Case 34-2006 — A 72-Year-Old Woman with Nausea Followed by Hypotension and Respiratory Failure
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《新英格兰医药杂志》
Presentation of Case
Dr. David S. Frankel (Medicine): A 72-year-old woman was admitted to this hospital because of respiratory failure and hypotension.
During the week before admission, the patient and other members of her family had symptoms of an upper respiratory tract infection. Five days before admission, the results of a routine annual checkup by her primary care physician were normal. Two days before admission, she awoke early in the morning with severe, intractable nausea and anorexia, without vomiting or diarrhea. During the next 24 hours, the symptoms worsened; a cough developed that was initially dry and was later productive of yellow sputum. The cough was accompanied by chills, sweats, malaise, lightheadedness, aching in the teeth, anorexia, and insomnia. She did not have a fever, wheezing, shortness of breath, crushing chest pain, dizziness, or urinary symptoms. The next afternoon, her family took her to the emergency department of another hospital.
The patient appeared uncomfortable. The blood pressure was 90/50 mm Hg, the pulse 107 beats per minute, and the temperature 36.7°C; the respiratory rate was 22 to 33 breaths per minute, and the oxygen saturation was 85 to 92% while the patient was breathing ambient air. No jugular venous distention or bruits in the neck were noted; the breath sounds were diminished bilaterally, with fine scattered crackles. Examination of the heart revealed a rapid rhythm; the sounds and point of maximal impulse were normal. The remainder of the physical examination was normal. A chest radiograph showed diffuse infiltrates, which were most prominent in the right middle lobe and both upper lobes; the heart size was normal. The results of laboratory tests are shown in Table 1 and Table 2. Intravenous fluids, ceftriaxone, azithromycin, and methylprednisolone were administered. The patient was admitted to the other hospital 9 hours after arrival in the emergency department.
Table 1. Results of Hematologic Laboratory Tests.
Table 2. Results of Chemical Laboratory Tests.
Hypoxemia persisted, and acidosis and hypercapnia developed. The patient was sedated, the airway was intubated, and mechanical ventilation was initiated 4 hours after admission. Pink secretions were suctioned from the endotracheal tube. The rate of normal saline infusion was decreased, and furosemide (80 mg) was administered intravenously. Worsening hypotension developed during the next 2 hours; an intravenous dobutamine drip was started, but it was discontinued because of increased tachycardia without improvement in the blood pressure; phenylephrine and norepinephrine were administered. An electrocardiogram revealed a sinus rate of 125 beats per minute, a 1-mm ST-segment elevation in lead aVL, and a 2-mm ST-segment depression in leads II, III, and aVF. The patient's condition did not improve, and 22 hours after her arrival at the other hospital, she was transferred to this hospital and admitted to the coronary care unit.
Seven months earlier, the patient had had a transient ischemic attack that was manifested as diplopia, slurred speech, and imbalance and resolved after 15 minutes. An inpatient evaluation by the neurology service at this hospital showed that the body-mass index (the weight in kilograms divided by the square of the height in meters) was 22.3, and the blood pressure was 163/72 mm Hg. The results of a neurologic examination were normal. The results of laboratory tests from that admission are shown in Table 1. Computed tomography (CT), CT angiography, and magnetic resonance imaging of the brain showed no stenosis or occlusion of the intracranial or cervical arteries and no evidence of acute infarction; there were microangiopathic white-matter changes. Chest radiographs and electrocardiograms showed no abnormalities. Echocardiography revealed an ejection fraction of 68%, trace mitral regurgitation, and thickening and prolapse of the mitral leaflets. A Holter monitor showed no evidence of arrhythmias during a 24-hour period. The patient was discharged on the second hospital day, with instructions to take aspirin and omeprazole. An exercise tolerance test with thallium performed 3 months later showed a normal exercise capacity (7 metabolic equivalents ; stage 2 of 7 stages of graduated exercise on a standard Bruce protocol), with no evidence of ischemia. Because of persistently elevated blood pressure, she began to receive lisinopril 1 month later. Consultants in neurology and cardiology recommended the addition of a statin.
The patient had a history of Graves' disease that had been treated with radioactive iodine, gastroesophageal reflux disease, peptic ulcer disease, diverticulitis, several cesarean sections, a total abdominal hysterectomy, and vocal-cord polyps. She did not have allergies to medications. She had smoked two to three cigarettes per week for 50 years, but stopped after the transient ischemic attack. Her mother had died of a myocardial infarction at age 75. She lived with her husband. She had not traveled recently.
The patient had been taking levothyroxine, fexofenadine, lisinopril, omeprazole, and aspirin at home. When she was transferred to this hospital, her medications included vancomycin, ceftriaxone, azithromycin, methylprednisolone, phenylephrine (200 μg per minute), norepinephrine (25 μg per minute), and intravenous heparin.
The patient was intubated and sedated. The blood pressure was 92/41 mm Hg, the pulse 154 beats per minute, the temperature 38.9°C, the respiratory rate 22 breaths per minute while the patient was receiving assisted ventilation, and the oxygen saturation 91%, with the fraction of inspired oxygen 1.0. The first and second heart sounds were normal; an S3 gallop and a grade 2/6 holosystolic murmur that radiated from the apex to the axilla were heard. Crackles were heard throughout both lungs. The results of laboratory tests are listed in Table 1 and Table 2. An electrocardiogram showed sinus tachycardia at 146 beats per minute with a 2-mm ST-segment elevation in leads I and aVL and a 2-mm ST-segment depression in leads II, III, and aVF.
A diagnostic procedure was performed.
Differential Diagnosis
Dr. Paula A. Johnson: This 72-year-old woman experienced the sudden onset of nausea and anorexia 2 days before admission; during a 48-hour period, hypoxemia and hypotension developed. Initial evaluation suggested the presence of pneumonia and sepsis. May we see the chest radiograph?
Dr. Jo-Anne O. Shepard: The chest radiograph (Figure 1A) obtained at the other hospital shows pulmonary opacities that are diffuse, bilateral, and symmetric. These opacities are characteristic of pulmonary edema. Because of its extent, the edema could obscure an underlying pneumonia.
Figure 1. Radiographs of the Chest.
A radiograph obtained at the other hospital 1 day before admission to this hospital (Panel A) reveals bilateral perihilar air-space disease, most likely representing pulmonary edema, which may obscure an underlying pneumonia. An endotracheal tube, a nasogastric tube, and a central catheter are in place. A chest radiograph obtained at this hospital (Panel B) after catheterization and before electrocardiography was performed shows slight improvement in the peripheral edema. The patient remains intubated, and an intraaortic balloon pump and a Swan–Ganz catheter have been inserted.
