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Partial Papillary Muscle Rupture: A Cause of Acute Mitral Regurgitation
Special Feature CARDIOLOGY GRAND ROUNDS FROM EMORY UNIVERSITY
Partial Papillary Muscle Rupture: A Cause of Acute Mitral Regurgitation
Authors Peter B. Flueckiger, MD, Alan C. Cheng, MD, Jonathan M. Patton, MD and Stephen D. Clements, Jr, MD Editor Stamatios Lerakis, MD Abstract: A 56-year-old woman presented to the cardiology clinic with a 7-day history of dyspnea and chest pressure. An echocardiogram showed a flail posterior mitral valve leaflet, and subsequent left heart catheterization showed complete occlusion of the first obtuse marginal coronary artery. Further investigation demonstrated the culprit lesion to be ischemic partial rupture of the posteromedial papillary muscle. Timely recognition of this condition allowed for an optimal clinical outcome. In this Cardiology Grand Rounds, the authors further describe the above presentation of ischemic partial papillary muscle rupture and provide a brief review of the pathophysiology, diagnosis and treatment of this condition. Key Indexing Terms: Partial papillary muscle rupture; Mitral regurgitation; Acute myocardial infarction. [Am J Med Sci 2013;345(6):478– 481.]
P
apillary muscle rupture (PMR), either complete or partial, is an uncommon cause of acute mitral regurgitation, occurring in 1% of cases. PMR is also a rare complication of acute myocardial infarction (AMI).1 Clinical presentation may be varied and requires early recognition and high suspicion, given the increased mortality if left untreated.2 Early echocardiographic visualization of PMR, assessment of coronary artery disease and surgical intervention is necessary. We present a case of a patient with a partial PMR secondary to AMI with discussion of the pathophysiology, diagnosis and treatment of PMR (Table 1).
From the Department of Medicine (PBF, ACC, JMP, SDC), Emory University, Atlanta, Georgia; and Division of Cardiology, Department of Medicine (ACC, JMP, SDC), Emory University, Atlanta, Georgia. Submitted June 28, 2012; accepted in revised form September 25, 2012. The authors state that they have no funding or conflicts of interest to disclose. Correspondence: Peter B. Flueckiger, MD, Department of Medicine, Emory University, 69 Jesse Hill Jr. Drive, Atlanta, GA 30303 (E-mail: pbfl[email protected]).
478
CASE PRESENTATION A 56-year-old woman was referred to the cardiology clinic for further evaluation of dyspnea, mild chest pressure and palpitations present for the last 7 days. At the onset of her symptoms, she was able to continue walking on a treadmill at her home. However, her activity became increasingly limited and she began to experience shortness of breath at rest that worsened when lying in the supine position. She denied a cough or fever. Medical history included hypertension, hyperlipidemia and ductal carcinoma in situ of the left breast that was subsequently treated with lumpectomy and radiation therapy 9 months before the above presentation. Her family history was remarkable for her father having an AMI at age 57 years and mother having an aortic dissection at age 70 years.
