Objectives: 1) To present a case of a patient with aortic dissection. 2) To show how the case arrived to its plausible diagnosis. 3) To discuss other illnesses discovered in the case. Case Summary This is a case of a 54-year old, female, Filipino, Catholic, who presented with severe chest pain, substernal in location, with pain intensity of 8/10 associated with diaphoresis and dyspnea leading to fainting spells. Initial impression was cardiogenic shock secondary to Non-ST elevated myocardial infarction. On physical examination, the patient was drowsy and in cardio-respiratory distress. She had symmetrical chest expansion and no retractions were noted. Clear breath sounds were noted in all lung fields. She had an adynamic precordium with normal rate and regular rhythm, however with distant heart sounds. There was no murmur, heave or thrill appreciated. Vital signs at the emergency room showed a blood pressure of 110/80 which eventually became 80/50 mmH, respiratory rate of 22 cycles per minute, heart rate of 80-100 beats per minute and was febrile. Patient was scheduled for a stat coronary angiography, however on further reassessment, repeat ECG showed resolution of the inferolateral wall ischemia but this could not explain her fluctuating blood pressure. When the patient underwent the scheduled bedside 2D echo, a moderate cardiac tamponade was discovered with a 4.5 cm aortic dissection. With these findings, patient underwent aortic repair, graft insertion with evacuation of hematoma. She was discharged stable and with no recurrence of chest pain.
Cardiac Tamponade ; Aortic Dissection

Humans ; Aortic Dissection ; Aorta

Aortic Dissection/complications* ; Aortic Rupture/etiology* ; Humans

Aortic Dissection ; Aortic Aneurysm, Thoracic ; Humans ; Models, Theoretical

Humans ; Aortic Dissection/surgery* ; Aortic Rupture/surgery* ; Death ; Treatment Outcome

Aortic Dissection/surgery* ; Aortic Aneurysm, Thoracic/surgery* ; Blood Vessel Prosthesis Implantation ; Endovascular Procedures ; Humans ; Treatment Outcome

OBJECTIVE: To explore whether the differentiation of vascular stem cells (VSC) into smooth muscle cells (SMC) in aortic dissection (AD) is dysregulated, and to verify the role of Notch3 pathway in this process. METHODS: Aortic tissues were obtained from AD patients undergoing aortic vascular replacement and heart transplant donors at Department of Cardiovascular Surgery, Guangdong Provincial People's Hospital Affiliated to Southern Medical University. VSC were isolated by enzymatic digestion and c-kit immunomagnetic beads. The cells were divided into normal donor-derived VSC group (Ctrl-VSC group) and AD-derived VSC group (AD-VSC group). The presence of VSC in the aortic adventitia was detected by immunohistochemical staining, and VSC was identified by stem cell function identification kit. The differentiation model of VSC into SMC established in vitro was induced by transforming growth factor-β1 (10 μg/L) for 7 days. They were divided into normal donor VSC-SMC group (Ctrl-VSC-SMC group), AD VSC-SMC group (AD-VSC-SMC group) and AD VSC-SMC+Notch3 inhibitor DAPT group (AD-VSC-SMC+DAPT group,DAPT 20 μmol/L was added during differentiation induction). The expression of contractile marker Calponin 1 (CNN1) in SMC derived from aortic media and VSC were detected by immunofluorescence staining. The protein expressions of contractile markers α-smooth muscle actin (α-SMA), CNN1 as well as Notch3 intracellular domain (NICD3) in SMC derived from aortic media and VSC were detected by Western blotting. RESULTS: Immunohistochemical staining showed there was a population of c-kit-positive VSC in the adventitia of aortic vessels, and VSC from both normal donors and AD patients had the ability to differentiate into adipocytes and chondrocytes. Compared with normal donor vascular tissue, the expressions of SMC markers α-SMA and CNN1 of tunica media contraction in AD were down-regulated (α-SMA/β-actin: 0.40±0.12 vs. 1.00±0.11, CNN1/β-actin: 0.78±0.07 vs. 1.00±0.14, both P < 0.05), while the protein expression of NICD3 was up-regulated (NICD3/GAPDH: 2.22±0.57 vs. 1.00±0.15, P < 0.05). Compared with Ctrl-VSC-SMC group, the expressions of contractile SMC markers α-SMA and CNN1 were down-regulated in AD-VSC-SMC group (α-SMA/β-actin: 0.35±0.13 vs. 1.00±0.20, CNN1/β-actin: 0.78±0.06 vs. 1.00±0.07, both P < 0.05), the protein expression of NICD3 was up-regulated (NICD3/GAPDH: 22.32±1.22 vs. 1.00±0.06, P < 0.01). Compared with AD-VSC-SMC group, the expressions of contractile SMC markers α-SMA, CNN1 were up-regulated in AD-VSC-SMC+DAPT group (α-SMA/β-actin: 1.70±0.07 vs. 1.00±0.15, CNN1/β-actin: 1.62±0.03 vs. 1.00±0.02, both P < 0.05). CONCLUSIONS Dysregulation of VSC differentiation into SMC occurs in AD, while inhibition of Notch3 pathway activation can restore the expression of contractile proteins in VSC-derived SMC in AD.
Humans ; Actins ; Platelet Aggregation Inhibitors ; Signal Transduction ; Aortic Dissection ; Cell Differentiation ; Myocytes, Smooth Muscle ; Stem Cells

