Outcomes of abdominal false lumen embolization for chronic aortic dissection after prior proximal repair with stent-graft.

BACKGROUND: Persistent false lumen (FL) perfusion with aneurysmal formation is common after thoracic endovascular aortic repair (TEVAR) for typical extended aortic dissection and is associated with poor outcomes. Endovascular FL embolization (FLE) has recently been tried for treatment of postdissection aortic aneurysm (PDAA). However, most reports address thoracic rather than abdominal FLE. In this study, we present the results of abdominal FLE in patients with residual patent abdominal FL following stent-graft repair for aortic dissection. METHODS: Between 2015 and 2019, 24 patients (mean age: 56.7 ± 11.8 years, range: 40-84 years, 18 male) received endovascular abdominal FLE using vascular plugs, coils, or candy plugs as the main surgery (5 patients) or auxiliary procedure (19 patients) after earlier stent-graft repair for aortic dissection (Type A: 9, Type B: 15). The medical records were reviewed and aortic remodeling was examined comparing the preembolization computed tomography (CT) and the most recent CT before reintervention. RESULTS: Technical success was achieved without any intraoperative complications, early morbidity, or mortality. Median follow-up was 34.4 months (range: 12-71). Regarding thoracic FL, 15 patients exhibited complete thrombosis before the procedure and did not change status thereafter except for 1 patient with distal stent-graft-induced new entry. In the other 9 patients, 6 exhibited increased thrombosis. With regard to the abdominal aorta, increased FL thrombosis only occurred in 8 patients with 3 (12.5%) achieving complete thrombosis. The maximal thoracic aortic diameter did not change (1.4 ± 5.6 mm) statistically, but the abdominal diameter increased significantly (4.3 ± 3.7 mm, p < 0.005). CONCLUSION: From our results, abdominal FLE is a safe procedure. However, covering all the re-entry tears is complex and the possibility of complete FL thrombosis is low. The abdominal aortic diameter appears to become enlarged in these patients. Continuous follow-up is necessary after FLE.

Distinct Roles of DRP1 in Conventional and Alternative Mitophagy in Obesity Cardiomyopathy.

BACKGROUND: Obesity induces cardiomyopathy characterized by hypertrophy and diastolic dysfunction. Whereas mitophagy mediated through an Atg7 (autophagy related 7)-dependent mechanism serves as an essential mechanism to maintain mitochondrial quality during the initial development of obesity cardiomyopathy, Rab9 (Ras-related protein Rab-9A)-dependent alternative mitophagy takes over the role during the chronic phase. Although it has been postulated that DRP1 (dynamin-related protein 1)-mediated mitochondrial fission and consequent separation of the damaged portions of mitochondria are essential for mitophagy, the involvement of DRP1 in mitophagy remains controversial. We investigated whether endogenous DRP1 is essential in mediating the 2 forms of mitophagy during high-fat diet (HFD)-induced obesity cardiomyopathy and, if so, what the underlying mechanisms are. METHODS: Mice were fed either a normal diet or an HFD (60 kcal %fat). Mitophagy was evaluated using cardiac-specific Mito-Keima mice. The role of DRP1 was evaluated using tamoxifen-inducible cardiac-specific Drp1knockout (Drp1 MCM) mice. RESULTS: Mitophagy was increased after 3 weeks of HFD consumption. The induction of mitophagy by HFD consumption was completely abolished in Drp1 MCM mouse hearts, in which both diastolic and systolic dysfunction were exacerbated. The increase in LC3 (microtubule-associated protein 1 light chain 3)-dependent general autophagy and colocalization between LC3 and mitochondrial proteins was abolished in Drp1 MCM mice. Activation of alternative mitophagy was also completely abolished in Drp1 MCM mice during the chronic phase of HFD consumption. DRP1 was phosphorylated at Ser616, localized at the mitochondria-associated membranes, and associated with Rab9 and Fis1 (fission protein 1) only during the chronic, but not acute, phase of HFD consumption. CONCLUSIONS: DRP1 is an essential factor in mitochondrial quality control during obesity cardiomyopathy that controls multiple forms of mitophagy. Although DRP1 regulates conventional mitophagy through a mitochondria-associated membrane-independent mechanism during the acute phase, it acts as a component of the mitophagy machinery at the mitochondria-associated membranes in alternative mitophagy during the chronic phase of HFD consumption.

