Transesophageal Echocardiographic Assessment of Papillary Muscle Rupture
Background In some patients with papillary muscle rupture, the ruptured head may not prolapse into the left atrium, which makes diagnosis by transthoracic or transesophageal echocardiography difficult.
Methods and Results In an attempt to find additional or more definite diagnostic echocardiographic features, we analyzed intraoperative transesophageal echocardiograms of 21 consecutive patients with papillary muscle rupture (20 involved the left ventricle and 1 involved the right ventricle) confirmed at surgery. In 7 (35%) of 20 patients with left ventricular papillary muscle rupture, the ruptured head was not seen to prolapse into the left atrium. In these patients, examination of the left ventricle proved most useful. Abnormal, large-amplitude erratic motion (1 to 5 cm in 17 patients; 0.5 cm in 1 patient) of a large echo density in the left ventricle consistent with the ruptured head was noted in 18 (90%) of these 20 patients. This included all 7 patients with nonprolapse of the ruptured papillary muscle head into the left atrium. Less prominent erratic motion or flutter of the papillary muscle still attached to the left ventricular wall was also noted but was less sensitive in the diagnosis of papillary muscle rupture. The single patient with right ventricular papillary muscle rupture showed erratic motion as well as prolapse of the ruptured head into the right atrium.
Conclusions Transesophageal echocardiographic examination of the left ventricle is useful in the diagnosis of papillary muscle rupture, especially in those patients in whom the ruptured head does not prolapse into the left atrium. The left ventricle should be scrutinized thoroughly during transesophageal echocardiographic examination for erratic papillary muscle motion in all patients with suspected rupture.
Rupture of PM after acute MI, although rare, has an unacceptably high mortality if surgical intervention is delayed.1 It has been reported that without surgery, 50% of patients with this complication are dead within 24 hours2 3 ; this is nearly twice the mortality seen in those with a ventricular septal defect after an acute infarct.4 Hence, it is crucial to arrive rapidly at a definitive diagnosis in these patients.
Clinically, it is possible only to suspect the occurrence of this complication in the setting of acute MI because the appearance of a new systolic murmur could be due to PM dysfunction or an acute ventricular septal defect other than PM rupture, and at times, no murmur may be heard in patients with severe hemodynamic disturbance.5 Furthermore, it is not possible clinically to differentiate the rupture of chordae tendineae from PM rupture, which may occasionally result after an acute MI.6 Because patients are too ill for immediate invasive procedures, TTE has come to be used as an initial diagnostic modality to diagnose acute PM rupture. Features suggestive of PM rupture that have been described by TTE include a flail mitral valve leaflet with systolic prolapse into the left atrium, a mobile mass attached to the chordae tendineae and to the mitral valve, and an abnormal cutoff of one PM.2 7 8 9 Some of these features are nonspecific; for example, a mobile mass could simulate a tumor, vegetation, or thrombus, and a flail mitral valve may be seen as a result of chordal rupture. Moreover, a diagnosis may not be possible in some patients owing to technical difficulties in obtaining adequate quality images by TTE.5 As a result, the use of TEE for final diagnosis of such critically ill patients has gained support, but recognition of PM rupture with this technique has appeared in the literature only in the form of short case reports because the complication is uncommon.10 11 12 13 14
Diagnosis of PM rupture by TEE in the published case reports was made by observation of an echogenic mass attached to the mitral valve11 or when a mobile mass was seen to prolapse into the left atrium during systole and to move back into the left ventricle during diastole.12 We and others13 have observed that in some patients with complete PM rupture, the ruptured PM head is not visualized to prolapse into the left atrium. Therefore, we attempted to find additional echocardiographic features that could help make a more reliable diagnosis of PM rupture, particularly in the absence of prolapse of the ruptured head into the left atrium. For this purpose, we retrospectively analyzed the data in each of our 21 consecutive patients who had undergone both TTE and intraoperative TEE and in whom confirmation of PM rupture had been made at surgery.
