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How Does Sudden Cardiac Death Occur In Familial Hypertrophic Cardiomyopathy?
Funder
National Health and Medical Research Council
Funding Amount
$1,312,606.00
Summary
Familial hypertrophic cardiomyopathy is a leading cause of sudden cardiac death but the mechanisms for the induction of arrhythmia are unknown. This proposal has the potential to impact sudden death in the young and enable significant expansion of Australia’s research capacity into the treatment of familial hypertrophic heart disease in humans.
The L-type Calcium Channel In Cardiovascular Health And Disease
Funder
National Health and Medical Research Council
Funding Amount
$631,370.00
Summary
Calcium influx into cardiac muscle cells occurs via the L-type calcium channel. The channel is essential to life but when function is altered it can contribute to the development of sudden death and heart failure. I have made significant discoveries in understanding the role of the channel in disease and I have exploited this knowledge to design therapy including a novel class of calcium channel antagonists to prevent the development of heart failure.
Despite dramatic improvements in diagnosis, prevention and treatment of heart disease, cardiovascular disease remains the commonest cause of death in Australia. The continuing decline in mortality from ischaemic heart disease has been offset by an increase in the incidence of sudden cardiac death due to abnormal heart rhythms. By understanding the basic mechanisms underlying cardiac arrhythmias we are seeking to develop more effective therapies to treat and/or prevent sudden cardiac death.
Dynamic Action Potential Clamp Studies Of Drugs That Affect The Cardiac Action Potential
Funder
National Health and Medical Research Council
Funding Amount
$343,976.00
Summary
The development of drugs to treat and.or prevent cardiac arrhythmias have been plagued by the side-effect of actually increasing the risk of sudden death. One of the reasons for this is that drugs that work well in one part of the heart may cause problems in another part. We are developing a system called “dynamic action potential clamp” that will make it easier for researchers to assess the effect of drugs in different regions of both normal and diseased hearts.
Anthracyclines Disrupt Ca2+ Signalling In Cardiomyocytes: A Contribution To Cardiac Toxicity
Funder
National Health and Medical Research Council
Funding Amount
$525,620.00
Summary
Anthracyclines are one of the most effective drugs used in chemotherapy, but cause side effects resulting in serious heart problems which can be fatal. The link between anthracycline therapy and the problems they cause in the heart is not fully defined. We will investigate mechanisms leading to these side effects and define specific targets of anthracyclines in the heart. It is hoped this will lead to the design of new drugs which counteract the side effects of anthracycline treatment.
New CaMKII Therapeutic Targets In Heart Failure With Preserved Ejection Fraction
Funder
National Health and Medical Research Council
Funding Amount
$740,335.00
Summary
Deaths associated with impaired heart muscle relaxation and unstable cardiac cycle rhythm are increasing. The mechanisms by which these pathologies occur are not understood and clinical therapies are lacking. We have novel evidence to suggest that a key signalling protein, CaMKII, is critically involved in the development of these forms of heart pathology. This goal of this project is to identify how CaMKII is implicated in heart failure and dysrhythmia as a basis for designing new therapies.
A Novel Therapy For The Prevention And Treatment Of Familial Hypertrophic Cardiomyopathy
Funder
National Health and Medical Research Council
Funding Amount
$835,972.00
Summary
Familial hypertrophic cardiomyopathy is a genetic disorder that leads to enlargement of the heart, cardiac failure and sudden death. No treatment exists that can reverse or prevent the cardiomyopathy. In this proposal we will determine whether a peptide (Patent WO2013/113060) targeting a calcium channel can prevent or reverse the cardiomyopathy as a novel treatment for the disease.
Optimising Efficacy Of A Peptide Derived Against The Alpha-interacting Domain Of The L-type Calcium Channel In Reduction Of Ischemia-reperfusion Injury
Funder
National Health and Medical Research Council
Funding Amount
$405,063.00
Summary
A heart attack is associated with an increase in free radicals and calcium in heart muscle cells. The function of the L-type calcium channel, a protein responsible for calcium entry into cells, is altered by free radicals and this contributes to the development of heart disease. We now have considerable proof of concept that a peptide derived against the L-type calcium channel can decrease heart injury. We will optimise efficacy and delivery of the peptide to prevent heart failure.
Regulation Of RyR2 Channels By Calmodulin In Healthy And Diseased Hearts
Funder
National Health and Medical Research Council
Funding Amount
$614,421.00
Summary
In the heart, RyR2 is responsible for intracellular Ca2+ release. The RyR2 is comprised of a Ca2+ channel and accessory proteins such as CaM that regulate channel activity. Evidence suggests that RyR2 regulation by CaM is altered in heart failure and human arrhythmia syndromes, but there has been no direct evidence for this. We will provide this direct evidence plus determine how CaM regulates RyR2 channels and intracellular Ca2+ release and how this leads to cardiac arrhythmias.
Disturbances to the normal rhythm of the heart beat cause ~15% of deaths in our community. We wish to understand why the electrical signals in the heart can become chaotic. We will study a particular heart rhythm disturbance called acquired long QT syndrome to see if it is possible to develop a computer model that can accurately predict when and how arrhythmias will occur.