Repair of a right coronary artery rupture with perforated right ventricle following spontaneous pseudoaneurysm: a case report.

BACKGROUND: Following the rupture of a coronary artery, a patient's condition usually deteriorates rapidly due to cardiac tamponade. A pseudoaneurysm due to a coronary artery rupture is rare; however, when a spontaneous coronary artery pseudoaneurysm occurs without tamponade, it creates a fistula in the right ventricle, often requiring surgical repair. CASE PRESENTATION: This report describes the case of a 68-year-old man who presented with chest discomfort after a 12-day course of antibiotic treatment for bacteremia. Following coronary angiography, echocardiography, and enhanced computed tomography, he was diagnosed with a right coronary artery pseudoaneurysm accompanied with perforation of the right ventricle. Severe adhesions were observed during emergency surgery surrounding the entire heart. The patient presented with risk factors for coronary artery disease, including hypertension and smoking history. His coronary artery was severely calcified due to end-stage renal failure requiring dialysis; thus, a covered stent could not fit inside the arterial lumen. Consequently, coronary artery bypass grafting to the right coronary artery and right ventricle repair were performed. Unfortunately, the patient died postoperatively due to sepsis from intestinal translocation. This rare development was hypothesized to be an incidental result of the combination of severe post-inflammatory adhesions, extensive coronary artery calcification, and rupture of the calcification crevices. CONCLUSIONS: In the case of a severe post-inflammatory response, shock without cardiac tamponade may require further scrutiny by assuming the possibility of inward rupture. For patients in poor condition, two-stage surgical treatment might be considered after stabilization with a covered stent.

Early Clinical Results From the Japanese Prospective Multicenter Study to Evaluate Zenith Alpha Abdominal Stent Graft for Abdominal Aortic Aneurysm (JUSTICE) Registry Demonstrate Acceptable Limb Patency at 12 Months.

PURPOSE: Recent reports of the Zenith Alpha abdominal endovascular graft (Zenith Alpha AAA, Cook, Inc., Bloomington, Indiana) have demonstrated an unexpectedly high incidence of limb graft occlusion (LGO). The purpose of this study was to prospectively evaluate the performance of the Zenith AAA in Japan, with a specific focus on LGO. MATERIALS AND METHODS: All endovascular aneurysm repairs (EVARs) for abdominal aortic aneurysms performed using the Zenith Alpha AAA from July 2020 to October 2021 in 23 Japanese hospitals were prospectively evaluated. All computed tomographic images were analyzed in the core laboratory. Late complications were defined as any aneurysm-related events occurring >30 days after EVAR, including aneurysm sac enlargement of >5 mm and any reinterventions performed. Endoleaks without sac enlargement or reintervention were excluded as late complications. RESULTS: During the study period, 147 EVARs were performed using the Zenith Alpha AAA. The mean patient age was 76.5±7.7 years, 84.4% of patients were male, and the mean aneurysm diameter was 52.4±9.2 mm. Instruction-for-use violations were observed in 76 patients (51.7%), primarily associated with a severely angulated proximal neck (>60°). There were six intraoperative complications and 62 additional intraoperative treatments reported, most of which involved preemptive coil embolization of the inferior mesenteric artery (37 cases). Technical success, defined as the absence of type 1 or 3 endoleaks on final angiography, was achieved in 99.3% of patients. At 12 months, there was only one case of type 1/3 endoleak (0.8%) and one aneurysm sac enlargement exceeding 5 mm (0.8%); however, a high incidence of type 2 endoleaks was observed in 35.2% of patients, and aneurysm sac regression exceeding 5 mm was achieved in 30.1% of patients. Nine late complications were observed, and the rate of freedom from late complications at 12 months was 93.5%, encompassing four LGOs and one limb graft stenosis (3.4%). CONCLUSIONS: In contrast to recent reports, our Japanese multicenter prospective study demonstrated satisfactory early clinical results, including an acceptable LGO rate, for the low-profile Zenith Alpha AAA. Long-term follow-ups will be performed to confirm the persistence of these outcomes. CLINICAL IMPACT: This study prospectively evaluated the performance of 147 Zenith Alpha AAAs used for endovascular aneurysm repair with core-lab adjudication focusing especially on limb graft occlusion (LGO). At 12 months, aneurysm sac regression exceeding 5 mm was achieved in 30.1% of patients, and there was only one type 1/3 endoleak, one aneurysm sac enlargement (>5 mm), and nine late complications including five LGOs (3.4%), resulting in rate of freedom from late complications at 93.5%. Satisfactory early clinical results, including an acceptable rate of LGO can be achieved, particularly with cautious usage of the Zenith Alpha Spiral-Z Endovascular Leg." 5mm), and nine late complications including five LGOs (3.4%), resulting in rate of freedom from late complications at 93.5%. Satisfactory early clinical results, including an acceptable rate of LGO can be achieved, particularly with cautious usage of the Zenith Alpha Spiral-Z Endovascular Leg.

