A 75-year-old man presented to the emergency department with a 6-day history of dyspnea and substernal exertional chest pain with radiation to the jaw and left arm. He reported managing his chest pain with ibuprofen, but the chest pain continued, which prompted him to present for further evaluation. His medical history included diabetes mellitus type 2 complicated by neuropathy, hypertension, and hyperlipidemia. He had a 20-year 1.5 pack per day smoking history and did not use alcohol or illicit drugs. He did not have any family history of coronary artery disease. His medications included metformin, insulin, hydrochlorothiazide, and atorvastatin. Examination revealed an elderly man with a body mass index of 26 kg/m2 who was in no acute distress. He was afebrile and had a pulse rate of 76 beats/min, blood pressure of 138/88 mm Hg, respiratory rate of 17 breaths/min, and oxygen saturation of 100% while breathing room air. Cardiac and pulmonary examination findings were unremarkable. There was no elevated jugular venous distention or lower extremity edema. He did not report any change in chest pain with an adjustment in position, respiration, or palpation of the anterior chest wall. Electrocardiography revealed evidence of T-wave inversion and 1-mm downsloping ST-segment depression in leads V5, V6, I, and aVL. His initial troponin T level was elevated at 0.04 ng/mL. He was given 324 mg of aspirin and supplemental oxygen. After administration of sublingual nitroglycerin, he stated that his chest pain improved. Troponin T level at 3 hours was 0.09 ng/mL.1.Which one of the following diagnoses is most consistent with this patient’s clinical picture?a.Acute pericarditisb.Costochondritisc.Stress cardiomyopathyd.Pulmonary embolisme.Acute coronary syndrome Acute pericarditis is a potential cause of new-onset chest pain that is often difficult to distinguish from other causes of chest pain. However, the chest pain of acute pericarditis is typically sharp, pleuritic, and improved by sitting up and leaning forward. Additionally, a pericardial friction rub, characterized by a scratching or grating quality, may be present and is best heard with the diaphragm of the stethoscope during held inspiration. Electrocardiographic findings are characterized by widespread concave ST elevation or PR depression as well as PR elevation in the aVR lead. Troponin elevation in patients with acute pericarditis suggests myocardial involvement, and such patients should be considered to have myopericarditis. Costochondritis is less likely in this patient given that his pain was not reproducible by palpation nor reduced with nonsteroidal anti-inflammatory drug therapy, and the elevation in cardiobiomarker levels also pointed against such a diagnosis. The onset of stress cardiomyopathy is typically preceded by a physical or emotional stress and should be considered a diagnosis of exclusion based on invasive angiographic evaluation. Among patients with massive and submassive pulmonary embolism, troponin elevation occurs 1 in 3 and 1 in 7 patients, respectively.1Meyer T. Binder L. Hruska N. Luthe H. Buchwald A.B. Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction.J Am Coll Cardiol. 2000; 36: 1632-1636Crossref PubMed Scopus (279) Google Scholar However, the patient’s improvement in chest pain with nitroglycerin, the presence of numerous cardiac risk factors, and major troponin delta over time suggested an alternative diagnosis. The patient’s clinical presentation was consistent with acute coronary syndrome, specifically non–ST-segment elevation myocardial infarction. He underwent cardiac catheterization and was found to have a critical stenosis of the first obtuse marginal branch as well as the circumflex artery. Additionally, disease was present in the right coronary artery and left anterior descending artery. He underwent drug-eluting stent placement in the circumflex and second obtuse marginal artery. He had an uneventful hospital course postcatheterization until 2 days later when he experienced recurrence of shortness of breath and substernal, nonpleuritic, and nonpositional chest pain. Repeated blood pressure measurement revealed a blood pressure of 85/40 mm Hg. Cardiac auscultation revealed a harsh early systolic murmur loudest at the apex without a thrill when the patient was laying in the left lateral decubitus position. Chest radiography revealed bilateral pulmonary