TIMP-1 in the prognosis of patients who underwent coronary artery bypass surgery: a 12-year follow-up study.

Introduction: Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) have been linked to clinical outcomes in patients with coronary artery disease (CAD). However, the prognostic value of TIMP-1 in patients with CAD who underwent coronary artery bypass grafting (CABG) has not been elucidated. We aimed to investigate the correlations of TIMP-1 with high-sensitivity C-reactive protein (hs-CRP) and N-terminal pro-brain natriuretic peptide (NT-proBNP) in the long-term prognosis of consecutive patients who underwent CABG. Methods: A total of 234 patients (age: 70.4 ± 10.5 years, 84.6% men) with CAD who underwent CABG were prospectively enrolled. Preoperative levels of MMPs, TIMP-1, hs-CRP, and NT-proBNP were recorded. Major adverse cardiovascular events (MACE) were defined as non-fatal myocardial infarction, non-fatal stroke, and cardiovascular death. Results: During a median follow-up of 12.1 years, 120 deaths were recorded. The deceased were older, had more manifest acute coronary syndrome (ACS), a lower left ventricular ejection fraction (LVEF), and an estimated glomerular filtration rate (eGFR), but significantly higher MMP13, TIMP-1, hs-CRP, and NT-proBNP compared with the survivors. After adjusting for age, sex, manifest ACS, eGFR, LVEF, total cholesterol, and triglycerides, TIMP-1 (hazard ratio and 95% confidence intervals per SD: 1.506, 1.183-1.917), hs-CRP (1.349, 1.183-1.561), and NT-ProBNP (1.707, 1.326-2.199) were all independently associated with all-cause mortality. The mediation analysis revealed that the mortality risks of TIMP-1 were partially mediated by NT-proBNP (62.2%) and hs-CRP (25.3%). The associations of TIMP-1 with MACE were partially mediated by NT-proBNP (54.4%) but not hs-CRP. Conclusions: TIMP-1 was an independent predictor of long-term outcomes after CABG, with possible roles in subclinical inflammation and postoperative cardiac remodeling.

PERM1 regulates genes involved in fatty acid metabolism in the heart by interacting with PPARα and PGC-1α.

PERM1 (PGC-1/ERR-induced regulator in muscle 1) is a muscle-specific protein induced by PGC-1 and ERRs. Previous studies have shown that PERM1 promotes mitochondrial biogenesis and metabolism in cardiomyocytes in vitro. However, the role of endogenous PERM1 in the heart remains to be investigated with loss-of-function studies in vivo. We report the generation and characterization of systemic Perm1 knockout (KO) mice. The baseline cardiac phenotype of the homozygous Perm1 KO mice appeared normal. However, RNA-sequencing and unbiased pathway analyses showed that homozygous downregulation of PERM1 leads to downregulation of genes involved in fatty acid and carbohydrate metabolism in the heart. Transcription factor binding site analyses suggested that PPARα and PGC-1α are involved in changes in the gene expression profile. Chromatin immunoprecipitation assays showed that PERM1 interacts with the proximal regions of PPAR response elements (PPREs) in endogenous promoters of genes involved in fatty acid oxidation. Co-immunoprecipitation and reporter gene assays showed that PERM1 promoted transcription via the PPRE, partly in a PPARα and PGC-1α dependent manner. These results suggest that endogenous PERM1 is involved in the transcription of genes involved in fatty acid oxidation through physical interaction with PPARα and PGC-1α in the heart in vivo.

Cardiac Dopamine-Secreting Paraganglioma with Involved Skull Base and Retroperitoneum After a History of Pheochromocytoma Post Adrenalectomy.

