Acute Aortic Dissection Group Research Articles

Pericoronary adipose tissue attenuation in patients with acute aortic dissection based on coronary computed tomography angiography.

Periaortic fat is associated with coronary disease. Thus, it was hypothesized that the inflammation associated with acute aortic dissection (AAD) spreads to pericoronary adipose tissue (PCAT) via thoracic periaortic fat. Pericoronary adipose tissue attenuation (PCATa) serves as a marker for inflammation of perivascular adipose tissue (PVAT). This study sought to examine PCATa in individuals diagnosed with AAD. Consecutive patients with chest pain from May 2020 to September 2022 were prospectively enrolled in this study and underwent coronary computed tomography angiography (CCTA) and/or aorta computed tomography angiography (CTA). Based on the results of the CTA, the patients were divided into the following two groups: (I) the AAD group; and (II) the non-AAD group. PCATa of the right coronary angiography (RCA), left anterior descending (LAD), and left circumflex (LCx) was quantified for each patient using semi-automated software. The PCATa values were compared between the AAD and non-AAD patients according to the atherosclerosis of the coronary arteries. Similarly, the PCATa values of the AAD patients were compared between the preoperative and postoperative steady states. A total of 136 patients (42 female, 94 male; mean age: 63.3±11.9 years) were divided into the two groups according to the presence of aortic dissection on CTA. The RCAPCATa, LADPCATa, and LCxPCATa values were significantly higher in the AAD subjects than the non-AAD subjects, regardless of the presence or absence of atherosclerosis in the coronary arteries [-85.1±9.3 vs. -92.9±10.0 Hounsfield unit (HU); -83.2±7.4 vs. -89.9±9.1 HU; -77.5±8.4 vs. -85.6±7.9 HU, all P<0.001). The preoperative RCAPCATa, LADPCATa, and LCxPCATa values were higher in the AAD patients than the postoperative steady-state patients (-82.9±8.7 vs. -97.6±8.8 HU; -79.8±7.6 vs. -92.8±6.8 HU; -74.6±7.1 vs. -87.7±6.9 HU, all P<0.001). According to the multivariable logistic regression analysis, high RCAPCATa and LADPCATa values were associated with AAD regardless of the degree of stenosis [odds ratio (OR) =0.014; 95% confidence interval (CI): 0.001-0.177; P=0.001 and OR =0.010; 95% CI: 0.001-0.189; P=0.002]. PCATa on computed tomography was increased in patients with AAD regardless of the presence or absence of coronary artery disease (CAD). This suggests that vascular inflammation is present in AAD independent of CAD. Further research should be conducted to investigate the potential of this imaging biomarker to predict AAD and monitor patients' responses to therapies for AAD.

Where next for type B aortic dissection?

In April 2021 the acute aortic dissection toolkit was launched by NHS England.1 It was designed to improve the care of patients with acute aortic dissection (AD) by raising awareness of the condition and introduced seven key principles of management including better governance, 24/7 rotas and specialist care. Each NHS region in England was encouraged to form an AD group, benchmark their current service against the toolkit principles and then try to improve their management of these patients by addressing deficiencies. The toolkit provided tools for self-assessment together with protocols to improve deficiencies by sharing best practice. A regular series of regional meetings has been held with clinicians and managers to advise and help progress – engagement with the process and feedback has been good. National key performance indicators are being developed to monitor the overall effect of the toolkit. Although the toolkit applies to all dissections, there is inevitably a bias towards management of type A dissections because many need urgent cardiac surgical repair. So where next and what about type B dissections?