Relationship between false lumen morphology and entry tear in acute type A aortic dissection.

OBJECTIVES: This study aimed to investigate the relationship between false lumen morphology and the size, aortic segment and position of the entry tear for acute type A aortic dissection. METHODS: The records of patients who underwent emergency operation for acute type A aortic dissection in our institution between April 2011 and May 2022 were examined. Data regarding size, location and position of the entry tear and preoperative computed tomography findings were reviewed. The relationship of these variables with false lumen morphology was examined and retrospectively compared according to tear size. RESULTS: Of 243 cases, characteristics of the entry tear, visualized during surgery, were confirmed in 134 cases (age = 70.9 ± 12.6 years, male = 45.5%). Tear sizes at different aortic segments were not significantly different (P = 0.376). Tears posterior to the lesser curvature were significantly smaller than those anterior to the greater curvature (P = 0.004). A thrombosed false lumen was associated with a significantly smaller tear size and position on the posterior to the lesser curvature side in aortic cross-section (all P < 0.001). Multivariate analysis showed that tear size, the presence of re-entry and tear position anterior to the greater curvature were independent predictors of a patent false lumen. CONCLUSIONS: In acute type A aortic dissection, larger tear size, the presence of re-entry and tear position anterior to the greater curvature are risk factors for a patent false lumen. Although the results of this study are valid only for patients in whom intimal tears were detected during aortic surgery, this trend may provide information for pathophysiology of the disease.

[Mitral Valve Plasty Late after Tetrology of Fallot Repair:Report of a Case].

The case was a 32-year-old man. Blalock-Taussig shunt was performed at five months-old for tetralogy of Fallot, and intracardiac repair was performed at four years-old. He was admitted with a diagnosis of infective endocarditis. Preoperative echocardiography showed vegetations on the mitral valve and severe mitral regurgitation. Severe right heart pressure load findings, pulmonary valve stenosis and regurgitation, and residual ventricular septal defect were also observed. The surgery included mitral valve repair, reconstruction of the right ventricular outflow tract, pulmonary valve replacement, and closure of the ventricular septal defect. The postoperative course was favorable. The cause of mitral regurgitation was an abnormal chordae tendineae attached to the interventricular septum and valve destruction by infective endocarditis.

Nitric oxide synthesis stimulated by arachidonic acid accumulation via PPARα in acetylcholine-stimulated gastric mucous cells.

NEW FINDINGS: What is the central question of this study? Arachidonic acid (AA) stimulates NO production in antral mucous cells without any increase in [Ca2+ ]i . Given that the intracellular AA concentration is too low to measure, the relationship between AA accumulation and NO production remains uncertain. Is AA accumulation a key step for NO production? What is the main finding and its importance? We demonstrated that AA accumulation is a key step for NO production. The amount of AA released could be measured using fluorescence-HPLC. The intracellular AA concentration was maintained at < 1 µM. Nitric oxide is produced by AA accumulation in antral mucous cells, not as a direct effect of [Ca2+ ]i . ABSTRACT: In the present study, we demonstrate that NO production is stimulated by an accumulation of arachidonic acid (AA) mediated via peroxisome proliferation-activated receptor α (PPARα) and that the NO produced enhances Ca2+ -regulated exocytosis in ACh-stimulated antral mucous cells. The amount of AA released from the antral mucosa, measured by fluorescence high-performance liquid chromatography (F-HPLC), was increased by addition of ionomycin (10 µM) or ACh, suggesting that AA accumulation is stimulated by an increase in [Ca2+ ]i . The AA production was inhibited by an inhibitor of cytosolic phospholipase A2 (cPLA2-inhα). GW6471 (a PPARα inhibitor) and cPLA2-inhα inhibited NO synthesis stimulated by ACh. Moreover, indomethacin, an inhibitor of cyclooxygenase, stimulated AA accumulation and NO production. However, acetylsalicylic acid did not stimulate AA production and NO synthesis. An analogue of AA (AACOCF3) alone stimulated NO synthesis, which was inhibited by GW6471. In antral mucous cells, indomethacin enhanced Ca2+ -regulated exocytosis by increasing NO via PPARα, and the enhancement was abolished by GW6471 and cPLA2-inhα. Thus, AA produced via PLA2 activation is the key step for NO synthesis in ACh-stimulated antral mucous cells and plays important roles in maintaining antral mucous secretion, especially in Ca2+ -regulated exocytosis.