The study comprised 21 consecutive patients (19 men and 2 women; mean age, 63.2±9 years; range, 42 to 76 years) with PM rupture confirmed at surgery who had undergone preoperative TTE and intraoperative TEE (Table 1⇓). Twelve of these patients (patients 1 through 12) were studied at the University of Alabama Medical Center and the remaining 9 (patients 13 through 21) were examined at the Hospital Universitario San Carlos in Madrid, Spain. Twenty of 21 patients were diagnosed to have sustained an acute MI by the standard ECG and enzymatic criteria (Table 1⇓) and had developed a new systolic mitral murmur and severe dyspnea (NYHA class IV). The remaining 52-year-old male patient (patient 11) did not have an acute MI on the ECG or by serial cardiac enzyme rise but had a mitral systolic murmur and congestive cardiac failure and was found to have isolated posterior PM infarction at pathology. Five (24%) of 21 patients died, 3 intraoperatively and 2 postoperatively, in the hospital.
At surgery, 20 patients had a left ventricular PM rupture, and 1 had a right ventricular posterior PM rupture together with an acute ventricular septal defect. Among those with left ventricular PM rupture, in 3 patients, there was rupture of the anterior PM; in 16, the posterior PM had ruptured; and in 1 (patient 4), a rupture of one head of the PM was reported to have been seen without a clear mention of whether the anterior or posterior PM was involved. In 3 patients (patients 15, 20, and 21), the PM head remained attached to the rest of the PM body by a thin strand of fibrous tissue of variable length, as seen at surgery.
TTE was performed in all patients by use of commercially available phased-array systems and a 2.5-MHz transducer within 24 hours before cardiac surgery except in 1 patient in whom surgery was performed after an interval of 5 days. Intraoperative TEE was undertaken after informed consent was obtained. The probe was inserted after induction of anesthesia and the examination performed in the standard manner in all patients with the use of a 5-MHz transducer and a Hewlett-Packard Sonos 1000/1500 (9 patients), Toshiba 140 (9 patients), or Aloka-SSD-870 (3 patients) ultrasound machine.15 16 17 Imaging was undertaken by multiplane transducer in 7 patients, by biplane in 13, and by single-plane probe in 1 patient.
The TEE images of patients with left ventricular PM rupture were analyzed for the following:
1. Visualization of a mobile echo density in the left atrium consistent with ruptured PM head and its maximal size and excursion.
2. Visualization of a mobile echo density in the left ventricular body (not attached to the ventricular wall) with an erratic motion (out of phase with ventricular wall motion) consistent with ruptured PM head, its maximal size and maximal excursion, and the imaging plane in which this was visualized.
3. Erratic motion (out of phase with ventricular wall motion) or a flutter of PM(s) attached to the left ventricular wall, the maximal excursion, and the imaging plane in which this was visualized.
4. Prolapse of mitral valve cusps into the left atrium and their extent relative to one another.
5. Presence of mitral regurgitation, whether freestanding or along the leaflets or wall, its direction in the left atrium evaluated in three planes (two chamber, four chamber, and five chamber), and assessment of its severity as measured by jet size and by systolic backflow into the left and/or right upper pulmonary veins.
6. Left and right ventricular wall motion abnormalities.
TTE findings of patients with left ventricular PM rupture were analyzed in the same manner as TEE studies except for mitral regurgitation severity, which was graded by the maximal jet area expressed as a ratio of left atrial size, as described previously.18
The TEE and TTE findings of the patient with right ventricular PM were analyzed similarly, with the following assessments: (1) size of the ruptured head in the right atrium; (2) any erratic motion of the PM(s) in the right ventricle; (3) extent of prolapse of tricuspid valve leaflets into the right atrium; (4) presence of tricuspid regurgitation and assessment of its severity, as described previously19 ; and (5) ventricular wall-motion abnormalities.