Serum Sema7A is increased in patients with acute aortic dissection

ABSTRACT Background To observe the level of serum Sema7A in acute aortic dissection (AAD) and its diagnostic value for AAD. Research design and methods Patients with sudden chest pain including AAD, acute myocardial infarction (AMI) or pulmonary embolism (PE) were enrolled. Patients without chest pain or cardiovascular diseases were included as the controls. Serum Sema7A and plasma D-dimer were detected and compared in each group. Results 85 AAD patients, 55 AMI patients, 15 PE patients, and 30 controls were enrolled. The concentration of Serum Sema7A in the AAD group was significantly higher than that in the control, AMI and PE group. Serum Sema7A was positively correlated with D-dimer. In AAD patients who underwent invasive intervention therapy, serum Sema7A levels were significantly decreased after the intervention. Serum Sema7A was an independent risk factor for the presence of AAD. The areas under the ROC curve of Sema7A and D-dimer for differential diagnosis of AAD from other chest pain disorders were 0.842 (0.776, 0.909) and 0.788 (0.714, 0.862), respectively. Conclusions Sema7A is highly expressed in patients with AAD. Sema7A might be a valuable biomarker for the early diagnosis of AAD and has the potential to differentiate AAD from AMI and PE.

Analysis on tissue-related biomarkers in patients with acute aortic dissection

Objective: To explore the clinical implication of tissue-related biomarkers in patients with acute aortic dissection (AAD). Methods: It was a cross-sectional study. Ten Stanford Type A AAD patients, who were diagnosed and surgically treated in the Department of Cardiology, First Affiliated Hospital of Xinjiang Medical University, from December 2018 to August 2019, were selected as the case group. Meanwhile, 10 patients with atherosclerotic heart disease, who underwent coronary artery bypass grafting (CABG), were selected as control group. The ascending aorta tissue specimens from patients of the two groups were collected during the operation. Four-dimensional non-standard quantitative proteomics technology (4D-LFQ) was used to detect the protein profile of ascending aorta tissue specimens of the two groups and to screen out differentially expressed proteins and analyze their biological functions. Precise quantification of the selected target proteins was achieved by parallel response monitoring (PRM). Results: A total of 3 985 proteins were identified by 4D-LFQ technology, among which 3 350 proteins could be quantified. There were 39 proteins were significantly upregulated and 47 proteins were significantly downregulated in AAD group. The results of biological function analysis showed that most of the differentially expressed proteins were located in the extracellular, and their functions were mainly involved in cell migration and proliferation, inflammatory cell activation, cell contraction, and muscle organ development. The 15 selected proteins underwent precise quantification by PRM, and the results showed that integrin α-Ⅱb (ITGA2B), integrin α-M (ITGAM), integrin β-2 (ITGB2), integrin β-3 (ITGB3) were significantly upregulated in the ascending aorta tissue of AAD patients. Conclusion: ITGA2B, ITGAM, ITGB2, and ITGB3 are highly expressed in aortic tissues of patients with AAD, which may be used as biomarkers for the diagnosis of AAD patients.

Reduced Number and Activity of Circulating Endothelial Progenitor Cells in Acute Aortic Dissection and Its Relationship With IL-6 and IL-17.

This study investigates the alteration in function and number of circulating endothelial progenitor cells (EPCs) in patients with aortic dissection (AD), compared with hypertensive patients, and its possible mechanism. Thirty-four patients with acute aortic dissection (AAD) and 20 patients with primary hypertension were involved. Flow cytometry analysis was performed to detect the number of CD34+/KDR+ cells, and acetylated low density lipoprotein (ac-LDL) and lectin fluorescent staining method was applied to test the number of cultured EPCs. In addition, EPC migration and proliferation were measured, and plasma interleukin 6 (IL-6) and interleukin 17 (IL-17) levels were investigated. The number of circulating EPCs in the AAD group was lower than that in the non-AD group, and the proliferation and migration of circulating EPCs in the AAD group were lower than that in the non-AD group. In addition, the number, proliferation, and migration of circulating EPCs were significantly inversely correlated with the aortic dissection detection risk score (ADD-RS). More importantly, increased plasma IL-6 and IL-17 level was found in the AAD group, and the two inflammatory factors were inversely associated with the function and number of circulating EPCs in the AAD group. We first demonstrated that the number and function of circulating EPCs are reduced in the AAD group, which may be partly related to upregulated plasma IL-6 and IL-17. Our study provides novel insight on the underlying mechanism and potential therapeutic target of AAD.

