Heart Foundation

The Heart Foundation wants hearts fit for life. To ensure this happens, its mission is to stop all people in New Zealand dying prematurely from heart disease and enable people with heart disease to live full lives. With more than 186,000 people in New Zealand living with heart disease, they intend to continue to fund life-saving heart research and maintain our vital work in local communities. To achieve this vision they have three goals – enable people to make heart healthy choices; better outcomes for people and whānau impacted by heart disease; fund New Zealand heart research and training.

Why is diabetes associated with high rates of heart disease?

Supervisors

Kim Mellor
Parisa Koutsifeli

Discipline

Heart Foundation

Project code: MHS003

Heart disease is the leading cause of morbidity and mortality in diabetic patients. In diabetes, cardiac complications are evident even in the absence of vascular abnormalities and represent a primary manifestation of the disease. Understanding the mechanisms of cardiac pathology in diabetes is important for the development of new targeted treatment therapies. We have recently reported that a particular type of programmed cell death, autophagy, is upregulated in diabetic hearts but an understanding of how autophagy contributes to cardiac pathology in diabetes is lacking. Preliminary evidence suggests that the disturbed balance of systemic glucose, fructose and insulin levels in diabetes modifies key signaling pathways involved in autophagy induction. This project aims to investigate the molecular mechanisms underlying heart dysfunction in diabetes.

Investigating exercise intolerance in hypertension

Supervisor

Rohit Ramchandra (ext 85183)

Discipline

Heart Foundation

Project code: MHS037

Exercise improves outcomes for people of all ages. However, tolerance to exercise appears to be significantly limited in patients with cardiovascular disease, in particular in patients with hypertension. What drives this intolerance is not clear and this project will investigate the role of blood flow to the heart in limiting exercise tolerance.

We will utilise a large animal model to explore changes in heart muscle blood flow and autonomic drive during exercise. The consequences of hypertension for perfusion of coronary blood vessels will be explored. This project will introduce the student to a number of experimental techniques in conscious animals. Preference will be given to students who WANT to continue on with a Masters project.

Memory of previous cell damage

Supervisors

Assoc Prof Qi Chen (ext 85645)
Prof Larry Chamley

Discipline

Heart Foundation

Project code: MHS064

Preeclampsia, a human specific hypertensive disorder during pregnancy affects 5-8% of all pregnancies worldwide. There is rapidly growing evidence suggesting that women with a history of preeclampsia have an increased risk for recurrent preeclampsia and developing cardiovascular diseases later.This is despite the clinical symptoms and signs of hypertension resolving within a few weeks after delivery. However, the underlying mechanisms of this association have not been well understood. Dysfunction of endothelial cells is a fundamental feature of hypertension in pregnancy, and cardiovascular diseases. After the birth, dysfunction of endothelial cells in women who developed preeclampsia is still present and remains for many years. This slow recovery may indicate that endothelial cells memorise previous damage, a memory which persists for a long time. To date there is no intervention or prevention programmes for women with a history of preeclampsia, in order to reduce the risk of developing cardiovascular diseases later. In this project we will investigate whether calcium supplementation or aspirin treatment can prevent the transferring of previous damage onto the next generation, as both treatments have showed significant reduction of recurrent preeclampsia. In this project, general laboratory, and cell and tissue culture skills are required.

The little brains on the heart: Pioneering 3D imaging of human cardiac neurons in health and disease

Supervisors

Jesse Ashton (09 373 7599 ext 83259)
Johanna Montgomery

Discipline

Heart Foundation

Project code: MHS092

Interconnecting clusters of neurons - termed ganglia - situated in fat on the surface of the heart constitute the final node in a sophisticated network that controls heart rhythm. Maladaptive changes in cardiac neuronal function are associated with development of abnormal heart rhythms in conditions of cardiovascular disease and with aging. Nerve stimulation which reverses this neuronal plasticity has emerged as a viable therapeutic strategy for treating abnormal heart rhythms. This project will help advance this treatment strategy by improving our understanding of human cardiac ganglia structure and function.

Biopsies of cardiac fat are obtained with consent from patients undergoing open heart surgery at Auckland Hospital. We then make electrophysiological recordings from neurons in intact ganglia to describe how they function and communicate, and then use microscopy to image single neurons in 3D to determine expression of proteins involved in synaptic communication. This project will involve scaling up our methods to image interconnecting ganglia and testing specific antibodies to help delineate functional classes of neurons involved in heart rhythm control. The student will develop skills in immunolabelling and 3D confocal microscopy. Preference will be given to students wishing to continue on to an Honours degree project.

How many hours per night is enough? A systematic integrative review to identify optimal hours of CPAP therapy use for sleep apnoea

Supervisor

Kim Ward

Discipline

Heart Foundation

Project code: MHS096

Obstructive sleep apnoea (OSA) is a global health issue and continuous positive airway pressure (CPAP), delivered overnight via face-mask is the go to treatment worldwide. However, concern exists that patients under-utilise this therapy, despite a lack of consensus about what is good therapy use. An array of studies are available regarding the hours per night and nights per week required for CPAP use, but which differ in opinion about what is optimal.

This systematic review aims to identify from the current literature what constitutes optimal CPAP use for OSA.

Skills developed include:

  • Literature search and review
  • Basic research skills including data collection methods and data quality appraisal
  • Data interpretation and presentation
  • Professional scientific writing and the publication process
  • The student will be based at the School of Nursing, University of Auckland.