Cardiac paragangliomas are exceedingly rare. Herein, we describe a patient with a large dopaminesecreting cardiac paraganglioma who had a history of pheochromocytoma after right adrenalectomy. The cardiac surgery was uneventful and without blood pressure fluctuations.The measurement of plasma-free metanephrines or urinary fractionated metanephrines is used as an initial screening test for pheochromocytoma or paraganglioma detection. However, these results must be combined with those of a plasma 3-methoxytyramine test to accurately establish the rare dopaminergic phenotype of pheochromocytomas or paragangliomas, if suspected. F-FDOPA (6-[18F]-L-fluoro-L-3, 4-dihydroxyphenylalanine)-based positron emission tomography (PET) and PET-computed tomography are relatively sensitive and specific; therefore, these techniques are recommended for patients with pheochromocytomas or paragangliomas before operation or during postoperative follow-up.

Aortic remodeling of the provisional extension to induce complete attachment technique in DeBakey type IIIb aortic dissection.

BACKGROUND/PURPOSE: Data about volumetric remodeling of the provisional extension to induce complete attachment (PETTICOAT) technique on DeBakey type IIIb aortic dissection in acute and subacute phases were scarce. The proper timing to perform this technique to promote false lumen reduction was also unknown. METHODS: Patients with DeBakey type IIIb aortic dissection who underwent the PETTICOAT technique between December 2005 and March 2017 were reviewed and divided into acute (treatment occurred ≦14 days after symptom onset) and subacute (15-90 days) groups. Remodeling parameters of the true and false lumens were analyzed. Receiver operating characteristic curve was used to deduce the timing of this technique. RESULTS: In the 2-year follow-up, the acute group (N = 20) demonstrated significant true lumen expansion and false lumen regression in the thoracic, abdominal, and total aorta. However, the subacute group (N = 20) only showed significant shrinkage in the false lumen of the thoracic and total aorta. Using PETTICOAT technique within 36 days after the aortic event may result in better total false lumen reduction. CONCLUSION: For DeBakey type IIIb aortic dissection, more prominent true lumen expansion and false lumen reduction were noted when using the PETTICOAT technique in the acute phase. When performed within 36 days after symptoms onset, the PETTICOAT technique may potentiate better total false lumen regression.

Atypical antipsychotic drugs deregulate the cholesterol metabolism of macrophage-foam cells by activating NOX-ROS-PPARγ-CD36 signaling pathway.

BACKGROUND: Clinical reports indicate that schizophrenia patients taking atypical antipsychotic drugs suffer from metabolism diseases including atherosclerosis. However, the mechanisms underlying the detrimental effect of atypical antipsychotic drugs on atherosclerosis remain to be explored. METHODS: In this study, we used apolipoprotein E-deficient (apoe-/-) hyperlipidemic mice and apoe-/-cd36-/- mice to investigate the underlying mechanism of atypical antipsychotic drugs on atherosclerosis and macrophage-foam cells. RESULTS: In vivo studies showed that genetic deletion of cd36 gene ablated the pro-atherogenic effect of olanzapine in apoe-/- mice. Moreover, in vitro studies revealed that genetic deletion or siRNA-mediated knockdown of cd36 or pharmacological inhibition of CD36 prevented atypical antipsychotic drugs-induced oxLDL accumulation in macrophages. Additionally, olanzapine and clozapine activated NADPH oxidase (NOX) to generate reactive oxygen species (ROS) which upregulated the activity of peroxisome proliferator-activated receptor γ (PPARγ) and subsequently elevated CD36 expression. Inhibition of NOX activity, ROS production or PPARγ activity suppressed CD36 expression and abolished the detrimental effects of olanzapine and clozapine on oxLDL accumulation in macrophages. CONCLUSION: Collectively, our results suggest that atypical antipsychotic drugs exacerbate atherosclerosis and macrophage-foam cell formation by activating the NOX-ROS-PPARγ-CD36 pathway.

Hyperuricemia induces endothelial dysfunction and accelerates atherosclerosis by disturbing the asymmetric dimethylarginine/dimethylarginine dimethylaminotransferase 2 pathway.

