Stanford Type A Acute Aortic Dissection with Left Coronary Artery Involvement: Computed Tomography Angiography Findings

A 48-year-old female presented to the emergency department with complaints of acute onset chest pain radiating to the back and breathlessness for the past 24 hours. The patient reported no significant past medical history but had a family history of hypertension. On examination, her blood pressure was markedly elevated at 200/160 mmHg and she appeared distressed and diaphoretic. Auscultation revealed diminished breath sounds in the left lung base. An Electrocardiogram (ECG) revealed sinus tachycardia. Given the clinical suspicion of aortic dissection, urgent imaging studies were performed. A Computed Tomography Angiography (CTA) of the chest was conducted, revealing a Stanford Type A aortic dissection extending from the ascending aorta to the abdominal aorta. A thin, oblique intimal flap was noted, extending from the aortic root just above the right sinus of Valsalva through the entire course of the ascending aorta, arch of the aorta, descending thoracic aorta and abdominal aorta, up to the common iliac artery [Table/Fig-1a-d]. An extension of the flap transversely into the left sinus of Valsalva, involving the osteoproximal segment of the left main coronary artery, was observed [Table/Fig-2]. Diffuse consolidations involving bilateral perihilar regions of both lung fields suggested pulmonary oedema [Table/Fig-3a]. Bilateral pleural effusions were also noted [Table/Fig-3b]. Despite the immediate initiation of antihypertensive therapy and arrangements for surgical consultation, the patient’s condition rapidly deteriorated. She developed profound hypotension and loss of consciousness within two hours of admission. Despite aggressive resuscitative measures, including fluid resuscitation and vasopressor support, the patient could not be stabilised. Cardiopulmonary resuscitation was initiated, but unfortunately, the patient succumbed to cardiac arrest.

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Publication Details

Journal
JOURNAL OF CLINICAL AND DIAGNOSTIC RESEARCH
Published
2025-03-01
DOI
https://doi.org/10.7860/jcdr/2025/77915.20710
Primary Topic
Aortic Disease and Treatment Approaches
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article

Stanford Type A Acute Aortic Dissection with Left Coronary Artery Involvement: Computed Tomography Angiography Findings

Deepthi Arunkumar, Revathi Rajagopal, Senthil Kumar Aiyappan, Jubin Joseph et al.
JOURNAL OF CLINICAL AND DIAGNOSTIC RESEARCH
Aortic Disease and Treatment Approaches
article

Stanford Type A Acute Aortic Dissection with Left Coronary Artery Involvement: Computed Tomography Angiography Findings

Deepthi Arunkumar, Revathi Rajagopal, Senthil Kumar Aiyappan, Jubin Joseph, Nishant Narendra Kumar
article en

Abstract

A 48-year-old female presented to the emergency department with complaints of acute onset chest pain radiating to the back and breathlessness for the past 24 hours. The patient reported no significant past medical history but had a family history of hypertension. On examination, her blood pressure was markedly elevated at 200/160 mmHg and she appeared distressed and diaphoretic. Auscultation revealed diminished breath sounds in the left lung base. An Electrocardiogram (ECG) revealed sinus tachycardia. Given the clinical suspicion of aortic dissection, urgent imaging studies were performed. A Computed Tomography Angiography (CTA) of the chest was conducted, revealing a Stanford Type A aortic dissection extending from the ascending aorta to the abdominal aorta. A thin, oblique intimal flap was noted, extending from the aortic root just above the right sinus of Valsalva through the entire course of the ascending aorta, arch of the aorta, descending thoracic aorta and abdominal aorta, up to the common iliac artery [Table/Fig-1a-d]. An extension of the flap transversely into the left sinus of Valsalva, involving the osteoproximal segment of the left main coronary artery, was observed [Table/Fig-2]. Diffuse consolidations involving bilateral perihilar regions of both lung fields suggested pulmonary oedema [Table/Fig-3a]. Bilateral pleural effusions were also noted [Table/Fig-3b]. Despite the immediate initiation of antihypertensive therapy and arrangements for surgical consultation, the patient’s condition rapidly deteriorated. She developed profound hypotension and loss of consciousness within two hours of admission. Despite aggressive resuscitative measures, including fluid resuscitation and vasopressor support, the patient could not be stabilised. Cardiopulmonary resuscitation was initiated, but unfortunately, the patient succumbed to cardiac arrest.

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