Clinical Characteristics, Incidences, and Mortality Rates for Type A and B Aortic Dissections: A Nationwide Danish Population-Based Cohort Study From 1996 to 2016.

BACKGROUND: Population-based epidemiologic studies of aortic dissections (ADs) are needed. This study aimed to report clinical characteristics, incidences, and mortality rates for adult patients admitted to Danish hospitals with type A AD (TAAD) or type B AD (TBAD) from 1996 through 2016. METHODS: We conducted a nationwide, population-based register study. All cases of AD registered with International Classification of Diseases, Tenth Revision codes in the Danish National Patient Registry at time of admission to a hospital with available medical records underwent validation. Data were merged between nationwide health registries including the cause of death registry. Patients with validated AD were matched 1:10 on sex and age with patients with hypertension from the general Danish population. RESULTS: Of 5018 registered cases of AD, 4183 cases underwent review and 3023 (60.2%) were validated as AD. After exclusions, the distribution of validated TAAD and TBAD was 1620 (60.5%) and 1059 (39.5%; P<0.001), 67.5% and 67.0% of patients were men, and mean ages at dissection were 63.5±12.9 and 67.5±12.2 years (P<0.001), respectively. The most prevalent comorbidities for TAAD were hypertension (55.2%), thoracic aortic aneurysms (14.6%), and chronic obstructive pulmonary disease (13.1%); for TBAD, the most prevalent comorbidities were hypertension (64.1%), aortic aneurysms at any location (7.5% to 12.0%), and chronic obstructive pulmonary disease (15.7%). The overall mean annual incidence rate was 4.2/100 000 patient-years. Incidence was significantly higher for TAAD (2.2/100 000) compared with TBAD (1.5/100 000; P<0.001). The 30-day mortality rates for validated TAAD and TBAD were 22.0% and 13.9% (P<0.001), respectively, with no significant changes over time or between sexes. Adjusted 5-year overall mortality rates for TAAD and TBAD were hazard ratio 3.2 (2.9 to 3.5; P<0.001; aortic-related cause of death, 57.0%) and hazard ratio 2.1 (1.9 to 2.4; P<0.001; aortic-related cause of death, 42.8%), respectively, compared with the general hypertensive population. Among patients who survived 30 days from dissection, the adjusted 5-year overall mortality rates were hazard ratio 1.1 (1.0 to 1.3; P=0.12; aortic-related cause of death, 23.2%) and hazard ratio 1.4 (1.2 to 1.6; P<0.001; aortic-related cause of death, 25.6%) for TAAD and TBAD, respectively. CONCLUSIONS: Hypertension, aortic aneurysms, and chronic obstructive pulmonary disease were the most prevalent comorbidities. The 30-day mortality frequencies were consistent over time with no significant differences between sexes. The 5-year mortality rate was higher for TAAD than TBAD. If the patient survived 30 days from dissection, the mortality rate for patients with TAAD was comparable with that of the general hypertensive population, but the mortality rate was significantly higher in patients with TBAD.

Blood Pressure, Hypertension, and the Risk of Aortic Dissection Incidence and Mortality: Results From the J-SCH Study, the UK Biobank Study, and a Meta-Analysis of Cohort Studies.

BACKGROUND: Hypertension or elevated blood pressure (BP) is an important risk factor for aortic dissection (AD); however, few prospective studies on this topic have been published. We investigated the association between hypertension/elevated BP and AD in 2 cohorts and conducted a meta-analysis of published prospective studies, including these 2 studies. METHODS: We analyzed data from the J-SHC study (Japan-Specific Health Checkups) and UK Biobank, which prospectively followed up 534 378 and 502 424 participants, respectively. Multivariable Cox regression was used to estimate hazard ratios and 95% CIs for the association of hypertension/elevated BP with AD incidence in the UK Biobank and AD mortality in the J-SHC Study. In the meta-analysis, summary relative risks were calculated with random-effects models. A potential nonlinear dose-response relationship between BP and AD was tested with fractional polynomial models, and the best-fitting second-order fractional polynomial regression model was determined. RESULTS: In the J-SHC study and UK Biobank, there were 84 and 182 ADs during the 4- and 9-year follow-up, and the adjusted hazard ratios of AD were 3.57 (95% CI, 2.17-6.11) and 2.68 (95% CI, 1.78-4.04) in hypertensive individuals, 1.33 (95% CI, 1.05-1.68) and 1.27 (95% CI, 1.11-1.48) per 20-mm Hg increase in systolic BP (SBP), and 1.67 (95% CI, 1.40-2.00) and 1.66 (95% CI, 1.46-1.89) per 10-mm Hg increase in diastolic BP (DBP), respectively. In the meta-analysis, the summary relative risks were 3.07 (95% CI, 2.15-4.38, I2=76.7%, n=7 studies, 2818 ADs, 4 563 501 participants) for hypertension and 1.39 (95% CI, 1.16-1.66, I2=47.7%, n=3) and 1.79 (95% CI: 1.51-2.12, I2 = 57.0%, n=3) per 20-mm Hg increase in SBP and per 10-mm Hg increase in DBP, respectively. The AD risk showed a strong, positive dose-response relationship with SBP and even more so with DBP. The risk of AD in the nonlinear dose-response analysis was significant at SBP >132 mm Hg and DBP >75 mm Hg. CONCLUSIONS: Hypertension and elevated SBP and DBP are associated with a high risk of AD. The risk of AD was positively dose dependent, even within the normal BP range. These findings provide further evidence for the optimization of BP to prevent AD.