Synthesising evidence on predictive factors for CPAP use and non-use for sleep apnoea using systematic integrative review

Supervisor

Kim Ward

Discipline

Heart Foundation

Project code: MHS098

Obstructive sleep apnoea (OSA) is a global health issue and continuous positive airway pressure (CPAP), delivered overnight via face-mask is the go-to treatment worldwide. However, concern exists that patients under-utilise this therapy, despite a lack of consensus about what is good therapy use. An array of studies are available regarding interventions to support CPAP use, but which factors leverage CPAP use the best?
This systematic review aims to identify from the current literature what key predictive factors support CPAP use and which predict non-use for OSA.

Skills developed include:

Literature search and review

  • Basic research skills including data collection methods and data quality appraisal
  • Data interpretation and presentation
  • Professional scientific writing and the publication process
  • The student will be based at the School of Nursing, University of Auckland

Quantification of exchange proteins activated by cAMP (Epac) in rat hearts with right ventricular hypertrophy

Supervisors

Dr Marie-Louise Ward (09 923 4889)
Dr Sarbjot Kaur

Discipline

Heart Foundation

Project code: MHS178

Heart disease is a global burden, responsible for 31% of all mortalities worldwide. However, little is known of the contribution of the right ventricle to heart disease that progresses to heart failure and premature death. Right heart disease frequently arises as a result of increased right ventricular afterload in response to pulmonary arterial hypertension. Research using an animal model of pulmonary artery hypertension suggests that the development of right ventricular hypertrophy results in subcellular changes in the cardiomyocytes that impair cardiac function. Recent studies have shown that exchange proteins activated by cAMP (known as “Epac”) induce alterations in intracellular Ca2+ regulation when activated in many cell types, including cardiomyocytes. Cyclical changes in intracellular Ca2+ are key in controlling cardiomyocyte contraction and relaxation, which enables the heart to function as a pump. Previously we have shown that Epac activation of healthy cardiomyocytes causes Ca2+ leak from the sarcoplasmic reticulum, which is the intracellular Ca2+ store. This in turn means less Ca2+ is available for activating the cross bridges and force production.

The aim of this summer studentship project is to quantify the relative abundance and distribution of Epac proteins in ventricular tissue from healthy control hearts and in hearts with right ventricular hypertrophy. Fixed tissue samples will be sectioned and antibody labelled with specific Epac antibodies and key excitation-contraction coupling proteins. Images will be taken using confocal microscopy and quantification carried out.

This project would ideally suit a student with a strong background in cardiac muscle physiology who are considering a research career.

Skills developed include:

  • Cryosectioning
  • Immunolabelling 
  • Confocal microscopy
  • Data collection and statistical analysis
  • Literature review and scientific report writing 
  • Presentation of results

Nanoscale fibrosis and intracellular remodelling of cardiac myocytes in heart failure

Supervisor

David Crossman (ext 89964 )

Discipline

Heart Foundation

Project code: MHS182

Heart failure is the inability of the heart to pump enough blood to supply the body’s energetic demands. A notable pathological feature of the failing heart is fibrosis, where excessive production of proteins, including collagen, fills the extra-cellular matrix (ECM). The ECM can be thought of as flexible scaffold that organises the cardiac myocytes into functional pump. At a macroscopic level fibrosis leads to both impaired relaxation and impaired contraction. However, limited data exists on the organisation of collagen at the nanoscale. Recent data from the Cardiac Nanobiology Group (https://www.fmhs.auckland.ac.nz/en/sms/about/our-departments/physiology/research-groups/cardiac-nanobiology-group.html) demonstrates excessive production of the rarely studied type VI collagen appears to disrupt nanoscale intra-cellular organisation of the calcium signally apparatus that controls contraction. In this project you will use cutting edge microscopy to characterise fibrosis and myocyte remodelling at the nanoscale. This will provide new insight on the structural changes that drive heart failure.

Does the ABO blood group A afford immunoprotection to cardiac valvular bioprostheses?

Supervisors

Dr Steve Waqanivavalagi
Professor Jillian Cornish
Mr Paget Milsom

Discipline

Heart Foundation

Project code: MHS215

The problem
Bioprosthetic heart valves, such as those derived from pigs, are limited by a short lifespan because they elicit a chronic inflammatory response that leads to progressive calcification and graft failure. Pigs possess a unique AO blood group system that is similar to the human ABO blood group. The A antigen from pigs and the A antigen from humans are similar. Therefore, it is possible that patients with an A blood group do not develop the same degree of graft rejection as patients with other blood group types.

The project
The aim of this project is to record and correlate the ABO and rhesus blood group statuses, demographic data, and clinical risk factors, with the longevity of bioprosthetic cardiac valves for patients who have undergone redo valve replacement surgery at Green Lane Cardiothoracic Surgical Unit.

Examination of the Immunogenicity of a Tissue Engineered Heart Valve using a Novel Surgical Model in Rats

Supervisors

Dr Steve Waqanivavalagi
Professor Jillian Cornish
Mr Paget Milsom

Discipline

Heart Foundation

Project code: MHS218

Background

Our group is tissue engineering a novel heart valve that we hope will outperform and outlive prostheses currently used for valve replacement surgery. A preliminary scaffold has been engineered using bovine pericardium and decellularised to remove the genetic material of the animal. This scaffold has surpassed preliminary laboratory investigations and is now at a point where its immunogenicity must be interrogated.

Project

To answer this question, experimental samples will be surgically implanted subcutaneously in rats and then harvested at designated time points. Experimental tissue samples will be compared to industry standard samples using histological, biochemical, and architectural techniques that have been perfected within our laboratory.

A surgical rat model has been designed specifically for this project last summer and animal ethics application has been initiated.

Outcomes

The main aim of the study is to prove that the surgical rat model can be used to satisfactorily examine the immunogenicity of experimental tissue engineered heart valves. This summer project will set the scene for a strong Honours project. The project will suit biomedical students interested in regenerative medicine and translational science or clinical students interested in Cardiology or Cardiothoracic Surgery.