Abstract 265: Extracorporeal Cardiopulmonary Resuscitation for Acute Aortic Dissection During Cardiac Arrest: A Nationwide Retrospective Observational Study

Aim: Acute aortic dissection has been considered a contraindication for extracorporeal cardiopulmonary resuscitation (ECPR). However, studies are lacking regarding the epidemiology and effectiveness of ECPR for this condition. We aimed to examine whether ECPR for acute aortic dissection during cardiac arrest is effective or not. Methods: Using the Japanese Diagnosis Procedure Combination inpatient database from July 2010 to March 2018, we identified all emergently hospitalized adults who received ECPR on the day of admission. ECPR was defined as receiving both chest compressions and percutaneous extracorporeal membrane oxygenation on the day of hospital admission. In-hospital mortality and neurological outcomes were compared between patients with and without acute aortic dissection. We also calculated the incremental cost-effectiveness ratio of ECPR for acute aortic dissection. Results: We identified 10,238 patients who received ECPR on the day of admission. Of these, 398 patients (3.9%) had acute aortic dissection. In-hospital mortality was 98% in the acute aortic dissection group and 79% in the non-acute aortic dissection group. Seven patients (1.8%) in the acute aortic dissection group survived to discharge after ECPR; of these, six patients had good neurological outcomes at discharge. The incremental cost-effectiveness ratio of ECPR for patients with acute aortic dissection was estimated at 159,337 US dollars per quality-adjusted life year gained. Conclusion: ECPR successfully rescued a small number of acute aortic dissection patients with cardiac arrest; however, the cost burden of ECPR for acute aortic dissection patients was unacceptably high.

Evaluation of Common Carotid Stiffness via Echo Tracking in Hypertensive Patients Complicated by Acute Aortic Dissection.

ObjectivesTo evaluate the common carotid stiffness via echo tracking in patients with hypertension and acute aortic dissection (AD) and to investigate the independent predictors for the occurrence of AD in hypertensive (HP) patients.MethodsFifty HP patients complicated by acute AD (AD group), 50 HP patients without AD (HP group), and 50 age‐matched healthy volunteers (control group) were enrolled to assess the common carotid stiffness index (β), single‐point pulsed wave velocity (PWVβ), and arterial compliance (AC) via echo tracking.ResultsThe intima‐media thickness, diameter, β and PWVβ of the common carotid artery (CCA) in the AD group were significantly higher than those in the HP and control groups, whereas AC in the AD group was significantly lower (P < .05). In a multivariate logistic regression analysis, the systolic blood pressure (SBP; odds ratio [OR], 2.316; 95% confidence interval [CI], 2.033–2.563; P < .001), β (OR, 2.140; 95% CI, 1.931–2.367; P < .001), PWVβ (OR, 1.212; 95% CI, 1.004–1.397; P = .023), and AC (OR, 0.565; 95% CI, 0.339–0.654; P < .001) were significantly related to the occurrence of AD in HP patients. The area under the curve values for the AC, SBP, β, and PWVβ were 0.822, 0.806, 0.778, and 0.741, respectively, and the area under the curve was up to 0.943 when these parameters were combined.ConclusionsThe compliance of the CCA decreased, and the stiffness of the CCA increased significantly in HP patients complicated by AD. The AC, β, and PWVβ of the CCA, together with the SBP, were independent predictors of the occurrence of AD in HP patients.

MicroRNA microarray analysis to detect biomarkers of aortic dissection from paraffin-embedded tissue samples.