Hyperuricemia is closely associated with the mobility and mortality of patients with cardiovascular diseases. However, how hyperuricemia accelerates atherosclerosis progression is not well understood. The balance between asymmetric dimethylarginine (ADMA) and dimethylarginine dimethylaminotransferases (DDAHs) is crucial to regulate vascular homeostasis. Therefore, we investigated the role of the ADMA/DDAH pathway in hyperuricemia-induced endothelial dysfunction and atherosclerosis and the underlying molecular mechanisms in endothelial cells (ECs) and apolipoprotein E-knockout (apoe-/-) mice. Our results demonstrated that uric acid at pathological concentrations increased the intracellular levels of ADMA and downregulated DDAH-2 expression without affecting DDAH-1 expression. Excess uric acid also reduced NO bioavailability and increased monocyte adhesion to ECs, which were abolished by using the antioxidant N-acetylcysteine, the nicotinamide adenine dinucleotide phosphate oxidase inhibitor apocynin, or DDAH-2 overexpression. In apoe-/- mice, treatment with oxonic acid, a uricase inhibitor, increased the circulating level of uric acid, cholesterol, and lipid peroxidation; exacerbated systemic and aortic inflammation; and worsened atherosclerosis compared with vehicle-treated apoe-/- mice. Furthermore, oxonic acid-treated apoe-/- mice exhibited elevated ADMA plasma level and downregulated aortic expression of DDAH-2 protein. Notably, DDAH-2 overexpression in the ECs of apoe-/- mice prevented hyperuricemia-induced deleterious effects from influencing ADMA production, lipid peroxidation, inflammation, and atherosclerosis. Collectively, our findings suggest that hyperuricemia disturbs the balance of the ADMA/DDAH-2 axis, results in EC dysfunction, and, consequently, accelerates atherosclerosis.

Flow density of computed tomography aortography for predicting early unfavorable aortic remodeling after TEVAR in type IIIb aortic dissection.

OBJECTIVE: Patients diagnosed of DeBakey type III aortic dissection with partial thrombosis of false lumen (FL) have a higher mortality rate. However, IIIb dissections with full patent FL tend to exhibit a partially thrombosed FL quickly after thoracic endovascular aortic repair (TEVAR); thus, we investigated survival and aortic remodeling in this population. METHODS: We reviewed computed tomography aortograms (CTAs) of 123 patients with TEVAR-treated IIIb aortic dissections from July 2006 to June 2015; contrast density of CTAs represented intraluminal flow. Patients were selected to fit in 2 groups of FL in term of FL contrast density: low flow (LF) group (non-opacification in the midway of FL) and high flow (HF) group (full patent FL). RESULTS: Surgical mortality was 10.3% in the HF group and 4.5% in the LF group (n = 61; LF = 22; HF = 39). 3 patients in the HF group suffered from lethal aortic rupture in 10 days postoperatively. The HF group showed significant increase in maximal diameter, and had larger thoracic (+4.00 ± 2.68 vs -1.16 ± 3.42 mm, P < .001) aortic diameter expansion from preoperation to one week postoperation. Both groups exhibited significant favorable thoracic TL expansion and maximal aortic diameter shrinkage in postoperative one week to one year. However, HF group displayed less thoracic aortic FL regression (-70.9 ± 83.5 vs -113.9 ± 95.0 cm3, P = .1) and TL expansion (+14.5 ± 27.2 vs +36.8 ± 28.3 cm3, P = .008) when compared to LF group. CONCLUSIONS: Preoperative HF in the FL has an unfavorable effect on thoracic aortic diameter in one week post-TEVAR. This might increase the risk of aortic rupture.

Midterm result of custom-made iliac branch device for common iliac aneurysm with and without abdominal aortic aneurysm.

OBJECTIVES: Although commercial iliac branch devices offer a new and valid endovascular approach to treating iliac aneurysm and effectively preserve antegrade flow of the internal iliac artery, their use may not be suited for all types of challenging anatomy, especially isolated common iliac artery aneurysm. Our custom-made iliac bifurcation device has a unique design and excludes both combined and isolated iliac branch aneurysm. This study validated the efficacy and safety of the custom device by comparing clinical outcomes between groups receiving commercial and custom devices. METHODS: Data of consecutive patients receiving iliac bifurcation device implantation for iliac aneurysm with or without concomitant endovascular repair for abdominal aortic aneurysm from January 2010 to May 2019 were reviewed. RESULTS: Iliac bifurcation device implantation with or without concomitant abdominal aortic aneurysm stent grafting was completed in 46 patients (commercial, n = 35; custom, n = 11). No significant differences were observed regarding postoperative complications, occlusion or endoleak. Comparisons of primary (80.8% vs 85.7%, P = 0.88) and secondary (86.5% vs 85.7%, P = 0.85) patency and freedom from reintervention (88.2% vs 100%, P = 0.33), all-cause mortality (78.6% vs 100%, P = 0.25) and aneurysm-related mortality (100% vs 100%, P = 1.00) also indicated no differences at a 5-year surveillance point. Furthermore, the iliac aneurysms of the groups displayed similar shrinkage 1 year after procedures. CONCLUSIONS: For iliac aneurysm, the novel custom-made iliac bifurcation device is an adaptable design not inferior to commercial devices with regard to postoperative complications, bridge occlusion, endoleak and short-term aneurysm remodelling. It provides an alternative for treatment, particularly when certain anatomic challenges are present. CLINICAL TRIAL REGISTRATION: 2018-07-050BC, 2017-01-023ACF.