Legumain Is an Endogenous Modulator of Integrin αvß3 Triggering Vascular Degeneration, Dissection, and Rupture.

BACKGROUND: The development of thoracic aortic dissection (TAD) is closely related to extracellular matrix degradation and vascular smooth muscle cell (VSMC) transformation from contractile to synthetic type. LGMN (legumain) degrades extracellular matrix components directly or by activating downstream signals. The role of LGMN in VSMC differentiation and the occurrence of TAD remains elusive. METHODS: Microarray datasets concerning vascular dissection or aneurysm were downloaded from the Gene Expression Omnibus database to screen differentially expressed genes. Four-week-old male Lgmn knockout mice (Lgmn-/-), macrophage-specific Lgmn knockout mice (LgmnF/F;LysMCre), and RR-11a-treated C57BL/6 mice were given BAPN (ß-aminopropionitrile monofumarate; 1 g/kg/d) in drinking water for 4 weeks for TAD modeling. RNA sequencing analysis was performed to recapitulate transcriptome profile changes. Cell interaction was examined in macrophage and VSMC coculture system. The reciprocity of macrophage-derived LGMN with integrin αvß3 in VSMCs was tested by coimmunoprecipitation assay and colocalization analyses. RESULTS: Microarray datasets from the Gene Expression Omnibus database indicated upregulated LGMN in aorta from patients with TAD and mice with angiotensin II-induced AAA. Elevated LGMN was evidenced in aorta and sera from patients with TAD and mice with BAPN-induced TAD. BAPN-induced TAD progression was significantly ameliorated in Lgmn-deficient or inhibited mice. Macrophage-specific deletion of Lgmn alleviated BAPN-induced extracellular matrix degradation. Unbiased profiler polymerase chain reaction array and Gene Ontology analysis displayed that LGMN regulated VSMC phenotype transformation. Macrophage-specific deletion of Lgmn ameliorated VSMC phenotypic switch in BAPN-treated mice. Macrophage-derived LGMN inhibited VSMC differentiation in vitro as assessed by macrophages and the VSMC coculture system. Macrophage-derived LGMN bound to integrin αvß3 in VSMCs and blocked integrin αvß3, thereby attenuating Rho GTPase activation, downregulating VSMC differentiation markers and eventually exacerbating TAD development. ROCK (Rho kinase) inhibitor Y-27632 reversed the protective role of LGMN depletion in vascular dissection. CONCLUSIONS: LGMN signaling may be a novel target for the prevention and treatment of TAD.

Microcalcification and Thoracic Aortopathy: A Window Into Disease Severity.