Dr. Johnson: On admission to this hospital, the patient clearly had an acute myocardial infarction with pulmonary edema and shock. Although I am aware of the diagnosis, it is important to think about the timing of the event. I suspect that the nausea and anorexia that developed suddenly 2 days before admission marked the onset of the myocardial infarction. The development of pulmonary edema and shock during the next 24 hours could have resulted from extension of the infarction. It is possible that she also had pneumonia, and there may have been a component of septic shock.
I shall focus on the possible cardiac causes of the patient's presentation. The differential diagnosis of cardiogenic shock due to myocardial infarction has three major categories: mechanical causes, including papillary muscle rupture, ventricular septal rupture, and rupture of the left ventricular free wall with tamponade1; ischemia or infarction involving a large area of the myocardium; and endocarditis with valvular dysfunction.
Mechanical Causes of Cardiogenic Shock
In this patient, major mechanical causes are foremost in the differential diagnosis, given the probable onset of the myocardial infarction 2 days before admission. Ventricular septal rupture occurs in 1 to 4% of myocardial infarctions. Reperfusion by means of either thrombolytic therapy or primary angioplasty has decreased the incidence of ventricular septal rupture. It usually occurs 3 to 7 days after myocardial infarction and is characterized by a harsh holosystolic murmur, an S3 gallop, and a thrill, which was not present in this patient. Rupture of the left ventricular free wall with tamponade occurs with similar frequency and within a similar time frame; physical examination reveals jugular venous distention, pulseless electrical activity, and a pulsus paradoxus, none of which were present in this patient.
Rupture of a papillary muscle occurs in about 1% of patients, usually between 2 and 7 days after myocardial infarction. A murmur of mitral regurgitation is heard in about 50% of such patients, but it tends to be soft rather than harsh. A thrill is rare. In this patient, both the physical findings and the timing are consistent with a rupture of a papillary muscle. The posterior papillary muscle ruptures more often than the anterior papillary muscle because its blood supply is typically from a single vessel, either the right coronary artery or a tributary; the rupture is usually associated with an inferior myocardial infarction. The anterior papillary muscle is usually perfused by two sources, which are often an obtuse marginal branch and the first diagonal branch of the left coronary artery, and a rupture is usually associated with an anterior myocardial infarction. A papillary muscle rupture can occur in the absence of a large myocardial infarction.
Extensive Ischemia or Infarction
Cardiogenic shock due to infarction or ischemia of a large area of the myocardium should be considered. Three-vessel disease or disease of the left main coronary artery is usually involved in such cases. Mitral regurgitation can occur when left ventricular dysfunction due to ischemia involves the mitral-valve apparatus. This patient presented with symptoms and signs that were consistent with septic shock; circulating cytokines in this condition could further decrease left ventricular function. Hypotension can also be associated with an extensive right ventricular infarction, especially in the setting of volume depletion. This patient initially had volume depletion with a hematocrit of 50.2%, but the hypotension did not respond to the administration of fluids. Thus, although we do not have information about right-sided electrocardiographic leads, I think right ventricular infarction is unlikely.
Endocarditis
Endocarditis should be considered in this case, since the patient had an abnormal myxomatous mitral valve. Even in the setting of possible sepsis, however, this cause is less likely than the others mentioned because there is no history of an event that might have led to entry of an organism likely to cause endocarditis.
In this patient with a 2-day-old myocardial infarction, hypotension, pulmonary edema, and a holosystolic murmur, the most likely diagnosis is rupture of the anterior papillary muscle and cardiogenic shock. I also think that there is probably concomitant septic shock.
Dr. Nancy Lee Harris (Pathology): Dr. Semigran, what was your impression at the time of admission?
Dr. Gail E. Semigran (Cardiology): On admission to the coronary care unit, the patient was intubated and sedated; she had fever, hypotension, and tachycardia, and pressors were being administered. The differential diagnosis included both septic and cardiogenic shock. Since the electrocardiographic changes and elevated levels of cardiac enzymes indicated ischemic myocardial damage, we proceeded with immediate cardiac catheterization.
Clinical Diagnosis
Acute myocardial infarction with cardiogenic shock and possible septic shock.
Dr. Paula A. Johnson's Diagnosis
Myocardial infarction, 48 hours old, with rupture of the anterior papillary muscle and cardiogenic shock; probable septic shock.
Pathological Discussion
Dr. Farouc A. Jaffer: Right-sided cardiac catheterization revealed a right atrial pressure of 12 mm Hg, right ventricular pressure of 41/13 mm Hg, pulmonary arterial pressure of 41/26/32 mm Hg, pulmonary-capillary wedge pressure of 21 mm Hg (with mild V waves), cardiac output of 7.9 liters per minute, cardiac index of 4.9 liters per minute per square meter of body-surface area, and calculated systemic vascular resistance of 527 dyne·sec·cm–5. These findings suggested a combination of cardiogenic shock and septic shock.
Coronary arteriography (Figure 2A) revealed subtotal occlusion of the ostium of the ramus artery, with compromised blood flow. There was also severe stenosis of the ostium of the dominant right coronary artery with superimposed spasm. Because the degree of shock was out of proportion to the extent of coronary artery disease, left ventriculography was performed (Video 1, available with the full text of this article at www.nejm.org). The left ventricular ejection fraction was 45%, with anterolateral hypokinesis. In addition, 3+ (moderate-to-severe) mitral regurgitation was present.
Figure 2. Coronary Angiographic Images in the Left Anterior Oblique Cranial Projection.
The diagnostic coronary angiogram (Panel A) shows a hazy subtotal occlusion of the ramus branch (arrow) with reduced blood flow. A pulmonary arterial catheter (asterisk) is also present. Percutaneous transluminal coronary angioplasty with the use of a 2-mm balloon catheter (Panel B) improves the flow into the lateral wall of the heart (arrow). An inflated intraaortic balloon pump (asterisk overlying a cylindrical air-filled structure) is also present.
These findings suggested an acute anterolateral myocardial infarction with mitral regurgitation due to dysfunction or rupture of an ischemic papillary muscle. An intraaortic balloon pump was immediately placed through the right femoral artery. Since the anterolateral hypokinesis indicated that the ramus artery was the culprit vessel, we proceeded with percutaneous transluminal coronary angioplasty of the lesion of the ramus artery (Figure 2B). This procedure restored coronary blood flow and resulted in resolution of the lateral ST-segment elevation on the electrocardiogram. Transesophageal echocardiography and cardiac surgical consultation were requested. We did not administer clopidogrel or glycoprotein IIb/IIIa antagonists because of the potential need for urgent cardiac surgery. The patient was transferred to the coronary care unit.
