Heart disease is the biggest killer in the society today. The function of the heart is governed by the cell biology and molecular physiology of the heart muscle. As such, the heartbeat, the rhythm, the force of the contraction, and irregularities thereof are controlled by the network of cells that make up the heart. In my laboratory, we study the heart muscle and its constituent cells under normal conditions, during pathologic conditions such as myocardial infarction, heart failure, and cardiac myopathies, as well as after exercise training in both health and disease. We do this to understand the heart better, and therefore be able to generate better therapies for the heart when something goes wrong and ultimately to reduce the impact of heart disease to the patient as well as the society as a whole. This includes studying the cellular and molecular events that underlie and translate into first a reduced and secondly an improved function. In order to do this, we employ a range of experimental models that mimic normal function, dysfunction, disease and exercise, as well as physiological, biophysical, electrophysiological, biochemical, and molecular laboratory methods.
CVD & Diabetes Trials
Professor John McMurray's research focuses on testing new treatments in patients with various types of heart diseases, type 2 diabetes mellitus and chronic kidney disease. This usually involves large studies involving substantial numbers of patients and investigators in many different countries. The aim is to advance the management of some of the most common, disabling and deadly diseases facing the developed world today.
Heart Failure and Cardiovascular Trials
Heart failure is the term used to describe a set of symptoms and findings on examination that occur when the heart fails to pump as well as it should. There are many reasons why the heart may not pump properly including weakness and/or stiffness of the heart muscle, narrowed or leaking valves and abnormal heart rhythms. The commonest cause is narrowing of the arteries of the heart and heart attacks. Therefore, heart failure is a very common condition. Around 1% of people under 65 years of age have heart failure, but 7% of 75-84 year olds have heart failure and this increases to 15% in people older than 85. It is one of the most common causes of hospitalisation in patients over 65 years of age and it is an extremely costly condition for health services around the world. Heart failure can be a deadly condition, and the life expectancy of patients with heart failure is as poor as patients with some of the most common types of cancer.
Human Atrial Fibrillation
Atrial fibrillation (AF) is the most common cardiac arrhythmia, affecting ~1% of the general population. It substantially increases the risk of stroke, heart failure and death. Currently available anti-arrhythmic drugs are only moderately effective and safe. The re-entrant and non-re-entrant electrophysiological mechanisms that initiate and sustain AF are multiple, complex and interacting. An improved understanding of these mechanisms at atrial cell and tissue level, and of how they are influenced by atrial remodelling from myocardial disease and chronic AF, will aid the search for new drug targets for preventing AF.
The Loughrey group has substantial expertise in experimental cardiology using an integrative approach to study the pathophysiology of heart disease. In particular, they focus on the cellular mechanisms contributing to altered heart architecture and function following myocardial infarction, myocarditis and hypertension and how this adverse cardiac remodelling leads to heart failure. The overall aim is to identify new therapeutic targets with translational potential for limiting the progression to heart failure by attenuating adverse cardiac remodelling.
Ventricular Arrhythmia Mechanisms
Patients with heart failure (HF) are at risk of sudden death due to abnormally fast heart rhythms (ventricular arrhythmias), which are produced by imbalances in the electrical system of the heart. At present, the only effective treatment is to implant a defibrillator (ICD) which can terminate ventricular arrhythmias by delivering a shock. In order to develop treatments which prevent these life-threatening arrhythmias, we must understand the mechanisms by which these conditions cause electrical imbalances in the heart.