The aim of this study was to explore the differential expression profiles of microRNAs (miRNAs) in paraffin-embedded acute aortic dissection (AAD) tissues to find potential biomarkers for this disease. A total of 92 paraffin-embedded tissue specimens were collected from 92 patients with AAD who underwent surgical replacement. Among these specimens, 54 had partial normal aortic segments (smooth intima surface, non-atherosclerotic lesions) in proximal crevasse of aorta. Samples of these segments were taken 1 cm away from aortic lesions as the control group, after eliminating the tunica adventitia tissues. miRNA expression profiles were obtained by miRNA microarray analysis. Differentially expressed miRNAs were found by comparing the AAD group with the control group and were verified by fluorescence real-time quantitative polymerase chain reaction and by fluorescence in situ hybridization. A total of 71 differentially expressed miRNAs were detected. Twenty-two were up-regulated and 49 were down-regulated. Four up-regulated miRNAs (hsa-miR-636, hsa-miR-142-3p, hsa-miR-425-3p, hsa-miR-191-3p) were selected for validation by real-time fluorescence quantitative polymerase chain reaction and fluorescence in situ hybridization. In the fluorescence real-time quantitative polymerase chain reaction analysis, only hsa-miR-636 showed a statistically significant difference in the AAD versus control comparison (3.3-fold, P = 0.012). The fluorescence in situ hybridization validation showed that the expression level of hsa-miR-636 was significantly increased in the AAD versus control comparison (P < 0.001), with average optical densities of 61.29 ± 16.83 in the AAD group and 9.30 ± 3.98 in the control group. Hsa-miR-636 is involved in the pathogenesis of AAD and may be a potential biomarker for this disease.

Identification of Vinculin as a Potential Diagnostic Biomarker for Acute Aortic Dissection Using Label-Free Proteomics.

Acute aortic dissection (AAD) is an emergent vascular disease. Currently, its diagnosis depends on clinical and radiological investigations but lacking of serum biomarkers. In this study, we aimed to identify potential serum biomarkers for AAD using label-free proteomics approach. A total of 90 serum samples were collected from three groups: patients with acute aortic dissection (AAD, n = 30), patients with acute myocardial infarction (AMI, n = 30), and healthy controls (n = 30), and the first four samples from each group were selected for label-free proteomics analysis. Using label-free approach, a total of 22 differentially expressed proteins were identified in the serum samples of the AAD group, of which 15 were upregulated and 7 were downregulated as compared to the AMI and healthy control groups. The most prominent increased protein was vinculin, which was selected to validate in total samples. The level of vinculin was significantly elevated in AAD patients (15.8 ng/ml, IQR: 9.3-19.9 ng/ml) than that in AMI patients (8.6 ng/ml, IQR:5.3-11.4 ng/ml) and healthy volunteers (5.3 ng/ml, IQR:2.8-7.6 ng/ml), P < 0.0001. Furthermore, the concentration of vinculin both increased in type A and B dissection. At the early stage of AAD, vinculin maintained a high level to 48 hours compared with that of AMI. Our study demonstrated that vinculin may play a role in the early diagnosis of AAD.

Changes in Aortic Wall Thickness at a Site of Entry Tear on Computed Tomography before Development of Acute Aortic Dissection.

Objective: To determine if there are changes in the aortic wall before acute aortic dissection (AD) that can be observed on contrast-enhanced computed tomography (CECT).Materials and Methods: Twenty-two patients with AD who underwent CECT before developing AD were retrospectively identified and enrolled as the AD group. Twenty-five consecutive patients who underwent CECT and did not develop AD were enrolled as the control group. In the AD group, the site of entry tear was detected on CECT images; the aortic wall thickness at this site, defined as the dissection-related wall thickness (D-T), was then measured on CECT images acquired before AD. Moreover, the mean thickness of the ascending, thoracic descending, and abdominal aortic walls before AD was defined as the non-dissection-related wall thickness (non-D-T). In the control group, the aortic wall thickness was measured similarly and defined as the control wall thickness (C-T). The D-T, non-D-T, and C-T values were compared using one-way analysis of variance with the Games–Howell pairwise comparison test.Results: The D-T (2.17±0.75 mm) was significantly greater than the non-D-T (1.58±0.22 mm; P<.01) and C-T (1.53±0.15 mm; P<.01).Conclusion: The aortic wall may have become thicker prior to the onset of AD.

Monocyte Subsets, Stanford-A Acute Aortic Dissection, and Carotid Artery Stenosis: New Evidences.