Dr. Shepard: A chest radiograph obtained after the catheterization (Figure 1B) shows some clearing of the peripheral pulmonary edema, but central opacification in the typical "bat wing" distribution of pulmonary edema remains.
Dr. Semigran: Although angioplasty of the ramus resulted in an improvement in the anterolateral wall motion, confirming the contribution of ischemia to that lesion, the severe mitral regurgitation and cardiogenic shock persisted, and we proceeded to obtain a transesophageal echocardiogram.
Dr. Tomas G. Neilan: On the transesophageal echocardiogram (Figure 3A), the left atrium appears dilated. Both leaflets of the mitral valve are thickened and flail. A mobile echodensity in the left ventricle is attached to the mitral-valve apparatus and also appears to be partially tethered to the left ventricle (Video 2). Color Doppler ultrasonography shows a broad jet of eccentric mitral regurgitation directed toward the left upper pulmonary vein (Figure 3B and Video 3).
Figure 3. Transesophageal Echocardiogram and Color Doppler Ultrasonographic Images.
The midesophageal long-axis view (Panel A) focuses on the left atrium (LA), the left ventricle (LV), the mitral valve (MV), and the papillary muscle (PM). The left atrium appears dilated. Both leaflets of the mitral valve are thickened and flail. A mobile echodensity is attached to the mitral-valve apparatus and is also partially tethered to the wall of the left ventricle. Color Doppler ultrasonography in the same view (Panel B) shows an eccentric jet of severe mitral regurgitation (MR).
Dr. Semigran: At this point, I went looking for a cardiac surgeon.
Dr. Jennifer D. Walker (Cardiac Surgery): We hesitated to take this patient to the operating room while she was in a hyperdynamic state with possible sepsis, since cardiopulmonary bypass can cause refractory hypotension in a patient with sepsis, and it may be difficult to remove the patient from cardiopulmonary bypass. Since an intra-aortic balloon pump had been inserted, we decided to monitor her condition overnight and see whether it improved. As expected, the serum creatinine level fell, the cardiac enzyme levels began a downward trend, and the need for pressors decreased. The next morning, we thought that we had a window of opportunity to operate, and we did so after an extensive discussion with the patient's family. A transesophageal echocardiogram obtained in the operating room confirmed the findings from the previous study.
Given the severe stenosis of the right coronary artery, we thought that the ramus branch had probably provided collateral flow to that artery, so that the ramus occlusion was causing global hypokinesis and the ST-segment changes in the inferior leads. We first bypassed the right coronary artery and then excised the anterior leaflet of the mitral valve. We then saw that the papillary muscle had ruptured near its attachment to the anterior lateral mitral-valve leaflet. We left the posterior leaflet intact except for a small piece with the posterior medial papillary muscle (Figure 4A), and we placed a 27-mm porcine valve. This leaflet-sparing valve replacement preserves the geometry of the ventricle, which is important in a patient who has had a recent myocardial infarction and is in shock. After this procedure, the patient's heart rate slowed, and the ventricular walls moved normally. The cardiopulmonary bypass was removed; her cardiac output was 6.5 liters per minute with no inotropic support, and there was no mitral regurgitation or stenosis when we left the operating room.
Figure 4. Resected Mitral-Valve Leaflet with Anterolateral Papillary Muscle.
Panel A (courtesy of Dr. Jennifer Walker) shows a portion of the mitral valve with attached, ruptured papillary muscle. A low-power view of a section stained with hematoxylin and eosin (Panel B) shows a blue band of inflammatory cells (arrow) adjacent to the rupture site. A high-power view (Panel C) shows necrotic muscle, extensive infiltration by neutrophils, and early myocyte removal.
Dr. James R. Stone: A portion of the mitral valve with attached chordae tendineae and papillary muscle was received for pathological examination (Figure 4B). Histologic analysis revealed acute infarction of the papillary muscle. There was myxomatous degeneration of the mitral valve with expansion of the spongiosa; such valvular changes can occur as a result of chronic ischemic heart disease that causes alterations in the left ventricular geometry. There were also proliferative, onlay lesions on the valve surfaces; this finding was indicative of chronic mitral regurgitation. There was no evidence of infective endocarditis.
After an acute myocardial infarction, there is a well-characterized progression of the histologic changes in the tissue.2,3,4 Necrotic myocytes start to appear approximately 12 hours later, with the maximal number present 2 to 5 days after the acute myocardial infarction (Figure 4C). Neutrophils appear in appreciable numbers 1 day after the injury, and the maximal number is present at 3 to 5 days. Myocyte removal first begins at approximately 4 to 5 days and is maximal at 2 weeks. The formation of granulation tissue is maximal at 3 weeks, and scar formation becomes prominent after 4 weeks. The histologic changes present in the papillary muscle in this patient indicate that the infarct was 3 to 5 days old.
Dr. Walker: The patient's postoperative course was complicated by the delayed recovery of consciousness, aspiration pneumonia, and ischemia of the right foot due to a popliteal arterial thrombus, which resolved with anticoagulation therapy. Despite these complications, the patient had a remarkable recovery and was discharged to a rehabilitation facility on the 23rd day and went home 8 days later. During the next month, she resumed exercising at home; 30 months after discharge, she entered a cardiac rehabilitation program at the cardiovascular disease prevention center at this hospital. This program includes supervised exercise sessions, cardiac education, nutrition counseling, and stress management and relaxation classes. Her medications include aspirin, warfarin, metoprolol, and simvastatin; the results of blood-pressure testing and the lipid profile were normal at the last follow-up visit.
Discussion of Management
Dr. Johnson: This case illustrates some of the special considerations in the diagnosis and management of coronary artery disease in women. These considerations include assessment of the risk of coronary artery disease, stress testing, atypical presentations of coronary artery disease, treatment of myocardial infarction and its timing, and secondary prevention.
