Several scientific and technical activities are run simultaneously by the CARDIOTRIALS research group.
We have created a semi-automatic procedure for segmenting CT scans to get cardiac anatomies timely. The procedure combines automatic algorithms (running in a few seconds) and human operations for better accuracy and assessment of the results.
The resulting cardiac anatomies are the input computational domain of our multiphyics solver. The latter is a groundbreaking computational model of the whole human heart, including all four chambers, valves, and the initial sections of major arteries and veins. The model simulates the complex mechanics of heart dynamics, including blood flow, muscle motion, and electrical signals, using high-performance-computing. To ensure high accuracy, it handles up to one billion spatial degrees of freedom and half a million-time steps per heartbeat.
First, we have used the model to replicate the cardiac dynamics of a healthy heart. Then, to simulate the left bundle branch block condition by disrupting the heart’s electrical signals between the atrioventricular node and the left bundle branch. This causes a decline in cardiovascular performance, reflecting real-life clinical symptoms. Pacemaker therapy is then simulated to resynchronize the heart. By testing different positions for the pacemaker lead in the left ventricle, the study generates a small-scale clinical trial to analyze therapy outcomes.
The model is also applied to study the effects of aortic stenosis (AS), a condition where the aortic valve narrows, restricting blood flow. The simulations reveal how AS increases blood velocity and pressure differences across the valve, known as transvalvular pressure drop (TPD). Severe cases result in peak jet velocities of 4.9 m/s and TPDs of 42.5 mmHg, aligning well with clinical and experimental data. Additionally, the model measures wall shear stress (WSS), a factor that cannot be directly observed in patients. High WSS levels are linked to severe AS, particularly in the aortic valve and ascending aorta, potentially damaging red blood cells and activating platelets, which raises the risk of blood clots.
Finally, the model has been exploited to study heart performance after an ischemic event (heart attack), where part of the heart muscle is damaged due to a lack of oxygen. This damaged region affects the heart muscle’s ability to contract and conduct electrical signals. The study examines various scenarios by changing the size and location of the damaged area, depending on which coronary artery is blocked. It evaluates heart efficiency in terms of blood pressure differences, cardiac output, and WSS, aiming to identify key factors influencing disease progression and detection.
In summary, this advanced heart model offers valuable insights into cardiac disorders and therapies, helping to improve the understanding and treatment of conditions like electrophysiology disfunctions, aortic stenosis, and ischemic heart disease.
