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Heart Failure Pharmacology

Slowing the progression of heart failure

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Laboratory head

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Latest Achievements

NHMRC Level A Senior Research Fellowship (2014–18)

American Heart Association International Fellow (2013– )

NHMRC Senior Research Fellowship Level A (2008)

NHMRC Biomedical Career Development Award (2002)

Foundation for High Blood Pressure Research Fellowship (2000)

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Professor Rebecca Ritchie NHMRC Senior Research Fellow
Identifying new therapeutic strategies to prevent, delay or arrest the progression of heart failure.



Mr Charles Cohen Mr Thomas Giddy Ms Cao-Uyen Lam Ms Nimna Perez


About the Heart Failure Pharmacology laboratory

Heart failure is a major cause of death worldwide, for which there is no cure. The over-arching goal of the Heart Failure Pharmacology laboratory is to prevent human heart failure, and to delay or arrest its progression. The team is focusing its research on developing new treatments for heart failure resulting from interruptions in coronary blood supply (such as in heart attack) and/or as a result of diabetes. They have chosen to focus on these as both are major causes of heart failure. Delaying the onset and progression of heart failure will enrich the quality and length of life for over three million Australians at risk of, or already affected by, this debilitating disorder.

Heart attack (myocardial infarction) and the heart failure that then develops in heart attack survivors are the major cause of death in Western societies; this is now expanding to all corners of the globe. Following heart attack, some cardiac muscle cells (cardiomyocytes) die. A scar (fibrosis) then develops to replace the dead muscle cells. The remaining surviving heart muscle cells then become abnormally enlarged (hypertrophy), to try and compensate for the loss of cardiac muscle. As a result, the heart is stiffer and becomes less efficient at contracting, so its ability to deliver blood to the body is suboptimal. These impairments can then further progress, increasing risk of heart failure and death. Indeed, myocardial contractile function often remains impaired in patients after an infarction, despite clinical advances that accelerate restored cardiac blood supply (reperfusion). New therapeutic strategies specifically targeted at preserving myocardial function in this context are thus essential.

Diabetes mellitus is a global epidemic. The major cause of death in affected patients is cardiovascular complications. The disease has been diagnosed in almost one million Australians, but current estimates suggest diabetes remains undetected in almost the same number. The markedly increasing incidence of both type 1 and type 2 diabetes imposes an exponential healthcare burden as a result of cardiovascular complications-induced morbidity and mortality. Whilst good blood glucose control is essential for delaying the onset and progression of the cardiovascular complications of diabetes, the impact of diabetes on the heart can be regarded as a silent predator. Even in patients who manage their blood glucose levels well and have no obvious cardiovascular symptoms (e.g. high blood pressure, atherosclerosis), the ability of the heart to recover from each cardiac contraction can be impaired. The diabetic heart can take longer to relax and to fill again with blood in readiness for the next cardiac contraction. Known as diastolic dysfunction, this may not manifest in obvious symptoms but is associated with increased heart failure risk and poor prognosis. Causal factors in diastolic function include cardiomyocyte hypertrophy and death, as well as cardiac fibrosis. Diabetes increases heart failure risk 2.5-fold, even when adjusted for coronary artery disease. Moreover, heart failure presents earlier in diabetic patients, with heart failure prevalence increased 5–8-fold in 45–65 year-old diabetic subjects. New therapies for restoring cardiac function in the diabetic heart are thus essential.

The Heart Failure Pharmacology research program seeks to develop better pharmacotherapies to prevent and treat myocardial dysfunction and heart failure from these causes, exploiting the team’s recent key discoveries. A key common thread to the group’s research is the important role of toxic molecules known as oxygen-derived free radicals (reactive oxygen species, ROS) in triggering abnormalities in cardiac structure and function. The group’s recent internationally-recognised discoveries from the preclinical research models in the laboratory include the first evidence that:

  1. The anti-inflammatory protein annexin-A1 is an endogenous regulator of cardiac muscle survival and recovery of cardiac contractile function, which utilise a different mechanism to its anti-inflammatory actions
  2. Nitroxyl-triggered signalling downregulates abnormal cardiac remodelling and ROS generation
  3. Coenzyme Q10 supplementation rescues cardiomyopathy induced by type 1 and 2 diabetes
  4. Enhancing physiological growth signalling through the p110α isoform of phosphoinositide 3-kinase (PI3Kα) can prevent diabetes-induced impairments in cardiac structure and function, via novel counter-regulation of myocardial ROS

Research focus

  • Identify which receptors for annexin-A1 are attractive targets for survival of myocardial tissue in the first few days after moderate myocardial infarction.
  • To use the group’s annexin-A1 cardioprotection research as a platform to develop new therapeutic opportunities for protecting cardiac function after more severe cardiac events, while the injury caused by the heart attack is still evolving.
  • Identify novel ways of exploiting nitric oxide signalling to preserve function of the diabetic and/or failing heart.
  • Examine the role of glucose-induced changes in the structure of key cardiac proteins in diabetes-induced cardiac remodelling and dysfunction.
  • Identify new mediators of diabetes-induced myocardial damage.

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With the rising number of Australians affected by diabetes, heart disease and stroke, the need for research is more critical than ever.

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