A control group of 31 patients (mean age, 62.5±8 years; range, 37 to 81 years) who did not have PM rupture but who had mitral regurgitation and had undergone intraoperative TEE was analyzed in the same manner as patients with left ventricular PM rupture. Of these, diagnosis at surgery showed that 10 patients had anterior chordal rupture, 9 had posterior chordal rupture, and 4 had both anterior and posterior chordal ruptures. The remaining 8 patients with mitral regurgitation and coronary artery disease were suspected by the surgeon to have PM dysfunction.
The clinical data of patients included in the present study are detailed in Table 1⇑.
Left Ventricular PM Rupture
The TEE features analyzed and the measurements made in all 20 patients with left ventricular PM rupture and the 1 patient with right ventricular posterior PM rupture are shown in Tables 2⇓ and 3.⇓ The ruptured PM head was observed to prolapse into the left atrium in only 13 (65%) of 20 patients with left ventricular PM rupture (Fig 1⇓). In the remaining 7 patients (35%), the ruptured PM head could not be visualized in the left atrium even though the left atrium was imaged in multiple planes (Figs 2 and 3⇓⇓). However, the ruptured PM head could be identified in the left ventricular body by its large, erratic motion (range, 1.0 to 5.0 cm in 17 patients; 0.5 cm in 1 patient) in as many as 18 (90%) of the 20 patients with left ventricular PM rupture. This included all 7 patients in whom the ruptured PM head was not seen in the left atrium. In the remaining 2 patients with no erratic motion, the ruptured PM head could be seen in the left atrium. In contrast to the motion of the ruptured head, erratic motion of the PM(s) attached to the ventricular wall was observed in a smaller number of patients (14 [70%] of 20), and the amplitude of the motion was much smaller (0.2 to 1.5 cm). Indeed, in 6 (43%) of these 14 patients, it consisted of a very-low-amplitude fluttering motion (0.2 to 0.3 cm). Thus, in the present study, PM rupture could be diagnosed by TEE examination of the left ventricular body in 19 (95%) of 20 patients by notation of the large-amplitude erratic motion of the ruptured PM head in the left ventricle in 18 patients and the erratic motion of the PM attached to the ventricular wall in 1 patient. On the other hand, PM rupture could be diagnosed by TEE examination of the left atrium in only 13 (65%) of 20 patients.
None of the 31 patients in the control group (23 with chordal rupture and 8 with PM dysfunction) demonstrated erratic motion or flutter of their PMs.
Comparison of the maximal size of the ruptured PM head in the left ventricle between patients in whom it was visualized in the left atrium (0.25 to 2.0 cm) and those in whom it was not (0.5 to 2.0 cm) showed no statistically significant difference. For this comparison, the 3 patients (patients 15, 20, and 21) in whom the PM head remained attached to the rest of the PM body by a thin strand of tissue were excluded because this could be a potential reason that the ruptured PM heads did not prolapse into the left atrium.
All patients with left ventricular PM rupture showed prominent mitral valve cusp prolapse. The posterior cusp prolapsed into the left atrium more than the anterior in 11 (55%) of 20 patients, and in 8 (73%) of these, the mitral regurgitation jet was directed medially. In the remaining 9 patients, the anterior mitral cusp prolapse into the left atrium was greater than (8 patients) or equal to (1 patient) the posterior cusp prolapse, and the mitral regurgitation jet was directed laterally in 7 (78%) of these 9 patients. In all 6 of the patients in whom both the left and right upper pulmonary veins were visualized, systolic backflow indicative of severe mitral regurgitation was detected in both veins. In 13 of the remaining 14 patients, only one pulmonary vein was imaged, which also showed systolic backflow, and in 1 patient, no pulmonary vein was visualized. The color Doppler mitral regurgitation jet was large and practically filled the whole of the imaged left atrium in all patients, consistent with severe mitral regurgitation.
