|Year : 2013 | Volume
| Issue : 2 | Page : 154-157
DeBakey type 1 acute aortic dissection presenting as inferior myocardial infarction: A case report and review of literature
Solomon S Danbauchi1, Philip O Ibinaiye2, Chiasaokwu A Anyiam1, Mohammed A Alhassan1, Albert I Oyati1
1 Department of Medicine (Cardiology unit), Ahmadu Bello University Teaching Hospital, Zaria, Nigeria
2 Department of Radiology, Ahmadu Bello University Teaching Hospital, Zaria, Nigeria
|Date of Web Publication||13-Dec-2013|
Philip O Ibinaiye
Department of Radiology, Ahmadu Bello University Teaching Hospital, Zaria
Source of Support: None, Conflict of Interest: None
Acute dissection of the aorta is one of the most dramatic presentation of cardiovascular emergencies. It has a varying presentation and it is described as deceptive and dangerous. It is reported as rare, and most cases are discovered during autopsies. Prompt recognition and appropriate intervention is crucial. However, not all aortic dissections (AoD) present with classic symptoms of abrupt chest, back, or abdominal pain, and the diagnosis may be missed. We have reported here a 68-year-old man who presented with 18 hours of severe chest pain radiating to the left shoulder and was associated with shortness of breath, palpitations, sweating, and feeling of an impending doom. A diagnosis of inferior myocardial infarction was made based on ST-Segment elevation >2 mm in the Leads II, III and aVF on electrocardiogram (ECG). However, further evaluation with computed tomographic angiogram done revealed DeBakey's type 1 or Stanford type A AoD. He was later referred to a cardiothoracic centre, where he had an aortic root and valve replacement 2 months after the first presentation. He is currently doing fine at 2-year follow-up. Although, AoD is a rare entity and can masquerade in different forms, a high index of suspicion will enhance diagnosis and prompt appropriate intervention.
Keywords: Aortic dissection, DeBakey type 1, myocardial infarction
|How to cite this article:|
Danbauchi SS, Ibinaiye PO, Anyiam CA, Alhassan MA, Oyati AI. DeBakey type 1 acute aortic dissection presenting as inferior myocardial infarction: A case report and review of literature. Arch Int Surg 2013;3:154-7
|How to cite this URL:|
Danbauchi SS, Ibinaiye PO, Anyiam CA, Alhassan MA, Oyati AI. DeBakey type 1 acute aortic dissection presenting as inferior myocardial infarction: A case report and review of literature. Arch Int Surg [serial online] 2013 [cited 2019 Oct 17];3:154-7. Available from: http://www.archintsurg.org/text.asp?2013/3/2/154/122945
| Introduction|| |
Acute thoracic aortic dissection (AoD), one of the most common and serious diseases of the aorta, carries a high morbidity and mortality rate when not recognized or treated promptly. The mortality of untreated AoD may be as high as 1% within 1 h and 40-50% of the patients die within 48 h. , For those fortunate enough to survive the initial 48 h, the disease may carry a 90% 1-year mortality rate. , Since the introduction of modern treatment regimens, the fatality rate has declined dramatically. Patients with proximal ascending dissection who rapidly undergo surgery in experienced tertiary centers have a 30-day survival rate of 80-85% and a 10-year survival of 55%.  Realizations of the significant benefits of early intervention is dependent upon rapid establishment of the diagnosis of AoD.
The classic symptoms of AoD such as abrupt chest, back, or abdominal pain are non-specific as other clinical conditions could mimic these symptoms. Hence, this makes the diagnosis of AoD difficult, especially in countries like Nigeria, where this disease entity is rare and modern diagnostic equipments are not readily available. By understanding the pathophysiology of AoD, the clinician may better understand the relationship between the dissection process and the resulting symptomatology. We present here a case of DeBakey type 1 AoD presenting with features of acute inferior myocardial infarction.
| Case Report|| |
A 68-year-old man presented with crushing chest pain that started 18 h before presentation following coitus. The pain radiated to the left shoulder and was associated with shortness of breath, palpitations, sweating, and feeling of an impending doom. He noted occasional painless swelling of feet and legs. He was diagnosed hypertensive 2 years prior to presentation, but was non-compliant to his medication. He did not have diabetes or a history suggestive of peripheral vascular disease, angina, stroke, transient ischemic attack (TIAS), or myocardial infarction. He smoked about 30 pack-years and consumed high cholesterol diet but denied alcohol consumption. No family history of similar disease was noted.