infiltrates consistent with pulmonary edema.2.Based on this patient’s history and physical examination findings, which one of the following complications of myocardial infarction is most likely?a.Dressler syndromeb.Ventricular septal rupturec.Left ventricular aneurysmd.Acute mitral regurgitatione.Right ventricular failure Typical physical examination findings in Dressler syndrome include pleuritic chest pain, fever, leukocytosis, and elevation in markers of inflammation including erythrocyte sedimentation rate and C-reactive protein.2Dressler W. A post-myocardial infarction syndrome: preliminary report of a complication resembling idiopathic, recurrent, benign pericarditis.J Am Med Assoc. 1956; 160: 1379-1383Crossref PubMed Scopus (119) Google Scholar Most commonly, there is a latent period of weeks to months between the initial injury and the development of symptoms. These symptoms and time frame are not consistent with those our patient experienced. Chest radiography should be performed in all patients with suspected Dressler syndrome and may reveal a postoperative pericardial effusion, which warrants further evaluation by echocardiography. Ventricular septal rupture manifests with onset of hypotension, biventricular failure (most often right-sided), and a new harsh holosystolic murmur loudest at the lower left or possibly right sternal borders. There may also be a loud pulmonic component of the second heart sound and a palpable thrill, which occur due to increased pulmonic flow resulting in pulmonary hypertension.3Jones B.M. Kapadia S.R. Smedira N.G. et al.Ventricular septal rupture complicating acute myocardial infarction: a contemporary review.Eur Heart J. 2014; 35: 2060-2068Crossref PubMed Scopus (138) Google Scholar Left ventricular aneurysm is typically the result of myocardial infarction, more often in the setting of a large anterior infarct. The presence of a left ventricular aneurysm should be suspected in patients with an extensive anterior myocardial infarction who experience heart failure symptoms, ventricular arrhythmias, or systemic embolization. Acute mitral regurgitation may manifest with a mid, late, or holosystolic murmur loudest at the apex; a thrill is generally not present. However, approximately 50% of patients with acute ischemic mitral regurgitation do not have an audible murmur.4Bursi F. Enriquez-Sarano M. Nkomo V.T. et al.Heart failure and death after myocardial infarction in the community: the emerging role of mitral regurgitation.Circulation. 2005; 111: 295-301Crossref PubMed Scopus (429) Google Scholar Causes of acute mitral regurgitation after myocardial infarction most commonly involve papillary muscle dysfunction. Clinical manifestations include acute onset of hypotension and pulmonary edema. In contradistinction, patients with right ventricular failure classically manifest with a triad of hypotension, jugular venous distention, and lack of pulmonary edema. The patient was determined to likely have acute mitral regurgitation based on auscultation in the left lateral decubitus position and chest radiographic findings of new pulmonary edema.3.Which one of the following diagnostic tests is the most appropriate next step in management of this patient?a.Chest computed tomographyb.Cardiac magnetic resonance imagingc.Right- and left-sided heart catheterizationd.Electrocardiographye.Transthoracic echocardiography Acute mitral regurgitation is rarely evaluated by cardiac computed tomography and magnetic resonance imaging, and importantly, patients must be stable in order to utilize these imaging modalities.5Morris M.F. Maleszewski J.J. Suri R.M. et al.CT and MR imaging of the mitral valve: radiologic-pathologic correlation.Radiographics. 2010; 30: 1603-1620Crossref PubMed Scopus (50) Google Scholar Left-sided heart catheterization would not be indicated at this stage because the new clinical findings are likely not secondary to a new coronary event but rather a mechanical complication of the original infarction. Right-sided heart catheterization allows for invasive assessment of circulatory hemodynamics. Large V waves in the pulmonary wedge pressure curve can be seen in 60% of patients with papillary muscle rupture, but a large V wave alone is nondiagnostic because it can also be seen in patients with ventricular septal rupture or severe left ventricular dysfunction.6Goldman A.P. Glover M.U. Mick W. et al.Role