Even though all 20 patients were known to have suffered an MI, only 1 showed evidence for akinesis at the ECG infarct site, and none showed dyskinetic wall motion. Seventeen of the remaining 19 patients showed hypokinesis that involved the inferior wall in 13, the anterior wall in 1, and the right ventricular wall in 3 patients. All patients showed normal to hyperdynamic motion of the noninvolved ventricular walls. The patient with no evidence of MI by ECG and serum enzyme criteria but with isolated posterior PM infarction at pathology had hypokinesis of the inferior wall.
In only 2 of 20 patients with left ventricular PM rupture, the ruptured PM head was seen to prolapse into the left atrium. None showed erratic motion of the ruptured PM head or the PM attached to the ventricular wall. Prolapse of mitral valve cusps was seen in 6 (30%) of 20 patients. However, all patients showed severe mitral regurgitation with mitral regurgitation area/left atrium size >40%. Wall-motion abnormalities were noted in 12 of 20 patients and consisted of hypokinesis that involved the inferior wall in 9 and the anterior wall in 3 patients. None of the patients showed akinesis or dyskinesis.
Right Ventricular PM Rupture
TTE and TEE
In the patient with right ventricular posterior PM rupture, the ruptured head was visualized by both TTE and TEE in the right atrium and right ventricle, and both the ruptured head and the PM attached to the right ventricular wall exhibited an erratic motion and prominent prolapse of the tricuspid valve. The tricuspid regurgitation jet filled practically all of the right atrium, which indicated severe tricuspid regurgitation. This patient also had an associated ventricular septal defect that was diagnosed by both TTE and TEE. There was severe hypokinesis of the left ventricular inferior wall and right ventricular diaphragmatic wall in this patient as assessed by both TEE and TTE.
Coronary arteriography was performed in 18 of 21 patients. Two of the 3 patients with anterior PM rupture had isolated circumflex coronary artery stenosis, and the remaining patient had both left anterior descending and circumflex coronary artery stenoses. Of 15 patients with posterior PM rupture, 6 had isolated right coronary artery stenosis, 4 had isolated circumflex coronary artery stenosis, 3 had combined circumflex and right coronary artery stenoses, and 2 had combined left anterior descending and right coronary artery stenoses.
The conventional diagnosis of left ventricular PM rupture by TEE is made when a mobile mass attached to the mitral valve is seen to prolapse into the left atrium during systole.10 12 However, in some patients, this mass may not be seen in the left atrium, which makes the diagnosis difficult or even impossible. In the present study, in as many as 35% of patients, the ruptured PM head was not visualized in the left atrium even though all patients were examined by biplane or multiplane TEE and none by the single-plane approach. The results of our data indicate that the diagnostic accuracy of TEE in patients with PM rupture could be improved by careful examination of the left ventricular body. In 90% of patients, the ruptured PM head showed a relatively large-amplitude erratic motion in the left ventricular body; this included all patients in whom the PM head was not visualized in the left atrium. In addition, in 70% of the patients, an erratic motion of the PM attached to the ventricular wall was also noted, although this was generally less prominent than the erratic motion of the ruptured PM head. Thus, by careful TEE examination of the left atrium and left ventricle, a diagnosis of left ventricular PM rupture could be made in all 20 patients. Also, in no patient among the control group did we observe an erratic motion of the PM in the left ventricular body. The chaotic motion of a flail, unsupported, ruptured PM head in the left ventricle easily explains the large-amplitude erratic motion seen by TEE and appears to be a highly specific diagnostic finding. The less prominent erratic motion or flutter of the remaining component of the PM still attached to the ventricular wall may be related to the loss of a part of its anchoring support to the mitral valve leaflets. However, this was a less consistent finding and may not be highly specific.
