According to recent study presented in PLOS Computational Biolog, researchers have developed a comprehensive computer model of a heart that reveals the electrophysiology of congestive heart failure.
Congestive heart failure (CHF) is a major cause of death in the United States. According to the Centers for Disease Control and Prevention (CDC), about 5.7 million people in America have heart failure.
Around 50% of the individuals who are diagnosed with this problem survive for just about 5 years post diagnosis.
Heart failure doesn’t imply that the heart has stopped, or will stop, entirely. It refers to a situation in which the heart is not capable to pump sufficient blood for the body to function normally.
As an outcome of heart failure, fluid and blood can back into the lungs, the individual may experience weakness, shortness of breath, and edema, or accumulation of fluid in the legs, ankles, and feet.
Heart failure can occur as an outcome of coronary artery disease, high blood pressure, and diabetes.
It is more probably to impact individuals above the age of 65 years, and specifically those who are overweight. Individuals who have earlier had a heart attack are more vulnerable. It is likely to impact men over women.
However, the mechanisms that lead to it, which includes its electrophysiological (EP) mechanisms, are not fully understood.
It is expected that the new “virtual heart” could help in the development of new medicines to treat the condition.
Tweaking an existing design provides insight into heart’s workings
The investigators, from the University of California-San Diego, improved an established design of a healthy rabbit heart to develop their simulation.
The model is capable to simulate small modifications in the heart, from the cellular and tissue levels, up to the whole heart.
An electrocardiogram (ECG) is a tool generally utilized by doctors to diagnose heart problems.
The research team hopes to use the numerical model they have designed to link modifications that take place at the cellular and tissue level when a heart fails to a numerically computed ECG. This, they wish, will assist to determine what it is that triggers ventricular fibrillation (VF), and to recognize the risk of VF.
At the cellular and tissue levels, the model can duplicate the heart’s responses to changes in the levels and flow of calcium, sodium, and potassium. In addition, it can take into consideration the pace at which the ion channels – which take in those ions – function.
At the whole heart level, it can also present what happens in a healthy, working heart as an outcome of variations in the various critical chemicals and electro physiologic components.
New understanding into VF
VF is a frequent reason for sudden death. While in VF, the electrical waves that take place in the heart break up chaotically. When this occurs, it impacts the timing of the heart’s pumping action. The heart can no longer contract and supply blood to the rest of the body.
Using the new model, investigators in the present study identified that this fragmentation and loss of co-ordination can be triggered by a slowdown in cellular processes at the top of the heart. This can result in heart failure.
To learn more regarding the reasons for VF in an individual with heart failure, the research team set-up a test that would simulate an individual with heart failure performing physical exercise.
The outcomes recommend that an individual with heart failure who experiences a fast heart rate and varying pacing will be more vulnerable to VF. This, they say, is because of a recently identified mechanism that blocks conduction.
The investigators have demonstrated that the model can be utilized to develop a new drug strategy to prevent the kind of fibrillation that is connected with heart failure.