Objective: Near-infrared spectroscopy (NIRS) is widely used for intraoperative cerebral oxygen saturation monitoring in patients with acute type A aortic dissection. This study aimed to investigate the correlation between NIRS-derived oxygen saturation and risk of postoperative stroke. Methods: This study included 193 patients with acute type A aortic dissection undergoing emergency surgery and elective unilateral cerebral perfusion via the right axillary artery at the Department of Cardiothoracic Surgery, Nanjing Drum Tower Hospital, Nanjing, China, from 2018 to 2020. NIRS was used for intraoperative cerebral oxygen saturation monitoring, and the basal values and the lowest values of cerebral oxygen saturation during deep hypothermic circulatory arrest (DHCA) were recorded. The patients were divided into no-stroke group (n=178, 92.2%) and stroke group (n=15, 7.8%) according to the absence or presence of postoperative stroke. The differences in preoperative, operative and postoperative clinical differences between the two groups were compared, and the relationship between the lowest cerebral oxygen saturation value and the change in cerebral oxygen saturation value ((base-lowest)/basal) and postoperative stroke were analyzed. Results: The proportion of preoperative atrial fibrillation (6.7% vs. 0.6%, P=0.026), and the proportion of preoperative hypotension (26.7% vs. 9.0%, P=0.031) were significantly higher in the stroke group than no-stroke group. There were no differences in the surgical approach between the two groups. Cardiopulmonary bypass (CPB) time ((256.1±84.8) h vs.(217.8±58.4) h, P=0.020), postoperative mechanical ventilation time ((139.3±172.8) h vs. (35.6±45.6) h, P<0.001) were significantly longer in stroke group as compared to no-stroke group. Incidence of postoperative tracheotomy (20.0% vs. 1.1%, P<0.001), acute kidney injury (73.3% vs. 30.3%, P=0.001) and continuous renal replacement therapy (46.7% vs. 11.8%, P<0.001) as well as mortality (20.0% vs. 5.1%, P=0.022) were significantly higher in the stroke group than in non-stroke group. There was no significant difference in the basal NIRS value and the lowest NIRS value during DHCA between the two groups. Patients in the stroke group had a significantly greater intraoperative change rate of right NIRS as compared to no-stroke group (15.2%±15.7% vs. 9.2%±7.0%, P=0.006). Conclusions: NIRS is valuable for monitoring cerebral oxygen saturation during acute type A aortic dissection surgery, and the rate change of NIRS during operation correlates significantly with postoperative stroke.
Aortic Dissection/surgery* ; Humans ; Monitoring, Intraoperative/methods* ; Oxygen ; Oxygen Saturation ; Spectroscopy, Near-Infrared/methods* ; Stroke

Thoracic aortic dissection (TAD) is one of the most lethal aortic diseases due to its acute onset, rapid progress, and high rate of aortic rupture. The pathogenesis of TAD is not completely understood. In this mini-review, we introduce three emerging experimental mouse TAD models using β-aminopropionitrile (BAPN) alone, BAPN for a prolonged duration (four weeks) and then with added infusion of angiotensin II (AngII), or co-administration of BAPN and AngII chronically. We aim to provide insights into appropriate application of these three mouse models, thereby enhancing the understanding of the molecular mechanisms of TAD.
Aminopropionitrile/toxicity* ; Aortic Dissection/pathology* ; Angiotensin II/toxicity* ; Animals ; Aortic Aneurysm, Thoracic/pathology* ; Disease Models, Animal ; Male ; Mice ; Mice, Inbred C57BL

Humans ; Endovascular Aneurysm Repair ; Stents ; Blood Vessel Prosthesis ; Aortic Dissection/surgery* ; Endovascular Procedures ; Aortic Aneurysm, Thoracic/surgery* ; Treatment Outcome ; Blood Vessel Prosthesis Implantation ; Retrospective Studies