Risk Assessment and Modification
Cardiovascular disease is the leading cause of death, and the absolute number of deaths per year is higher among women than among men. More than 30% of deaths among persons who are this patient's age (72 years) are caused by cardiovascular disease.5 Individual risk can be estimated with the use of the global risk score for women, which is based on data from the Framingham Heart Study.6 Data from the Women's Ischemic Syndrome Evaluation (WISE) study suggest that the use of a new strategy for screening asymptomatic women at intermediate or high risk for cardiovascular disease might improve the ability to detect subclinical disease and result in a more precise assessment of the risk of cardiovascular events.7
Before this patient's infarction, she was in the high-risk group, with a risk of a cardiovascular event of more than 20% in the next 10 years. Her risk factors included hypertension, a family history of cardiovascular disease (although it does not meet all the classic criteria for familial risk, since we do not know when her mother's cardiovascular disease began), a history of smoking, and a history of a transient ischemic attack. The class 1 recommendations (i.e., those based on more than one study, including randomized, controlled trials) that applied to this patient before her infarction are lifestyle modifications, including smoking cessation, physical activity, diet, and weight control. The patient was not overweight. She stopped smoking and started taking an angiotensin converting–enzyme inhibitor for blood-pressure control after the transient ischemic attack. Lipid control and statin therapy are now recommended for all patients in the high-risk category. Although statin therapy had been recommended in this case, the patient was not taking one. She was taking aspirin but not a beta-blocker. The data that form the basis for recommending n–3 fatty acids in the diet to prevent ischemic heart disease are not strong. A recent recommendation is that women at high risk for cardiovascular disease be evaluated for depression, because depression increases the risk of a recurrent cardiac event among patients who have had a myocardial infarction.8 Overall, this patient was well cared for in terms of the management of her risk factors for cardiovascular disease after the transient ischemic attack.
Stress testing was performed in this patient to determine whether ischemia could be provoked. She exercised on the treadmill to a level of about 7 MET, equivalent to an oxygen uptake of 3.5 ml per kilogram of body weight per minute (stage 2 according to a standard Bruce protocol). In elderly women, who tend to have poor exercise capacity, it is important to look not only at the end result of provokable ischemia, but also at the level of exercise they are able to attain. Women who cannot reach an exercise level of 5 MET (completion of stage 1 according to a standard Bruce protocol) have higher rates of death per year than women who can reach the 5-MET level.9 The current recommendation for a patient who cannot reach an exercise level of 5 MET is pharmacologic stress testing, which results in a more predictive result.
Symptoms of Coronary Artery Disease and Myocardial Infarction
The symptoms of myocardial ischemia in this patient were nausea and anorexia; the absence of chest pain undoubtedly contributed to a delay in the diagnosis. Although chest pain is the most common symptom in both men and women with acute myocardial infarction, among patients without chest pain, women are more likely than men to have dyspnea, nausea and vomiting, indigestion, fatigue, and sweating, as well as arm and shoulder pain.10 The incidence of inferior myocardial infarction may be higher in women than in men; this could explain the higher incidence of gastrointestinal symptoms among women. However, this patient had an anterior infarction.
Both women and health care providers need to know that symptoms of myocardial ischemia other than chest pain are especially prevalent among women. Consideration of the diagnosis of acute myocardial ischemia in the absence of chest pain, especially when other risk factors are present, is critical if women are to survive myocardial infarction; in the era of reperfusion, every minute counts. Among other factors, the absence of chest pain and female sex are associated with delays in performing primary angioplasty (the so-called door-to-balloon time).11 If this patient had sought medical attention when her nausea began, and if her symptoms of ischemia had been recognized, reperfusion might have prevented rupture of the papillary muscle. It is unlikely that this rupture could have been prevented by the time she presented to the other hospital; however, reperfusion is always better when it is performed earlier rather than later.
Postinfarction Care
This patient's postinfarction care will be very important. She should be screened for depression. Cardiac rehabilitation is underused in women. In one study,12 women were less than half as likely as men to be enrolled in a cardiac rehabilitation program after myocardial infarction. Women with myocardial infarction tend to be older than men; this fact may contribute to a delay in treatment and may make referral to a cardiac rehabilitation program less likely.
Dr. Arnold N. Weinberg (Infectious Diseases): This patient had a white-cell count of 38,200 per cubic millimeter, with increased band forms, fever, and hemorrhagic pulmonary edema fluid. A Gram's stain of the pulmonary edema fluid might have led to a specific understanding of what was causing the leukocytosis and increased band forms.
A Physician: Does myxomatous mitral-valve disorder lead to rupture of the papillary muscle?
Dr. Johnson: No, it is associated with rupture of the chordae tendineae; rupture of the papillary muscle is associated predominantly with ischemia.
Dr. Harris: Should an electrocardiogram be obtained for every 72-year-old woman with unexplained nausea?
Dr. Johnson: Yes, we should obtain electrocardiograms for all 72-year-old women presenting to the office or emergency department with symptoms that are suggestive of ischemia, even women with less common symptoms, especially if they have risk factors for cardiovascular disease.
Anatomical Diagnosis
Acute myocardial infarction (3 to 5 days old) with rupture of the anterolateral papillary muscle.
Dr. Johnson reports having received consulting fees from Fujisawa and Guidant and being an independent director of West Pharmaceutical Services. Dr. Stone reports having received consulting fees from MuscleTech. No other potential conflict of interest relevant to this article was reported.
Source Information
From the Division of Women's Health, Brigham and Women's Hospital (P.A.J.); the Cardiology Division (F.A.J., T.G.N.) and the Departments of Radiology (J.-A.O.S.) and Pathology (J.R.S.), Massachusetts General Hospital; and the Departments of Medicine (P.A.J., F.A.J., T.G.N.), Radiology (J.-A.O.S.), and Pathology (J.R.S.), Harvard Medical School — all in Boston.
References
Birnbaum Y, Fishbein MC, Blanche C, Siegel RJ. Ventricular septal rupture after acute myocardial infarction. N Engl J Med 2002;347:1426-1432.
Mallory GK, White PD, Salcedo-Salgar J. The speed of healing of myocardial infarction: a study of the pathologic anatomy of 72 cases. Am Heart J 1939;18:647-671.
Lodge-Patch I. The ageing of cardiac infarcts, and its influence on cardiac rupture. Br Heart J 1951;13:37-42.
Fishbein MC, Maclean D, Maroko PR. The histopathologic evolution of myocardial infarction. Chest 1978;73:843-849.
Mortality from coronary heart disease and acute myocardial infarction -- United States, 1998. MMWR Morb Mortal Wkly Rep 2001;50:90-93.
Mosca L, Appel LJ, Benjamin EJ, et al. Evidence-based guidelines for cardiovascular disease prevention in women. Circulation 2004;109:672-693.
Shaw LJ, Bairey Merz CN, Pepine CJ, et al. Insights from the NHLBI-Sponsored Women's Ischemia Syndrome Evaluation (WISE) Study. I. Gender differences in traditional and novel risk factors, symptom evaluation, and gender-optimized diagnostic strategies. J Am Coll Cardiol 2006;47:Suppl:S4-S20.
