Abstract:
Heart Failure due to Acute Myocardial Infarction (HF AMI) has emerged as prevalent heart disease with a high risk of short-term and long-term mortality rates. HF AMI has been associated with a progressively impaired interaction between the left ventricle (LV) and the systemic arteries. The progression of HF AMI and the key factors contributing to this process is an area of active research. Since the structural and functional changes of the Left Ventricle (LV) govern the progression of HF AMI, computational models have emerged as a robust tool to study the features of HF AMI and develop an effective treatment plan in recent years. FE model of LV would help assess the contributions of the critical factors to the progression of HF AMI. In the present study, a coupled LV FE-lumped parameter circulatory modelling framework has been calibrated with the measurements acquired from literature for a healthy subject and HF AMI patient. Both the healthy and HF AMI case models reproduced the literature datasets within acceptable limits. After that, the HF AMI model parameters such as geometry (Infarct Size: 9% to 27% of healthy LV volume, and Infarct Location: -3.5 cm to -5.5 cm), stiffness (up to 24% of healthy LV stiffness have been increased), and contractility (up to 30% of healthy LV contractility have been decreased) were varied to reproduce the effects of these parameters on the progression of HF AMI. The model predicts key features of HF AMI progression. The increase in infarct size produced a reduction in ejection fractions accompanied by a decrease in peak circumferential, longitudinal, and radial strains. Similar outcomes have been found by shifting the infract zone location towards the base of the LV (case: z = -3.5 cm). At the extreme basal location of infarct zone (z = -3.5 cm) with 9% of left ventricle volume (LVV) infarct size, the LV's dysfunction behaves like the extreme infarct size of 27% of LVV located at the mid-plane. The increase in infarct size increases the stiffness and reduces the contractility of LV. While isolated variations in these parameters have been shown to contribute to the severity of HF AMI, multiple mechanisms must likely be combined to reproduce all the pathophysiological features observed during the progression of HF AMI.