Examination revealed an elderly man in respiratory and painful distress. He had mild pedal edema and diaphoresis. He was not pale, jaundiced, or centrally cyanosed, but had basal crepitations in both the lungs. His pulse rate was 110 per minute, regular, and full volume with arterial wall thickening, blood pressure was 150/90 mmHg, and apex beat was in the 6 th LICS lateral to the mid clavicular line. The heart sounds revealed normal S1 and S2, but loud A2 and S3 at the apex. There was a systolic murmur in the apex, but no pericardial friction rub. The abdomen and central nervous system were unremarkable. An electrocardiogram (ECG) revealed ST-Segment elevation >2 mm in Leads II, III and aVF consistent with inferior myocardial infarction.
The patient declined admission with all entreaties. He however received thrombolysis with streptokinase 1.5 ml in 100 ml of normal saline, which ran for 1 h due to the inferior wall myocardial infarction, and he was subsequently placed on aspirin. He was also placed on furosemide and lisnopril due to the ensuing heart failure. He had non-steroidal anti-inflammatory drug due to crushing chest pain. The patient presented a week later with worsening chest pain and symptoms and signs of cardiac failure. ECG continued to show inferior wall myocardial infarction, echocardiogram showed depressed left ventricle (LV) systolic function (EF = 46%), diastolic dysfunction, and severe aortic and mild mitral regurgitation. Chest radiograph showed cardiomegaly and pulmonary edema [Figure 1]. The computed tomographic angiogram done as a part of his work-up revealed DeBakey type 1 or Stanford type A AoD [Figure 2]. The coronary angiogram showed no coronary artery disease, and the aortic arch branches and renal arteries were normal. He later had an aortic root and valve replacement 2 months after the first presentation. He is currently doing fine at 2-year follow-up.
|Figure 2: Showing aortic dissection, true lumen (black arrow), false lumen (white arrow), and intimal fl ap (arrow head)|
Click here to view
| Discussion|| |
AoD has varying presentation, and it is described as deceptive and dangerous. It is reported as rare, and most cases are discovered during autopsies. Dissection of the aorta begins with a tear in the intimal layer. This tear permits blood to enter the aortic wall, creating an intramural hematoma that is progressing distally in the aorta. A common site for the initiation of an intimal tear is at the proximal portion of the ascending aorta due to the thrust of blood ejecting from the LV. Upon intimal disruption, blood enters the media permitting dissection. Most patients with AoD have hypertension (80%). , The index case was diagnosed hypertensive 2 years prior to presentation. Physical effort or emotional stress elevating pulse pressure is a common trigger of acute AoD,  in the index case, acute AoD was triggered by physical exertion during sexual intercourse.
Because a dissection of the aorta has high morbidity and mortality, its protean symptoms must be appreciated. The symptoms may be secondary to the involvement of branch vessels or adjacent structures by the expanding aneurysm. The symptoms and signs may include abrupt chest pain, abdominal pain, back pain, acute myocardial infarction, intra-abdominal disorders and peripheral arterial occlusion disease. ,,,,,,, In the present case, AoD was not considered at first presentation because of the rarity of this disease entity in our country and the low index of suspicion despite the fact that the patient presented with crushing chest pain and inferior myocardial infarction changes on ECG.
Dissection of the thoracic aorta has been classified anatomically by 2 different methods. The more commonly used system is the Stanford classification,  which is based on the involvement of the ascending aorta and simplifies the DeBakey classification.  The Stanford classification divides dissections into 2 types: Type A and type B. Type A involves the ascending aorta (DeBakey types I and II), while type B does not (DeBakey type III). This system helps to delineate treatment. Usually, type A dissections require surgery, while type B dissections may be managed medically under most conditions.
The DeBakey classification divides dissections into 3 types, as follows:
- Type I involves the ascending aorta, aortic arch, and descending aorta
- Type II is confined to the ascending aorta
- Type III is confined to the descending aorta distal to the left subclavian artery
Type IIIa originates distal to the left subclavian artery, but extend proximally and distally above the diaphragm.
Type IIIb dissections that originate distal to the left subclavian artery, extend only distally, and may extend below the diaphragm.
