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A 70-year-old woman presented to the emergency department with prolonged precordial chest tightness that was not affected by exertion and not relieved by sublingual nitroglycerin. Associated symptoms were bilateral arm soreness, dyspnea, and generalized weakness. During the 4 months before presentation, she had been hospitalized 3 times for chest pain, and myocardial infarction had been excluded on each admission.
The patient had known coronary artery disease and had undergone coronary artery bypass grafting 6 months previously because of accelerated angina (a squeezing sensation across her chest induced by exertion and relieved within minutes by sublingual nitroglycerin). Early postoperatively, she developed atrial fibrillation and experienced relatively constant chest tightness. Additional complaints included shortness of breath, abdominal discomfort, nau sea, and severe generalized weakness. During multiple evaluations at another institution, she was noted to have an elevated jugular venous pressure, a diastolic murmur along the left sternal edge, and an enlarged, slightly tender liver. A ventilation-perfusion lung scan was interpreted as showing low probability for pulmonary embolism. An echocardiogram demonstrated near-normal left ventricular systolic function and evidence of at least moderate aortic regurgitation. Courses of therapy with diuretics, amiodarone, and nitrates produced little symptomatic relief.
The patient's medical history included long-standing hypertension and hyperlipidemia. Her surgical history included a hysterectomy for endometriosis, prior resection of a benign intraductal papilloma from the right breast, and prior cholecystectomy. She had a known infrarenal abdominal aortic aneurysm (2.8 cm). Medications at presentation included torsemide and transdermal nitroglycerin. She did not smoke or drink alcohol. There was no family history of coronary artery disease, but her father and a half sister had a ruptured aortic aneurysm.
Physical examination revealed a woman in moderate respiratory distress. Her blood pressure was 120/58 mm Hg, pulse rate was 79/min and regular, respirations were 32/min, and temperature was 36.4°C. The oxygen saturation was 98% while she was breathing room air. Jugular venous distention was absent. There were decreased breath sounds and dullness to percussion at the left lung base. She had a regular heart rate and rhythm with a high-pitched grade 3/6 diastolic murmur at the right and left upper sternal borders, a grade 2/6 systolic murmur at the right upper sternal border, and a grade 2/6 holosystolic murmur over the apex. Third and fourth heart sounds were absent. No hepatosplenomegaly or enlargement of the abdominal aorta was evident. She had mild pitting edema of the left ankle. Peripheral pulses were bounding in all extremities, with a positive Quincke sign. The patient had no delay, decrease, or asymmetry in arterial pulses, and findings on the rest of the examination were normal.
Which one of the following would be least likely to cause a high-pitched diastolic murmur in this patient?
Rupture ofsinus of Valsalva
Mitral valve prolapse
Endocarditis of the aortic valve can cause acute aortic regurgitation and a high-pitched diastolic murmur if the aortic leaflets are disrupted by vegetations or perforated during infection. Aortic dissection can also cause aortic regurgitation if an ascending aortic dissection ruptures the aortic valve annulus or results in dilatation of the aortic root and valve annulus. The International Registry of Acute Aortic Dissection (IRAD) series, which included 464 consecutive patients with acute aortic dissections (both type A and type B) from 1996 to 1998, reported that 44% of patients with acute ascending aortic dissection presented with a new murmur of aortic regurgitation.
Pulmonary hypertension, either idiopathic or secondary to left ventricular failure, mitral stenosis, or acute pulmonary embolism, may be associated with both dilatation of the pulmonic valve. Rupture of the sinus of Valsalva causes a diastolic or continuous murmur and may occur spontaneously or after trauma, usually in a sinus that has been weakened by aneurysm formation. Mitral valve prolapse, however, would cause a systolic murmur, not the diastolic murmur heard in this patient, unless accompanied by severe mitral regurgitation. In this setting, a low-pitched diastolic flow murmur may accompany the grade 4/6 systolic murmur expected from severe mitral regurgitation. Nevertheless, the patient had no prior history of mitral valve prolapse to suggest this diagnosis.
Initial testing in our patient revealed a troponin-I level of less than 0.5 ng/mL (reference ranges shown parenthetically) (<0.5 ng/mL). Blood counts, electrolytes, and coagulation study results were normal except for a creatinine level of 1.3 mg/dL (0.6-0.9 mg/dL). Blood cultures were obtained. An electrocardiogram revealed a normal sinus rhythm with poor R-wave progression across the precordial leads but with no ischemic changes. Chest radiography showed a left pleural effusion.
Which one ofthe following is the most likely cause of this patient's symptoms?