Berkman LF, Blumenthal J, Burg M, et al. Effects of treating depression and low perceived social support on clinical events after myocardial infarction: the Enhancing Recovery in Coronary Heart Disease Patients (ENRICHD) Randomized Trial. JAMA 2003;289:3106-3116.
Mieres JH, Shaw LJ, Arai A, et al. Role of noninvasive testing in the clinical evaluation of women with suspected coronary artery disease: consensus statement from the Cardiac Imaging Committee, Council on Clinical Cardiology, and the Cardiovascular Imaging and Intervention Committee, Council on Cardiovascular Radiology and Intervention, American Heart Association. Circulation 2005;111:682-696.
Milner KA, Funk M, Richards S, Wilmes RM, Vaccarino V, Krumholz HM. Gender differences in symptom presentation associated with coronary heart disease. Am J Cardiol 1999;84:396-399.
Angeja BG, Gibson CM, Chin R, et al. Predictors of door-to-balloon delay in primary angioplasty. Am J Cardiol 2002;89:1156-1161.
Witt BJ, Jacobsen SJ, Weston SA, et al. Cardiac rehabilitation after myocardial infarction in the community. J Am Coll Cardiol 2004;44:988-996.(Paula A. Johnson, M.D., M)
Dr. David S. Frankel (Medicine): A 72-year-old woman was admitted to this hospital because of respiratory failure and hypotension.
During the week before admission, the patient and other members of her family had symptoms of an upper respiratory tract infection. Five days before admission, the results of a routine annual checkup by her primary care physician were normal. Two days before admission, she awoke early in the morning with severe, intractable nausea and anorexia, without vomiting or diarrhea. During the next 24 hours, the symptoms worsened; a cough developed that was initially dry and was later productive of yellow sputum. The cough was accompanied by chills, sweats, malaise, lightheadedness, aching in the teeth, anorexia, and insomnia. She did not have a fever, wheezing, shortness of breath, crushing chest pain, dizziness, or urinary symptoms. The next afternoon, her family took her to the emergency department of another hospital.
The patient appeared uncomfortable. The blood pressure was 90/50 mm Hg, the pulse 107 beats per minute, and the temperature 36.7°C; the respiratory rate was 22 to 33 breaths per minute, and the oxygen saturation was 85 to 92% while the patient was breathing ambient air. No jugular venous distention or bruits in the neck were noted; the breath sounds were diminished bilaterally, with fine scattered crackles. Examination of the heart revealed a rapid rhythm; the sounds and point of maximal impulse were normal. The remainder of the physical examination was normal. A chest radiograph showed diffuse infiltrates, which were most prominent in the right middle lobe and both upper lobes; the heart size was normal. The results of laboratory tests are shown in Table 1 and Table 2. Intravenous fluids, ceftriaxone, azithromycin, and methylprednisolone were administered. The patient was admitted to the other hospital 9 hours after arrival in the emergency department.
Table 1. Results of Hematologic Laboratory Tests.
Table 2. Results of Chemical Laboratory Tests.
Hypoxemia persisted, and acidosis and hypercapnia developed. The patient was sedated, the airway was intubated, and mechanical ventilation was initiated 4 hours after admission. Pink secretions were suctioned from the endotracheal tube. The rate of normal saline infusion was decreased, and furosemide (80 mg) was administered intravenously. Worsening hypotension developed during the next 2 hours; an intravenous dobutamine drip was started, but it was discontinued because of increased tachycardia without improvement in the blood pressure; phenylephrine and norepinephrine were administered. An electrocardiogram revealed a sinus rate of 125 beats per minute, a 1-mm ST-segment elevation in lead aVL, and a 2-mm ST-segment depression in leads II, III, and aVF. The patient's condition did not improve, and 22 hours after her arrival at the other hospital, she was transferred to this hospital and admitted to the coronary care unit.
Seven months earlier, the patient had had a transient ischemic attack that was manifested as diplopia, slurred speech, and imbalance and resolved after 15 minutes. An inpatient evaluation by the neurology service at this hospital showed that the body-mass index (the weight in kilograms divided by the square of the height in meters) was 22.3, and the blood pressure was 163/72 mm Hg. The results of a neurologic examination were normal. The results of laboratory tests from that admission are shown in Table 1. Computed tomography (CT), CT angiography, and magnetic resonance imaging of the brain showed no stenosis or occlusion of the intracranial or cervical arteries and no evidence of acute infarction; there were microangiopathic white-matter changes. Chest radiographs and electrocardiograms showed no abnormalities. Echocardiography revealed an ejection fraction of 68%, trace mitral regurgitation, and thickening and prolapse of the mitral leaflets. A Holter monitor showed no evidence of arrhythmias during a 24-hour period. The patient was discharged on the second hospital day, with instructions to take aspirin and omeprazole. An exercise tolerance test with thallium performed 3 months later showed a normal exercise capacity (7 metabolic equivalents ; stage 2 of 7 stages of graduated exercise on a standard Bruce protocol), with no evidence of ischemia. Because of persistently elevated blood pressure, she began to receive lisinopril 1 month later. Consultants in neurology and cardiology recommended the addition of a statin.
The patient had a history of Graves' disease that had been treated with radioactive iodine, gastroesophageal reflux disease, peptic ulcer disease, diverticulitis, several cesarean sections, a total abdominal hysterectomy, and vocal-cord polyps. She did not have allergies to medications. She had smoked two to three cigarettes per week for 50 years, but stopped after the transient ischemic attack. Her mother had died of a myocardial infarction at age 75. She lived with her husband. She had not traveled recently.
The patient had been taking levothyroxine, fexofenadine, lisinopril, omeprazole, and aspirin at home. When she was transferred to this hospital, her medications included vancomycin, ceftriaxone, azithromycin, methylprednisolone, phenylephrine (200 μg per minute), norepinephrine (25 μg per minute), and intravenous heparin.
The patient was intubated and sedated. The blood pressure was 92/41 mm Hg, the pulse 154 beats per minute, the temperature 38.9°C, the respiratory rate 22 breaths per minute while the patient was receiving assisted ventilation, and the oxygen saturation 91%, with the fraction of inspired oxygen 1.0. The first and second heart sounds were normal; an S3 gallop and a grade 2/6 holosystolic murmur that radiated from the apex to the axilla were heard. Crackles were heard throughout both lungs. The results of laboratory tests are listed in Table 1 and Table 2. An electrocardiogram showed sinus tachycardia at 146 beats per minute with a 2-mm ST-segment elevation in leads I and aVL and a 2-mm ST-segment depression in leads II, III, and aVF.