ASSESSMENT Initially, the patient was hypertensive (148/94 mm Hg), tachypneic (respiratory rate of 28 breaths per minute), tachycardic (102 beats per minute), afebrile and hypoxic with oxygen saturation 91% on room air. There was marked distention of the internal jugular vein to the level of her earlobes when reclined at a 30° angle. Cardiac examination revealed mild lateral displacement of the apical impulse, a regular rhythm and a 4/6 holosystolic murmur heard best at the apex with radiation to the left axilla. There were faint crackles heard in the bilateral lower lung fields. No abdominal tenderness, ascites or hepatomegaly was noted. Trace pretibial edema was appreciated on examination of her lower extremities, but no lesions consistent with Osler nodes or Janeway lesions were present. Basic laboratory evaluation demonstrated her complete blood count and comprehensive metabolic panel to be within the normal range. Cardiac laboratory studies showed a brain natriuretic peptide of 1378 pg/mL, troponin I of 0.80 ng/mL, creatinine kinase of 43 units/L and creatinine kinase-MB fraction of 1 ng/mL. Electrocardiogram showed sinus tachycardia, biatrial enlargement and S-T segment depression in the inferior leads
The American Journal of the Medical Sciences
Volume 345, Number 6, June 2013
Partial Papillary Muscle Rupture
TABLE 1. Potential causes of PMR/dysfunction Myocardial infarction Trauma (blunt or iatrogenic) Myocarditis Endocarditis Connective tissue disease
as well as V3-V6. A 2-D transthoracic echocardiogram was performed, revealing a left ventricular ejection fraction of 60% to 65%, moderate to severe mitral valve (MV) regurgitation with an anteriorly directed regurgitant jet, moderate to severe tricuspid valve regurgitation, severely elevated right ventricular systolic pressure (estimated at 70–75 mm Hg) and a dilated inferior vena cava with decreased respiratory collapse. Repeat examination revealed worsening hypoxia with oxygen saturation 88% on room air, an irregular rapid pulse and increasingly prominent bibasilar lung crackles. A subsequent electrocardiogram showed atrial fibrillation with a ventricular rate of 173 beats per minute and more pronounced S-T segment depression (Figure 1).
DIAGNOSIS
Due to the patient’s atrial fibrillation with rapid ventricular response and increasing dyspnea, she was admitted to the cardiac intensive care unit. She received an intravenous diltiazem drip and intravenous furosemide with subsequent spontaneous conversion to sinus rhythm. A transesophageal echocardiogram (TEE) performed to assess the etiology of her MV regurgitation revealed severe prolapse of the posterior mitral leaflet (Figures 2A and 2B). The patient subsequently underwent a left heart catheterization demonstrating complete occlusion of the first obtuse marginal (OM1) branch from the left circumflex coronary artery and 50% stenosis of the midsegment of the left anterior descending (LAD) coronary artery (Figure 3). The finding of an occluded OM1 suggested ischemic PMR as the etiology of her symptoms. On reexamination of the TEE, partial rupture of the posteromedial papillary muscle was seen.
MANAGEMENT An intra-aortic balloon pump was inserted in the catheterization laboratory. She was taken emergently to the operating room, where partial rupture of the posteromedial
papillary muscle was found. A bioprosthetic valve was placed in the MV position, and coronary bypass was performed with an in situ left internal mammary artery graft to the LAD and a saphenous vein graft to the OM1. The patient recovered nicely.
ISCHEMIC PMR Ischemic PMR is a rare etiology of mitral regurgitation (MR), occurring in 1% of patients with myocardial ischemia.1 Acute MR due to rupture of the papillary muscle typically occurs within 5 days of the initial acute ischemic event and leads to flail of 1, or rarely, both of the MV leaflets.1,3,4 PMR can occur in either the posteromedial or anterolateral muscle heads. The posteromedial papillary muscle is 6 to 12 times more likely to rupture than the anterolateral muscle due to the typical solitary blood supply to the posteromedial head from the posterior descending artery and the dual blood supply to the anterolateral head from the LAD and the left circumflex arteries.5,6 Risk factors for PMR differ compared with those associated with other etiologies of acute MR. Patients with PMR are more likely to have an absence of previous angina, an inferoposterior AMI, single-vessel disease and no history of diabetes mellitus. Patients without PMR are more likely to have recurrent myocardial ischemia, multi-vessel disease, previous AMI and larger infarct area.1 The clinical presentation of PMR differs from that of other ischemic MR etiologies, typically presenting with acute severe pulmonary edema and hypotension. Often patients with PMR have an inconsequential murmur due to the larger orifice and lack of pressure gradient between the left ventricle and left atrium (LA).1,7 The symptoms may be less dramatic in a partial rupture. Specific transthoracic echocardiogram (TTE) findings in PMR include a flail mitral leaflet that prolapses into the LA during systole and/or a mobile mass attached to the chordae and MV.8 TEE is necessary to evaluate other conditions that could be mistaken for PMR, including endocarditis and chordal rupture. The diagnosis of partial PMR may be more difficult to make than complete rupture and should be closely investigated in the setting of a flail mitral leaflet.9 TEE still may not clearly visualize subvalvular mitral structures, requiring a high suspicion of partial PMR in the appropriate clinical setting.10
FIGURE 1. Electrocardiogram reveals atrial fibrillation with a ventricular rate of approximately 170 and S-T segment depression in leads II, III, aVF and V2-V6.