Persistence of angina after revascularization could explain recurrent chest pain if early bypass grafting failed or revascularization was incomplete. However, our patient's chest pain at presentation had a different quality than her preoperative angina (see previous description of symptoms), and she had negative cardiac enzymes on numerous occasions when presenting with chest pain. At the current presentation, her troponin-I value was normal, and the electrocardiogram revealed no ischemic changes or Q waves. The postcardiotomy or Dressler syndrome includes fever, pericarditis, and an elevated sedimentation rate that may occur 2 weeks to 2 years after cardiac surgery or myocardial infarction.
Although she developed chest pain early after her operation, the pain did not fluctuate with positional changes as is typical of pericarditis. She had no pericardial friction rub, fever, or electrocardiographic changes suggesting pericarditis. Aortic dissection, although rare after bypass, could account for her continued chest pain. Chest pain is the most common symptom in patients with acute ascending aortic dissection, occurring in 78.9%,
and in our patient it was accompanied by a murmur of aortic regurgitation, which had not been noted before coronary artery bypass grafting. When aortic dissection occurs after cardiac surgery, it is usually at the site of aortic cross-clamping, cannulation for cardiopulmonary bypass, or proximal graft anastomoses. Pulmonary embolus could result in dyspnea, chest pain, and a diastolic murmur of pulmonic regurgitation, but a recent Doppler ultrasound study of the extremities showed normal findings, and a ventilation-perfusion scan was interpreted as showing a low probability for pulmonary embolus. In addition, a previous echocardiogram did not demonstrate right ventricular enlargement or pulmonic regurgitation; thus, this diagnosis is less likely. Constrictive pericarditis may also occur as a late complication of cardiac surgery (<1%), causing chest pain, dyspnea, and fatigue.
However, patients with constrictive pericarditis also commonly have peripheral edema (90%), elevated jugular venous pressure (86%), and other signs of right-sided heart failure such as hepatomegaly, third heart sound, pulsus paradoxus, and Kussmaul sign. Although our patient had previously experienced an episode of congestive heart failure, jugular venous distention was not evident at presentation and would be expected in the setting of constrictive pericarditis. Diuretic therapy may mask physical signs of constriction, but a new prominent diastolic murmur should not be a feature of constrictive pericarditis.
In the emergency department, the patient received oxygen, intravenous furosemide, and a nitroglycerin infusion. This therapeutic regimen decreased her pain somewhat, and intravenous morphine relieved her pain completely.
Which one of the following is the least appropriate initial test for this patient?
Transthoracic Doppler echocardiography
Transesophageal Doppler echocardiography
Computed tomography (CT) ofthe chest
Magnetic resonance imaging (MRI) ofthe chest
Contrast aortography, the past gold standard for diagnosing aortic dissection, has an estimated sensitivity of at least 80% to 90%, but it is associated with procedural complications and is rarely used today for diagnosis (<5%) because of the availability and accuracy of noninvasive diagnostic modalities.
Echocardiography enables visualization of the ascending aorta, the heart, and pericardium in real time. The sensitivities of transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) for detection of ascending aortic dissection are 75% and 96%,
respectively. Both are commonly used in patients suspected of having acute ascending aortic dissection. Echocardiography was the initial diagnostic test in 122 of the 289 patients (42%) with acute ascending aortic dissection in the IRAD series.
Although TTE is less sensitive for detecting dissection than TEE, CT, or MRI, it is a reason annulus and a high-pitched diastolic murmur of pulmonic regurgitation. Transthoracic echocardiography revealed normal left ventricular size with low-normal systolic function, moderate to severe aortic regurgitation, and mild to moderate mitral regurgitation. An aneurysm (6.5 em) of the ascending aorta with a mobile intimal flap was identified and subsequently confirmed by TEE (Figure 1).
Which one ofthe following is least likely to be associated with the TEE findings in our patient?
Cystic medial necrosis
Cystic medial necrosis, associated with aortic dissection in Marfan syndrome and other connective tissue disorders, is a cause of arterial wall weakness. Although our patient had no history of a connective tissue disorder, a family history of aortic aneurysm rupture suggests an inherited tendency for arterial wall weakness. Advanced atherosclerosis may also predispose to aortic wal1 disruption and is found in a substantial number of patients (>20%) who present with ascending aortic dissections.
including our patient. In addition to arterial wall weakness, factors that increase the stress on the arterial wall may also predispose to aortic dissection. This includes arterial hypertension, found in our patient and most patients with aortic dissection (approximately 70%):
Trauma to the arterial wall due to aortic cross-clamping, partial-occlusion clamping, cannulation, cardioplegia injection, and proximal graft anastomosis during cardiac surgery may leave an undetected localized intimal disruption that may precipitate aortic dissection. Syphilis, however, has been classically associated with ascending and transverse aortic aneurysms with fibrous scarring, making dissection rare. Furthermore, syphilitic aneurysms typically spare the sinuses (our patient's dissection involved the sinus of Valsalva) and may be associated with calcification of the aortic root, which can be seen on chest radiography.