A diagnostic procedure was performed.
Differential Diagnosis
Dr. Paula A. Johnson: This 72-year-old woman experienced the sudden onset of nausea and anorexia 2 days before admission; during a 48-hour period, hypoxemia and hypotension developed. Initial evaluation suggested the presence of pneumonia and sepsis. May we see the chest radiograph?
Dr. Jo-Anne O. Shepard: The chest radiograph (Figure 1A) obtained at the other hospital shows pulmonary opacities that are diffuse, bilateral, and symmetric. These opacities are characteristic of pulmonary edema. Because of its extent, the edema could obscure an underlying pneumonia.
Figure 1. Radiographs of the Chest.
A radiograph obtained at the other hospital 1 day before admission to this hospital (Panel A) reveals bilateral perihilar air-space disease, most likely representing pulmonary edema, which may obscure an underlying pneumonia. An endotracheal tube, a nasogastric tube, and a central catheter are in place. A chest radiograph obtained at this hospital (Panel B) after catheterization and before electrocardiography was performed shows slight improvement in the peripheral edema. The patient remains intubated, and an intraaortic balloon pump and a Swan–Ganz catheter have been inserted.
Dr. Johnson: On admission to this hospital, the patient clearly had an acute myocardial infarction with pulmonary edema and shock. Although I am aware of the diagnosis, it is important to think about the timing of the event. I suspect that the nausea and anorexia that developed suddenly 2 days before admission marked the onset of the myocardial infarction. The development of pulmonary edema and shock during the next 24 hours could have resulted from extension of the infarction. It is possible that she also had pneumonia, and there may have been a component of septic shock.
I shall focus on the possible cardiac causes of the patient's presentation. The differential diagnosis of cardiogenic shock due to myocardial infarction has three major categories: mechanical causes, including papillary muscle rupture, ventricular septal rupture, and rupture of the left ventricular free wall with tamponade1; ischemia or infarction involving a large area of the myocardium; and endocarditis with valvular dysfunction.
Mechanical Causes of Cardiogenic Shock
In this patient, major mechanical causes are foremost in the differential diagnosis, given the probable onset of the myocardial infarction 2 days before admission. Ventricular septal rupture occurs in 1 to 4% of myocardial infarctions. Reperfusion by means of either thrombolytic therapy or primary angioplasty has decreased the incidence of ventricular septal rupture. It usually occurs 3 to 7 days after myocardial infarction and is characterized by a harsh holosystolic murmur, an S3 gallop, and a thrill, which was not present in this patient. Rupture of the left ventricular free wall with tamponade occurs with similar frequency and within a similar time frame; physical examination reveals jugular venous distention, pulseless electrical activity, and a pulsus paradoxus, none of which were present in this patient.
Rupture of a papillary muscle occurs in about 1% of patients, usually between 2 and 7 days after myocardial infarction. A murmur of mitral regurgitation is heard in about 50% of such patients, but it tends to be soft rather than harsh. A thrill is rare. In this patient, both the physical findings and the timing are consistent with a rupture of a papillary muscle. The posterior papillary muscle ruptures more often than the anterior papillary muscle because its blood supply is typically from a single vessel, either the right coronary artery or a tributary; the rupture is usually associated with an inferior myocardial infarction. The anterior papillary muscle is usually perfused by two sources, which are often an obtuse marginal branch and the first diagonal branch of the left coronary artery, and a rupture is usually associated with an anterior myocardial infarction. A papillary muscle rupture can occur in the absence of a large myocardial infarction.
Extensive Ischemia or Infarction
Cardiogenic shock due to infarction or ischemia of a large area of the myocardium should be considered. Three-vessel disease or disease of the left main coronary artery is usually involved in such cases. Mitral regurgitation can occur when left ventricular dysfunction due to ischemia involves the mitral-valve apparatus. This patient presented with symptoms and signs that were consistent with septic shock; circulating cytokines in this condition could further decrease left ventricular function. Hypotension can also be associated with an extensive right ventricular infarction, especially in the setting of volume depletion. This patient initially had volume depletion with a hematocrit of 50.2%, but the hypotension did not respond to the administration of fluids. Thus, although we do not have information about right-sided electrocardiographic leads, I think right ventricular infarction is unlikely.
Endocarditis
Endocarditis should be considered in this case, since the patient had an abnormal myxomatous mitral valve. Even in the setting of possible sepsis, however, this cause is less likely than the others mentioned because there is no history of an event that might have led to entry of an organism likely to cause endocarditis.
In this patient with a 2-day-old myocardial infarction, hypotension, pulmonary edema, and a holosystolic murmur, the most likely diagnosis is rupture of the anterior papillary muscle and cardiogenic shock. I also think that there is probably concomitant septic shock.
Dr. Nancy Lee Harris (Pathology): Dr. Semigran, what was your impression at the time of admission?
Dr. Gail E. Semigran (Cardiology): On admission to the coronary care unit, the patient was intubated and sedated; she had fever, hypotension, and tachycardia, and pressors were being administered. The differential diagnosis included both septic and cardiogenic shock. Since the electrocardiographic changes and elevated levels of cardiac enzymes indicated ischemic myocardial damage, we proceeded with immediate cardiac catheterization.
Clinical Diagnosis
Acute myocardial infarction with cardiogenic shock and possible septic shock.
Dr. Paula A. Johnson's Diagnosis
Myocardial infarction, 48 hours old, with rupture of the anterior papillary muscle and cardiogenic shock; probable septic shock.
Pathological Discussion
Dr. Farouc A. Jaffer: Right-sided cardiac catheterization revealed a right atrial pressure of 12 mm Hg, right ventricular pressure of 41/13 mm Hg, pulmonary arterial pressure of 41/26/32 mm Hg, pulmonary-capillary wedge pressure of 21 mm Hg (with mild V waves), cardiac output of 7.9 liters per minute, cardiac index of 4.9 liters per minute per square meter of body-surface area, and calculated systemic vascular resistance of 527 dyne·sec·cm–5. These findings suggested a combination of cardiogenic shock and septic shock.
Coronary arteriography (Figure 2A) revealed subtotal occlusion of the ostium of the ramus artery, with compromised blood flow. There was also severe stenosis of the ostium of the dominant right coronary artery with superimposed spasm. Because the degree of shock was out of proportion to the extent of coronary artery disease, left ventriculography was performed (Video 1, available with the full text of this article at www.nejm.org). The left ventricular ejection fraction was 45%, with anterolateral hypokinesis. In addition, 3+ (moderate-to-severe) mitral regurgitation was present.