Hybrid zone zero debranching thoracic endovascular aortic repair of ascending aortic injury after surgery and radiotherapy for breast cancer.

Thoracic endovascular aortic repair of the ascending aorta remains challenging. We have reported the case of an 81-year-old woman with ascending aortic injury who underwent a life-saving hybrid repair. The patient had previously undergone extended radical mastectomy and postoperative radiotherapy for breast cancer, which had resulted in a right thoracic wall defect and bone exposure and osteonecrosis of the sternum. Therefore, the ascending aorta was directly compressed by the sternum at the level of the brachiocephalic artery bifurcation, causing persistent bleeding from the thoracic wall. Hybrid zone 0 debranching thoracic endovascular aortic repair with a left subclavian artery inflow was emergently performed and achieved hemostasis.

[A Case of Internal Jugular Vein Thrombosis Caused by Gravity-Induced Catheter Excursion following Subcutaneous Implantable Central Venous Port Insertion for Colorectal Cancer Treatment].

The patient was a 66-year-old woman. She underwent central venous port insertion as part of postoperative adjuvant chemotherapy for sigmoid colon cancer. At the beginning of the 2 cycle, she experienced discomfort in the neck, and computed tomography was performed. As a result, catheter deviation and a thrombus in the internal jugular vein were observed. It was considered that breast displacement due to gravity caused the catheter deviation and that the position of the tip of the catheter deviating to immediately above the venous valve caused thrombus formation. We examined the factors that may cause catheter deviation.

Transgraft embolization by using long needle for the treatment of type II endoleaks after endovascular abdominal aortic repair.

We used a long custom needle (LCN) to improve transgraft embolization (TGE) in 10 reported cases that underwent TGE with LCN for type II endoleak (T2E) treatment after endovascular abdominal aortic aneurysm repair. TGE was performed with a LCN enabling the usage of microcatheter and embolization coils in 10 cases with T2E after endovascular abdominal aortic aneurysm repair. Embolization was successfully achieved in the nidus in all 10 cases. The aneurysmal sac diameter significantly decreased by TGE, and none of the 7 of 10 cases exhibited recurrence of sac expansion or T2E throughout the 2-year follow-up period.

Two-Year Results of a Multicenter Prospective Observational Study of the Zenith Spiral-Z Limb Deployed in the External Iliac Artery During Endovascular Aneurysm Repair.

BACKGROUND: Limited data is available on the use of a polyester graft limb with a helical stent configuration deployed in the external iliac artery (EIA) during endovascular aneurysm repair (EVAR), so we prospectively analyzed the efficacy of the Zenith Spiral-Z limb deployed in the EIA.Methods and Results:Patients undergoing EVAR using a Zenith stent-graft and Spiral-Z limb deployed in the EIA were prospectively registered in 24 Japanese institutions from June 2017 to November 2017. In total, 65 patients (74 limbs) (mean age: 77.1±8.0 years, 87.7% men, mean abdominal aortic aneurysm (AAA) diameter: 51.9±7.2 mm, mean iliac artery aneurysm (IAA) diameter: 38.3±10.0 mm) were registered and followed up. The most common reason for deployment in the EIA was a common IAA (43 limbs, 58.1%), and 8 limbs (10.8%) had a bare nitinol stent placed at the Spiral-Z limb. A total of 61 patients (70 limbs) completed a 24-month follow-up. There were 2 Spiral-Z limb stenoses and 1 occlusion, leading to a primary patency of 95.5% and a secondary patency of 100%, at 24 months. Buttock claudication occurred in 24.3% of the limbs treated at 1 month but decreased to 4.3% at 24 months. CONCLUSIONS: Our multicenter prospective study showed that Spiral-Z limb deployed in the EIA was associated with satisfactory results and seems to be a durable option, even in the era of iliac branch devices.

Carbocisteine stimulated an increase in ciliary bend angle via a decrease in [Cl-]i in mouse airway cilia.