Monocytes are a heterogeneous cell population distinguished into three subsets with distinctive phenotypic and functional properties: “classical” (CD14++CD16-), “intermediate” (CD14++CD16+), and “nonclassical” (CD14+CD16++). Monocyte subsets play a pivotal role in many inflammatory systemic diseases including atherosclerosis (ATS). Only a low number of studies evaluated monocyte behavior in patients affected by cardiovascular diseases, and data about their role in acute aortic dissection (AAD) are lacking. Thus, the aim of this study was to investigate CD14++CD16-, CD14++CD16+, and CD14+CD16++ cells in patients with Stanford-A AAD and in patients with carotid artery stenosis (CAS). Methods. 20 patients with carotid artery stenosis (CAS group), 17 patients with Stanford-A AAD (AAD group), and 17 subjects with traditional cardiovascular risk factors (RF group) were enrolled. Monocyte subset frequency was determined by flow cytometry. Results. Classical monocytes were significantly increased in the AAD group versus CAS and RF groups, whereas intermediate monocytes were significantly decreased in the AAD group versus CAS and RF groups. Conclusions. Results of this study identify in AAD patients a peculiar monocyte array that can partly explain depletion of T CD4+ lymphocyte subpopulations observed in patients affected by AAD.

Identification of Lysophosphatidylcholines and Sphingolipids as Potential Biomarkers for Acute Aortic Dissection via Serum Metabolomics

Acute aortic dissection (AAD) is a severe clinical emergency with a high mortality, and is easily misdiagnosed in its early stage. This study aimed at discovering serum metabolomic markers with the potential to diagnose AAD and distinguish between two subtypes of AAD. Thirty-five patients with AAD, including 20 with Stanford type A and 15 with Stanford type B were enrolled in this study, together with 20 healthy controls. All patients with AAD were admitted within 72 h of onset. Serum metabolomics profiles were determined by ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry and the data were analysed by principal component analysis and partial least squares discriminant analysis. A total of 17 metabolites differing between the control and AAD groups were finally screened and identified as lysophosphatidylcholines (LPC) and sphingolipids including sphinganine, phytosphingosine, sphingomyelin, and ceramide. Compared with those in the healthy control group, LPC levels were significantly lower in both the Stanford type A and type B AAD groups. Interestingly, sphingolipids, including sphinganine, phytosphingosine, and ceramide, were remarkably reduced in the Stanford type A AAD group, but not in the Stanford type B AAD group. Subgroup analysis showed that the changes in LPC and sphingolipid levels were unrelated to hypertension or gender. The present results indicate that LPCs and sphingolipids are significantly altered in patients with AAD, and several sphingolipids, such as sphinganine, phytosphingosine, and ceramide, were dramatically decreased in patients with Stanford type A AAD. A combination of these two families of metabolites could serve as a potential biomarker for the diagnosis of AAD and distinguishing between Stanford type A and Stanford type B.

Stanford Tip B Akut Aortik Diseksiyon Hastalarında Kısa Orta Dönem Tedavi Sonuçlarımız.

Aim: Stanford Type B acute aortic dissection (Type B-AAD) has a higher mortality among the cardiovascular diseases and the complexity of its treatment is an important challenge. The duration of dissection, whether it is complicated or uncomplicated play a determinant role in the treatment of the disease. In this study, we evaluated the results of the patients that we followed and we treated due to the Type B acute aortic dissection.Materials and Methods: The study was conducted in a single center and retrospectively. The treatment strategy of the patients was determined with respect to be acute or chronic and to be complicated or uncomplicated. The patients were treated via medical treatment, thoracic endovascular aortic repair (TEVAR) or open surgery and then they were followed. The mortality and the morbidity causes of the patients were recorded.Result:Totally, 23 patients were treated due to Type B acute aortic dissection. The mean age of the patients was 58.21±14.17. The majority of the followed patients (16 patients (69.5%)) were followed with medical treatment. The patients who were followed with TEVAR treatment were in the second rank. The number of the TEVAR patients was 5 (21.7%). Two patients were treated with open surgery. 30-day survival was observed in 20 (86.9%) patients. The total mortality was seen in 3 (13%) patients.Conclusion: The twenty five percent of the patients who refer due to Type B acute aortic dissection admit due to malperfusion syndrome or hemodynamic instability. Organ malperfusion and hemodynamic instability are the most important causes of deaths of these patients. Hence, the early diagnosis of the patient and its optimal treatment is life-saving. If the patients who are treated due to the Type B acute aortic dissection are in uncomplicated type, medical treatment is in the forefront. In complicated patients, TEVAR or open surgery are recommended. In our Type B acute aortic dissection group which consists of 23 patients, the total mortality ratio was seen in 3 (13%) patients. The ratios for renal failure and for plegia were found as 4.3%. In thoracic endovascular aortic repair, no mortality was found.In conclusion, we primarily recommend conventional medical treatment for the patients in uncomplicated type in the treatment of the Type B acute aortic dissection patients. In the patients in complicated type we recommend TEVAR treatment. Since the necessary equipment for the TEVAR could not be ensured, we recommend open surgery for the emergency cases.

