Heart failure affects an estimated 26 million people worldwide, and at any one time 300,000 Australians. Whilst the gold standard treatment for heart failure is heart transplantation, a shortage of donor hearts limits the availability of this lifesaving intervention. Mechanical circulatory support devices offer a promising alternative treatment for not only patients on the transplantation waiting list, but also as a destination therapy for patients who are not eligible for transplantation. Ventricular assist devices (VADs) are a form of mechanical circulatory support used to support the function of the failing heart when the heart is unable to maintain adequate cardiac output. Most commonly a VAD will work in parallel with the native left ventricle (LV), with inflow cannula implantation performed through the apex of the LV and secured to the epicardium with a suture ring. Common complications of VAD implantation and support, such as surgical bleeding, can be attributed in part to inflow cannula design or placement. Extended time on cardiopulmonary bypass (utilised during VAD implantation) is also associated with inferior postoperative outcomes. To address the complications influenced by extended surgical time, and inflow cannula design and placement, Shaun Gregory developed a novel sutureless cannula through his doctoral research. The cannula was introduced in a chapter of his thesis and awarded a provisional patent (now lapsed). Gregory’s research involved the design and manufacture of a proof-of-concept device, and its implantation within cadaveric hearts connected to an ex-vivo mock circulation loop that evaluated the ability of the device to provide a blood-tight seal through the compression of the myocardium between the internal and external components. In 2016 a paper was published that evaluated different inflow cannula tip geometries for thrombus risk within an in-silico heart model, from the same research group. One of the five cannulae modelled had an inferiorly flared internal geometry, indicative of Gregory’s cannula, however it was only a representative model with an idealised internal geometric shape. Beyond this publication there has been no further research, device development, or device evaluation undertaken or published involving the sutureless inflow cannulae (SLIC) until this doctoral research. The doctoral research presented within this thesis aimed to continue the development beyond proof-of-concept and undertake a critical evaluation of the SLIC. To undertake further evaluation of the SLIC a critical review of the cannula developed by Gregory was undertaken, where the limitations of the design were addressed, and the device progressed through design changes. For development of an implantable medical device one of the evaluations conducted is implantation within an animal in the acute setting. To continue with its evaluation the SLIC was implanted in-vivo (within pigs) through an acute study and evaluated against parameters such as the ability of the SLIC to be implanted in under 2 minutes, for the SLIC to provide a secure haemostatic seal across the myocardial wall, and there to be no bleeding at the site of SLIC implantation. To investigate the impact the compressive seal of the SLIC had on the myocardium, histology review was conducted on sectioned cardiac tissue from all five animals against markers for myocardial injury. Whilst the initial two animals in the acute in-vivo study had successful outcomes across all areas evaluated, the following three animals all suffered adverse events due to internal cardiac geometry incompatible with SLIC implantation (hypertrophic cardiomyopathy), or surgical error (near-complete oversew of the outflow graft). The final animal implanted with the SLIC had undiagnosed severe hypertrophic cardiomyopathy that resulted, during attempted implantation, in critical breakage of the SLIC within the LV. Histological review against immunohistochemical markers for early onset myocardial injury also produced positive results, primarily seen at the site of implantation through expression of Tumor Necrosis Factor Alpha, and depletion of Cardiac Troponin T and Myoglobin. Haematoxylin and Eosin staining also revealed changers indicative of early onset damage such as wavy fibres, interstitial oedema, granulation formation, and hypereosinophilia of some cardiomyocytes. These results, in combination with the in-vitro testing determining forces applied by the SLIC onto the cardiac tissue, provide indication that the current implantation securement mechanism of the SLIC causes myocardial injury. The final research conducted and described in this doctoral thesis details the redesign process of the SLIC, that extracts the outcomes from the research and formulates new device development inputs. A proof-of-concept device is introduced in the final research chapter. The main finding of this doctoral research indicates that a SLIC that is capable of rapid implantation, without the reliance on suturing into place for secure fixation is feasible and capable of working in conjunction with a VAD to support cardiac function. However, the impact that the compressive locking mechanism has on the tissue it is implanted within requires attention and consideration in any future work design parameters to ensure development of an implantable medical device suitable for long-term implantation.