## 1 Introduction  
According to an EU Health report from 2014 [1], cardiovascular diseases (CVDs) account for almost 40% of all deaths in EU countries and are present in more than 30% of the population in the United States (US) [2]. Therefore, many studies have been conducted in this area in the past to better understand the cardiac cycle and vasculature. Special interest is given to cardiomyopathies, which is a general name for all anomalies in the ventricular endocardiup leading to a stretched, thickened, or stiff heart chamber. There are four types of cardiomyopathies [3] but the greatest attention is paid to hypertrophic (HCM) and dilated (DCM) [4]. HCM is characterized by thickened heart muscle that produces an increased heart size. It is estimated that HCM occurs in 1 in 500 adults, mostly young healthy people, and athletes, and is the leading cause of sudden death. DCM is characterized by the dilation of the heart, with the muscle wall progressively thinning. Decreased systolic function and an ejection fraction \(<\) 50% are common in DCM [5]. The treatment of cardiomyocytesopathy using existing types of therapies may only partially improve outcomes; hence, it is still necessary to introduce new and efficient types of treatment. Different types of cardiomyocytesopathies require the use of different drugs and methods of treatment. With the recently developed MUSICO platform [6; 7], which is capable of simulating the effects of genetic mutations on muscle activity, it became possible to understand how small molecules (drugs) affect muscle contraction. According to simulations of the muscles at the micro level performed using the MUSICO software ([[https://www.solindies.com/](https://www.solindies.com/)]([https://www.solindies.com/](https://www.solindies.com/)), accessed on 23 October 2023) and based on the main activity performed by drugs, it was found that drugs can be divided into three groups: namely, drugs that modulate the calcium transient and affect muscle contractility (disopyramide and digoxin), drugs that change kinetic parameters (mavacamten and dATP), and drugs that affect macroscopic parameters (Entresto(tm)), Table 1.  
Disopyramide is a drug that slows the speeding-up of the LV ejection flow, extends the flow acceleration time [16], and in HCM patients, can affect the level of Ca2+ transient, which reduces the contractility of the heart muscle [8]. Digoxin can be used in DCM patients, and it increases the intracellular calcium concentration transient [17; 18; 19], but also myocardial contractility, stroke volume, and blood pressure [9]. It is proven that mavacamten affects the contractility of the heart muscle, and produces a significant decrease in tension during resting [4; 20]. The influence of this drug is still under investigation in HCM patients. 2-deoxy adenosine triphosphate (dATP) is proven to be a molecule with a lot of potential in the treatment of DCM [21; 22]. dATP has been shown to increase the contractility of heart tissue in heart failure patients [12], and systolic pressure in heart failure [13]. Finally, it was shown in [15] that Entresto(tm) contributes to the remodelling of the walls of the heart chambers and to changes in the elasticity of blood vessels, which leads to a decrease in the resistance to blood flow. The changes in calcium concentration in the muscle cells, obtained for the aforementioned drugs and presented in Figure 1, represent the basis for further application in in silico clinical trials. In silico clinical trials allow for testing drugs in \"virtual patients\" using computational modelling and a variety of simulation techniques. Among the computer methods, the finite element (FE) method is the most frequently used for investigating the effects of various drugs on cardiac function, as described in papers [4; 23]. A recently introduced methodology presented in [24] couples macro and micro scales using the FE modelling of fluid-solid interaction (FSI) and molecular drug interactions in the cardiac muscle cells using the MUSICO [6] platform.