ABC | Volume 111, Nº3, September 2018

Case Report Partial Papillary Muscle Rupture after Myocardial Infarction and Early Severe Obstructive Bioprosthetic Valve Thrombosis: an Unusual Combination Inês Silveira, Marta Oliveira, Catarina Gomes, Sofia Cabral, André Luz, Severo Torres Centro Hospitalar do Porto, Porto – Portugal Mailing Address: Inês Silveira • Largo Prof. Abel Salazar, 4099-001 Porto - Portugal E-mail: Ines.c.silveira@gmail.com Manuscript receivde December 02, 2017, revised manuscript April 04, 2018, accepted April 25, 2018 Keywords Myocardial Infarction/complications; Thrombolytic Therapy; Atrioventricular Block/complications; Pacemaker Artificial; Heart Arrest; Heart Rupture.Post-Infarction; Bioprosthesis DOI: 10.5935/abc.20180179 Introduction Mechanical complications after myocardial infarction (MI) have become uncommon since the introduction of primary angioplasty. 1 They can lead to a rapid clinical deterioration and a fatal outcome, with patient’s survival being dependent on their prompt recognition and intervention. We describe a case of two rare mechanical complications: a partial papillary muscle rupture after MI, followed by an early severe obstructive thrombosis of the implanted bioprosthetic valve. Case report We report a case of a 70 year-old male, with a history of dyslipidaemia and smoking habits, who suffered an inferior ST elevation myocardial infarction (STEMI). Given the impossibility to achieve a timely percutaneous coronary artery intervention, thrombolysis was performed within 4 hours of symptoms onset. Advanced atrioventricular block requiring a transcutaneous pacemaker occurred soon after, followed by cardiorespiratory arrest in ventricular fibrillation, which was reversed after one cycle of advanced life support. The patient was transported by airplane to a percutaneous coronary intervention (PCI)-capable centre. Coronary angiography showed a 50-60% stenosis in the proximal segment of the right coronary artery, which was treated with a bare metal stent. Echocardiography showed a moderate left ventricular systolic dysfunction (estimated ejection fraction of 35%), with inferior, inferolateral and inferoseptal akinesia and moderate mitral regurgitation. On the fifth day, the patient was transferred to our centre, after a 10-hour flight. On admission to intensive care unit, the patient was in cardiogenic shock with inotropes and non-invasive ventilation. A bedside transthoracic echocardiography revealed a severe mitral valve regurgitation of uncertain mechanism, along with moderate left ventricle systolic dysfunction and right ventricle systolic compromise. Additional characterisation by transoesophageal echocardiography revealed a 9 mm disruption of the posteromedial papillary muscle consistent with a contained, albeit morphologically imminent, rupture. The instability of the sub-valvular apparatus, leading to a broad posterior leaflet prolapse, caused severe mitral regurgitation with an eccentric jet with Coanda effect, reaching the left atria roof (Figure 1). The patient underwent urgent mitral valve replacement with a biological prosthetic valve (St. Jude #29), with preservation of anterior and posterior leaflets. The patient experienced a favourable post-operative recovery and was discharged 12 days after surgery with anticoagulant therapy for three months, in addition to dual antiplatelet therapy. On the fourth month after surgery, the patient initiated progressive heart failure symptoms (NYHA class III) without any further complaints. Additional transthoracic and transoesophageal evaluations were performed, revealing a significant restriction of the prosthetic mitral valve leaflets mobility due to thrombotic material deposition, leading to severe obstruction, with a mean gradient of 19 mmHg and an effective orifice area estimated by PISA method of 0.4 cm. 2 Additionally, in continuity with the prosthesis, a large mural thrombus was present covering the left atrial posteroseptal wall (Figure 2). Urgent surgery, within twenty‑four hours after diagnosis, was performed involving mitral bioprosthesis replacement with another biologic prosthesis with significant improvement in clinical status. After an extensive study, no evidence was found of atrial fibrillation or thrombotic disorders. Pathology examination of the excised prosthetic material confirmed prosthetic thrombosis, with no signs of endocarditis. Discussion In the current era of early mechanical reperfusion, the incidence of papillary muscle rupture (PMR) after MI has decreased, being less than 0.5%. Although rare, complete or partial PMR is a serious complication which can lead to rapid clinical deterioration and death. 1,2 A great deal of foresight is essential for an early recognition of this condition, especially in uncommon scenarios, like the case reported. Moreover, the patient was submitted to thrombolytic therapy and prolonged air travel in the acute phase of MI, which could have contributed to additional ischemia and injury. Transthoracic echocardiography (TTE) is of critical importance in the evaluation of patients in cardiogenic shock after MI, and so it is the initial imaging modality used. It has a sensitivity of 65–85% for the diagnosis of PMR. 3 However, in some cases TTE is insufficient to accurately ascertain the mechanism causing mitral regurgitation, so an additional characterization with transoesophageal echocardiogram (TEE) becomes crucial to establish diagnosis. TEE can offer superior visibility and characterization of the posterior structures – such as mitral valve apparatus – with a diagnostic yield between 95% and 430