Carbocisteine (CCis), a mucoactive agent, is widely used to improve respiratory diseases. This study demonstrated that CCis increases ciliary bend angle (CBA) by 30% and ciliary beat frequency (CBF) by 10% in mouse airway ciliary cells. These increases were induced by an elevation in intracellular pH (pHi; the pHi pathway) and a decrease in the intracellular Cl- concentration ([Cl-]i; the Cl- pathway) stimulated by CCis. The Cl- pathway, which is independent of CO2/HCO3-, increased CBA by 20%. This pathway activated Cl- release via activation of Cl- channels, leading to a decrease in [Cl-]i, and was inhibited by Cl- channel blockers (5-nitro-2-(3-phenylpropylamino) benzoic acid and CFTR(inh)-172). Under the CO2/HCO3--free condition, the CBA increase stimulated by CCis was mimicked by the Cl--free NO3- solution. The pHi pathway, which depends on CO2/HCO3-, increased CBF and CBA by 10%. This pathway activated HCO3- entry via Na+/HCO3- cotransport (NBC), leading to a pHi elevation, and was inhibited by 4,4'-diisothiocyano-2,2'-stilbenedisulfonic acid. The effects of CCis were not affected by a protein kinase A inhibitor (1 µM PKI-A) or Ca2+-free solution. Thus, CCis decreased [Cl-]i via activation of Cl- channels including CFTR, increasing CBA by 20%, and elevated pHi via NBC activation, increasing CBF and CBA by 10%.

Author Correction: Normothermic Microwave Irradiation Induces Death of HL-60 Cells through Heat-Independent Apoptosis.

A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper.

Normothermic Microwave Irradiation Induces Death of HL-60 Cells through Heat-Independent Apoptosis.

Microwaves have been used in various cancer therapies to generate heat and increase tumor cell temperature; however, their use is limited by their side-effects in normal cells and the acquisition of heat resistance. We previously developed a microwave irradiation method that kills cultured cancer cells, including a human promyelomonocytic leukemia (HL-60) cell line, by maintaining a cellular temperature of 37 °C during treatment. In the present study, we investigated the mechanisms underlying HL-60 cell death during this treatment. The microwave-irradiated HL-60 cells appear to undergo caspase-independent apoptosis, whereby DNA fragmentation was induced by mitochondrial dysfunction-related expression of apoptosis-inducing factor (AIF). Caspase-dependent apoptosis was also interrupted by the loss of apoptotic protease-activating factor 1 (Apaf-1) and caspase 9. Moreover, these cells did not exhibit a heat-stress response, as shown by the lack of heat shock protein 70 (HSP70) upregulation. Alternatively, in HL-60 cells heated at 42.5 °C, HSP70 expression was upregulated and a pathway resembling death receptor-induced apoptosis was activated while mitochondrial function was maintained. Collectively, these results suggest that the cell death pathway activated by our 37 °C microwave irradiation method differs from that induced during other heating methods and support the use of normothermic microwave irradiation in clinical cancer treatments.

A low [Ca2+]i-induced enhancement of cAMP-activated ciliary beating by PDE1A inhibition in mouse airway cilia.

This study demonstrated that PDE1 (phosphodiesterase 1) existing in the ciliary beat frequency (CBF)-regulating metabolon regulates CBF in procaterol-stimulated lung airway ciliary cells of mouse. Procaterol (an ß2-agonist) increased the ciliary bend angle (CBA) and CBF via cAMP accumulation in the ciliary cells of mice: interestingly, the time course of CBF increase was slower than that of CBA increase. However, IBMX (3-isobutyl-1-methylxanthine, an inhibitor of PDE) increased CBA and CBF in an identical time course. Lowering an intracellular Ca2+ concentration ([Ca2+]i) caused by switching to an EGTA-containing Ca2+-free solution from normal one elevated the procaterol-induced increasing rate of CBF. These observations suggest that Ca2+-dependent PDE1 controls cAMP-stimulated CBF increase. Either application of 8MmIBMX (8-methoxymethyl-IBMX, a selective PDE1 inhibitor), BAPTA-AM (an intracellular Ca2+ chelator), or calmidazolium (an inhibitior of calmodulin) alone increased CBA and CBF in the lung airway ciliary cells and increased cAMP contents in the isolated lung cells, and like IBMX, each application of the compound made the time courses of CBA and CBF increase stimulated by procaterol identical. The immunoelectron microscopic examinations revealed that PDE1A exists in the space between the nine doublet tubules ring and plasma membrane in the lung airway cilium, where the outer dynein arm (a molecular motor regulating CBF) functions. In conclusion, PDE1A is a key factor slowing the time course of the procaterol-induced increase in CBF via degradation of cAMP in the CBF-regulating metabolon of the mouse lung airway cilia.