BACKGROUND: Patients with thoracic aortopathy are at increased risk of catastrophic aortic dissection, carrying with it substantial mortality and morbidity. Although granular medial calcinosis (medial microcalcification) has been associated with thoracic aortopathy, its relationship to disease severity has yet to be established. METHODS: One hundred one thoracic aortic specimens were collected from 57 patients with thoracic aortopathy and 18 control subjects. Standardized histopathologic scores, immunohistochemistry, and nanoindentation (tissue elastic modulus) were compared with the extent of microcalcification on von Kossa histology and 18F-sodium fluoride autoradiography. RESULTS: Microcalcification content was higher in thoracic aortopathy samples with mild (n=28; 6.17 [2.71-10.39]; P≤0.00010) or moderate histopathologic degeneration (n=30; 3.74 [0.87-11.80]; P<0.042) compared with control samples (n=18; 0.79 [0.36-1.90]). Alkaline phosphatase (n=26; P=0.0019) and OPN (osteopontin; n=26; P=0.0045) staining were increased in tissue with early aortopathy. Increasingly severe histopathologic degeneration was related to reduced microcalcification (n=82; Spearman ρ, -0.51; P<0.0001)-a process closely linked with elastin loss (n=82; Spearman ρ, -0.43; P<0.0001) and lower tissue elastic modulus (n=28; Spearman ρ, 0.43; P=0.026).18F-sodium fluoride autoradiography demonstrated good correlation with histologically quantified microcalcification (n=66; r=0.76; P<0.001) and identified areas of focal weakness in vivo. CONCLUSIONS: Medial microcalcification is a marker of aortopathy, although progression to severe aortopathy is associated with loss of both elastin fibers and microcalcification.18F-sodium fluoride positron emission tomography quantifies medial microcalcification and is a feasible noninvasive imaging modality for identifying aortic wall disruption with major translational promise.

Inherited Thoracic Aortic Disease: New Insights and Translational Targets.

Inherited thoracic aortopathies denote a group of congenital conditions that predispose to disease of the thoracic aorta. Aortic wall weakness and abnormal aortic hemodynamic profiles predispose these patients to dilatation of the thoracic aorta, which is generally silent but can precipitate aortic dissection or rupture with devastating and often fatal consequences. Current strategies to assess the future risk of aortic dissection or rupture are based primarily on monitoring aortic diameter. However, diameter alone is a poor predictor of risk, with many patients experiencing dissection or rupture below current intervention thresholds. Developing tools that improve the risk assessment of those with aortopathy is internationally regarded as a research priority. A robust understanding of the molecular pathways that lead to aortic wall weakness is required to identify biomarkers and therapeutic targets that could improve patient management. Here, we summarize the current understanding of the genetically determined mechanisms underlying inherited aortopathies and critically appraise the available blood biomarkers, imaging techniques, and therapeutic targets that have shown promise for improving the management of patients with these important and potentially fatal conditions.

Familial Clustering of Aortic Size, Aneurysms, and Dissections in the Community.

BACKGROUND: Ruptured aortic aneurysm and aortic dissections are potentially preventable disorders associated with high mortality. Screening of individuals at risk may translate into elective surgical interventions and lowered mortality. It is uncertain if the risk of aortic dilation of varying degrees aggregates within families. METHODS: We investigated the risk of having thoracic and abdominal aortic sizes in the highest quartile (measured by computed tomography scans and indexed for body size) if at least 1 parent did so in the Framingham Heart Study cohorts, and estimated the incidence rates and hazard ratios of developing aortic aneurysm or dissection among first-degree relatives of those with aortic aneurysm or dissection, in comparison with age- and sex-matched controls (1:10 for aortic aneurysm and 1:100 for aortic dissection) using the Danish nationwide administrative registries. RESULTS: In the Framingham Heart Study, offspring (n=235) whose parent(s) had a sex- and age-standardized aortic size in the upper quartile had a multivariable-adjusted ≈3-fold increased odds ratio of belonging to the upper quartile themselves. In Denmark, a total of 68 939 individuals (mean age, 42 years) had a first-degree relative with aortic aneurysm and 7209 persons (mean age, 39 years) had a first-degree relative with aortic dissection. During an average follow-up of 7 years, first-degree relatives of patients with aortic aneurysm and dissection had a hazard ratio of 6.70 (95% CI, 5.96-7.52) for developing aortic aneurysm and a hazard ratio of 9.24 (95% CI, 5.53-15.44) for dissection in comparison with matched controls. These estimates remained unchanged on adjusting for several comorbidities, including prevalent hypertension, bicuspid aortic valve, and the Marfan syndrome. For both aortic aneurysm and dissections, the absolute event rates approached 1 per 1000 person-years for first-degree relatives versus 11 to 13 (aortic aneurysm) and 2 to 3 (aortic dissections) per 100 000 person-years among controls. CONCLUSIONS: Increased aortic size, a precursor of aortic aneurysm and a risk factor for dissection, clusters in families. The incidence rates of aortic aneurysm and dissections approach the incidence rates of other common cardiovascular conditions in first-degree relatives, supporting the use of systematic screening for these conditions.

High Salt Intake Worsens Aortic Dissection in Mice: Involvement of IL (Interleukin)-17A-Dependent ECM (Extracellular Matrix) Metabolism.

