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| CASE REPORT |
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| Year : 2019 | Volume
: 5
| Issue : 2 | Page : 122-124 |
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Chronic painless stanford type a aortic dissection involving whole of the aorta in an elderly female
Kunal Mahajan, Rajeev Bhardwaj, Sachin Sondhi
Department of Cardiology, Indira Gandhi Medical College and Hospital, Shimla, Himachal Pradesh, India
| Date of Submission | 19-Mar-2019 |
| Date of Decision | 13-May-2019 |
| Date of Acceptance | 31-May-2019 |
| Date of Web Publication | 19-Aug-2019 |
Correspondence Address:
Rajeev Bhardwaj
Department of Cardiology, Indira Gandhi Medical College and Hospital, Shimla - 171 001, Himachal Pradesh
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jpcs.jpcs_14_19
Stanford type A aortic dissection (AD) is a rapidly progressive disease associated with a very high mortality rate, especially in the absence of emergent surgical repair. However, very rarely, few cases remain undiagnosed in acute phase because of atypical or absent symptoms. We present such an atypical case of a chronic painless type A AD in an elderly female, who is still surviving at 6 months follow-up without any surgical/catheter-based intervention. This case emphasizes that chronic type A ADs have different natural history and could potentially be managed differently from the acute lesions.
Keywords: Aortic dissection, chronic, painless, Stanford type A
How to cite this article:
Mahajan K, Bhardwaj R, Sondhi S. Chronic painless stanford type a aortic dissection involving whole of the aorta in an elderly female. J Pract Cardiovasc Sci 2019;5:122-4 |
How to cite this URL:
Mahajan K, Bhardwaj R, Sondhi S. Chronic painless stanford type a aortic dissection involving whole of the aorta in an elderly female. J Pract Cardiovasc Sci [serial online] 2019 [cited 2023 Jun 4];5:122-4. Available from: https://www.j-pcs.org/text.asp?2019/5/2/122/264620 |
| Introduction | |  |
Aortic dissection (AD) is a catastrophic condition which can be classified according to the Stanford classification into type A and type B. Type A involves the ascending aorta (with or without extension into descending aorta), while type B are those which do not involve ascending aorta.[1] Acute type A AD has a mortality of 50% within the first 48 h and 90% at 1 month, if not operated.[2] This is despite the fact that many cases are still missed because of incorrect diagnoses, prehospital mortality, or failure to recognize dissection as the cause of a complication.[3] Surgery reduces 1-month mortality from 90% to 30%.[4] Despite improvements in surgical and anesthetic techniques, perioperative mortality (25%) and neurological complications (18%) remain high.[2],[3],[4] It is extremely rare to find a patient with chronic type A AD involving the whole of the aorta and its branches and still surviving without surgery at 6 months after diagnosis. Such patients are likely to have different pathophysiological mechanisms compared to acute lesions.
| Case Report | | |
A 75-year-old hypertensive female presented with insidious-onset, progressively increasing dyspnea of 12 weeks' duration. No history of chest pain or syncope was recorded. On examination, her pulse rate was 100/min and blood pressure was 190/30 mmHg. All the peripheral pulses were palpable. Chest auscultation revealed bilateral basal crepitations. An early diastolic murmur of aortic regurgitation (AR) was auscultated. Electrocardiogram did not show any significant ST-T changes. Echocardiogram showed a dilated ascending aorta (67 mm) with a dissection flap. The dissection flap extended to the arch of the aorta and then along the descending aorta and abdominal aorta [Figure 1] to the femoral artery on the right side and common iliac artery on the left side [Figure 2]a,[Figure 2]b, [Figure 2]c. Dissection also extended into the right common carotid artery up to the level of bifurcation [Figure 2]d and into the proximal part of the left subclavian artery. Moderate AR was present [Figure 3]. The patient was classified as having Stanford type A AD. Multidetector computerized tomographic angiography confirmed the echocardiographic findings [Figure 4] and [Figure 5]. The patient declined surgical intervention and has been managed by medical therapy in the form of high-dose beta-blocker, angiotensin receptor antagonist, and diuretics. She continues to be stable at 6 months follow-up. | Figure 1: (a) Parasternal long-axis view demonstrating a dilated ascending aorta with a dissection flap. (b) Suprasternal view revealing a dissection flap at the level of aortic arch. (c) Suprasternal view showing the extension of dissection flap into the left subclavian artery (white arrow) and along the descending thoracic aorta (yellow arrow). (d) Subcoastal view demonstrating a dissection flap in the abdominal aorta.
