Future Participants of The Baird Institute’s Kenyan Fellowship Program

Two future participants of The Baird Institute’s Kenyan Fellowship program visit Australia

Pictured: (Left to right)  photographed in front of RPAH; Dr Nikita Mehta, Dr Fredrick Mitema, Ambassador Isaiya Kabiya, Prof Paul Bannon & Dr Victor Kwasi

In November we hosted two future participants of The Baird Institute’s Kenyan Fellowship Program in Australia; Dr Nikita Mehta and Dr Fredrick Mitema from Nairobi.  They came to Australia on a “travelling scholarship”.  While here they attended the annual conference of the Association of Thoracic and Cardiovascular Surgeons of Asia in Melbourne, then came to Sydney to visit Royal Prince Alfred Hospital (RPAH) and The Baird Institute’s research programs and research facilities. During the reception and tour, Dr Mehta and Dr Mitema were joined by the Kenyan High Commissioner from Canberra, Ambassador Isaiya Kabiya.

Nikita is the first locally trained female cardiothoracic surgeon in East and Central Africa and is a graduate of the program at The University of Nairobi that The Baird Institute helped establish around 5 years ago.  Dr Mehta completed her undergraduate and post-graduate training at the University of Nairobi last year, graduating with a Master’s degree in cardiothoracic and vascular surgery. She will return to Sydney in 2018/2019 to commence her 2 year surgical trainee fellowship at RPAH under the guidance of Professor Paul Bannon, the Chair of The Baird Institute. Nikita hopes this will give her the skills and knowledge to one day set up a self-sustained cardiothoracic centre of excellence in Kenya specialising in clinical care, training and research.

Please take a look at our interview with Nikita and Fred.

In Kenya, we are still in the infantile stage when it comes to cardiac surgery. This is partly because of the lack of skilled personnel, as well as the numerous challenges of providing super specialised care in a resource constrained environment. Working at RPA will give me exposure to cardiac surgeries which are not routinely performed back home.

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.

“The best surgeon will eventually be a robot”

Professor Michael Wilson of The Baird Institute, recently spoke to Matt Peacock of the ABC’s 7.30 Report.

The revolution in robotics and artificial intelligence has made its way into surgery. Patients needing coronary artery bypasses would normally require open heart surgery but now, thanks to robots, they are facing far less traumatic surgery and a much faster recovery.

The “Da Vinci” robot is used by Professor Wilson to minimise the invasive chest surgery normally associated with a bypass operation.  Also talking to Matt Peacock on the 7.30 Report was Professor Vipul Patel from the “Global Robotics Institute” at Florida Hospital in the USA.  Professor Patel is world-renowned for his contribution to the field of robotic-assisted surgery and is one of the most experienced robotic surgeons in the world.  He has personally performed more than 10,000 robotic prostatectomies.

Professor Patel was the plenary speaker and guest of honour at the recent Sydney Robotic Summit on the future of Robotic Surgery.  The Summit hosted some of the world’s best Robotic Surgeons from across multiple surgical specialities. In his session, Professor Patel examined where we would be 10 years from now in the operating rooms of hospitals. Many of the surgeons associated with the Baird Institute also presented at the Robotics Summit; Professor Paul Bannon, Chair of The Baird Institute, spoke on adopting innovation ethically, while Professor Michael Wilson spoke on when to do open heart surgery, thoracoscopic surgery or surgery using the Da Vinci robot.  One of our past Research Fellows, Dr Michael Seco, presented on robotic cardiac surgery at the Summit.

‘When I first saw pictures of it, I couldn’t believe it. There was a surgeon to the side and the patient on the table. And the surgeon was controlling the whole thing through a robot at some remove from the operating table itself.”

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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