Identification of Lysophosphatidylcholines and Sphingolipids as Potential Biomarkers for Acute Aortic Dissection via Serum Metabolomics

Acute aortic dissection (AAD) is a severe clinical emergency with a high mortality, and is easily misdiagnosed in its early stage. This study aimed at discovering serum metabolomic markers with the potential to diagnose AAD and distinguish between two subtypes of AAD. Thirty-five patients with AAD, including 20 with Stanford type A and 15 with Stanford type B were enrolled in this study, together with 20 healthy controls. All patients with AAD were admitted within 72h of onset. Serum metabolomics profiles were determined by ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry and the data were analysed by principal component analysis and partial least squares discriminant analysis. A total of 17 metabolites differing between the control and AAD groups were finally screened and identified as lysophosphatidylcholines (LPC) and sphingolipids including sphinganine, phytosphingosine, sphingomyelin, and ceramide. Compared with those in the healthy control group, LPC levels were significantly lower in both the Stanford type A and type B AAD groups. Interestingly, sphingolipids, including sphinganine, phytosphingosine, and ceramide, were remarkably reduced in the Stanford type A AAD group, but not in the Stanford type B AAD group. Subgroup analysis showed that the changes in LPC and sphingolipid levels were unrelated to hypertension or gender. The present results indicate that LPCs and sphingolipids are significantly altered in patients with AAD, and several sphingolipids, such as sphinganine, phytosphingosine, and ceramide, were dramatically decreased in patients with Stanford type A AAD. A combination of these two families of metabolites could serve as a potential biomarker for the diagnosis of AAD and distinguishing between Stanford type A and Stanford type B.

Usefulness of Fibrinogen/Fibrin Degradation Products Value in Differential Diagnosis Between Acute Ischemic Stroke and Acute Aortic Dissection.

A post-marketing surveillance study reported fatalities following tissue plasminogen activator administration in acute aortic dissection (AAD) with the symptoms of acute ischemic stroke (AIS) patients. Therefore, it is important to discriminate AAD from AIS. The present study aimed to investigate whether fibrinogen/fibrin degradation products (FDP) value can be useful in differential diagnosis between AAD and AIS. The study group comprised 20 AAD patients (10 men and 10 women; age 63.9 ± 13.6 years) and 159 AIS patients (91 men and 68 women; age 74.2 ± 10.6 years) who were transported to our hospital from 2007 to 2012. The AAD cases were further divided into patent-type AAD and thrombosed-type AAD. FDP values were significantly higher in the AAD group than in the AIS group (18.15 [5.2 - 249.9] μg/ml vs. 2.3 [1.5 - 4.45] μg/ml ; P < 0.001). In AAD groups, FDP values were significantly higher in the patent-type AAD group (n = 9) than in the thrombosed type AAD group (n = 11) (293.2 μg/ml [63.1 - 419.6 μg/ml ] vs. 5.6 μg/ml [3.8 - 7.9 μg/ml ]. FDP values were significantly higher in patients with AAD than in those with AIS, especially those with patent-type AAD compared with AIS patients. High FDP values may be a useful marker for differential diagnosis between patent-type AAD and AIS.

Painless Acute Aortic Dissection May Present as a Stroke; Risky Markers that Could be Identified on Hospital Arrival.

