Fig 1.
(a) CircAdapt model for simulation of cardiovascular mechanics and hemodynamics. (b) Two-degree- of-freedom model used for heart sound generation and embedded in CircAdapt. For each valve the same model was used albeit with different proximal and distal mechanical and hemodynamic values. Panel (a): LA: left atrium, LV: left ventricle, MV: mitral valve, PV: pulmonary valve, RA: right atrium, RV: right ventricle, TV: tricuspid valve. Panel (b): c: damping factor, dis: distal to valve, f: driving force, k: spring factor, m: blood mass, prox: proximal to valve, v: valve, x: movement of mass.
Table 1.
Mechanical properties of tissues.
Fig 2.
Heart sounds and their relationship with cardiovascular hemodynamics under resting conditions in simulation and recording on myocardium.
Dashed lines indicate beginning/ending of LV isovolumic contraction/relaxation phase. In experiment, volumetric data was used to estimate start of isovolumic phases. Since the sensor was remotely placed from the heart which caused a delay in the Ao pressure, the Ao-LV pressure cross-over could not be used as an indicator of aortic valve closure. Ao: Aorta, LA: Left atrium, LV: Left ventricle, Pu: Pulmonary artery, Ra: Right atrium, RV: Right ventricle, S1: first component of heart sound, S2: second component of heart sound, HS: heart sound, M1: mitral component of first heart sound, T1: tricuspid component of first heart sound, A2: aortic component of second heart sound, P2: pulmonary component of second heart sound.
Fig 3.
Frequency spectrum of simulated normal heart sound and its comparison with the pattern of PCG recorded on apical area and with frequency ranges of S1 and S2.
Fig 4.
Simulated heart sounds and pressures at reference and left/right heart failures.
EF: ejection fraction.
Fig 5.
Relationship between heart rate and amplitudes of S1 and S2.
The amplitudes are normalized to the control. All the experimental data (black dots and lines) are adapted from the figures in the article by Bergman and Blomqvist 1975 [25] in which patients have at least one major coronary artery with reduced vessel diameter by 50%. (a) A linear relationship between S1 amplitude and exercise level in normal condition for both simulation and experiment. (b) Simulated biventricular heart failure causes a reduction in S1 amplitude which is in agreement with the abnormal experimental data. (c) Average of S1 amplitude for both normal and abnormal simulations is within the range of experimental data. (d) Exercise doesn’t change S2 amplitude significantly compared to S1. APO: average of patient observations, BPM: beat per minute, BiVHF1-5: biventricular heart failure levels, HR: heart rate, IPO: individual patient observations, Ref: reference, YNS: young normal subjects.
Fig 6.
Relation between LV dp/dtmax and the first heart sound amplitude in simulations and reported experimental observations [26].
Conditions used in the experiment are: Aortic insufficiency, Aortic occlusion, Atropine, Artery occlusion, Epinephrine, Haemorrhage, Histamine, Isoprenaline, Methoxamine, Myocardial infarction, Norepinephrine, Phenylephrine, Pulmonary Rapid saline infusion, Pitressin, Veratridine, Venae cavae occlusion. BiVHF1-5: biventricular heart failure levels, LV dp/dt max: maximum of first derivative of left ventricular pressure, Ref: reference.
Fig 7.
(a) A2-P2 splitting interval for left ventricular heart failure of various severity levels and exercise levels. (b) A2-P2 splitting interval for right ventricular heart failure of various severity levels and exercise levels. Positive values indicate reverse splitting.