OBJECTIVE: Aortic dissection (AD) is a fatal disease that occurs suddenly without preceding clinical signs or symptoms. Although high salt intake is a proposed risk factor for cardiovascular diseases, the relationship between AD and high salt intake has not been clarified. We examined the effect of high-salt challenge on a mouse AD model. Approach and Results: AD was induced in male mice by continuous infusion of ß-aminopropionitrile and Ang II (angiotensin II). High-salt challenge exacerbated aortic wall destruction in AD. Deletion of Il17a (IL-17KO [IL (interleukin)-17A knockout]) did not affect the AD phenotype at baseline, but it abolished the high salt-induced worsening of the aortic destruction. Unexpectedly, aortas of IL-17KO mice exhibited global changes in ECM (extracellular matrix)-related genes without alteration of proinflammatory genes, altered architecture of collagen fibers, and reduced stiffness before AD induction. The aortas of IL-17KO mice were less sensitive to AD-inducing stimuli, as shown by the induction of phenotypic modulation markers SMemb and vimentin, suggesting a reduced stress response. The aortas of IL-17KO mice had a higher population of smooth muscle cells with nuclear-localized phosphorylated Smad2, indicative of TGFß (transforming growth factor-beta) signal activation. Consistently, pretreatment of smooth muscle cells in culture with IL-17A blunted the activation of Smad2 by TGFß1. CONCLUSIONS: These findings indicate that high salt intake has a worsening effect on AD in the context of high aortic wall stiffness, which is under the control of IL-17A through ECM metabolism. Therefore, salt restriction may represent a low-cost and practical way to reduce AD risk.

Interfacility Transfer of Medicare Beneficiaries With Acute Type A Aortic Dissection and Regionalization of Care in the United States.

BACKGROUND: The feasibility and effectiveness of delaying surgery to transfer patients with acute type A aortic dissection-a catastrophic disease that requires prompt intervention-to higher-volume aortic surgery hospitals is unknown. We investigated the hypothesis that regionalizing care at high-volume hospitals for acute type A aortic dissections will lower mortality. We further decomposed this hypothesis into subparts, investigating the isolated effect of transfer and the isolated effect of receiving care at a high-volume versus a low-volume facility. METHODS: We compared the operative mortality and long-term survival between 16 886 Medicare beneficiaries diagnosed with an acute type A aortic dissection between 1999 and 2014 who (1) were transferred versus not transferred, (2) underwent surgery at high-volume versus low-volume hospitals, and (3) were rerouted versus not rerouted to a high-volume hospital for treatment. We used a preference-based instrumental variable design to address unmeasured confounding and matching to separate the effect of transfer from volume. RESULTS: Between 1999 and 2014, 40.5% of patients with an acute type A aortic dissection were transferred, and 51.9% received surgery at a high-volume hospital. Interfacility transfer was not associated with a change in operative mortality (risk difference, -0.69%; 95% CI, -2.7% to 1.35%) or long-term mortality. Despite delaying surgery, a regionalization policy that transfers patients to high-volume hospitals was associated with a 7.2% (95% CI, 4.1%-10.3%) absolute risk reduction in operative mortality; this association persisted in the long term (hazard ratio, 0.81; 95% CI, 0.75-0.87). The median distance needed to reroute each patient to a high-volume hospital was 50.1 miles (interquartile range, 12.4-105.4 miles). CONCLUSIONS: Operative and long-term mortality were substantially reduced in patients with acute type A aortic dissection who were rerouted to high-volume hospitals. Policy makers should evaluate the feasibility and benefits of regionalizing the surgical treatment of acute type A aortic dissection in the United States.

Outcomes of open repair of postdissection abdominal aortic aneurysms.

BACKGROUND: Evidence to guide management of postdissection abdominal aortic aneurysms (PDAAA) is lacking. This study describes the outcomes of open repair of PDAAA. METHODS: A retrospective cohort study was conducted of all consecutive patients treated with open repair for PDAAA after a Stanford type A or type B thoracic aortic dissection between January 2006 and December 2017 in two vascular referral centers. Preceding type B dissection treatment could include conservative or surgical management. Primary outcomes were 30-day mortality, complication rates, survival, and reintervention-free survival. Survival and reintervention-free survival were analyzed using the Kaplan-Meier method. Reintervention was defined as any endovascular or surgical intervention after the index procedure. RESULTS: Included were 36 patients (27 men [75%]) with a median age of 64 years (range, 35-81 years). The 30-day mortality was 2.7%. The median follow-up was 16 months (range, 0-88 months). The postoperative course was uneventful in 21 patients (58%). The most frequent complications were postoperative bleeding requiring repeat laparotomy (n = 4), pneumonia (n = 3), congestive heart failure (n = 2), new-onset atrial fibrillation (n = 2), mesenteric ischemia requiring left hemicolectomy (n=1), and ischemic cerebrovascular accident (n = 1). Renal failure requiring hemodialysis developed in one patient. The overall survival at 1 year was 88.8%. Reintervention-free survival was 95.5% after 1 year and 88.6% after 2 years. CONCLUSIONS: Open repair of PDAAA can be performed with a low mortality rate and an acceptable complication rate, comparable with elective open repair of abdominal aortic aneurysms without dissection.