Acute aortic dissection (AAD) is a life-threatening emergency. A small portion of AAD patients presents as an acute stroke without chest pain. A missed or delayed diagnosis of AAD often brings catastrophic outcome. We aimed to identify clinical markers suggestive of the presence of painless AAD in acute stroke patients. From January 2007 through December 2014, painless AAD patients were retrospectively collected from our stroke registry. We expanded the search by reviewing Medline and the Science Citation Index Expanded from 1981 until March 2015. We enrolled 200 consecutive cases of acute ischemic stroke without AAD as the control. Univariate analyses were performed to compare clinical markers, followed by logistic regression to analyze the markers with signifi cant differences. The AAD group had more female, younger patients and fewer co-morbidities. They more frequently had consciousness disturbances (p < 0.001), were brought to the hospital sooner (p < 0.001), arrived more frequently with impaired consciousness (p = 0.001), hypotension and bradycardia (p < 0.001) and left-sided weakness (70.2%; p < 0.001). In the risk factor analysis, hypotension (OR 48.86, 95% CI 5.70-420.28), bradycardia (OR 8.11, 95% CI 2.71-24.24), initial loss of consciousness (OR 5.27, 95% CI 1.88-14.76), andleft-sided weakness (OR 3.31, 95% CI 1.17-9.40) were observed more frequently in the AAD group. Consider to rule out a painless AAD in stroke patients presenting with hypotension, bradycardia, initial loss of consciousness, or left-sided weakness.

Prognostic Value of Neutrophil to Lymphocyte Ratio and Risk Factors for Mortality in Patients with Stanford Type A Aortic Dissection.

Neutrophil to lymphocyte ratio (NLR) is a prognostic predictor in a wide range of cardiovascular disease. Acute aortic dissection (AD) is an uncommon but fatal cardiovascular disease. In this study, we investigated both prognostic factors in patients with AD and whether NLR can be a predictor for mortality.Methods: We analyzed retrospectively the data of 57 patients with AD who had undergone emergent surgery in our hospital and included 128 consecutive patients with chest pain admitted to the emergency room as a control group. Also, patients who were operated on due to aortic dissection as another subgroup were compared to NLR values. Baseline clinical features, cardiovascular risk factors, and surgical and laboratory parameters were obtained from the hospital database.Results: Patients with AD had higher NLR than the control group (1.7 ± 0.5 versus 7.6 ± 3.3, P < .001). In the AD group, 15 deaths occurred and non-survivors had significantly higher NLR, compared to survivors (11.6 ± 2.4 versus 6.6 ± 2.3, P < .001). In multivariate analysis, high NLR (odds ratio [OR] 1.913, 95% CI 1.030-1.081, P = .04) and cross-clamp time (OR 1.265, 95% CI 1.003-1.596, P = .04) were determined as independent predictors of in-hospital mortality. In receiver operating characteristics curve analyses, the NLR > 9.3 predicted the mortality in AD with a specificity of 91% and a sensitivity of 86% (P < .001). This study shows that high NLR can be used as a marker for prognosis in short-term mortality of patient with AD. Additionally, increased lactate level in perioperative period, prolonged cardiopulmonary bypass time, and additional cardiac procedures are strong independent predictors of short-term mortality in patients with acute AD.

Consumption coagulopathy in acute aortic dissection: principles of management

BackgroundThe effect of acute aortic dissection itself on coagulopathy or surgery-related coagulopathy has never been specifically studied. The aim of the present study was to perioperatively describe consumption coagulopathy in patients with acute aortic dissection.MethodsSixty-six patients with acute type A aortic dissection were enrolled in this study from January 2015 to September 2016. Thirty-six patients with thoracic aortic aneurysms were used as a control group during the same period. Consumption coagulopathy was evaluated using standard laboratory tests, enzyme-linked immunosorbent assay and thromboelastograghy at five perioperative time-points.ResultsA significant reduction in clotting factors and fibrinogen was observed at the onset of acute aortic dissection. Enzyme-linked immunosorbent assay and thromboelastograghy also revealed a persistent systemic activation of the coagulation system and the consumption of clotting factors. In contrast, although platelet counts were consistently low, we did not find that platelet function was more impaired in the acute aortic dissection group than the control group.ConclusionsAfter surgery, clotting factors and fibrinogen were more impaired than platelet function. Thus, we proposed that hemostatic therapy should focus on the rapid and sufficient supplementation of clotting factors and fibrinogen to improve consumption coagulopathy in patients with acute aortic dissection.

