Master of the Masquerade: An Atypical Presentation of Acute Aortic Dissection.
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ABSTRACT:
SUBMITTER: Mando R
PROVIDER: S-EPMC7054764 | biostudies-literature | 2020
REPOSITORIES: biostudies-literature
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Master of the Masquerade: An Atypical Presentation of Acute Aortic Dissection.
Mando Ramy R Tim Daniel D DeCicco Anthony A Trivax Justin J Hanson Ivan I
Case reports in cardiology 20200220
Acute aortic dissection (AAD) is associated with unacceptably high mortality rate. As such, early diagnosis and aggressive management are essential in order to avoid life-threatening complications. Herein, we report an atypical presentation of AAD and clinical sequelae. ...[more]
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Project description:Acute type A aortic dissection (ATAAD) is a life-threatening disease. The understanding of its pathogenesis and treatment approaches remains unclear. In the present work, differentially expressed genes (DEGs) from two ATAAD datasets GSE52093 and GSE98770 were filtered. Transcription factor TEAD4 was predicted as a key modulator in protein-protein interaction (PPI) network. Weighted correlation network analysis (WGCNA) identified five modules in GSE52093 and four modules in GSE98770 were highly correlated with ATAAD. 71 consensus DEGs of highly correlated modules were defined and functionally annotated. L1000CDS2 was executed to predict drug for drug repositioning in ATAAD treatment. Eight compounds were filtered as potential drugs. Integrative analysis revealed the interaction network of five differentially expressed miRNA and 16 targeted DEGs. Finally, master DEGs were validated in human ATAAD samples and AD cell model in vitro. TIMP3 and SORBS1 were downregulated in ATAAD samples and AD cell model, while PRUNE2 only decreased in vitro. Calcium channel blocker and glucocorticoid receptor agonist might be potential drugs for ATAAD. The present study offers potential targets and underlying molecular mechanisms ATAAD pathogenesis, prevention and drug discovery.
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Project description:BackgroundType A acute aortic dissection (AAD) is an extremely severe condition, having a high risk of mortality. Initial diagnosis can be deceptive, especially in patients with other confounding presentations.Case summaryWe present the case of a 60-year-old male with a history of endovascular aortic repair for abdominal aortic dissection, in whom a diagnosis of AAD was made, but almost missed, after he presented with stroke signs and left coronary myocardial infarction. Thorough clinical evaluation and point-of-care ultrasound (POCUS) were fundamental to the diagnosis of the underlying condition, which showed the intimal flap in the ascending aorta, aortic insufficiency, and a dissected left common carotid artery. The diagnosis was confirmed with a head and thoracic computed tomography scan, which also showed bilateral haemorrhagic strokes. Treatment options can be limited in patients with AAD with associated complications. After a careful multidisciplinary evaluation, life-sustaining therapy was withdrawn and the patient passed away.DiscussionOur case depicts the diagnosis challenge presented by patients with AAD. We emphasize the importance of clinical suspicion and POCUS examination for the diagnosis of the underlying condition, as it is frequently missed during first evaluation. We discuss the available literature regarding the prevalence and described mechanisms by which AAD can associate occlusion myocardial infarction, which more commonly involves the right coronary artery, as well as haemorrhagic stroke. We briefly mention management options, which are limited and controversial.
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Project description:Acute aortic dissection (AAD) is one of the major aortic diseases that occurs without a preceding symptom and often results in sudden death. Despite the recent advances in cardiovascular medicine, AAD remains a serious problem because its molecular pathogenesis is largely unknown. In this paper, we report our serendipitous discovery that stress-induced expression of tenascin C (TNC), a member of matricellular proteins, is the protection mechanism of aorta to prevent AAD. The aortic wall stress imposed by the aortic stiffening and the angiotensin II infusion caused the strong induction of TNC in wild type mouse aorta without gross morphological changes. While TNC knockout mice at the baseline showed no morphological, histological or biomechanical abnormalities of aorta, deletion of TNC gene rendered the aorta susceptible to AAD upon the aortic stress. The stressed TNC-null aorta showed the loss of the tensile strength due to the insufficient expression of extracellular matrix proteins and the exaggerated proinflammatory response before the onset of AAD. Therefore, TNC works as a stress-activated molecular damper both by reinforcing the tensile strength and by limiting the excessive proinflammatory response in aorta. Thus far, the molecular event that leads to the AAD development has been unclear because of the unpredictable nature of the AAD onset. This study sheds light on the previously unrecognized tissue protection mechanism that converts the potentially harmful stress response into the active reinforcement of the aorta, of which failure leads to the development of AAD. Although TNC is expressed in various tissues