Figure 2. Coronary Angiographic Images in the Left Anterior Oblique Cranial Projection.
The diagnostic coronary angiogram (Panel A) shows a hazy subtotal occlusion of the ramus branch (arrow) with reduced blood flow. A pulmonary arterial catheter (asterisk) is also present. Percutaneous transluminal coronary angioplasty with the use of a 2-mm balloon catheter (Panel B) improves the flow into the lateral wall of the heart (arrow). An inflated intraaortic balloon pump (asterisk overlying a cylindrical air-filled structure) is also present.
These findings suggested an acute anterolateral myocardial infarction with mitral regurgitation due to dysfunction or rupture of an ischemic papillary muscle. An intraaortic balloon pump was immediately placed through the right femoral artery. Since the anterolateral hypokinesis indicated that the ramus artery was the culprit vessel, we proceeded with percutaneous transluminal coronary angioplasty of the lesion of the ramus artery (Figure 2B). This procedure restored coronary blood flow and resulted in resolution of the lateral ST-segment elevation on the electrocardiogram. Transesophageal echocardiography and cardiac surgical consultation were requested. We did not administer clopidogrel or glycoprotein IIb/IIIa antagonists because of the potential need for urgent cardiac surgery. The patient was transferred to the coronary care unit.
Dr. Shepard: A chest radiograph obtained after the catheterization (Figure 1B) shows some clearing of the peripheral pulmonary edema, but central opacification in the typical "bat wing" distribution of pulmonary edema remains.
Dr. Semigran: Although angioplasty of the ramus resulted in an improvement in the anterolateral wall motion, confirming the contribution of ischemia to that lesion, the severe mitral regurgitation and cardiogenic shock persisted, and we proceeded to obtain a transesophageal echocardiogram.
Dr. Tomas G. Neilan: On the transesophageal echocardiogram (Figure 3A), the left atrium appears dilated. Both leaflets of the mitral valve are thickened and flail. A mobile echodensity in the left ventricle is attached to the mitral-valve apparatus and also appears to be partially tethered to the left ventricle (Video 2). Color Doppler ultrasonography shows a broad jet of eccentric mitral regurgitation directed toward the left upper pulmonary vein (Figure 3B and Video 3).
Figure 3. Transesophageal Echocardiogram and Color Doppler Ultrasonographic Images.
The midesophageal long-axis view (Panel A) focuses on the left atrium (LA), the left ventricle (LV), the mitral valve (MV), and the papillary muscle (PM). The left atrium appears dilated. Both leaflets of the mitral valve are thickened and flail. A mobile echodensity is attached to the mitral-valve apparatus and is also partially tethered to the wall of the left ventricle. Color Doppler ultrasonography in the same view (Panel B) shows an eccentric jet of severe mitral regurgitation (MR).
Dr. Semigran: At this point, I went looking for a cardiac surgeon.
Dr. Jennifer D. Walker (Cardiac Surgery): We hesitated to take this patient to the operating room while she was in a hyperdynamic state with possible sepsis, since cardiopulmonary bypass can cause refractory hypotension in a patient with sepsis, and it may be difficult to remove the patient from cardiopulmonary bypass. Since an intra-aortic balloon pump had been inserted, we decided to monitor her condition overnight and see whether it improved. As expected, the serum creatinine level fell, the cardiac enzyme levels began a downward trend, and the need for pressors decreased. The next morning, we thought that we had a window of opportunity to operate, and we did so after an extensive discussion with the patient's family. A transesophageal echocardiogram obtained in the operating room confirmed the findings from the previous study.
Given the severe stenosis of the right coronary artery, we thought that the ramus branch had probably provided collateral flow to that artery, so that the ramus occlusion was causing global hypokinesis and the ST-segment changes in the inferior leads. We first bypassed the right coronary artery and then excised the anterior leaflet of the mitral valve. We then saw that the papillary muscle had ruptured near its attachment to the anterior lateral mitral-valve leaflet. We left the posterior leaflet intact except for a small piece with the posterior medial papillary muscle (Figure 4A), and we placed a 27-mm porcine valve. This leaflet-sparing valve replacement preserves the geometry of the ventricle, which is important in a patient who has had a recent myocardial infarction and is in shock. After this procedure, the patient's heart rate slowed, and the ventricular walls moved normally. The cardiopulmonary bypass was removed; her cardiac output was 6.5 liters per minute with no inotropic support, and there was no mitral regurgitation or stenosis when we left the operating room.
Figure 4. Resected Mitral-Valve Leaflet with Anterolateral Papillary Muscle.
Panel A (courtesy of Dr. Jennifer Walker) shows a portion of the mitral valve with attached, ruptured papillary muscle. A low-power view of a section stained with hematoxylin and eosin (Panel B) shows a blue band of inflammatory cells (arrow) adjacent to the rupture site. A high-power view (Panel C) shows necrotic muscle, extensive infiltration by neutrophils, and early myocyte removal.
Dr. James R. Stone: A portion of the mitral valve with attached chordae tendineae and papillary muscle was received for pathological examination (Figure 4B). Histologic analysis revealed acute infarction of the papillary muscle. There was myxomatous degeneration of the mitral valve with expansion of the spongiosa; such valvular changes can occur as a result of chronic ischemic heart disease that causes alterations in the left ventricular geometry. There were also proliferative, onlay lesions on the valve surfaces; this finding was indicative of chronic mitral regurgitation. There was no evidence of infective endocarditis.
After an acute myocardial infarction, there is a well-characterized progression of the histologic changes in the tissue.2,3,4 Necrotic myocytes start to appear approximately 12 hours later, with the maximal number present 2 to 5 days after the acute myocardial infarction (Figure 4C). Neutrophils appear in appreciable numbers 1 day after the injury, and the maximal number is present at 3 to 5 days. Myocyte removal first begins at approximately 4 to 5 days and is maximal at 2 weeks. The formation of granulation tissue is maximal at 3 weeks, and scar formation becomes prominent after 4 weeks. The histologic changes present in the papillary muscle in this patient indicate that the infarct was 3 to 5 days old.
