The Difficult Diagnosis of Ischaemic Papillary Muscle Rupture Case report from an urban emergency department

We present a rare case of severe ischaemic papillary muscle rupture in a 67-year-old male patient who was admitted to the Emergency Department of the University Hospital Bern, Switzerland, in November 2013 with acute chest pain. On admission, the patient’s blood pressure was 60/40 mm/Hg, his pulse was 110 beats per minute and his respiratory rate was 20 breaths per minute. An electrocardiogram was normal and focused assessment with sonography in trauma was negative. Transthoracic echocardiography showed possible thickening of the mitral valve leaflet with no indications of severe mitral insufficiency or wall motion abnormalities. Triple-ruleout computed tomography angiography revealed no pulmonary emboli or aortic dissection, although coronary atherosclerosis was present. Finally, severe insufficiency of the mitral valve with rupture of the papillary muscle, likely due to ischaemia, was observed via transoesophageal echocardiography. The patient underwent a successful surgical intervention and was discharged 10 days later in stable condition.

A physical examination of the patient on arrival indicated regular heart sounds with a systolic murmur; the heart sounds were heard most clearly above Erb's point.Auscultation of the lung, examination of the abdomen and a preliminary neurological examination were all normal.An electrocardiogram was normal with no evidence of acute ischaemia.Focused assessment with sonography in trauma was negative.Transthoracic echocardiography performed by cardiologists revealed a thickened mitral valve leaflet with mild mitral insufficiency and, most importantly, no wall motion abnormalities or pericardial effusion [Figure 1].The left ventricular ejection fraction was estimated to be 65%.Creatine kinase (1,319 U/L; normal value: <190 U/L), creatine phosphokinase-MB (119.2 µg/L; normal value: <4.9 µg/L) and high-sensitivity cardiac troponin T (2.150 µg/L; normal value: <0.014 µg/L) levels were all substantially elevated.Although the patient was becoming increasingly haemodynamically unstable, the diagnosis remained unclear.Consequently, triplerule-out computed tomography was performed.No evidence of pulmonary emboli or aortic dissection was noted, although there were signs of general coronary atherosclerosis with plaques and without any luminal occlusion.The scan also revealed an infiltrate in the left upper lobe, perhaps due to aspiration pneumonia, with a small amount of left pleural effusion.
After diagnostic and laboratory testing, the patient was prescribed vasopressin before being intubated and receiving analgaesics.He was in a progressively unstable state and was re-evaluated by an interdisciplinary team, including intensive care physicians, cardiologists and emergency physicians.Although there were marked increases in heart enzymes, due to the lack of segmental wall motion abnormalities on transthoracic echocardiography, a coronary angiogram was not immediately performed.The patient was transferred to the intensive care ward for further monitoring.While there, he rapidly developed cardiogenic shock and it was not possible to stabilise him.As a result, transoesophageal echocardiography was performed.This demonstrated severe mitral valve insufficiency with rupture of the papillary muscle, dilatation of the left atrium and severe secondary pulmonary hypertension.The left ventricular ejection fraction remained the same (65%) and there were still no signs of any regional wall motion abnormalities [Table 1].
A coronary angiograph was subsequently carried out which showed that the papillary muscle rupture was caused by a distally occluded right coronary artery (RCA).As the patient remained unstable, cardiac surgery was performed.The mitral valve was replaced with a biological prosthesis and a coronary artery bypass graft was undertaken.The postoperative course was uneventful and the patient was discharged in a stable condition 10 days later.

Discussion
This report presents an unusual case of ischaemic papillary muscle rupture.Firstly, it is rare for cardiogenic shock to develop only a few hours after the onset of symptoms; the highest risk of shock is normally two to seven days after the myocardial infarction, when healing has begun. 5In this particular

Conclusion
Corresponding with previous findings in the literature, the current case report supports the view that transoesophageal echocardiography is a valuable tool to confirm the diagnosis of ischaemic papillary muscle rupture.In these cases, several diagnostic measures may often be needed.As such, the utilisation of transoesophageal, rather than transthoracic, echocardiography may lead to a life-saving diagnosis for patients who are cardiovascularly unstable.
case, the short interval of time could potentially be explained by a silent ischaemic event occurring one or two days previously.Alternatively, the papillary muscle may have already been affected for some unrelated reason. 6Secondly, the lack of regional wall motion abnormalities is an uncommon finding, particularly in a hypotensive patient; the only possible explanation for this would be an acute papillary muscle rupture with severe acute mitral regurgitation.As in this case, the posteromedial papillary muscle is often affected during a myocardial infarction in the area perfused by the RCA; in comparison, the anterolateral papillary muscle has a dual blood supply and therefore very rarely exhibits ischaemic complications. 1 Thirdly, it is rare for cases of papillary muscle rupture with severe mitral regurgitation to have an uncomplicated postoperative course, as observed with the current patient.This condition usually carries a high mortality rate; Schroeter et al. determined a 30-day postoperative mortality rate of 39.3%, while another study reported rates of 4.2% and 25.0% for intraoperative and in-hospital mortality, respectively. 7,8hocardiography is the imaging modality of choice for the non-invasive assessment of mechanical cardiac complications such as acute mitral regurgitation in the setting of a myocardial infarction. 6n these cases, the appearance of mitral regurgitation, often in relation to papillary muscle rupture, is an important sign of poor prognosis. 9Consequently, echocardiography plays an essential role in the early diagnosis, estimation of severity and determination of the pathomechanisms of ischaemic mitral regurgitation in patients with acute myocardial infarctions. 9ransoesphageal echocardiography has been well established as the initial diagnostic tool for identifying papillary muscle rupture, with a diagnostic sensitivity of 65-85%. 6Due to the close proximity of the ultrasound transducer to the mitral apparatus, transoesophageal echocardiography is often used to improve reliability when diagnosing the cause of mitral regurgitation; it has been found to increase the diagnostic yield to approximately 95-100%. 10 Christ et al. described a case of partial papillary muscle rupture diagnosed solely by transoesophageal echocardiography; previous transthoracic echocardiographs had shown no pathologies or only posterior mitral leaflet prolapse. 3Similar experiences have been reported for patients with acute septal ruptures in the acute stage of a myocardial infarction.Maillier et al. found that only eight out of 15 septal ruptures could be visualised directly by conventional transthoracic echocardiography; in contrast, transoesophageal echocardiography successfully diagnosed 14 of the same

Figure 1 :
Figure 1: Transthoracic echocardiography showing a thickened posterolateral mitral leaflet (arrow) in a 67-year-old male patient with ischaemic papillary muscle rupture.Note the lack of wall motion abnormalities or pericardial effusion.

Table 1 :
Comparison of transthoracic and transoesophageal echocardiographic findings for a 67-year-old male patient with ischaemic papillary muscle rupture *Using colour Doppler imaging.† Small jet of mitral regurgitation.‡ Large eccentric jet of mitral regurgitation.