It is unclear from analysis of the data of patients in the present study why the ruptured PM head was not visualized in the left atrium in approximately one third of the patients. In 3 patients, the ruptured PM head was still tenuously attached by a thin, long strand of tissue to the remnant of PM in the left ventricle, and it is possible that this was a contributing factor in prevention of its prolapse into the left atrium. However, in the remaining 4 patients, no such strand connecting the ruptured PM head to its ventricular component was reported to be seen at surgery. It is possible that in some patients, the ruptured PM head with its chordae had become trapped around the intact chordae or other PM in the left ventricle, resulting in its nonprolapse into the left atrium. We suggest this from our previous case report20 in which a left ventricular myxoma moved between the left ventricle and the left atrium with intermittent trapping of the mass in the left atrium. One group of authors11 in a single case report noticed an associated mitral stenosis and speculated that the narrowed mitral valve orifice may have prevented the ruptured PM from prolapsing into the left atrium. None of our patients had evidence of mitral stenosis, yet the ruptured PM head could not be visualized in the left atrium in 7 patients, and hence this appears to be an unlikely explanation. To determine whether a larger size of the ruptured PM heads had any bearing on this observation, we measured the maximal sizes of the ruptured PM heads seen in these patients. However, there was no significant difference between the size of the ruptured heads of patients in whom they were visualized in the left atrium and those in whom they were seen only in the left ventricle. Hence, we believe that the size of the ruptured PM heads has no direct relationship to this observation. One also needs to consider the possibility that in some patients, the ruptured PM head may not fall into the plane of interrogation by the ultrasonic beam. However, this is very unlikely, because in all our patients, the left atrium was well visualized in multiple planes with use of a biplane or multiple probe (Table 2⇑).
Roberts and Chen21 commented that right ventricular PM(s) may develop necrosis or fibrosis as a result of inferior MI, but their rupture is extremely rare.22 In a single patient in our series with right ventricular PM, the ruptured posterior PM head was clearly seen to prolapse into the right atrium. Also, examination of the right ventricle demonstrated an erratic motion of the ruptured PM head as well as that of the remaining PM still attached to the right ventricular diaphragmatic walls; these findings permitted easy diagnosis of PM rupture.
Interestingly, although all patients suffered from MI and many showed hypokinesis of the involved walls, only one patient demonstrated akinesis and none showed dyskinesis. We believe that absence of severe wall-motion abnormalities could have been due to the use of inotropic agents and tachycardia in these hemodynamically disturbed patients with PM rupture.
In conclusion, TEE examination of the left ventricle is useful in the diagnosis of PM rupture. It is particularly helpful in patients in whom the ruptured PM head does not prolapse into the left atrium. The left ventricle should be scrutinized thoroughly during TEE examination for erratic PM motion in all patients with suspected PM rupture.
Selected Abbreviations and Acronyms
Reprint requests to Navin C. Nanda, MD, University of Alabama at Birmingham, Heart Station SW/S102, Birmingham, AL 35233. E-mail firstname.lastname@example.org.
- Received October 30, 1995.
- Revision received February 27, 1996.
- Accepted March 4, 1996.
- Copyright © 1996 by American Heart Association
Buda AJ. The role of echocardiography in the evaluation of mechanical complications of acute myocardial infarction. Circulation. 1991;84:109-121.
Mintz GS, Victor MF, Kotler MN, Parry WR, Segal BL. Two-dimensional echocardiographic identification of surgically correctable complications of acute myocardial infarction. Circulation. 1981;64:91-96.
Helmcke F, Nanda NC, Hsiung MC, Soto B, Adey C, Goyal RG, Gatewood R. Color Doppler assessment of mitral regurgitation using orthogonal planes. Circulation. 1987;75:175-183.
Roberts WC, Chen LS. Left ventricular papillary muscles: description of the normal and a survey of conditions causing them to be abnormal. Circulation. 1972;26:138-154.
Maxted W, Nanda NC, Kim KS, Roychoudhury D, Pinheiro L. Transesophageal echocardiographic identification and validation of individual tricuspid valve leaflets. Echocardiography. 1994;11:585-596.