of echocardiography/Doppler in cardiogenic shock: silent mitral regurgitation.Ann Thorac Surg. 1991; 52: 296-299Abstract Full Text PDF PubMed Scopus (16) Google Scholar Furthermore, right-sided heart catheterization is invasive, and in contemporary practice there are more convenient noninvasive approaches to achieve the correct diagnosis. Electrocardiography in patients with chronic mitral regurgitation may exhibit left atrial enlargement, left ventricular hypertrophy, and atrial fibrillation. Furthermore, evidence of left ventricular enlargement may occur in patients with severe chronic mitral regurgitation. However, these findings may be absent in patients with acute mitral regurgitation. Two-dimensional transthoracic echocardiography is highly useful in assessing mitral regurgitation and should be the first test to pursue if the diagnosis is being contemplated because it can demonstrate the mechanism of mitral valve insufficiency. A ruptured papillary muscle or chordae can also be frequently seen moving in the left ventricle. However, in nearly 35% of patients with papillary rupture, the ruptured head does not prolapse into the left atrium, necessitating the need for other imaging modalities including transesophageal echocardiography.7Moursi M.H. Bhatnagar S.K. Vilacosta I. San Roman J.A. Espinal M.A. Nanda N.C. Transesophageal echocardiographic assessment of papillary muscle rupture.Circulation. 1996; 94: 1003-1009Google Scholar Furthermore, as the mitral apparatus is a posterior structure, transesophageal echocardiography has a greater sensitivity of 95% to 100% and should be considered in patients in whom transthoracic echocardiography could not fully delineate the mitral subvalvular apparatus. The addition of color flow Doppler to measure eccentric regurgitant jets increases the sensitivity of both transthoracic echocardiography and transesophageal echocardiography. The patient underwent transthoracic echocardiography, which was considered suboptimal due to limited acoustic windows, and subsequently underwent transesophegeal echocardiography, which demonstrated severe mitral regurgitation with evidence of papillary muscle rupture.4.Which one of the following therapies will provide the most definitive long-term management?a.Diuretic therapy and nitratesb.Insertion of intra-aortic balloon pumpc.Surgical mitral valve repair/replacementd.MitraClip proceduree.Coronary artery bypass grafting Once the diagnosis of papillary muscle rupture has been established, medical therapy should be initiated and urgent surgical intervention should be sought for definitive management. Medical therapy is centered on preload and afterload reduction with a traditional combination of loop diuresis and intravenous nitrates. Intra-aortic balloon pump counterpulsation placement during acute mitral regurgitation complicated by cardiogenic shock lowers aortic impedance, resulting in reduced mitral regurgitation and increased cardiac output. The mortality rate in patients with papillary muscle rupture undergoing surgical intervention is approximately 20% to 25%, but the mortality rate of patients who do not undergo surgical intervention approaches 100% at 2 months.8Sanders R.J. Neubuerger K.T. Ravin A. Rupture of papillary muscles: occurrence of rupture of the posterior muscle in posterior myocardial infarction.Dis Chest. 1957; 31: 316-323Abstract Full Text Full Text PDF Scopus (89) Google Scholar Although the superiority of mitral valve repair over mitral valve replacement has never been definitively shown due to conflicting data, small sample size, and prolonged recruitment periods, mitral valve repair is often performed if experienced surgeons are available. Furthermore, mitral valve repair should be performed only when there is no evidence of papillary muscle necrosis. The MitraClip (Abbott) is the only US Food and Drug Administration–approved device for transcatheter mitral valve repair, a minimally invasive technique for the treatment of symptomatic, chronic, moderate to severe mitral regurgitation. The 2014 American Heart Association/American College of Cardiology guidelines suggested patients should meet all of the following criteria to be considered for the MitraClip: (1) severely symptomatic (New York Heart Association class III or IV) heart failure despite medical therapy, (2) chronic moderate to severe or severe primary mitral regurgitation, (3) favorable anatomy for repair, (4) reasonable life expectancy, and (5) prohibitive surgical risk due to comorbidities.9Nishimura R.A. Otto C.M. Bonow R.O. et al.American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.J Am Coll Cardiol. 