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 | Figure 2: Demonstration of the extension of dissection flap into the right common iliac artery (a), right femoral artery (b), left common iliac artery (c) and the right common carotid artery (d).
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 | Figure 3: Transthoracic echocardiogram, parasternal long axis view, demonstrating the aortic regurgitation jet. Note the dilatation of ascending aorta and the moderate pericardial effusion (arrow).
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 | Figure 4: Multidetector 256 slice computed tomography three-dimensional reconstructed contrast aortogram showing dissection of aorta up to the right external iliac artery. Intimal flap has divided aorta into true lumen (white arrow) and false lumen (yellow arrow). True lumen is smaller in size as compared to false lumen (approximately 30:70). True lumen shows more contrast density and multifocal wall calcifications. False lumen is less dense owing to delayed contrast enhancement.
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 | Figure 5: Multidetector computed tomography contrast scan showing (a) an intimal flap arising at the level of aortic root (blue arrow) which is extending into ascending aorta, arch of aorta and descending thoracic aorta (black arrow). Note the extension of intimal flap into the right common carotid artery and left subclavian artery (pink arrows). (b) Intimal flap extending into the abdominal aorta (black arrow) and up to the right common iliac artery (pink arrow).
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| Discussion | | |
AD is classified as “acute” when present for <2 weeks and “chronic” when present for >2 weeks.[3] Acute type A AD is often fatal, so chronic type A AD is likely to have pathological and physiological differences that allow the disease process to settle down. In a recent review of 696 type A dissection repairs, it was observed that chronic type A ADs were more often associated with bicuspid aortic valve morphology and were less likely to extend beyond the arch, compared with acute lesions.[5] However, in the present case, dissection involved almost the whole of the aorta and extended up to the femoral artery.
Chest or back pain is the most common presenting complaint in acute AD, occurring in up to 96% of the cases.[6] However, no such history was recorded in the present case. Registry data show that in patients presenting without pain, the most common clinical presentation includes AR (40%–75%), syncope (15%), stroke (<10%), myocardial ischemia (10%–15%), acute renal failure (15%–20%), or congestive heart failure (<10%).[6] Heart failure that occurs in AD is commonly related to AR.[6]
Although surgery is the gold standard treatment of type A AD, acceptable outcomes in late-presenting patients with type A AD managed temporarily or permanently without operative intervention have been reported.[7] Histological evaluations have suggested that a remodeling process might stabilize the false lumen through the development of a new endothelial lining and thickening of the media by the production of new smooth muscle cells.[8] This remodeling process might explain the relative stability of chronic type A ADs and also provides logical support for the medical management of uncomplicated asymptomatic lesions. However, no significant data exist that adequately define the outcomes of nonoperative management for this subset of patients. In fact, many cases reportedly have been associated with sudden onset of delayed symptoms, false lumen expansion, and progressive aneurysmal dilatation.[3] The small number of cases continues to limit our understanding of treatment options in chronic type A ADs. The current body of evidence suggests operative modality as the most suitable treatment strategy for these chronic lesions.[3],[5]
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient has given her consent for her images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
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| 4. | Bachet J, Goudot B, Dreyfus GD, Brodaty D, Dubois C, Delentdecker P, et al. Surgery for acute type A aortic dissection: The hopital foch experience (1977-1998). Ann Thorac Surg 1999;67:2006-9. |
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| 6. | Di Eusanio M, Trimarchi S, Patel HJ, Hutchison S, Suzuki T, Peterson MD, et al. Clinical presentation, management, and short-term outcome of patients with type A acute dissection complicated by mesenteric malperfusion: Observations from the international registry of acute aortic dissection. J Thorac Cardiovasc Surg 2013;145:385-900. |
| 7. | Davies RR, Coe MP, Mandapati D, Gallo A, Botta DM, Elefteriades JA, et al. Thoracic surgery directors association award. What is the optimal management of late-presenting survivors of acute type A aortic dissection? Ann Thorac Surg 2007;83:1593-601. |
| 8. | Carnevale D, Lembo G, Frati G. Chronic type A aortic dissection: Could surgical intervention be guided by molecular markers? J Cell Mol Med 2011;15:1615-9. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
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