Clinical Challenge

Emergency Case

Thoracic aortic dissection

Distinguishing it from acute myocardial infarction

Harold Schubert, MD, MSC, CCFP

QUESTIONS

A 65-year-old man presents with severe chest pain. An electrocardiogram (EKG) shows ST segment elevations in leads I, aVL, and V1 to V6. Results from portable chest x-ray examination are normal. You consider initiating thrombolytic therapy.

Could this be dissection of the ascending thoracic aorta? What features in the history and examination are most helpful for distinguishing thoracic aortic dissection (TAD) from acute myocardial infarction (AMI)? Are laboratory tests, EKGs, or chest x-ray films helpful?

Thoracic aortic dissection and AMI can have nearly identical presentations, and both conditions require urgent therapies that differ greatly. Therapy for AMI (thrombolysis) can be catastrophic for patients with TAD. This paper reviews features of TAD that can help physicians distinguish it from AMI.

Aortic aneurysm and aortic dissection are distinct conditions (Figure 11,2). Both aneurysm and dissection result from degeneration of the media, the middle layer of the aortic wall. Aortic aneurysm is a general widening of the aorta due to weakening of the media. This widening develops slowly and can progress over years without symptoms.1

Figure 1. Two distinct diseases of the ascending aorta: Thoracic aortic aneurysm and thoracic aortic dissection. Note Debakey classifications 1, 2, and 31,2 of the intimal tear.

Thoracic aortic dissection is a sudden event. It begins with a tear in the intima, the vessel lining, and progresses to hemorrhage into the media. The intimal tear is thought to result from hemodynamic forces acting on the intima and from the repetitive motion of 37 to 40 million heartbeats a year.2

Incidence of TAD in North America is about 5 to 10 cases per million people annually, about one thousand times lower than the incidence of AMI.1 Incidence figures are generally based on autopsy studies. Unfortunately, TAD continues to be underdiagnosed before death.3

Thoracic aortic dissection is the most common acute illness of the aorta, being two to three times more common than rupture of the abdominal aorta. The ascending aorta is most often involved.1

Mortality from untreated dissection of the ascending aorta is very high; 33% in the first 24 hours after onset of symptoms, 50% in the first 48 hours, and 75% within 2 weeks. Expressed another way, mortality is approximately 1% to 2% per hour for the first 48 hours after onset of symptoms.3

Thoracic aortic dissection was first repaired successfully by Debakey in 1955. He classified TAD according to the location of the intimal tear.1,2 Debakey classifications 1, 2, and 3 are shown in Figure 11,2. A more recent and more popular classification from Stanford University in California simply denotes whether the dissection includes the ascending aorta (class A) or is restricted to the descending aorta (class B).1,2 This classification divides TAD patients into two groups; those thought to do best with surgery (class A) and those thought to do best with medical management (class B). Stanford class A TAD can mimic AMI and is the focus of this paper. The TAD illustrated in Figure 11,2 is Stanford class A.

How TAD can look like AMI

Stanford class A TAD, by retrograde dissection, can impinge on one or both coronary ostia and thereby reduce coronary blood flow. The location and extent of ischemic changes on EKG will depend on which coronary ostia are affected, how much they are affected, and on left or right dominance of coronary circulation. Stanford class A TAD will give ST segment elevations suggesting AMI in up to 8% of cases.3,4 Some ST segment changes (elevation, depression, or nonspecific) are seen in up to 42% cases of class A TAD.4

Thoracic aortic dissection has been described in the literature for hundreds of years. Only recently have several publications reviewed large series of TAD patients in an effort to reveal the true incidence of various features of the condition: those that arise from the history or physical examination and those apparent from laboratory, EKG, and x-ray investigations. Most notably, in 2000, the International Registry of Acute Aortic Dissection (IRAD) reported on a series of 464 patients with TAD, 289 of whom had Stanford class A dissection.4 Table 14 lists some of the features of class A TAD and indicates how often they occurred in IRAD patients. Faced with the AMI or TAD dilemma and under pressure to start treatment promptly, physicians need to know what features define each condition and to what extent, to make the distinction.

No single criterion or group of criteria clearly distinguishes TAD from AMI. Physicians must rely on varying their level of clinical suspicion based on findings in the history, physical examination, and clinical tests.

Thoracic aortic dissection

Typical TAD patients are 60 to 65 years old, have a history of hypertension, and are twice as likely to be men as women.4 In the IRAD series, a few TAD patients had no pain; these were thought to be patients with neurologic conditions, such as diabetic neuropathy, or patients whose pain perception was blunted by cerebrovascular accident (CVA).1,4

Some features, such as chest pain with syncope or CVA, are uncommon. If they occur, these combinations are highly suggestive of TAD and physicians should pursue that diagnostic path aggressively. It is notable that normal chest x-ray results do not rule out TAD. A widened mediastinum, sometimes thought to be a consistent finding in TAD, was found in only 63% of class A TAD patients in the IRAD series. (On a portable anteroposterior chest x-ray film, a widened mediastinum is considered to be >8 cm.3)

The most consistently occurring features of TAD relate to the quality of the pain. The pain is clearly distinct from the type of pain associated with AMI.1

Suspicion of TAD, in the absence of a clear alternative diagnosis, should be quickly followed by a contrast-enhanced CT scan,1 which has good sensitivity and specificity for rapidly diagnosing TAD. The drawback is having to take a potentially unstable patient out of the emergency department.

ANSWERS

Acute myocardial infarction and TAD can present identically. For patients with chest pain, the most important first step in distinguishing AMI from TAD is to consider both as diagnostic possibilities. After that, the strongest and most reliable indicators for TAD are found in the history (Table 14). Results of EKG and chest x-ray investigations do not reliably discriminate between TAD and AMI. Blood tests are not helpful right after onset of symptoms when starting appropriate treatment rapidly is critical. A careful history focused on the quality of a patient’s pain is the most useful tactic for distinguishing TAD from AMI.

References

1. Chen K, Varon J, Wenker OC, Judge DK, Fromm RE Jr, Sternbach GL. Acute thoracic aortic dissection: the basics. J Emerg Med 1997;15(6):859-67.
2. Wheat MW. Acute dissection of the aorta. Cardiovasc Clin 1987;17(3):241-62.
3. Wiesenfarth J. Aortic dissection [monograph on-line]. Stanford, Calif: Stanford University School of Medicine; 2001. Updated May 9, 2001. Available at: http://www.emedicine.com/emerg. Accessed 2002 May 27.
4. Hagan PG, Nienaber CA, Isselbacher EM. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA 2000;283:897-903.

Dr Schubert practises emergency medicine at the University of British Columbia Hospital in Vancouver.