Research

Composite Y Grafts From the Left Internal Mammary Artery: Current Considerations

Paterson HS, Bannon PG

Heart Lung Circ 2018 Feb;27(2):133-137

PMID: 29126818

Abstract

The use of composite coronary artery bypass grafts from the left internal mammary artery (LIMA) has increased over the last 20 years. Total arterial revascularisation can be achieved with two arterial conduits and is associated with a reduced risk of stroke. However, the traditional coronary bypass graft configurations of the in situ LIMA and aorto-coronary saphenous vein grafts remain as the mainstay of coronary bypass surgery in most centres. Concerns regarding composite Y grafts relate to (1) the adequacy of a single inflow for all coronary bypass grafts; (2) the risk of compromising the LIMA flow to the left anterior descending coronary artery; (3) the effects of competitive flow on graft patency; and (4) the use of sequential coronary anastomoses. The evidence upon which these concerns are based will be discussed along with the evidence relating to the use of the various second conduit options.

A Time to Act and a Time to Watch: Severe Guide-Catheter Induced Proximal Coronary Dissection With Extensive Ascending Aorta and Arch Dissection, Managed by Immediate Coronary Stenting and Watchful Waiting

Lau JK, Roy P, Bing R, Bannon PG, Lowe HC

J Invasive Cardiol 2017 Sep;29(9):E99-E100

PMID: 28878100

Abstract

In this case, prompt stenting of the dissection entry flap allowed for stabilization and eventual healing of a severe catheter-induced aortic dissection, without resort to surgical intervention.

Surgical Management of Caseous Calcification of the Mitral Annulus

Fong LS, McLaughlin AJ, Okiwelu NL, Nordstrand IAJ, Newman M, Passage J, Joshi PV

Ann. Thorac. Surg. 2017 Sep;104(3):e291-e293

PMID: 28838533

Abstract

Caseous calcification of the mitral annulus (CCMA) is a rare variant of mitral annular calcification; it can manifest with conduction abnormalities or systemic embolization. It typically involves the posterior mitral annulus, and surgery is indicated for severe mitral valve dysfunction, for embolic complications or when the diagnosis is not certain. We describe a structured approach to the surgical management of CCMA using bovine pericardium to repair the defect.

Tricuspid leaflet repair: innovative solutions

Boyd JH, Edelman JJB, Scoville DH, Woo YJ

Ann Cardiothorac Surg 2017 May;6(3):248-254

PMID: 28706867

Abstract

Tricuspid regurgitation (TR) represents a significant disease process and when severe, is associated with increased mortality. Recent guidelines support a more aggressive approach to tricuspid valve (TV) surgery, especially when encountered with left-sided valvular pathology. While annuloplasty has been the standard treatment for TR, it may not provide as effective or durable a repair compared to annuloplasty combined with TV repair techniques. Several of these approaches are discussed including bicuspidalization, anterior leaflet augmentation, edge to edge repair, neochords, leaflet resection and combined approaches. Although patient cohorts in most of the studies examining these techniques are small, the long-term durability of TV repair is significant.

ARHGAP18 Protects Against Thoracic Aortic Aneurysm Formation by Mitigating the Synthetic and Proinflammatory Smooth Muscle Cell Phenotype

Liu R, Lo L, Lay AJ, Zhao Y, Ting KK, Robertson EN, Sherrah AG, Jarrah S, Li H, Zhou Z, Hambly BD, Richmond DR, Jeremy RW, Bannon PG, Vadas MA, Gamble JR

Circ. Res. 2017 Aug;121(5):512-524

PMID: 28701309

Abstract

RATIONALE: Thoracic aortic aneurysm (TAA) is a potentially lethal condition, which can affect individuals of all ages. TAA may be complicated by the sudden onset of life-threatening dissection or rupture. The underlying mechanisms leading to TAA formation, particularly in the nonsyndromal idiopathic group of patients, are not well understood. Thus, identification of new genes and targets that are involved in TAA pathogenesis are required to help prevent and reverse the disease phenotype.

OBJECTIVE: Here we explore the role of ARHGAP18, a novel Rho GAP expressed by smooth muscle cells (SMCs), in the pathogenesis of TAA.

METHODS AND RESULTS: Using human and mouse aortic samples, we report that ARHGAP18 levels were significantly reduced in the SMC layer of aortic aneurysms. Arhgap18 global knockout (Arhgap18(-/)(-)) mice exhibited a highly synthetic, proteolytic, and proinflammatory smooth muscle phenotype under basal conditions and when challenged with angiotensin II, developed TAA with increased frequency and severity compared with littermate controls. Chromatin immunoprecipitation studies revealed this phenotype is partly associated with strong enrichment of H3K4me3 and depletion of H3K27me3 at the MMP2 and TNF-α promoters in Arhgap18-deficient SMC. We further show that TAA formation in the Arhgap18(-/-) mice is associated with loss of Akt activation. The abnormal SMC phenotype observed in the Arhgap18(-/-) mice can be partially rescued by pharmacological treatment with the mTORC1 inhibitor rapamycin, which reduces the synthetic and proinflammatory phenotype of Arhgap18-deficient SMC.

CONCLUSION: We have identified ARHGAP18 as a novel protective gene against TAA formation and define an additional target for the future development of treatments to limit TAA pathogenesis.

Plasma activated coating immobilizes apolipoprotein A-I to stainless steel surfaces in its bioactive form and enhances biocompatibility

Vanags LZ, Tan JTM, Santos M, Michael PS, Ali Z, Bilek MMM, Wise SG, Bursill CA

Nanomedicine 2017 Oct;13(7):2141-2150

PMID: 28668625

Abstract

We utilized a plasma activated coating (PAC) to covalently bind the active component of high density lipoproteins (HDL), apolipoprotein (apo) A-I, to stainless steel (SS) surfaces. ApoA-I suppresses restenosis and thrombosis and may therefore improve SS stent biocompatibility. PAC-coated SS significantly increased the covalent attachment of apoA-I, compared to SS alone. In static and dynamic flow thrombosis assays, PAC+apoA-I inhibited thrombosis and reduced platelet activation marker p-selectin. PAC+apoA-I reduced smooth muscle cell attachment and proliferation, and augmented EC attachment to PAC. We then coated PAC onto murine SS stents and found it did not peel or delaminate following crimping/expansion. ApoA-I was immobilized onto PAC-SS stents and was retained as a monolayer when exposed to pulsatile flow in vivo in a murine stent model. In conclusion, ApoA-I immobilized on PAC withstands pulsatile flow in vivo and retains its bioactivity, exhibiting anti-thrombotic and anti-restenotic properties, demonstrating the potential to improve stent biocompatibility.

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