upon the mechanical and proinflammatory stimuli, its role has long been a mystery. Our data uncovered the adaptive role of TNC in aorta that must be resilient to the continuous hemodynamic and humoral stress for lifetime. We used periaortic application of 0.5 M CaCl2 to the infrarenal aorta or either wild type (WT) or tenascin C knockout (TNC-KO) mice to create the mouse model for stiffened aorta and infused the mice with AngII (1 µg/min/kg) for 1 week to apply the pathological stress on aorta (Ca+AngII). Mice were then killed with an overdose of pentobarbital to obtain the tissue samples. The suprarenal aortic samples, from the level of right renal artery to 10 mm above the right renal artery, and infrarenal aortic samples, from the level of left renal artery to 10 mm below the left renal artery, were collected and kept in RNAlater (Qiagen) until the extraction of total RNA using RNeasy (Qiagen). We obtained the RNA samples from 8 mice with Ca+AngII treatment and 5 mice without Ca+AngII treatment for each genotype. We pooled the RNA samples with the identical experimental condition to perform the transcriptome analysis using Mouse Genome 430 2.0 (Affymetrix). We obtained suprarenal aortic smooth muscle cells (ASMCs) from TNC-KO mice by enzymatic dispersion and cultured them in Dulbecco's modified Eagle medium (DMEM) supplemented with 10% fetal bovine serum. We cultured TNC-KO ASMCs in the presence or absence of exogenous TNC (10 µg/mL) and stimulated the cells with 10 ng/mL TNF-alpha for 24 h before obtaining total RNA using RNeasy. We used 3 independent ASMC cultures without the exogenous TNC and 4 independent cultures with the exogenous TNC. We hybridized each of the RNA samples individually to Mouse Genome 430 2.0 Array (Affymetrix).
2015-03-27 | E-GEOD-36899 | biostudies-arrayexpress
Project description:ObjectiveAortic calcification (AC) is associated with increased risks of cardiovascular events and mortality. Numerous studies have explored the association between calcification and abdominal artery aneurysm. However, evidence regarding the association between AC and acute aortic dissection (AAD) is limited. We aimed to evaluate the association between AC-related variables and the development of intimal tear (IT) in patients with AAD.MethodsWe conducted a retrospective observational study involving 64 patients with type A AAD and 32 patients with type B AAD from February, 2011 to January, 2017 at a tertiary referral medical center in Taiwan. We used the default analysis module "calcification score analysis" to calculate all the calcification variables, including AC scores and volume.ResultsWe identified an association between AC and AAD. Patients with AAD had a greater AC volume in the aortic arch and greater AC scores for both the ascending aorta and the aortic arch than did patients without AAD. However, hypertension and coronary artery disease, rather than AC remained to be the independent risk factor for AAD in multivariate analysis. Patients with type A AAD had greater mean and cumulative AC volumes in the aortic arch, greater cumulative AC volumes in the whole aorta and higher cumulative AC scores in the aortic arch than did patients with type B AAD. ACs were superimposed on ITs in nearly half of the patients with AAD. In patients with type A AAD, AC was more commonly located distal to the IT and farther from the IT.ConclusionsWe identified the associations between AC-related variables and the location of IT in patients with AAD. However, AC was not an independent risk factor for AAD. The distribution of AC was different between patients with type A and type B AAD.
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Project description:Background Octogenarians (≥80 years old) are high-risk patients for acute aortic dissection (AAD) surgery. However, no population-based study has investigated the late outcomes of AAD surgery in octogenarians. This study aimed to investigate the late outcomes of AAD surgery in octogenarians. Methods and Results A total of 3998 patients who received AAD surgery from 2005 to 2013 were identified from the Taiwan National Health Insurance Research Database. In-hospital complications and late outcomes including all-cause mortality, major adverse cardiac and cerebrovascular event, respiratory failure, and redo aortic surgery were evaluated. The risks of late outcomes between octogenarians and nonoctogenarians were compared using the multivariable Cox proportional hazard model or Fine and Gray competing model. The numbers of the octogenarians who underwent type A and B AAD surgeries were 206 (6%; 206/3423) and 79 (13.7%; 79/575), respectively. Compared with the nonoctogenarians, the type A octogenarians had higher risks of in-hospital mortality and several in-hospital complications, whereas the type B octogenarians did not. Furthermore, compared with the nonoctogenarians, the type A octogenarians had a higher risk of all-cause mortality (61.7% vs 32.5%; hazard ratio [HR], 2.35; 95% CI, 1.95-2.84) and a higher cumulative incidence of major adverse cardiac and cerebrovascular event and respiratory failure, and the type B octogenarians demonstrated a higher risk of all-cause mortality (44.3% vs 30.4%; HR, 1.74; 95% CI, 1.18-2.55). The octogenarians receiving AAD surgeries had higher mortality rates than the normal octogenarian population. Conclusions Octogenarians receiving AAD surgeries exhibit worse late outcomes than nonoctogenarian counterparts.
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