Aortic dissection is a relatively uncommon but potentially catastrophic condition.[2] The incidence of aortic dissection is estimated to be 5-30 cases per 1 million people per year. Aortic dissection can manifest in numerous ways; it has been described as "the great mimicker" because of its myriad of presentations. The symptom complex of aortic dissection depends on the direction and degree of propagation of the initial dissection tear.
For example, a dissection of the ascending aorta can propagate in a cephalad fashion to involve either of the carotid arteries, causing acute stroke symptoms. Also, the dissection plane can travel caudally and cause occlusion of either of the main coronary arteries, leading to acute myocardial infarction. If the dissection flap is below the insertion of the pericardial reflection on the ascending aorta, leakage of blood into the pericardial space can cause pericarditis and/or pericardial tamponade.[3] This proximal vascular disruption allows slow penetration of blood into the pericardial space, where it causes inflammatory pericarditis.[3,4] Symptoms of pericarditis may precede fatal aortic rupture by several days.[3] Dissection can also lead to accumulation of blood in the pleural space, with a risk for exsanguination. Finally, aortic dissection can cause aortic valve insufficiency resulting from mechanical disruption of leaflet malcoaptation.
The risk factors for aortic dissection include hypertension, Marfan syndrome, and bicuspid aortic valve, but surprisingly, patients with aortic dissection frequently have little coronary atherosclerosis. In addition, an increasing appreciation of genetics in aortic disease has been described.[2] Other variations of aortic dissection include penetrating aortic ulcer and intramural hematoma.
Differentiating aortic dissection from other causes of chest pain is important because the therapeutic strategies are completely different. For example, acute pericarditis is treated with anti-inflammatory medications and expectant observation, making it a diagnosis of exclusion. However, acute myocardial infarction is treated with antiplatelet and antithrombin agents, as well as prompt revascularization via either primary angioplasty or pharmacologic thrombolysis.
Lack of recognition of aortic dissection can lead to devastating therapeutic decisions, such as anticoagulation for presumed acute myocardial infarction. The use of heparin and/or thrombolytics in an acute aortic dissection can transform a meta-stable, contained dissection into an exsanguinating fatal event. Lack of prompt recognition of an acute aortic dissection may have led to the death of the actor John Ritter.
Dissection of the thoracic aorta is a cardiovascular emergency that has a high morbidity and mortality rate when it is not promptly recognized and treated. Untreated, this condition has a mortality rate of 28% within 24 hours, 50% at 48 hours, 70% within 1 week, and 90% within 3 months.[5,6] Most deaths in patients with proximal aortic dissection are caused by rupture, aortic insufficiency, or branch-vessel obstruction.[7]
The diagnosis of aortic dissection may not be straightforward and may challenge even experienced physicians. In fact, the diagnosis is missed on initial evaluation in 38% of all patients.[8,9] Further complicating the picture is the fact that at least 1% of patients with aortic dissection have concomitant coronary artery occlusions (from the dissection flap extending into the coronary os), which may precipitate acute myocardial infarction and left ventricular failure[8]; therefore, patients with aortic dissection may have ECG changes consistent with myocardial ischemia or injury, such as marked ST-segment elevation.
Other ECG abnormalities occurring with aortic dissection include changes consistent with left ventricular hypertrophy, left-axis deviation, heart blocks, or dysrhythmias.[10] Multiple diagnostic methods can be used to investigate for aortic dissection if the diagnosis is suspected. These diagnostic methods include chest radiography, transthoracic echocardiography, transesophageal echocardiography, MRI, or CT. Each method has its own strengths and drawbacks.
Chest radiography is quick and widely available, but it is not sensitive or specific. Transthoracic echocardiography is rapid, can be performed at bedside, and is noninvasive, but it is limited to evaluation of the proximal ascending aorta and the competency of the aortic valve. Transesophageal echocardiography can reliably view the proximal and descending thoracic aorta, but it is invasive, requires sedation of the patient, and may not be available at all institutions 24 hours per day. MRI provides excellent imaging characteristics but may not be available emergently in all institutions. CT is usually rapid and available and has good diagnostic accuracy, but it requires administration of intravenous contrast. In general, CT is usually the most expeditious and easily obtained imaging modality in the absence of contraindications, such as renal insufficiency.
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Any views expressed above are the author's own and do not necessarily reflect the views of WebMD or Medscape.
Cite this: Ryland P. Byrd, Thomas M. Roy. Dull Chest Pain in a 42-Year-Old Man - Medscape - Jun 12, 2017.
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