Ó 2013 Lippincott Williams & Wilkins
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Flueckiger et al
FIGURE 2. (A) Transesophageal echocardiogram (TEE) with a midesophageal view at 30˚ shows a flail posterior leaflet of the mitral valve. (B) TEE with a gastric view at 90˚ suggests partial posteromedial papillary muscle rupture (arrow).
Additionally, the conventional diagnosis of PMR (mobile mass attached to the MV visible in the LA) likely will not be present in partial rupture. The left ventricle needs to be examined for abnormal anatomy and motion of the papillary muscle.8 Acute mitral regurgitation due to ischemia requires not only repair or replacement of the MV but also revascularization of the culprit coronary lesion. A ruptured papillary muscle is a surgical emergency and causes up to 5% of deaths in AMI.6,11 Partial rupture of the papillary muscle may also be considered a surgical emergency as the majority of cases will progress to complete rupture.12 Approximately 50% of patients with PMR will die within the first day if surgical intervention is not per-
formed,2 and overall mortality with medical therapy alone may be up to 75% at 24 hours and 95% at 48 hours.13 Before bypass grafting, acute MR due to PMR had operative mortality rates up to 67%. However, coronary artery bypass grafting has decreased mortality rates to less than 10%.11 Initial medical management may include afterload reduction (either pharmacological or mechanical with an intra-aortic balloon pump), diuretics and inotropes to improve hemodynamic compromise.1 Ultimately, patients with complete or partial PMR and acute MR usually require MV repair or replacement. MV replacement is a common strategy to reestablish valve competency as it provides a more consistent and predictable surgical intervention with regard to duration of surgical repair, durability of repair and recovery.14 There has been an increasing trend in the use of MV repair in the setting of PMR, though surgical management depends significantly on the specific clinical circumstances.15 When a single, or partial, papillary muscle is involved without further extensive areas of necrosis, papillary muscle repair may be favored.16 However, extensive myocardial necrosis necessitates MV replacement. In a small series, MV repair was shown to have favorable outcomes, although repair did require longer cardiopulmonary bypass support time.11 There are no large trials to suggest a clear benefit of one strategy over another. What is clearer is the benefit of early revascularization therapy. Coronary artery bypass grafting is essential for improved outcome in patients with ischemic PMR.11,17 PMR, and specifically partial PMR, is rare but serious complication of myocardial ischemia. Due to the hemodynamics caused by acute PMR, emergent identification and treatment are necessary to improve patient outcomes. With the advancement of MV repair/replacement with coronary revascularization, patient outcomes have improved. Clinicians should consider ischemic PMR, either partial or complete, as a cause of acute MR even in patients who present without chest pain syndromes.
CONCLUSIONS
FIGURE 3. An anterior-posterior caudal view of the left coronary artery demonstrating an occluded first obtuse marginal (OM1) off the circumflex artery (single arrow) and a 50% proximal left anterior descending artery stenosis (double arrow).