Long-Term Outcomes of Bioprosthetic or Mechanical Valve Replacement in End-Stage Renal Disease: A Nationwide Population-Based Retrospective Study.

Background: Valve replacement is associated with worse outcomes in individuals who have end-stage renal disease (ESRD) and require a long-term renal replacement therapy. Prosthetic valve selection in patients with ESRD has remained controversial. Objective: We aimed to investigate long-term outcomes of mechanical and bioprosthetic valve replacement in individuals with ESRD. Methods: We conducted a population-based retrospective cohort study using data obtained from the Taiwan National Health Insurance Research Database. In total, 10,202 patients, including 912 ESRD and 9,290 non-ESRD patients, were selected after a 1:1 propensity-score matching based on the type of prosthetic valve used. The long-term mortality outcomes were then analyzed. Results: During a median follow-up period of 59.6 months, the Kaplan-Meier survival analysis revealed that ESRD patients who underwent mechanical valve replacement had higher rates of all-cause mortality and CV deaths than those who underwent bioprosthetic valve replacement (Log-rank test, p = 0.03 and 0.02, respectively). Multivariable regression analyses demonstrated that ESRD patients who underwent bioprosthetic valve replacement had lower rates of all-cause mortality (p < 0.001, hazard ratio: 0.88, 95% confidence interval: 0.82-0.93) and cardiovascular (CV) death (p < 0.001, hazard ratio: 0.83, 95% confidence interval: 0.76-0.90) than those who had mechanical valve replacement. Conclusion: Bioprosthetic valve replacement is significantly associated with lower rates of all-cause mortality and CV death in the ESRD population.

Feasibility and rationale of direct current cardioversion immediately after transcatheter percutaneous edge-to-edge mitral valve repair.

AIMS: Atrial fibrillation (AF) is a frequent comorbidity among patients with severe mitral regurgitation (MR). Direct current (DC) cardioversion is one of the strategies for rhythm control. However, the safety and feasibility of immediate DC cardioversion after MitraClip are not elucidated. METHODS AND RESULTS: In this study, patients with symptomatic severe MR who underwent MitraClip were included. After fixing the MR, synchronized DC cardioversion was attempted for those with AF. A total of consecutive 60 patients, 36 subjects (60%), comorbid with AF. DC cardioversion was performed in 30 patients (mean age of 76.0 ± 9.3 years), and the successful conversion was achieved in 15 patients (50%). There was no any adverse event related to the cardioversion. Subjects with sustained conversion to SR experienced significant improvement in 6MWT (failed: 285 ± 110-308 ± 135 m, P = .278; successful: 269 ± 109 m-328 ± 78, P = .047) and reduction in NT-proBNP level (failed: 4411 ± 7401-3296 ± 4299 ng/mL, P = .217; successful: 4094 ± 2735-2353 ± 2856 ng/mL, P = .026) at 1 month. CONCLUSIONS: Direct current cardioversion seemed to be safe and feasible immediately after the transcatheter edge-to-edge mitral valve repairs. Subjects who maintain SR experienced better functional improvement.

DDAH-2 alleviates contrast medium iopromide-induced acute kidney injury through nitric oxide synthase.