Usefulness of Measuring the Serum Elastin Fragment Level in the Diagnosis of an Acute Aortic Dissection

Previous reports have shown that serum elastin fragments (SEFs) may be a useful biomarker for the diagnosis of an acute aortic dissection (AAD). However, because the reference interval of SEFs has not been established, it has not been determined whether SEFs are really useful for the diagnosis of AAD. The purpose of this study was to determine the usefulness of measuring SEFs for the diagnosis of AAD. A total of 42 consecutive patients aged 68 ± 18years who were diagnosed with an AAD were studied. Patient background and SEF levels were examined on admission. SEF levels were also measured in patients undergoing a medical examination (n= 531, age 54 ± 17years) to compare with those with an AAD. In the control group, SEF levels increased with age (R= 0.725, p<0.001). Then, we defined the upper limit of the reference interval of SEF levels as the 97.5th percentile of control SEF grouped by decade of life from the sixth to ninth decade. The overall risk of AAD exceeding the upper limit of the reference interval at each decade was 10% (4 of 42). For patients in their 60s and 70s, median SEF levels in the AAD group (89 [77 to 104], 93 [60 to 123] ng/ml, respectively) were not significantly higher than those in the control group (79 [68 to 92], 90 [79 to 106] ng/ml, respectively; p= 0.081 and 0.990, respectively). Our data suggest that measuring SEF levels may not be useful in the diagnosis of an AAD as the upper limit of the reference interval of the SEF level was unexpectedly higher.

Clinical characteristics and outcomes of patients with acute aortic dissection: impact of hypertension

To observe the clinical characteristics and outcomes of patients with acute aortic dissection (AAD) and explore the impact of hypertension. The present study enrolled 1 087 consecutive patients with AAD who were confirmed by computed tomographic scanning in Fuwai Hospital from January 2008 to December 2010. The major endpoints were in-hospital death and long-term mortality during follow up. A total of 595 (54.7%) patients were Stanford type A and 492 (45.3%) patients were Stanford type B. The median length of follow-up was 24.2 months (interquartile range 10.9, 40.8 months). The prevalence of hypertension was 67.4%(733 cases), and was significantly higher in type B patients than in type A patients (71.3%(351/492) vs. 64.2%(382/595), P=0.01). Regardless of Stanford classification, patients complicating with hypertension were older, had higher comorbidities (coronary heart diseases or diabetes), and less likely to receive surgical treatment compared with those without hypertension (all P<0.05). In Stanford type A AAD group, patients with hypertension had higher levels of admission blood pressure, serum creatinine and inflammatory markers (including WBC count, D-dimer and CRP) than those without hypertension (all P<0.05). In-hospital death (9.9% (38/382)vs. 5.6%(12/213), P=0.07) and long-term mortality (9.0% (31/344) vs. 8.9% (18/201), P=0.98) were similar in hypertensive and normotensive AAD type A patients. In type B AAD group, the in-hospital death rate was significantly higher in patients with hypertension than those without hypertension (5.4%(19/351) vs. 0.7%(1/141), P=0.02), while the long-term mortality was similar (6.9%(23/332) vs. 7.9%(11/140), P=0.71) between patients with and without hypertension. Multiple logistic regression analysis showed that hypertension did not predict the increased risk of in-hospital death of type A or type B AAD patients. The main protective factor of in-hospital mortality was operation in patients with type A AAD. The independent predictors of in-hospital death were age and surgical treatment in patients with type B AAD. Hypertension is a common co-morbidity in patients with AAD. AAD patients with hypertension are usually elder, have higher comorbidities of cardiovascular diseases, and less likely to receive surgical treatment compared with those without hypertension, but hypertension is not associated with increased risk of in-hospital and long-term mortality in both AAD type A and type B patients.