480
Ischemic PMR, either partial or complete, is a rare sequella of myocardial ischemia that typically presents with severe acute shortness of breath and hypotension. Our patient illustrates a part of the spectrum of presentation in patients with ischemic PMR and the need for a high clinical suspicion in patients presenting with acute or subacute dyspnea, despite a lack of overt chest pain. Furthermore, the diagnosis of partial PMR needs to be considered when associated findings are present, Volume 345, Number 6, June 2013
Partial Papillary Muscle Rupture
despite lack of visualization on TTE or TEE. An atypical presentation of PMR may lead the clinician to miss a surgical emergency. Early recognition and identification of the underlying pathology in this patient allowed for an optimal clinical outcome. A partial rupture implies infarction of the papillary muscle and can lead to poor clinical outcomes if not identified early. Ischemic PMR is a serious complication of myocardial ischemia that usually demands timely medical and surgical intervention. REFERENCES
8. Moursi MH, Bhatnagar SK, Vilacosta I, et al. Transesophageal echocardiographic assessment of papillary muscle rupture. Circulation. 1996;94:1003–9. 9. Nishimura RA, Shub C, Tajik AJ. Two dimensional echocardiographic diagnosis of partial papillary muscle rupture. Br Heart J. 1982; 48:598–600. 10. Chirillo F, Totis O, Cavarzerani A, et al. Transesophageal echocardiographic findings in partial and complete papillary muscle rupture complicating acute myocardial infarction. Cardiology. 1992; 81:54–8.
1. Birnbaum Y, Chamoun AJ, Conti VR, et al. Mitral regurgitation following acute myocardial infarction. Coron Artery Dis. 2002;13: 337–44.
11. Russo A, Suri RM, Grigioni F, et al. Clinical outcome after surgical correction of mitral regurgitation due to papillary muscle rupture. Circulation. 2008;118:1528–34.
2. Nishimura RA, Gersh BJ, Schaff HV. The case for an aggressive surgical approach to papillary muscle rupture following myocardial infarction: “From paradise lost to paradise regained”. Heart. 2000;83:611–3.
12. Christ G, Siostrzonek P, Maurer G, et al. Partial papillary muscle rupture complicating acute myocardial infarction. Diagnosis by multiplane transoesophageal echocardiography. Eur Heart J. 1995;16: 1736–8.
3. Calvo FE, Figueras J, Cortadellas J, et al. Severe mitral regurgitation complicating acute myocardial infarction. Clinical and angiographic differences between patients with and without papillary muscle rupture. Eur Heart J. 1997;18:1606–10. 4. Figueras J, Calvo F, Cortadellas J, et al. Comparison of patients with and without papillary muscle rupture during acute myocardial infarction. Am J Cardiol. 1997;80:625–7. 5. Wilansky S, Moreno CA, Lester SJ. Complications of myocardial infarction. Crit Care Med. 2007;35(8 suppl):S348–S354.
13. Wei JY, Hutchins GM, Bulkley BH. Papillary muscle rupture in fatal acute myocardial infarction: a potentially treatable form of cardiogenic shock. Ann Intern Med. 1979;90:149–52. 14. Iung B. Management of ischaemic mitral regurgitation. Heart. 2003;89:459–64. 15. Stout KK, Verrier ED. Acute valvular regurgitation. Circulation. 2009;119:3232–41.
6. Fuster V, Walsh RA, Harrington RA, et al. Hurst’s The Heart. 13th ed. New York, NY: The McGraw Hill Companies; 2011.
16. Yamanishi H, Izumoto H, Kitahara H, et al. Clinical experiences of surgical repair for mitral regurgitation secondary to papillary muscle rupture complicating acute myocardial infarction. Ann Thorac Cardiovasc Surg. 1998;4:83–6.
7. Clements SD Jr., Story WE, Hurst JW, et al. Ruptured papillary muscle, a complication of myocardial infarction: clinical presentation, diagnosis, and treatment. Clin Cardiol. 1985;8:93–103.
17. Picard MH, Davidoff R, Sleeper LA, et al. Echocardiographic predictors of survival and response to early revascularization in cardiogenic shock. Circulation. 2003;107:279–84.
