BMJ  2003;326:1135-1136 (24 May), doi:10.1136/bmj.326.7399.1135

Commentary

Cardiovascular management

¹ University of Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria irene.lang{at}univie.ac.at

In the United States each year, aortic dissection causes two deaths per 100 000 men and 0.8 deaths per 100 000 women.¹ Predisposing factors include Marfan's, Ehlers-Danlos, and Turner's syndrome and mutation in the gene for type III collagen. The third trimester of pregnancy, bicuspid aortic valve (91% of dissected aortic aneurysms show bicuspid aortic valves²), coarctation of the aorta, arteritis, systemic lupus erythematosus, juvenile nephropathic nephrocalcinosis, Cushing's syndrome, and cocaine misuse are additional predisposing factors. Arterial hypertension, another common risk factor for aortic dissection, was mentioned by many respondents to the case.

The characteristic histological change in aortic dissection is cystic medial necrosis.² Apoptosis of medial smooth muscle cells leads to microscopic gunshot-like holes in the medial layer. The most widely used classification of aortic dissection is that of Stanford, with type A being proximal aortic dissection and type B aortic dissection distal to the left subclavian artery. This is of more practical use than the DeBakey classification.³ Surgeons like to remember that they need to act quickly in type A dissections but can delay surgery for type B dissections.

The site of initial pain may indicate the site of dissection. Descriptions include sensations of ripping, burning, splitting, cutting, or being hit in the chest. Transient syncope is often associated with the first onset of pain. Patients usually appear in distress, cold and clammy, and hypertensive because of damage to the aortic arch baroreceptors. An aortic regurgitation murmur may be an early physical sign of dissection. Three signs to alert physicians not to give early thrombolytic therapy are a history of hypertension, sudden onset of pain, and subsequent caudal migration of pain.

In a study population with a prevalence of aortic dissection over 50%, positive predictive values were 86% for angiography, 99% for computed tomography, 100% for magnetic resonance imaging, and 99% for transoesphageal echocardiography.⁴

Although it is known that untreated concomitant coronary disease decreases long term postoperative survival,⁵ Peter Hartl did not have diagnostic cardiac catheterisation because it would have delayed surgery. Early surgical repair was essential in Peter's case because 40% of patients with proximal dissection die immediately, 70% within the first 24 hours, 94% within one week, and all patients within five weeks. By contrast, about 75% of patients with distal dissection survive one month,⁶ and cardiac catheterisation is valuable in this group.

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Competing interests: None declared.

References

1. Demos TC, Posniak HV, Marsan RE. CT of aortic dissection. Semin Roentgenol 1989;24: 22-37.[CrossRef][Medline]
2. Roberts CS, Roberts WC. Aortic dissection with the entrance tear in transverse aorta: analysis of 12 autopsy patients. Ann Thorac Surg 1990;50: 762-6.[Abstract]
3. Svensson LG, Crawford ES. Aortic dissection and aortic aneurysm surgery: clinical observations, experimental investigations, and statistical analyses. Part II. Curr Probl Surg 1992;29: 913-1057.[Medline]
4. Barbant SD, Eisenberg MJ, Schiller NB. The diagnostic value of imaging techniques for aortic dissection. Am Heart J 1992;124: 541-3.[CrossRef][ISI][Medline]
5. Svensson LG, Crawford ES, Hess KR, Coselli JS, Safi HJ. Dissection of the aorta and dissecting aortic aneurysms. Improving early and long-term surgical results. Circulation 1990;82: IV24-38.[Medline]
6. Shennan T. Dissecting aneurysms. Med Res Clin Special Rep Ser 1934;193.

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