BACKGROUND: Contrast medium-induced acute kidney injury (CI-AKI) is one of the most common causes of hospital-acquired acute renal failure. However, the pathogenesis of CI-AKI remains unclear. Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase (NOS) inhibitor that is largely metabolised by dimethylarginine dimethylaminohydroxylase (DDAH) in humans. Two isoforms of DDAH exist, namely, DDAH-1 and DDAH-2. In the present study, we examined whether the DDAH-2/ADMA/NOS pathway is involved in the pathogenesis of CI-AKI. METHODS AND RESULTS: Exposure to the contrast medium iopromide led to increase in creatinine and blood urea nitrogen (BUN) levels, accumulation of ADMA, increase in reactive oxygen species (ROS) generation, and an inflammatory response in mice kidney tissue. The injection of adenovirus-harbouring DDAH-2 lowered renal ADMA levels and had a reno-protective effect against contrast-medium injury by decreasing cell apoptosis, ROS, and fibrosis. By contrast, contrast medium-induced renal injury was exacerbated in heterozygous DDAH-2 knockout mice. In the in vitro study, overexpression of DDAH-2 increased the levels of nitrite and intracellular cGMP, while the DDAH-2 knockdown induced the opposite effect. These findings were also observed in the in vivo sample. CONCLUSIONS: Our findings provide the first evidence that the DDAH-2/ADMA/NOS pathway is involved in the pathogenesis of CI-AKI and that the protective effect of DDAH-2 probably arises from the modulation of NOS activity, oxidative stress, and the inflammatory process.

Yes-Associated Protein (YAP) Facilitates Pressure Overload-Induced Dysfunction in the Diabetic Heart.

Patients with diabetes are more prone to developing heart failure in the presence of high blood pressure than those without diabetes. Yes-associated protein (YAP), a key effector of the Hippo signaling pathway, is persistently activated in diabetic hearts, and YAP plays an essential role in mediating the exacerbation of heart failure in response to pressure overload in the hearts of mice fed a high-fat diet. YAP induced dedifferentiation of cardiomyocytes through activation of transcriptional enhancer factor 1 (TEAD1), a transcription factor. Thus, YAP and TEAD1 are promising therapeutic targets for diabetic patients with high blood pressure to prevent the development of heart failure.

The detrimental effect of asymmetric dimethylarginine on cholesterol efflux of macrophage foam cells: Role of the NOX/ROS signaling.

BACKGROUND: Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase inhibitor and has been proposed to be an independent risk factor for cardiovascular diseases. However, little is known about its role in the regulation of lipid metabolism. In this study, we investigated the effect of ADMA on cholesterol metabolism and its underlying molecular mechanism. METHODS: Oxidized low-density lipoprotein (oxLDL)-induced macrophage foam cells were used as an in vitro model. Apolipoprotein E-deficient (apoE-/-) hyperlipidemic mice were used as an in vivo model. Western blot analysis was used to evaluate protein expression. Luciferase reporter assays were used to assess the activity of promoters and transcription factors. Conventional assay kits were used to measure the levels of ADMA, cholesterol, triglycerides, and cytokines. RESULTS: Treatment with oxLDL decreased the protein expression of dimethylarginine dimethylaminohydrolase-2 (DDAH-2) but not DDAH-1. Incubation with ADMA markedly increased oxLDL-induced lipid accumulation in macrophages. ADMA impaired cholesterol efflux following oxLDL challenge and downregulated the expression of ATP-binding cassette transporter A1 (ABCA1) and ABCG1 by interfering with liver X receptor α (LXRα) expression and activity. Additionally, this inhibitory effect of ADMA on cholesterol metabolism was mediated through the activation of the NADPH oxidase/reactive oxygen species pathway. In vivo experiments revealed that chronic administration of ADMA for 4 weeks exacerbated systemic inflammation, decreased the aortic protein levels of ABCA1 and ABCG1, and impaired the capacity of reverse cholesterol transport, ultimately, leading to the progression of atherosclerosis in apoE-/- mice. CONCLUSION: Our findings suggest that the ADMA/DDAH-2 axis plays a crucial role in regulating cholesterol metabolism in macrophage foam cells and atherosclerotic progression.

Can Elderly Patients with Severe Mitral Regurgitation Benefit from Trans-catheter Mitral Valve Repair?