Studies have shown that chest X-ray is not helpful in distinguishing between myocardial infarction and AoD, , as seen in our patient. Computed tomographic scan, , magnetic resonance imaging,  and transoesophageal echocardiography , are all validated and sensitive non-invasive procedures that are capable of confirming the diagnosis in over 90% of cases. Computed tomographic angiography was used to confirm diagnosis in the index case. These imaging modalities are used in preference to aortography because of their non-invasiveness, speed, and ease of use. However, the most important thing is to maintain a high index of suspicion, which is a vital lesson learnt in our patient. If a patient with a history of hypertension, presents with an acute and severe symptoms or signs suggestive of vascular origin, particularly if they include chest pain, then AoD should be considered and appropriate investigation and management should be pursued.
Urgent surgical intervention is required in type A dissections. , The area of the aorta with the intimal tear is usually resected and replaced with a Dacron graft. The operative mortality rate is usually less than 10%, and serious complications are rare with ascending AoDs. The development of more impermeable grafts, such as woven Dacron, collagen-impregnated Hemashield (Meadox Medicals, Oakland, NJ), aortic grafts, and gel-coated Carbo-Seal Ascending Aortic Prothesis (Sulzer CarboMedics, Austin, Tex), has greatly enhanced the surgical repair of thoracic AoDs. With the introduction of profound hypothermic circulatory arrest and retrograde cerebral perfusion, the morbidity and mortality rates associated with this highly invasive surgery have decreased.
Dissections involving the arch are more complicated than those involving only the ascending aorta, because the innominate, carotid, and subclavian vessels branch from the arch. Deep hypothermic arrest is usually required. If the arrest time is less than 45 min, the incidence of central nervous system complications is less than 10%. Aortic stent grafting is a challenging technique. It may prove feasible and has offered good results in a small series of patients. It may be a reasonable alternative in high-risk patients in the near future.
The definitive treatment for type B dissections is less clear.  Uncomplicated distal dissections may be treated medically to control blood pressure. Distal dissections treated medically have a mortality rate that is the same as or lower than the mortality rate in patients who are treated surgically. Surgery is reserved for distal dissections that are leaking, ruptured, or compromising blood flow to a vital organ. Acute distal dissections in patients with Marfan syndrome usually are treated surgically. Inability to control hypertension with medication is also an indication for surgery in patients with a distal thoracic AoD.
Endovascular stenting remains an option for the treatment of some type B dissections. Some studies recommend that patients with complicated acute type B dissections undergo endovascular stenting with the goal of covering the primary intimal tear. , Definitive treatment involves segmental resection of the dissection, with interposition of a synthetic graft.
When thoracic dissections are associated with aortic valvular disease, replace the defective valve. With combined reconstruction - valve replacement, the operative mortality rate is approximately 5%, with a late mortality rate of less than 10%. The index case had type I or type A AoD and was treated surgically by an aortic root and valve replacement.
In conclusion, AoD can masquerade in different forms. The rarity of this condition in our country may be due to lack of facilities for correct diagnosis. We suggest that a high index of suspicion will enhance diagnosis and that increased autopsies might highlight the cases hitherto misdiagnosed.
| References|| |
|1.||Hirst AE Jr, Johns VJ Jr, Kime SW Jr. Dissecting aneurysm of the aorta: A review of 505 cases. Medicine (Baltimore) 1958;37:217-279. |
|2.||DeSanctis RW, Doroghazi RM, Austin WG, Buckley MJ. Aortic dissection. N Engl J Med 1987;317:1060-7. |