Ó 2013 Lippincott Williams & Wilkins
481
Partial Papillary Muscle Rupture: A Cause of Acute Mitral Regurgitation
Authors Peter B. Flueckiger, MD, Alan C. Cheng, MD, Jonathan M. Patton, MD and Stephen D. Clements, Jr, MD Editor Stamatios Lerakis, MD Abstract: A 56-year-old woman presented to the cardiology clinic with a 7-day history of dyspnea and chest pressure. An echocardiogram showed a flail posterior mitral valve leaflet, and subsequent left heart catheterization showed complete occlusion of the first obtuse marginal coronary artery. Further investigation demonstrated the culprit lesion to be ischemic partial rupture of the posteromedial papillary muscle. Timely recognition of this condition allowed for an optimal clinical outcome. In this Cardiology Grand Rounds, the authors further describe the above presentation of ischemic partial papillary muscle rupture and provide a brief review of the pathophysiology, diagnosis and treatment of this condition. Key Indexing Terms: Partial papillary muscle rupture; Mitral regurgitation; Acute myocardial infarction. [Am J Med Sci 2013;345(6):478– 481.]
P
apillary muscle rupture (PMR), either complete or partial, is an uncommon cause of acute mitral regurgitation, occurring in 1% of cases. PMR is also a rare complication of acute myocardial infarction (AMI).1 Clinical presentation may be varied and requires early recognition and high suspicion, given the increased mortality if left untreated.2 Early echocardiographic visualization of PMR, assessment of coronary artery disease and surgical intervention is necessary. We present a case of a patient with a partial PMR secondary to AMI with discussion of the pathophysiology, diagnosis and treatment of PMR (Table 1).
From the Department of Medicine (PBF, ACC, JMP, SDC), Emory University, Atlanta, Georgia; and Division of Cardiology, Department of Medicine (ACC, JMP, SDC), Emory University, Atlanta, Georgia. Submitted June 28, 2012; accepted in revised form September 25, 2012. The authors state that they have no funding or conflicts of interest to disclose. Correspondence: Peter B. Flueckiger, MD, Department of Medicine, Emory University, 69 Jesse Hill Jr. Drive, Atlanta, GA 30303 (E-mail: pbfl[email protected]).
478
CASE PRESENTATION A 56-year-old woman was referred to the cardiology clinic for further evaluation of dyspnea, mild chest pressure and palpitations present for the last 7 days. At the onset of her symptoms, she was able to continue walking on a treadmill at her home. However, her activity became increasingly limited and she began to experience shortness of breath at rest that worsened when lying in the supine position. She denied a cough or fever. Medical history included hypertension, hyperlipidemia and ductal carcinoma in situ of the left breast that was subsequently treated with lumpectomy and radiation therapy 9 months before the above presentation. Her family history was remarkable for her father having an AMI at age 57 years and mother having an aortic dissection at age 70 years.