Dr. Walker: The patient's postoperative course was complicated by the delayed recovery of consciousness, aspiration pneumonia, and ischemia of the right foot due to a popliteal arterial thrombus, which resolved with anticoagulation therapy. Despite these complications, the patient had a remarkable recovery and was discharged to a rehabilitation facility on the 23rd day and went home 8 days later. During the next month, she resumed exercising at home; 30 months after discharge, she entered a cardiac rehabilitation program at the cardiovascular disease prevention center at this hospital. This program includes supervised exercise sessions, cardiac education, nutrition counseling, and stress management and relaxation classes. Her medications include aspirin, warfarin, metoprolol, and simvastatin; the results of blood-pressure testing and the lipid profile were normal at the last follow-up visit.
Discussion of Management
Dr. Johnson: This case illustrates some of the special considerations in the diagnosis and management of coronary artery disease in women. These considerations include assessment of the risk of coronary artery disease, stress testing, atypical presentations of coronary artery disease, treatment of myocardial infarction and its timing, and secondary prevention.
Risk Assessment and Modification
Cardiovascular disease is the leading cause of death, and the absolute number of deaths per year is higher among women than among men. More than 30% of deaths among persons who are this patient's age (72 years) are caused by cardiovascular disease.5 Individual risk can be estimated with the use of the global risk score for women, which is based on data from the Framingham Heart Study.6 Data from the Women's Ischemic Syndrome Evaluation (WISE) study suggest that the use of a new strategy for screening asymptomatic women at intermediate or high risk for cardiovascular disease might improve the ability to detect subclinical disease and result in a more precise assessment of the risk of cardiovascular events.7
Before this patient's infarction, she was in the high-risk group, with a risk of a cardiovascular event of more than 20% in the next 10 years. Her risk factors included hypertension, a family history of cardiovascular disease (although it does not meet all the classic criteria for familial risk, since we do not know when her mother's cardiovascular disease began), a history of smoking, and a history of a transient ischemic attack. The class 1 recommendations (i.e., those based on more than one study, including randomized, controlled trials) that applied to this patient before her infarction are lifestyle modifications, including smoking cessation, physical activity, diet, and weight control. The patient was not overweight. She stopped smoking and started taking an angiotensin converting–enzyme inhibitor for blood-pressure control after the transient ischemic attack. Lipid control and statin therapy are now recommended for all patients in the high-risk category. Although statin therapy had been recommended in this case, the patient was not taking one. She was taking aspirin but not a beta-blocker. The data that form the basis for recommending n–3 fatty acids in the diet to prevent ischemic heart disease are not strong. A recent recommendation is that women at high risk for cardiovascular disease be evaluated for depression, because depression increases the risk of a recurrent cardiac event among patients who have had a myocardial infarction.8 Overall, this patient was well cared for in terms of the management of her risk factors for cardiovascular disease after the transient ischemic attack.
Stress testing was performed in this patient to determine whether ischemia could be provoked. She exercised on the treadmill to a level of about 7 MET, equivalent to an oxygen uptake of 3.5 ml per kilogram of body weight per minute (stage 2 according to a standard Bruce protocol). In elderly women, who tend to have poor exercise capacity, it is important to look not only at the end result of provokable ischemia, but also at the level of exercise they are able to attain. Women who cannot reach an exercise level of 5 MET (completion of stage 1 according to a standard Bruce protocol) have higher rates of death per year than women who can reach the 5-MET level.9 The current recommendation for a patient who cannot reach an exercise level of 5 MET is pharmacologic stress testing, which results in a more predictive result.
Symptoms of Coronary Artery Disease and Myocardial Infarction
The symptoms of myocardial ischemia in this patient were nausea and anorexia; the absence of chest pain undoubtedly contributed to a delay in the diagnosis. Although chest pain is the most common symptom in both men and women with acute myocardial infarction, among patients without chest pain, women are more likely than men to have dyspnea, nausea and vomiting, indigestion, fatigue, and sweating, as well as arm and shoulder pain.10 The incidence of inferior myocardial infarction may be higher in women than in men; this could explain the higher incidence of gastrointestinal symptoms among women. However, this patient had an anterior infarction.
Both women and health care providers need to know that symptoms of myocardial ischemia other than chest pain are especially prevalent among women. Consideration of the diagnosis of acute myocardial ischemia in the absence of chest pain, especially when other risk factors are present, is critical if women are to survive myocardial infarction; in the era of reperfusion, every minute counts. Among other factors, the absence of chest pain and female sex are associated with delays in performing primary angioplasty (the so-called door-to-balloon time).11 If this patient had sought medical attention when her nausea began, and if her symptoms of ischemia had been recognized, reperfusion might have prevented rupture of the papillary muscle. It is unlikely that this rupture could have been prevented by the time she presented to the other hospital; however, reperfusion is always better when it is performed earlier rather than later.
Postinfarction Care
This patient's postinfarction care will be very important. She should be screened for depression. Cardiac rehabilitation is underused in women. In one study,12 women were less than half as likely as men to be enrolled in a cardiac rehabilitation program after myocardial infarction. Women with myocardial infarction tend to be older than men; this fact may contribute to a delay in treatment and may make referral to a cardiac rehabilitation program less likely.
Dr. Arnold N. Weinberg (Infectious Diseases): This patient had a white-cell count of 38,200 per cubic millimeter, with increased band forms, fever, and hemorrhagic pulmonary edema fluid. A Gram's stain of the pulmonary edema fluid might have led to a specific understanding of what was causing the leukocytosis and increased band forms.
A Physician: Does myxomatous mitral-valve disorder lead to rupture of the papillary muscle?
Dr. Johnson: No, it is associated with rupture of the chordae tendineae; rupture of the papillary muscle is associated predominantly with ischemia.
Dr. Harris: Should an electrocardiogram be obtained for every 72-year-old woman with unexplained nausea?
Dr. Johnson: Yes, we should obtain electrocardiograms for all 72-year-old women presenting to the office or emergency department with symptoms that are suggestive of ischemia, even women with less common symptoms, especially if they have risk factors for cardiovascular disease.
Anatomical Diagnosis
Acute myocardial infarction (3 to 5 days old) with rupture of the anterolateral papillary muscle.
Dr. Johnson reports having received consulting fees from Fujisawa and Guidant and being an independent director of West Pharmaceutical Services. Dr. Stone reports having received consulting fees from MuscleTech. No other potential conflict of interest relevant to this article was reported.
Source Information
From the Division of Women's Health, Brigham and Women's Hospital (P.A.J.); the Cardiology Division (F.A.J., T.G.N.) and the Departments of Radiology (J.-A.O.S.) and Pathology (J.R.S.), Massachusetts General Hospital; and the Departments of Medicine (P.A.J., F.A.J., T.G.N.), Radiology (J.-A.O.S.), and Pathology (J.R.S.), Harvard Medical School — all in Boston.
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