BACKGROUND AND OBJECTIVES: Age is a traditional risk factor for open-heart surgery. The efficacy and safety of transcatheter edge-to-edge mitral valve repair, using MitraClip (Abbott Vascular), has been demonstrated in patients with severe mitral regurgitation (MR). Since octogenarians or older patients are usually deferred to receive open-heart surgery, the main interest of this study is to elucidate the procedural safety and long-term clinical impact of MitraClip in elderly patients. METHODS: Patients with symptomatic severe MR were evaluated by the heart team. For those with high or prohibitive surgical risks, transcatheter mitral valve repair was performed in hybrid operation room. Transthoracic echocardiography (TTE), blood tests, and six-minute walk test (6MWT) were performed before, 1-month, 6-months, and 1 year after index procedure. RESULTS: A total of 46 consecutive patients receiving MitraClip procedure were enrolled. Nineteen patients (84.2±4.0 years) were over 80-year-old and 27 (73.4±11.1 years) were younger than 80. Compare to baseline, the significant reduction in MR severity was achieved after the procedure and sustained. All the patients benefited from significant improvement in New York Heart Association functional class. The 6-minute walk test (6MWT) increased from 259±114 to 319±92 meters (p=0.03) at 1 year. The overall 1-year survival rate was 80% in the elderly and 88% in those <80 years, p=0.590. Baseline 6MWT was a predictor for all-cause mortality (odds ratio, 0.99; 95% confidence interval, 0.982-0.999; p=0.026) after the MitraClip procedure. CONCLUSIONS: Trans-catheter edge-to-edge mitral valve repairs are safe and have positive clinical impact in subjects with severe MR, even in advanced age.

Efficacy of ascending aortic banding technique concomitant with type I hybrid aortic arch repair in high-risk patients.

Banding of the ascending aorta has been introduced as a less complex procedure to optimize the proximal landing zone of the stent graft in hybrid aortic arch surgery. However, data about the long-term results and effects of this technique are still limited. We aimed to study the efficacy of banding of the ascending aorta in hybrid aortic arch repair. The study included 11 high-risk patients with dilated ascending aorta (wider than 38 mm in diameter) undergoing ascending aortic banding for hybrid arch repair. Clinical outcomes, including technical success, endoleaks, perioperative mortality and morbidity, and sequential remodeling of the ascending aorta were investigated. The average diameter of the ascending aorta had been reduced (p = 0.02) from 42.1 mm (range = 39.0-46.4) to 37.2 mm (range = 35.6-38.6) after banding procedure. The technical success rate was 100.0%. No type I endoleak occurred, but 2 cases of distal stent graft-induced new entry required re-interventions. The 5-year survival and freedom from aortic events rates both were 81.8%. The ascending aortic diameter remained stable and no proximal migration of the stent graft was observed during the study period. The 5-year results validated the durability of this therapeutic modality, especially in high-risk patients.

Combined surgical and endovascular treatment with arch preservation of acute DeBakey type I aortic dissection.

BACKGROUND: DeBakey type I aortic dissection is a catastrophic event that presents a formidable challenge to cardiovascular surgeon. Here, we evaluate a new combined surgical and endovascular technique for acute condition. METHODS: Between December 2011 and December 2015, 12 patients with type I aortic dissection concomitant involving supra-aortic vessels underwent ascending aortic replacement and simultaneous stent grafts inserted into the descending aorta, left subclavian, and left carotid arteries, and into the innominate artery when possible, without arch replacement. The stent grafts, Gore TAG thoracic endoprosthesis and Viabahn, were deployed under visual guidance through opened aortic arch into the true lumen, with the techniques of circulatory arrest, moderate hypothermia, and bilateral antegrade cerebral perfusion. RESULTS: Operation was performed smoothly in all patients. There was one death, and the other 11 recovered without any neurological deficits. Follow-up computed tomography scans showed that the true lumen expanded and false lumen regressed in both arch and descending aortic segments in 1 year. The diameter did not increase in either arch or descending aortic segments. CONCLUSION: Ascending aortic replacement and stent graft for supra-aortic arteries and the descending aorta without arch replacement are feasible options for type I aortic dissection with satisfactory short-term aortic remodeling.