ASSESSMENT Initially, the patient was hypertensive (148/94 mm Hg), tachypneic (respiratory rate of 28 breaths per minute), tachycardic (102 beats per minute), afebrile and hypoxic with oxygen saturation 91% on room air. There was marked distention of the internal jugular vein to the level of her earlobes when reclined at a 30° angle. Cardiac examination revealed mild lateral displacement of the apical impulse, a regular rhythm and a 4/6 holosystolic murmur heard best at the apex with radiation to the left axilla. There were faint crackles heard in the bilateral lower lung fields. No abdominal tenderness, ascites or hepatomegaly was noted. Trace pretibial edema was appreciated on examination of her lower extremities, but no lesions consistent with Osler nodes or Janeway lesions were present. Basic laboratory evaluation demonstrated her complete blood count and comprehensive metabolic panel to be within the normal range. Cardiac laboratory studies showed a brain natriuretic peptide of 1378 pg/mL, troponin I of 0.80 ng/mL, creatinine kinase of 43 units/L and creatinine kinase-MB fraction of 1 ng/mL. Electrocardiogram showed sinus tachycardia, biatrial enlargement and S-T segment depression in the inferior leads
The American Journal of the Medical Sciences
Volume 345, Number 6, June 2013
Partial Papillary Muscle Rupture
TABLE 1. Potential causes of PMR/dysfunction Myocardial infarction Trauma (blunt or iatrogenic) Myocarditis Endocarditis Connective tissue disease
as well as V3-V6. A 2-D transthoracic echocardiogram was performed, revealing a left ventricular ejection fraction of 60% to 65%, moderate to severe mitral valve (MV) regurgitation with an anteriorly directed regurgitant jet, moderate to severe tricuspid valve regurgitation, severely elevated right ventricular systolic pressure (estimated at 70–75 mm Hg) and a dilated inferior vena cava with decreased respiratory collapse. Repeat examination revealed worsening hypoxia with oxygen saturation 88% on room air, an irregular rapid pulse and increasingly prominent bibasilar lung crackles. A subsequent electrocardiogram showed atrial fibrillation with a ventricular rate of 173 beats per minute and more pronounced S-T segment depression (Figure 1).
DIAGNOSIS
Due to the patient’s atrial fibrillation with rapid ventricular response and increasing dyspnea, she was admitted to the cardiac intensive care unit. She received an intravenous diltiazem drip and intravenous furosemide with subsequent spontaneous conversion to sinus rhythm. A transesophageal echocardiogram (TEE) performed to assess the etiology of her MV regurgitation revealed severe prolapse of the posterior mitral leaflet (Figures 2A and 2B). The patient subsequently underwent a left heart catheterization demonstrating complete occlusion of the first obtuse marginal (OM1) branch from the left circumflex coronary artery and 50% stenosis of the midsegment of the left anterior descending (LAD) coronary artery (Figure 3). The finding of an occluded OM1 suggested ischemic PMR as the etiology of her symptoms. On reexamination of the TEE, partial rupture of the posteromedial papillary muscle was seen.
MANAGEMENT An intra-aortic balloon pump was inserted in the catheterization laboratory. She was taken emergently to the operating room, where partial rupture of the posteromedial
papillary muscle was found. A bioprosthetic valve was placed in the MV position, and coronary bypass was performed with an in situ left internal mammary artery graft to the LAD and a saphenous vein graft to the OM1. The patient recovered nicely.
ISCHEMIC PMR Ischemic PMR is a rare etiology of mitral regurgitation (MR), occurring in 1% of patients with myocardial ischemia.1 Acute MR due to rupture of the papillary muscle typically occurs within 5 days of the initial acute ischemic event and leads to flail of 1, or rarely, both of the MV leaflets.1,3,4 PMR can occur in either the posteromedial or anterolateral muscle heads. The posteromedial papillary muscle is 6 to 12 times more likely to rupture than the anterolateral muscle due to the typical solitary blood supply to the posteromedial head from the posterior descending artery and the dual blood supply to the anterolateral head from the LAD and the left circumflex arteries.5,6 Risk factors for PMR differ compared with those associated with other etiologies of acute MR. Patients with PMR are more likely to have an absence of previous angina, an inferoposterior AMI, single-vessel disease and no history of diabetes mellitus. Patients without PMR are more likely to have recurrent myocardial ischemia, multi-vessel disease, previous AMI and larger infarct area.1 The clinical presentation of PMR differs from that of other ischemic MR etiologies, typically presenting with acute severe pulmonary edema and hypotension. Often patients with PMR have an inconsequential murmur due to the larger orifice and lack of pressure gradient between the left ventricle and left atrium (LA).1,7 The symptoms may be less dramatic in a partial rupture. Specific transthoracic echocardiogram (TTE) findings in PMR include a flail mitral leaflet that prolapses into the LA during systole and/or a mobile mass attached to the chordae and MV.8 TEE is necessary to evaluate other conditions that could be mistaken for PMR, including endocarditis and chordal rupture. The diagnosis of partial PMR may be more difficult to make than complete rupture and should be closely investigated in the setting of a flail mitral leaflet.9 TEE still may not clearly visualize subvalvular mitral structures, requiring a high suspicion of partial PMR in the appropriate clinical setting.10
FIGURE 1. Electrocardiogram reveals atrial fibrillation with a ventricular rate of approximately 170 and S-T segment depression in leads II, III, aVF and V2-V6.