Effects of Normothermic Conditioned Microwave Irradiation on Cultured Cells Using an Irradiation System with Semiconductor Oscillator and Thermo-regulatory Applicator.

We investigated the effects of microwave irradiation under normothermic conditions on cultured cells. For this study, we developed an irradiation system constituted with semiconductor microwave oscillator (2.45 GHz) and thermos-regulatory applicator, which could irradiate microwaves at varied output powers to maintain the temperature of cultured cells at 37 °C. Seven out of eight types of cultured cells were killed by microwave irradiation, where four were not affected by thermal treatment at 42.5 °C. Since the dielectric properties such as ε', ε" and tanδ showed similar values at 2.45 GHz among cell types and media, the degree of microwave energy absorbed by cells might be almost the same among cell types. Thus, the vulnerability of cells to microwave irradiation might be different among cell types. In HL-60 cells, which were the most sensitive to microwave irradiation, the viability decreased as irradiation time and irradiation output increased; accordingly, the decrease in viability was correlated to an increase in total joule. However, when a high or low amount of joules per minute was supplied, the correlation between cellular viability and total joules became relatively weak. It is hypothesized that kinds of cancer cells are efficiently killed by respective specific output of microwave under normothermic cellular conditions.

PPARα induced NOS1 phosphorylation via PI3K/Akt in guinea pig antral mucous cells: NO-enhancement in Ca(2+)-regulated exocytosis.

A PPARα (peroxisome proliferation activation receptor α) agonist (GW7647) activates nitric oxide synthase 1 (NOS1) to produce NO leading to cGMP accumulation in antral mucous cells. In this study, we examined how PPARα activates NOS1. The NO production stimulated by GW7647 was suppressed by inhibitors of PI3K (wortmannin) and Akt (AKT 1/2 Kinase Inhibitor, AKT-inh), although it was also suppressed by the inhibitors of PPARα (GW6471) and NOS1 (N-PLA). GW7647 enhanced the ACh (acetylcholine)-stimulated exocytosis (Ca(2+)-regulated exocytosis) mediated via NO, which was abolished by GW6471, N-PLA, wortmannin, and AKT-inh. The Western blotting revealed that GW7647 phosphorylates NOS1 via phosphorylation of PI3K/Akt in antral mucous cells. The immunofluorescence examinations demonstrated that PPARα existing with NOS1 co-localizes with PI3K and Akt in the cytoplasm of antral mucous cells. ACh alone and AACOCF3, an analogue of arachidonic acid (AA), induced the NOS1 phosphorylation via PI3K/Akt to produce NO, which was inhibited by GW6471. Since AA is a natural ligand for PPARα, ACh stimulates PPARα probably via AA. In conclusion, PPARα activates NOS1 via PI3K/Akt phosphorylation to produce NO in antral mucous cells during ACh stimulation.

Direct and transapical central cannulation for acute type a aortic dissection.

OBJECTIVE: The choice of cannulation site for the treatment of acute Stanford type A aortic dissection is much debated. We believe that central cannulation is quick to perform, easy to use, and safe to manage acute type A aortic dissection. MATERIALS AND METHODS: We retrospectively investigated 26 cases of acute aortic dissection performed using two different central cannulation methods between April 2011 and March 2012. Direct ascending aortic cannulation was performed using the Seldinger technique in 20 patients, and transapical ascending aortic cannulation was performed in six patients in whom puncture was difficult. RESULTS: Patients were 21-86 years old (mean age, 67 years). The surgical techniques used to treat aortic dissection were hemiarch repair in 21 patients and total arch replacement in 5 patients. The mean length of surgery was 393 min. One death (3.8%) was attributed to intestinal ischemia. CONCLUSION: During surgery for acute aortic dissection, central cannulation using either transapical or direct puncture can be performed quickly and safely, and satisfactory short-term outcomes can be obtained. Because acute aortic dissection can present with various conditions, there is no single perfect surgical or cannulation method; therefore, the choice of surgical procedure should be individualized for each patient.

PPARα autocrine regulation of Ca²âº-regulated exocytosis in guinea pig antral mucous cells: NO and cGMP accumulation.