Which one of the following is the most appropriate therapeutic option for this patient?
Observation and oral β-blocker therapy
Observation with serial echocardiograms
The most appropriate therapy for aortic dissection depends on the site and extent of injury. Immediate surgery is indicated for acutely presenting type A dissections (those involving the ascending aorta) because of the high risk of potentially fatal complications (in-hospital mortality for patients receiving medical therapy has been reported at 58% vs 26% mortality for. patients undergoing operative repair
Our patient presented with chest pain due to a large type A dissecting aneurysm and pronounced aortic regurgitation. Therefore, the most appropriate therapeutic option is surgery. Emergency medical management also includes reduction of aortic wall stress by decreasing the blood pressure but maintaining it at an adequate level that will ensure renal, myocardial, and cerebral perfusion. This is accomplished effectively with β-blockers, which also decrease the heart's intrinsic contractility and heart rate. Vasodilators may be added as second-line therapy. Type B dissections (distal to the left subclavian artery, sparing the ascending aorta) may be managed medically or surgically.
Endovascular stent-grafts have recently been used for nonsurgical repair of descending aortic aneurysms, including type B dissections,
although surgery is indicated in patients with persistent pain despite optimal medical therapy, with rapidly expanding aneurysms, or with compromise of important arterial side branches. Serial imaging to monitor aortic size is important for the long-term management of patients with type B aortic dissections managed with medication because late rupture is predicted by a serial increase in the diameter of the dissecting aneurysm. This strategy may be accomplished with serial CT or MRI scans every 3 to 12 months. If untreated, type A aortic dissection has a mortality of 37% at 48 hours and 90% at 3 months.
Our patient was treated with metoprolol and underwent operative repair of the dissection, aortic valve replacement, and reimplantation of the coronary bypass grafts. Transesophageal echocardiography performed at induction for surgery confirmed a type A aortic dissection arising from the level of the sinus of Valsalva and ending before the innominate artery. Both saphenous vein grafts connected to the false lumen. Complex atherosclerotic disease of the descending thoracic aorta was noted, but dissection was absent in that segment.
Pathologic study of the surgical specimen showed a chronic type A dissection of the ascending aorta with myxoid cystic medial degeneration, necrosis, and adventitial hemorrhage.
Sixteen months postoperatively, the patient was free of chest pain. On a recent follow-up, CT revealed a stable native descending thoracic aorta and ascending aortic graft.
Aortic dissection is a potentially fatal medical emergency in which presenting symptoms mimic other conditions. A high clinical index of suspicion and urgent anatomical imaging are essential to make a precise diagnosis and achieve a good outcome. In patients who have undergone cardiac surgery, the typical presentation of acute, severe retrosternal or interscapular pain may be mistaken for postoperative incisional pain or may be masked by analgesics. Patients may also present with various other manifestations, including back or abdominal pain (68.2%), syncope (12.7%), aortic regurgitation, or pulse deficits (18.7%).
In our patient, the occurrence of a new type of chest pain and detection of a new aortic insufficiency murmur several weeks after coronary artery bypass surgery raised the suspicion of aortic dissection due to intraoperative trauma.
The aim of imaging in patients with suspected dissection is to identify and localize an intimal tear, trace the extent of the double aortic lumen, and assess associated conditions such as rupture into the pericardium, aortic regurgitation, and aneurysm-pseudoaneurysm formation.
The initial imaging modality of choice varies and depends on factors such as availability and expertise in evaluation of acute dissection. Transthoracic echocardiography is widely available and can often be used to diagnose dissection, as in this case. However, normal findings on TTE do not exclude a diagnosis of dissection. Computed tomography, MRI, and TEE are more sensitive at evaluating aortic pathology than is TTE, and thus they are recommended to exclude dissection not identified by TTE or to confirm and clarify TTE findings before or after induction for surgery.
Aortic dissection occurs when patients have increased arterial wall stress (from aortic dilatation and thinning, hypertension, or trauma) and a weakened arterial wall (from cystic medial necrosis, severe atherosclerosis, aging, pregnancy, or surgery).
Intraoperative measures that reduce the risk of aortic dissectiou” are aimed at reducing aortic wall stress and include vigorous control of blood pressure to systolic levels lower than 100 to 110 mm Hg.'
We thank Dr Harold Snyder for his contributions to the management of this patient and the preparation of the submitted manuscript.
The International Registry of Acute Aortic Dissection (1RAD): new insights into an old disease.