Ó 2013 Lippincott Williams & Wilkins
479
Flueckiger et al
FIGURE 2. (A) Transesophageal echocardiogram (TEE) with a midesophageal view at 30˚ shows a flail posterior leaflet of the mitral valve. (B) TEE with a gastric view at 90˚ suggests partial posteromedial papillary muscle rupture (arrow).
Additionally, the conventional diagnosis of PMR (mobile mass attached to the MV visible in the LA) likely will not be present in partial rupture. The left ventricle needs to be examined for abnormal anatomy and motion of the papillary muscle.8 Acute mitral regurgitation due to ischemia requires not only repair or replacement of the MV but also revascularization of the culprit coronary lesion. A ruptured papillary muscle is a surgical emergency and causes up to 5% of deaths in AMI.6,11 Partial rupture of the papillary muscle may also be considered a surgical emergency as the majority of cases will progress to complete rupture.12 Approximately 50% of patients with PMR will die within the first day if surgical intervention is not per-
formed,2 and overall mortality with medical therapy alone may be up to 75% at 24 hours and 95% at 48 hours.13 Before bypass grafting, acute MR due to PMR had operative mortality rates up to 67%. However, coronary artery bypass grafting has decreased mortality rates to less than 10%.11 Initial medical management may include afterload reduction (either pharmacological or mechanical with an intra-aortic balloon pump), diuretics and inotropes to improve hemodynamic compromise.1 Ultimately, patients with complete or partial PMR and acute MR usually require MV repair or replacement. MV replacement is a common strategy to reestablish valve competency as it provides a more consistent and predictable surgical intervention with regard to duration of surgical repair, durability of repair and recovery.14 There has been an increasing trend in the use of MV repair in the setting of PMR, though surgical management depends significantly on the specific clinical circumstances.15 When a single, or partial, papillary muscle is involved without further extensive areas of necrosis, papillary muscle repair may be favored.16 However, extensive myocardial necrosis necessitates MV replacement. In a small series, MV repair was shown to have favorable outcomes, although repair did require longer cardiopulmonary bypass support time.11 There are no large trials to suggest a clear benefit of one strategy over another. What is clearer is the benefit of early revascularization therapy. Coronary artery bypass grafting is essential for improved outcome in patients with ischemic PMR.11,17 PMR, and specifically partial PMR, is rare but serious complication of myocardial ischemia. Due to the hemodynamics caused by acute PMR, emergent identification and treatment are necessary to improve patient outcomes. With the advancement of MV repair/replacement with coronary revascularization, patient outcomes have improved. Clinicians should consider ischemic PMR, either partial or complete, as a cause of acute MR even in patients who present without chest pain syndromes.
CONCLUSIONS
FIGURE 3. An anterior-posterior caudal view of the left coronary artery demonstrating an occluded first obtuse marginal (OM1) off the circumflex artery (single arrow) and a 50% proximal left anterior descending artery stenosis (double arrow).