Therapies for Thoracic Aortic Aneurysms and Acute Aortic Dissections.

Thoracic aortic aneurysms that progress to acute aortic dissections are often fatal. Thoracic aneurysms have been managed with treatment with ß-adrenergic blocking agents (ß-blockers) and routine surveillance imaging, followed by surgical repair of the aneurysm when the risk of dissection exceeds the risk for repair. Thus, there is a window to initiate therapies to slow aortic enlargement and delay or ideally negate the need for surgical repair of the aneurysm to prevent a dissection. Mouse models of Marfan syndrome-a monogenic disorder predisposing to thoracic aortic disease-have been used extensively to identify such therapies. The initial finding that TGFß (transformation growth factor-ß) signaling was increased in the aortic media of a Marfan syndrome mouse model and that its inhibition via TGFß neutralization or At1r (Ang II [angiotensin II] type I receptor) antagonism prevented aneurysm development was generally viewed as a groundbreaking discovery that could be translated into the first cure of thoracic aortic disease. However, several large randomized trials of pediatric and adult patients with Marfan syndrome have subsequently yielded no evidence that At1r antagonism by losartan slows aortic enlargement more effectively than conventional treatment with ß-blockers. Subsequent studies in mouse models have begun to resolve the complex molecular pathophysiology underlying onset and progression of aortic disease and have emphasized the need to preserve TGFß signaling to prevent aneurysm formation. This review describes critical experiments that have influenced the evolution of our understanding of thoracic aortic disease, in addition to discussing old controversies and identifying new therapeutic opportunities.

[Analysis of factors related to recanalization of intramural hematoma-type carotid artery dissection].

Objective: To investigate the factors related to recanalization of intramural hematoma-type carotid artery dissection (CAD). Methods: Retrospective analysis was performed on 56 patients (61 CADs) with intramural-hematoma type CAD confirmed by multimodal imaging examination based on cervical vascular ultrasound (CDU) in the Stroke Center of the First Affiliated Hospital of Suzhou University from August 2015 to May 2019. The clinical and imaging data were collected, and the time from onset to visit is bounded by 14 days. CDU follow-up was performed at 3, 6, and 12 months after the onset. According to the results of the 12-month follow-up, patients were divided into complete recanalization group and incomplete recanalization group. The clinical data, ultrasonic manifestations and drug treatment of patients between the two groups were compared. Multivariate logistic regression analysis was used to analyze the related factors affecting vascular recanalization. Results: Vascular recanalization: the rates of complete recanalization at 3, 6 and 12 months were 42.6% (26/61), 55.7% (34/61) and 59.0% (36/61), respectively. While among the 25 vessels in the incomplete recanalization group, 26.2% (16/61) showed residual stenosis and 14.8% (9/61) showed persistent occlusion. Comparison between the complete recanalization group and the incomplete recanalization group: the differences in the proportion of time from onset to visit ≤ 14 days, the echo type of intramural hematoma, and the proportion of vascular occlusion were statistically significant (all P<0.05). Multivariate logistic regression analysis showed that the time from onset to visit ≤14 days (OR=5.625, 95%CI: 1.302-24.293, P=0.021), and the hypoechoic intramural hematoma (OR=4.888, 95%CI: 1.304-18.320, P=0.019) were positively correlated with complete recanalization, while the dissection vascular occlusion (OR=0.234, 95%CI: 0.059-0.932, P=0.039) was negatively correlated with complete recanalization. Conclusions: CDU showed that hypoechoic intramural hematoma-type CAD treated with standard medications in the acute phase had a higher complete recanalization rate, while the recanalization rate of patients with dissecting vessel occlusion decreased. Early evaluation can provide a basis for clinical individualized treatment.

[Overview of multi-center registry of aortic dissection].

