Neuroendocrine Hormone Release in Acute Type B Aortic Dissection

Acute type B aortic dissection (TBAD) is a lethal condition associated with poor outcomes if not identified early and managed appropriately. Since the first description of aortic dissection back in the mid-18th century, the management of acute TBAD has changed tremendously. Initial management focused on open surgical techniques to repair the dissection or ‘tear’ in the aortic lumen; however, this was associated with high morbidity and mortality. As medicine continued to involve over the years, the management of acute TBAD shifted to focus on medical management as first line treatment in uncomplicated cases. The advancement of endovascular technology in recent decades have then superseded the open surgical management of TBAD with the utilisation of endografts to treat aortic dissection. In the acute setting, the initial step of management is focused on aggressive antihypertensive therapy to prevent further progression of the dissection or aortic dilatation. This can be difficult with majority of patients requiring multiple antihypertensive agents, both intravenous and oral therapy. Current literature is scarce in identifying the cause of this hypertensive drive in the acute phase. Chapter 1 provides a general overview of aortic dissection including its pathophysiology and management. Chapter 2 is aimed at assessing the current epidemiology of aortic dissection in Aotearoa New Zealand. The incidence of aortic dissection was shown to be increasing with major ethnic disparities seen affecting Maori and Pacific Islanders. Chapter 3 discusses the influence of cardiovascular-based neuroendocrine hormones on blood pressure in acute TBAD. The study sheds light on CNP and GDF-15 and the potential role of these two markers in the pathophysiology of aortic dissection and how these can be translated into the development of therapeutic agents to control blood pressure. Chapter 4 investigates the role of the sympathetic nervous system on blood pressure in acute TBAD. We found that there is an increased sympathetic nerve activity in acute TBAD and how this can be utilised in the development of both pharmaceutical or non-pharmaceutical therapy to reduce the central sympathetic outflow.