2014; 63 ([published correction appears in J Am Coll Cardiol. 2014;63(22):2489]): e57-e185Crossref PubMed Scopus (2085) Google Scholar Previous research has shown the addition of coronary artery bypass grafting in patients who underwent mitral valve surgery for ischemic papillary muscle rupture did not influence the acute postoperative course.10Schroeter T. Lehmann S. Misfeld M. et al.Clinical outcome after mitral valve surgery due to ischemic papillary muscle rupture.Ann Thorac Surg. 2013; 95: 820-824Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar Furthermore, this patient had complete percutaneous revascularization at the time of initial presentation. The patient was stabilized with medical therapy by administration of diuretics and nitrates before undergoing emergent bioprosthetic mitral valve replacement successfully.5.Which one of the following long-term anticoagulation regimens after mitral valve replacement is the most appropriate?a.Aspirinb.Warfarinc.Aspirin and warfarind.Dabigatrane.Low-molecular-weight heparin Anticoagulation is indicated in the setting of replacement of the mitral valve in order to preserve the longevity of the prosthesis and with the goal of preventing the adverse outcome of prosthetic valve thrombosis and dysfunction. Aspirin monotherapy does not provide adequate anticoagulation in the setting of mechanical mitral valve replacement. Instead, anticoagulation with a vitamin K antagonist (VKA), such as warfarin, is suggested to achieve a target international normalized ratio of 3 in addition to taking into account patient-specific thromboembolic risk factors. Additionally, aspirin therapy (75-100 mg/d) concurrent with a VKA has been suggested for all patients with a mechanical prosthetic valve. The benefit of antiplatelet therapy in addition to VKA therapy in patients with a mechanical prosthetic valve was summarized in previous work that found that combined antiplatelet and anticoagulant therapy reduced the risk of thromboembolism and mortality compared to anticoagulant therapy alone.11Massel D.R. Little S.H. Antiplatelet and anticoagulation for patients with prosthetic heart valves.Cochrane Database Syst Rev. 2013; 7: CD003464Google Scholar However, the need for anticoagulation for patients with bioprosthetic valves is less clear. It has been suggested that patients with a surgical bioprosthetic mitral valve should be anticoagulated with a VKA for the first 3 to 6 months to achieve an international normalized ratio of 2.5. The use of aspirin at 75 mg to 100 mg alone is recommended in all patients with a bioprosthetic mitral valve, consistent with the 2017 American Heart Association/American College of Cardiology focused update for the management of patients with valvular disease.12Nishimura R.A. Otto C.M. Bonow R.O. et al.2017 AHA/ACC focused update of the 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines.J Am Coll Cardiol. 2017; 70: 252-289Crossref PubMed Scopus (1812) Google Scholar Lifelong oral anticoagulation is recommended for patients with a mitral valve prosthesis who have other indications for anticoagulation, specifically atrial fibrillation, venous thromboembolism, hypercoagulable state, or an ejection fraction of less than 35%.13Baumgartner H. Falk V. Bax J.J. et al.ESC Scientific Document Group2017 ESC/EACTS guidelines for the management of valvular heart disease.Eur Heart J. 2017; 38: 2739-2791Crossref PubMed Scopus (2) Google Scholar Direct oral anticoagulants, such as rivaroxaban, should not be used in patients with mechanical valves based on findings of the RE-ALIGN (Randomised, Phase II Study to Evaluate the Safety and Pharmacokinetics of Oral Dabigatran Etexilate in Patients After Heart Valve Replacement) study that demonstrated increased bleeding and thrombotic complications compared to warfarin.14Eikelboom J.W. Connolly S.J. Brueckmann M. et al.RE-ALIGN InvestigatorsDabigatran versus warfarin in patients with mechanical heart valves.N Engl J Med. 2013; 369: 1206-1214Crossref PubMed Scopus (1002) Google Scholar Low-molecular-weight heparin is a useful injectable anticoagulant but is inconvenient and cost-ineffective to use as a long-term