Heart Views

: 2022  |  Volume : 23  |  Issue : 4  |  Page : 244--245

Ruptured head of papillary muscle complicating non-ST elevation myocardial infarction

Abdel Haleem Shawky Hamada, Mohammed A .A. Al-Hashemi, Smitha Anilkumar 
 Non-Invasive Cardiology, Heart Hospital, Hamad Medical Corporation, Doha, Qatar

Correspondence Address:
Dr. Abdel Haleem Shawky Hamada
Heart Hospital, Hamad Medical Corporation, P. O. Box 3050, Doha

How to cite this article:
Hamada AH, Al-Hashemi MA, Anilkumar S. Ruptured head of papillary muscle complicating non-ST elevation myocardial infarction.Heart Views 2022;23:244-245

How to cite this URL:
Hamada AH, Al-Hashemi MA, Anilkumar S. Ruptured head of papillary muscle complicating non-ST elevation myocardial infarction. Heart Views [serial online] 2022 [cited 2023 Dec 8 ];23:244-245
Available from: https://www.heartviews.org/text.asp?2022/23/4/244/361407

Full Text

A 74-year-old man presented to the emergency department for retrosternal chest pain and heaviness radiating to the left arm with progressive shortness of breath and orthopnea for the last 7 h before admission.

The patient had a past medical history of smoking, diabetes mellitus, hypertension, and hyperlipidemia. He had serial electrocardiograms (ECGs) in the past 7 years which showed right bundle branch block and a previous transthoracic echocardiography 5 years ago which was normal.

On initial assessment, he was conscious, alert, in pain, and on semi-sitting position, his temperature was 37.1°C, H.R 94/min, respiratory rate 25/min, and his blood pressure 80/50 mmHg. An oxygen saturation is 94% at room air. His initial laboratory investigations revealed elevated troponin-T HS: Chest X-ray showed interstitial and alveolar opacities in a butterfly pattern consistent with cardiogenic pulmonary edema. His ECG showed sinus tachycardia with upsloping ST segment depression in Leads II, AVF, V2-V3, and the posterior precordial leads were normal.

An urgent transthoracic echocardiography was done which revealed hyperdynamic left ventricle, flail anterior mitral leaflet with attached highly mobile bell-like mass suggestive of ruptured chordae and possible head of papillary muscle rupture, severe posteriorly directed torrential mitral regurgitation, and severe pulmonary HTN (70 mmHg). The cardiac chambers dimension was normal. Urgent transesophageal echocardiography (TEE) was needed to clarify the mechanism of mitral regurgitation.

In the Cath lab TEE was done which revealed ruptured head of anterolateral papillary muscle [Figure 1], flail anterior mitral leaflet, hyperdynamic left ventricle, torrential posteriorly directed mitral regurgitation swirling to the roof of the left atrium [[Figure 2]a, [Figure 2]b and Supplementary Video 1], systolic flow reversal in left pulmonary veins, and normal other cardiac valves.{Figure 1}{Figure 2}


Coronary angiography revealed 30% proximal left anterior descending (LAD), 70% proximal D2, 30% proximal left circumflex artery (LCX), and 60% mid right coronary artery (RCA) lesions [Figure 3]. An intra-aortic balloon pump was inserted. These nonsignificant obstructive coronary lesions did not require percutaneous coronary interventions and after discussion with cardiothoracic surgery team, the patient was immediately shifted to the operating room.{Figure 3}

In the operating room, the excision of the original valve was done and was replaced by a tissue valve size 31. The patient went off-pump and intraoperative TEE was done to assess the prosthesis. TEE showed moderate-to-severe central mitral regurgitation due to tethering and marked restriction of posterior leaflet mobility of MV Bio-prosthesis [[Figure 4]a, [Figure 4]b and Supplementary Video 2]. The patient went on the pump again and there was a stitch looped around the strut and the tethered leaflet causing its damage. The 31-size tissue valve was replaced with another tissue valve [Supplementary Video 3]. No coronary artery bypass grafting was done.{Figure 4}



The estimated incidence of papillary muscle rupture (PMR) is 0.5%–5% of myocardial infarction (MI) patients. PMR typically occurs 5–7 days after the onset of MI and is a rare complication of MI. It has poor prognosis (90% mortality) which depends on the extent of rupture.[1]

A high index of suspicion is warranted for early recognition and timely management of this catastrophic condition. Urgent echocardiography is the gold standard in the early diagnosis of this lethal condition and in guiding the management, which saves lives.[2],[3]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initial s will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed

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Conflicts of interest

There are no conflicts of interest.


1Roffi M, Patrono C, Collet JP, Mueller C, Valgimigli M, Andreotti F, et al. 2015 ESC guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task force for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 2016;37:267-315.
2Murad K, Missov E. Papillary muscle rupture following non-St-elevation myocardial infarction: A case report. Echocardiography 2016;33:923-5.
3Suarez K, Slicker K, Torres V. Diagnosis and management of papillary muscle rupture complicating acute myocardial infarction: A case report and review of the literature. Arch Cardiovasc Imaging 2015;3:e30490.