In antral mucous cells, acetylcholine (ACh, 1 µM) activates Ca(2+)-regulated exocytosis, consisting of a peak in exocytotic events that declines rapidly (initial phase) followed by a second slower decline (late phase) lasting during ACh stimulation. GW7647 [a peroxisome proliferation activation receptor α (PPARα) agonist] enhanced the ACh-stimulated initial phase, and GW6471 (a PPARα antagonist) abolished the GW7647-induced enhancement. However, GW6471 produced the delayed, but transient, increase in the ACh-stimulated late phase, and it also decreased the initial phase and produced the delayed increase in the late phase during stimulation with ACh alone. A similar delayed increase in the ACh-stimulated late phase is induced by an inhibitor of the PKG, Rp8BrPETcGMPS, suggesting that GW6471 inhibits cGMP accumulation. An inhibitor of nitric oxide synthase 1 (NOS1), N(5)-[imino(propylamino)methyl]-L-ornithine hydrochloride (N-PLA), also abolished the GW7647-induced-enhancement of ACh-stimulated initial phase but produced the delayed increase in the late phase. However, in the presence of N-PLA, an NO donor or 8BrcGMP enhanced the ACh-stimulated initial phase and abolished the delayed increase in the late phase. Moreover, GW7647 and ACh stimulated NO production and cGMP accumulation in antral mucosae, which was inhibited by GW6471 or N-PLA. Western blotting and immunohistochemistry revealed that NOS1 and PPARα colocalize in antral mucous cells. In conclusion, during ACh stimulation, a PPARα autocrine mechanism, which accumulates NO via NOS1 leading to cGMP accumulation, modulates the Ca(2+)-regulated exocytosis in antral mucous cells.

A case of type-2 endoleak from a bronchial artery after endovascular aortic repair for Kommerell diverticulum.

We describe a case of type-2 bronchial artery endoleak after endovascular aortic repair of Kommerell diverticulum (KD) involving right-sided aortic arch and aberrant left subclavian artery (LSA). A 68-year-old woman underwent an endovascular repair of KD with an aberrant LSA in our hospital. Follow-up computed tomography (CT) at 6 months after the procedure showed an endoleak. Digital subtraction angiography revealed a type-2 endoleak from a bronchial artery, but no type-1 or type-2 endoleak from the aberrant left subclavian artery. We performed coil embolization of the KD and the left subclavian artery. The endoleak disappeared in the postoperative CT.

Bio-imaging of hydroxyl radicals in plant cells using the fluorescent molecular probe rhodamine B hydrazide, without any pretreatment.

Rhodamine B hydrazide can be used to detect hydroxyl radicals in plant cells. RBH was easily inserted into plant cells without any pretreatment, and specifically reacted with intracellular hydroxyl radicals produced by antimycin A. RBH will be a powerful tool for detecting hydroxyl radicals in plant cells.

Safety and efficacy of ascending aorta cannulation during repair of acute type A aortic dissection (PA29-04): "Presented at the 65th Annual Scientific Meeting of the Japanese Association for Thoracic Surgery".

OBJECTIVE: Antegrade central perfusion for acute Stanford type A aortic dissection prevents malperfusion and retrograde cerebral embolism during cardiopulmonary bypass. Prompt establishment of antegrade perfusion via the ascending aorta may improve surgical results of type A dissections, especially in situations of hemodynamic instability. Thus, we evaluated the safety and efficacy of cannulation of the dissected ascending aorta in acute type A dissection. METHODS: We reviewed the medical charts of patients undergoing repair of acute ascending aortic dissection (n = 52) from April 2010 to April 2013. Cannulation was accomplished in 29 patients via the ascending aorta (central) and in 23 patients via the femoral or axillary artery (peripheral). The ascending aorta was routinely cannulated using Seldinger technique under epiaortic ultrasound guidance. Comorbidities, mortality, complications, and durations of hospital stays were compared for the groups. RESULTS: In all cases, routine cannulation of the ascending aorta was safely performed with no resultant malperfusion or thromboembolism. Mean operative duration, cardiopulmonary bypass time, intubation time, and intensive care unit stay were significantly shorter in the central group. Two patients (6.8 %) in the central group died compared with four patients (17.3 %) in the peripheral group (P = 0.005). CONCLUSIONS: Antegrade central perfusion via the ascending aorta, a simple and safe technique that enables rapid establishment of antegrade systemic perfusion, was as safe as peripheral cannulation in patients with type A acute aortic dissection.