480
Ischemic PMR, either partial or complete, is a rare sequella of myocardial ischemia that typically presents with severe acute shortness of breath and hypotension. Our patient illustrates a part of the spectrum of presentation in patients with ischemic PMR and the need for a high clinical suspicion in patients presenting with acute or subacute dyspnea, despite a lack of overt chest pain. Furthermore, the diagnosis of partial PMR needs to be considered when associated findings are present, Volume 345, Number 6, June 2013
Partial Papillary Muscle Rupture
despite lack of visualization on TTE or TEE. An atypical presentation of PMR may lead the clinician to miss a surgical emergency. Early recognition and identification of the underlying pathology in this patient allowed for an optimal clinical outcome. A partial rupture implies infarction of the papillary muscle and can lead to poor clinical outcomes if not identified early. Ischemic PMR is a serious complication of myocardial ischemia that usually demands timely medical and surgical intervention. REFERENCES
8. Moursi MH, Bhatnagar SK, Vilacosta I, et al. Transesophageal echocardiographic assessment of papillary muscle rupture. Circulation. 1996;94:1003–9. 9. Nishimura RA, Shub C, Tajik AJ. Two dimensional echocardiographic diagnosis of partial papillary muscle rupture. Br Heart J. 1982; 48:598–600. 10. Chirillo F, Totis O, Cavarzerani A, et al. Transesophageal echocardiographic findings in partial and complete papillary muscle rupture complicating acute myocardial infarction. Cardiology. 1992; 81:54–8.
1. Birnbaum Y, Chamoun AJ, Conti VR, et al. Mitral regurgitation following acute myocardial infarction. Coron Artery Dis. 2002;13: 337–44.
11. Russo A, Suri RM, Grigioni F, et al. Clinical outcome after surgical correction of mitral regurgitation due to papillary muscle rupture. Circulation. 2008;118:1528–34.
2. Nishimura RA, Gersh BJ, Schaff HV. The case for an aggressive surgical approach to papillary muscle rupture following myocardial infarction: “From paradise lost to paradise regained”. Heart. 2000;83:611–3.
12. Christ G, Siostrzonek P, Maurer G, et al. Partial papillary muscle rupture complicating acute myocardial infarction. Diagnosis by multiplane transoesophageal echocardiography. Eur Heart J. 1995;16: 1736–8.
3. Calvo FE, Figueras J, Cortadellas J, et al. Severe mitral regurgitation complicating acute myocardial infarction. Clinical and angiographic differences between patients with and without papillary muscle rupture. Eur Heart J. 1997;18:1606–10. 4. Figueras J, Calvo F, Cortadellas J, et al. Comparison of patients with and without papillary muscle rupture during acute myocardial infarction. Am J Cardiol. 1997;80:625–7. 5. Wilansky S, Moreno CA, Lester SJ. Complications of myocardial infarction. Crit Care Med. 2007;35(8 suppl):S348–S354.
13. Wei JY, Hutchins GM, Bulkley BH. Papillary muscle rupture in fatal acute myocardial infarction: a potentially treatable form of cardiogenic shock. Ann Intern Med. 1979;90:149–52. 14. Iung B. Management of ischaemic mitral regurgitation. Heart. 2003;89:459–64. 15. Stout KK, Verrier ED. Acute valvular regurgitation. Circulation. 2009;119:3232–41.
6. Fuster V, Walsh RA, Harrington RA, et al. Hurst’s The Heart. 13th ed. New York, NY: The McGraw Hill Companies; 2011.
16. Yamanishi H, Izumoto H, Kitahara H, et al. Clinical experiences of surgical repair for mitral regurgitation secondary to papillary muscle rupture complicating acute myocardial infarction. Ann Thorac Cardiovasc Surg. 1998;4:83–6.
7. Clements SD Jr., Story WE, Hurst JW, et al. Ruptured papillary muscle, a complication of myocardial infarction: clinical presentation, diagnosis, and treatment. Clin Cardiol. 1985;8:93–103.
17. Picard MH, Davidoff R, Sleeper LA, et al. Echocardiographic predictors of survival and response to early revascularization in cardiogenic shock. Circulation. 2003;107:279–84.
Ó 2013 Lippincott Williams & Wilkins
481