Aortic dissection is a life-threatening cardiovascular disease. Multi-center registration databases for aortic dissection have been established in many countries. The International Registry of Acute Aortic Dissection has produced a number of research results, which had a significant impact on the diagnosis and treatment of aortic dissection worldwide. The Society for Thoracic Surgeons Adult Cardiac Surgery Database summarizes perioperative data on aortic dissection. German Registry for Acute Aortic Dissection Type A has made remarkable achievements in the neurological protection and organ perfusion of type A aortic dissection. The Nordic Consortium for Acute Type A Aortic Dissection provides guidelines for perioperative administration of aortic dissection. However, the first Registry of Aortic Dissection in China (Sino-RAD) has not reported any new aortic dissection data in the past five years, although it has proposed a number of pathogenic characteristics of Chinese people. Therefore, it is necessary to establish our own aortic dissection database.

[Clinical analysis of 30 cases of traumatic aortic injury].

Objective: To examine the clinical treatment methods and short- and mid-term results of traumatic aortic injury (TAI). Methods: The clinical data of 30 patients suffering from TAI who were admitted to Department of Cardiothoracic Surgery, General Hospital of Eastern Theater Command from January 2010 to December 2018 were summarized and analyzed retrospectively. All patients were diagnosed as TAI by aortic CT angiography. There were 20 males and 10 females, aging (46.4±15.2) years (range: 17 to 76 years). One patient was diagnosed as extensive intramural hematoma (IMH). The other 29 cases had aortic intimal injury, and the primary intimal tear of all these patients was located in the isthmus of descending aorta. There were 2 cases of ulcer-like changes combined with IMH, and 27 cases of traumatic aortic dissection (TAD) including 23 cases of localized TAD and 4 cases of extensive TAD. Endovascular repair, artificial vascular replacement or conservative treatment were performed according to the patient's specific condition. The patients were followed up in outpatient or by telephone. The clinical data of all the patients of the in-hospital treatment and during follow-up period was analyzed retrospectively. Results: One patient with IMH was treated conservatively. Surgical intervention was performed in 29 cases with intimal injury, of which 14 cases underwent emergency surgery on the day of admission or the next day, and 15 cases underwent elective surgery. Twenty-seven cases underwent thoracic endovascular aortic repair (TEVAR), and 2 cases underwent artificial vascular replacement. Nine cases suffered combined operations in early or late stage. All patients were cured and discharged with in-hospital stay of (13.2±5.4) days (range: 7 to 30 days). There was no in-hospital death. Two patients underwent tracheotomy, and the rest had no serious complications. Up to the last follow-up in June 2019, 4 patients were lost to follow-up, and the remaining 26 patients were followed up for (50.6±34.1) months (range: 6 to 112 months) and survived healthily without new aortic events. Conclusions: Most of TAD cases are ascribed to Stanford type B aortic dissection, and a satisfactory short-term and mid-term result can be achieved by emergency TEVAR in most patients. Some patients can achieve good long-term results by open surgery with artificial vascular replacement.

[Surgical treatment for type Stanford A aortic dissection with Kommerell's diverticulum].

Objective: To examine the outcomes of surgical treatment in patients of type Stanford A aortic dissection with Kommerell's diverticulum. Methods: From January 2009 to August 2017, patients of type Stanford A aortic dissection with Kommerell's diverticulum who underwent the Sun procedure were enrolled. Patient demographic, preoperative, intraoperative, early morbidity and mortality data were collected from medical and electronic patient records. Clinical follow-up data, including late morbidity and mortality, were obtained by telephone interview with the patient. Results: A total of 13 patients (11 males and 2 females; mean age 47 years) were included. The mean maximum diameter of Kommerell's diverticulum was (21.8±7.7) mm. The Kommerell's diverticulum was repaired by direct suture of the orifice in 3 patients, ligation of the aberrant right subclavian artery in 9 patients, and suture and ligation in 1 patient, respectively. No perioperative death occurred. One patient underwent a reexploration for bleeding. There were 2 late deaths: unknown reason in 1 patient and septic shock secondary to renal abscess in 1 patient. Reintervention was performed in one patient for a persistent type Ⅱ endoleak. Conclusions: The Sun procedure with femoral artery cannulation for cardiopulmonary bypass, unilateral carotid artery cannulation for selective cerebral perfusion and ligation of aberrant right subclavian artery on the right side of the trachea is an appropriate therapeutic strategy for patients of type Stanford A aortic dissection with Kommerell's diverticulum.