agent. Its role in individuals with valve prosthesis is typically to help bridge toward a therapeutic level of anticoagulation with warfarin. After the patient underwent mitral valve replacement, an intra-aortic balloon pump and inotropic agents were used in the early postoperative period to aid in mechanical circulatory support. He was initiated on low-molecular-weight heparin as a bridge to warfarin in addition to aspirin. The patient was weaned from all intravenous medications and discharged to a rehabilitation facility to aid in strength training. The 3 main mechanical complications of acute myocardial infarction are ventricular septal rupture, left ventricular free wall rupture, and acute mitral regurgitation. The mechanisms of mitral regurgitation in the acute stage of myocardial infarction involve papillary muscle dysfunction, papillary muscle rupture, or rupture of the chordae tendineae. In patients with chronic mitral regurgitation after myocardial infarction, the etiology involves mitral annulus dilatation, tethering of mitral leaflets, and localized wall motion abnormalities. Papillary muscle rupture accounts for 5% of deaths in patients with acute myocardial infarction and usually occurs 2 to 7 days after the infarct.15Lavie C.J. Gersh B.J. Mechanical and electrical complications of acute myocardial infarction.Mayo Clin Proc. 1990; 65 ([published correction appears in Mayo Clin Proc. 1990;65(7):1032]): 709-730Abstract Full Text Full Text PDF PubMed Scopus (64) Google Scholar Rupture of the posteromedial papillary muscle occurs 6 to 12 times more frequently than rupture of the anterolateral papillary muscle because of differences in blood supply; the anterolateral papillary muscle receives dual blood supply from the first marginal artery of the circumflex artery and the first diagonal artery from the left anterior descending artery, whereas the posteromedial papillary muscle receives blood flow from the posterior descending artery alone.16Roberts W.C. Cohen L.S. Left ventricular papillary muscles: description of the normal and a survey of conditions causing them to be abnormal.Circulation. 1972; 46: 138-154Crossref PubMed Scopus (135) Google Scholar Papillary muscle rupture occurs in patients with both non–ST-elevation and ST-elevation infarcts. Although the development of a new systolic murmur may clue the clinician to a possible diagnosis of papillary rupture, patients with a complete papillary muscle rupture or with severe left ventricular dysfunction may not have an audible murmur secondary to early equalization of left ventricular and left atrial pressures. If there is clinical suspicion of acute mitral regurgitation, emergent bedside transthoracic echocardiography is warranted in addition to alerting a cardiovascular surgeon. Transesophegeal echocardiography may be necessary for complete delineation of the anatomic and physiologic perturbations observed in this setting. Prompt recognition, initiation of medical therapy, and emergent surgery are the cornerstones of treatment in patients with papillary muscle rupture secondary to acute myocardial infarction. Among patients who had papillary muscle dysfunction after acute myocardial infarction, the presence of a systolic murmur was associated with a higher hospital and 1-year mortality than those without systolic murmurs and had 2.5-fold shorter average time to reinfarction. Despite a mortality risk approaching 25% in patients undergoing surgery, medical therapy alone has poor results, with mortality rates reaching 75% and 95% at 24 hours and 2 weeks postinfarct, respectively.17Manning W.J. Waksmonski C.A. Boyle N.G. Papillary muscle rupture complicating inferior myocardial infarction: identification with transesophageal echocardiography.Am Heart J. 1995; 129: 191-193Google Scholar, 18Kishon Y. Oh J.K. Schaff H.V. Mullany C.J. Tajik A.J. Gersh B.J. Mitral valve operation in postinfarction rupture of a papillary muscle: immediate results and long-term follow-up of 22 patients.Mayo Clin Proc. 1992; 67: 1023-1030Abstract Full Text Full Text PDF PubMed Scopus (109) Google Scholar Furthermore, medical therapy with a delay in surgery has been associated with poor outcomes as well.17Manning W.J. Waksmonski C.A. Boyle N.G. Papillary muscle rupture complicating inferior myocardial infarction: identification with transesophageal echocardiography.Am Heart J. 1995; 129: 191-193Google Scholar