaflet, generating a severe TR that resolved by early revascularization.
Abstract P716 Figure. A: severe acute TR. B: few days after
P716 Acute chest pain and new onset severe and asymmetric functional tricuspid regurgitation: What is going on?