Small GTP-Binding Protein GDP Dissociation Stimulator Prevents Thoracic Aortic Aneurysm Formation and Rupture by Phenotypic Preservation of Aortic Smooth Muscle Cells.

BACKGROUND: Thoracic aortic aneurysm (TAA) and dissection are fatal diseases that cause aortic rupture and sudden death. The small GTP-binding protein GDP dissociation stimulator (SmgGDS) is a crucial mediator of the pleiotropic effects of statins. Previous studies revealed that reduced force generation in aortic smooth muscle cells (AoSMCs) causes TAA and thoracic aortic dissection. METHODS: To examine the role of SmgGDS in TAA formation, we used an angiotensin II (1000 ng·min-1·kg-1, 4 weeks)-induced TAA model. RESULTS: We found that 33% of Apoe-/- SmgGDS+/- mice died suddenly as a result of TAA rupture, whereas there was no TAA rupture in Apoe-/- control mice. In contrast, there was no significant difference in the ratio of abdominal aortic aneurysm rupture between the 2 genotypes. We performed ultrasound imaging every week to follow up the serial changes in aortic diameters. The diameter of the ascending aorta progressively increased in Apoe-/- SmgGDS+/- mice compared with Apoe-/- mice, whereas that of the abdominal aorta remained comparable between the 2 genotypes. Histological analysis of Apoe-/- SmgGDS+/- mice showed dissections of major thoracic aorta in the early phase of angiotensin II infusion (day 3 to 5) and more severe elastin degradation compared with Apoe-/- mice. Mechanistically, Apoe-/- SmgGDS+/- mice showed significantly higher levels of oxidative stress, matrix metalloproteinases, and inflammatory cell migration in the ascending aorta compared with Apoe-/- mice. For mechanistic analyses, we primary cultured AoSMCs from the 2 genotypes. After angiotensin II (100 nmol/L) treatment for 24 hours, Apoe-/- SmgGDS+/- AoSMCs showed significantly increased matrix metalloproteinase activity and oxidative stress levels compared with Apoe-/- AoSMCs. In addition, SmgGDS deficiency increased cytokines/chemokines and growth factors in AoSMCs. Moreover, expressions of fibrillin-1 ( FBN1), α-smooth muscle actin ( ACTA2), myosin-11 ( MYH11), MYLLK, and PRKG1, which are force generation genes, were significantly reduced in Apoe-/- SmgGDS+/- AoSMCs compared with Apoe-/- AoSMCs. A similar tendency was noted in AoSMCs from patients with TAA compared with those from control subjects. Finally, local delivery of the SmgGDS gene construct reversed the dilation of the ascending aorta in Apoe-/- SmgGDS+/- mice. CONCLUSIONS: These results suggest that SmgGDS is a novel therapeutic target for the prevention and treatment of TAA.

Insights From the International Registry of Acute Aortic Dissection: A 20-Year Experience of Collaborative Clinical Research.

Acute aortic dissection (AAD) is a life-threatening condition associated with high morbidity and mortality rates, and it remains a challenge to diagnose and treat. The International Registry of Acute Aortic Dissection was established in 1996 with the mission to raise awareness of this condition and provide insights to guide diagnosis and treatment. Since then, >7300 cases have been included from >51 sites in 12 countries. Although presenting symptoms and physical findings have not changed significantly over this period, the use of computed tomography in the diagnosis has increased, and more patients are managed with interventional procedures: surgery in type A AAD and endovascular therapy in type B AAD; with these changes in care, there has been a significant decrease in overall in-hospital mortality in type A AAD but not in type B AAD. Herein, we summarized the key lessons learned from this international registry of patients with AAD over the past 20 years.

Filtered back projection revisited in low-kilovolt computed tomography angiography: sharp filter kernel enhances visualization of the artery of Adamkiewicz.

PURPOSE: The reliability of assessment of the artery of Adamkiewicz before the aortic repair is highly dependent on the display of the continuity of this artery with the aorta, mainly around the vertebral pedicle, by computed tomography angiography (CTA). We hypothesized that the sharp filter kernel can improve visualization of this continuity of the vessel structure because of its edge enhancement and high-spatial resolution. This study was performed to compare the subjective and objective image quality of spinal CTA reconstructed with sharp and smooth filter kernels. METHODS: We retrospectively reviewed 40 consecutive patients who had undergone 80-kV CTA to detect the artery of Adamkiewicz before aortic repair. We measured the CT number and the contrast-to-noise ratio of the anterior spinal artery to the spinal cord. Furthermore, the continuity of the artery of Adamkiewicz was evaluated using a 3-point scale (2 points, absolute; 0 points, undetectable). RESULTS: CTA with the sharp filter kernel showed a significantly higher CT number and contrast-to-noise ratio of the spinal artery than did CTA with the smooth filter kernel (P < .001 for both). Moreover, the sharp filter kernel showed a significantly higher continuity of the artery of Adamkiewicz with the aorta than did the smooth filter kernel (P < .001). CONCLUSIONS: The sharp filter kernel significantly improved the image quality in low-tube-voltage CTA for the assessment of the artery of Adamkiewicz. Thus, CTA with the sharp filter kernel can generate a high-confidence level in the evaluation of the artery of Adamkiewicz.