|3.||Hagan PG, Neinaber CA, Isselbacher EM, Bruckman D, Karavite DJ, Russman PL, et al. The International Registry of Acute Aortic Dissection (IRAD): New insights into an old disease. JAMA 2000;283:897-903. |
|4.||Kaplan NM. Clinical hypertension. 7 th ed. Baltimore; 1998. p. 114. |
|5.||Isselbacher EM, Eagle KA, Desanctis RW. Diseases of the aorta. In: Braunwald E, editor. Heart Disease, USA: Saunders Company; 1997. p. 1558-64. |
|6.||Marek D, Nemec P, Herman M, Gwozdziewicz M, Troubil M, Lukl J. Mistakes in dealing with aortic dissection. Lessons from three warning cases. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 2008;152:283-7. |
|7.||Spittell PC, Spittell JA Jr, Joyce JW, Tajik AJ, Edwards WD, Schaff HV, et al. Clinical features and differential diagnosis of aortic dissection: Experience with 236 cases (1980 through 1990). Mayo Clin Proc 1993;68:642-51. |
|8.||Khan R, Amaram S, Gomes JA, Kelen GJ, Lynfield J, El-Sherif N. Myocardial infarction following acute aortic dissection. Cathet Cardiovasc Diagn 1980;6:181-4. |
|9.||Nordt TK, Rauch B, Mattfeldt T, Zimmermann R, Eberlein-Gonska M, Kübler W, et al. Acute myocardial infarction due to proximal aortic dissection in giant cell aortitis. Am Heart J 1991;122:1151-3. |
|10.||Cambria RP, Brewster DC, Gertler J, Moncure AC, Gusberg R, Tilson MD, et al.Vascular complication associated with spontaneous aortic dissection. J Vasc Surg 1988;7:199-209. |
|11.||Kellet MW, Young GR, Fletcher NA. Paraparesis due to syphilitic aortic dissection. Neurology 1997;48:221-3. |
|12.||Rosen SA. Painless aortic dissection presenting as spinal cord ischemia. Ann Emerg Med 1988;17:840-2. |
|13.||Pacifico L,s Spodick D. ILEAD-Ischemia of the lower extremities due to aortic dissection: The isolated presentation. Clin Cardiol 1999;22:353-6. |
|14.||Liu WP, Chen WK, Ng KC. Aortic dissection presenting as acute lower extremity ischemia: Report of a case. Yale J Biol Med 2002;75:211-4. |
|15.||Miller DC, Stinson EB, Oyer PE, Rossiter SJ, Reitz BA, Griepp RB, et al. Operative treatment of aortic dissections. Experience with 125 patients over a sixteen year period. J Thorac Cardiovasc Surg 1979;78:365-82. |
|16.||DeBakey ME, McCollum CH, Crawford ES, Morris GC Jr, Howell J, Noon GP, et al. Dissection and dissecting aneurysms of the aorta: Twenty-year follow-up of five hundred twenty-seven patient treated surgically. Surgery 1982;92:1118-34. |
|17.||Hartnell GG, Wakeley CJ, Tottle A, Papouhado M, Wilde RP. Limitation of chest radiography in discriminating between aortic dissection and myocardial infarction: implication of thrombolysis. J Thorac Imaging 1993;8:152-5. |
|18.||Vasile N, Mathieu D, Keita K, Lellouche D, Bloch G, Cachera JP. Computed tomography of thoracic aortic dissection: Accuracy and pitfalls. J Comput Assist Tomogr 1986;10:211-5. |
|19.||Thorsen MK, San Dretto MA, Lawson TL, Foley WD, Smith DF, Berland LL. Dissecting aortic aneurysms: Accuracy of computed tomographic diagnosis. Radiology 1983;148:773-7. |
|20.||Dinsmore RE, Liberthson RR, Winmer GL, Miller SW, Liu P, Thompson R, et al. Magnetic resonance imaging of thoracic aortic aneurysms: Comparison with other Imaging methods. AJR Am J Roentgenol 1986;146:309-14. |
|21.||Penco M, Paparoni S, Dagianti A, Fusilli C, Vitarelli A, De Remigis F, et al. Usefulness of transesophageal echocardiography in the assessment aortic dissections. Am J Cardiol 2000;86:53-6G. |
|22.||Adachi H, Kyo S, Takamoto S, Kimura S, Yokote Y, Omoto R. Early diagnosis and intervention of acute aortic dissection by transoesophageal color flow mapping. Circulation 1990;82 (5 Suppl):IV19-23. |
|23.||Isselbacher EM, Eagle KA, DeSanctis RW. Diseases of the aorta. In: Braunwald E, editor. Heart Disease. A Textbook of Cardiovascular Medicine, 5 th ed. Pheladelphia: W.B.Saunders Company; 1997. p. 1546-81. |
|24.||Masuda Y, Yamada Z, Morooka N, Watanade S, Inagaki Y. Prognosis of patient with medically treated aortic dissections. Circulation 1991;84 (5 Suppl):III7-13. |
|25.||Erbel R, Alfonso F, Boileru C, Dirsch O, Eber B, Haverich A, et al., Task Force on Aortic Dissection, European Society of Cardiology. Diagnosis and management of aortic dissection. Eur Heart J 2001;22:1642-81. |
[Figure 1], [Figure 2]