Aortic aneurysm and dissection in systemic lupus erythematosus.

Aortic aneurysm and dissection are rare complications of systemic lupus erythematosus (SLE). The incidence, etiology, risk factors, and outcomes of this entity were largely unknown.The study materials were based on the publications of aortic aneurysm or dissection due to SLE published between 2000 and 2017.A total of 36 articles reporting a single case or case series involving 40 patients were collected. The patients showed an absolute female dominance at a mean aneurysm age of 44.6 years. Steroid use was 13.3 ± 9.4 years prior to admission for management of aortic aneurysm or dissection. Aortic aneurysm occurred more commonly in abdominal than other segments of the aorta, whereas aortic dissection did not show any location predilection. Patients with open aortic operations showed a higher mortality rate than other groups; however, no statistical significance was reached. Interventional therapy was minimally invasive, but postinterventional endoleaks were a concerning problem.SLE patients had significant risks for developing aortic aneurysm and dissection. Hypertension, long-term steroid use, and aortic pathological changes related to SLE seemed to be predominant risk factors for the occurrence of aortic aneurysm and dissection. Upon diagnosis, a surgical, interventional, or hybrid treatment should be performed to prevent severe sequelae and sudden deaths.

[Numerical simulation study of type B aortic dissection using patient-specific reverse engineering and fluid-structure interaction].

Objective: To construct computational fluid model of type B aortic dissection using patient-specific reverse engineering and fluid-structure interaction, and evaluate the application of computational fluid model on aortic remodeling of type B aortic dissection. Methods: Consecutive computed tomographic angiograph data was acquired from a patient with type B aortic dissection at initial diagnosis, 1 week and 6 years after endovascular repair of primary tear entry and 3 months after endovascular repair of distal tear erosion. Three-dimensional model of aortic dissection was reversely reconstructed by Mimics, and then the model was smoothened by Geomagic. Computational fluid dynamic numerical simulation was performed in ANSYS by the means of two-way fluid-structure interaction, and the relation between blood dynamic characteristic and thrombosed remodeling of type B aortic dissection was evaluated. Results: The computational fluid model of type B aortic dissection using patient-specific reverse engineering and fluid-structure interaction method was successfully constructed. Local peak of blood pressure on the convex surface of junction at aortic arch and descending aorta was found. The wall stress was much higher at the false lumen than that at the true lumen, and the peak of wall stress converged on the edge and tear entry of false lumen. After the exclusion of proximal tear entry, the blood streamline was decreased significantly and flowed reversely. Blood flow in the remaining false lumen was retrograded from the entry at left iliac artery and formed turbulence at the top of false lumen, which was benefit for dissection thrombus remodeling. The higher pressure at the false lumen was associated with the new formation of aortic aneurysm at the distal tear. Conclusion: The computational fluid model of aortic dissection based on patient-specific reverse engineering and fluid-structure interaction method can successfully reveal the relatively truly blood dynamic and wall pressure characteristic of type B aortic dissection.

[Large clinical registries for acute aortic dissection: interpretation and comparison of latest results].

Despite the improvements in the diagnosis and management during the past six decades, acute aortic dissection (AAD) remains a life-threatening condition associated with significant morbidity and mortality rates. Due to the relatively rare occurrence of AAD, several clinical registries have been established to gain insights into this lethal disease in a large number of patients, such as the International Registry of Acute Aortic Dissection (IRAD), the German Registry for Acute Aortic Dissection Type A (GERAADA), and the Society of Thoracic Surgeons (STS) Adult Cardiac Surgery Database Aortic Section. This review aims to interpret and compare the latest results of the IRAD, STS and GERAADA database. It focuses on several controversial and key issues in the diagnosis and management of acute aortic dissection in hope of providing some insights and references for cardiovascular professionals engaged in the care of this deadly disease.