Simulation of left ventricular function during dyskinetic or akinetic aneurysm

Abstract

The purpose of our study was to simulate the hemodynamics of left ventricular function after left ventricular aneurysm (LVA) of various sizes and to validate the results of this computer based simulation with patient data. We developed an equivalent electronic circuit (EEC) that reflects the hemodynamic conditions of LVA (after acute myocardial infraction) while taking into consideration the resetting of the sympathetic nervous tone in the heart and systemic circuit, the fluctuating intrathoracic pressure during respiration and passive relaxation of the ventricle during diastole. The key feature of the EEC was a subcircuit representing the LVA, with a subcircuit to measure ventricular blood volume (i.e. intraventricular "shunting" of blood flow during systole and diastole) between the unaffected section of the left ventricle and its aneurysm. This EEC model can simulate akinetic or dyskinetic LVAs of different sizes and provides realistic beat-to-beat ventricular blood flow and pressure tracings that were validated by pressure-volume loop diagrams and by published patient data. In agreement with published data, simulated dyskinetic LVAs have a considerably greater impact on ventricular function than akinetic LVAs. The hemodynamic effects of ventricular systolic dysfunction following LVA were also evaluated. We conclude that the EEC model qualitatively and to a significant degree quantitatively represents conditions in patients with a dyskinetic or an akinetic LVA and provides realistic beat-to-beat ventricular blood flow and pressure tracings.

FIGURE 1

Electronic circuit of the left ventricle subdivided in section S1 (with initial normal function) and S2 (developing infarction and aneurysm). The time setting of switches in S2 determine whether S1 and S2 operate as a single unit, or as two distinctly separate units.

FIGURE 2

The time course of cardiovascular variables showing initially normal conditions when ejection fraction (EF) is 44. 4%, the effects of reduced contractility in 50% of left ventricle mass (in section S2) due to development of myocardial infarction and aneurysm (EF is 26.8%) and finally if in section S2 the distensibility is decreased in two steps (step I and step II) thus improving EF first to 27.7% and later to 29.2%. Acronyms are explained in Table 1.

FIGURE 3

The time course of cardiovascular variables showing initially normal conditions when ejection fraction (EF) is 44.4%, the effects of a strongly decreased contractility in 50% of left ventricle mass (in section S2) due to development of LVAMI with LVA (EF is 26.8%) and finally after contractility in section S1 is decreased, first mildly and later severely (i.e. development of systolic dysfunction in the ventricle section S1 initially unaffected by AMI and the subsequent LVA) decreasing EF first to 24% and then to 20.6%. Acronyms are explained in Table 1.

FIGURE 4

Pressure-Volume loop diagrams of left ventricle (LV) in normal conditions (N) aneurysm formation (Aneurysm), after distensibility of aneurysm is maximally decreased (STEP II) and after severe systolic dysfunction of section S1 (i.e. in the LV section that did not develop an aneurysm). Top graph: aneurysm in 20% of left ventricle mass. Bottom graph: aneurysm in 50% of left ventricle mass.

FIGURE 5

The effect of aneurysm size - measured as its end-diastolic volume (EDVS2) - on left ventricle end-diastolic volume (EDVLV) and left ventricle end-diastolic pressure (EDPLV). Symbols: S1 (section of left ventricle initially unaffected by aneurysm), S2 (section of left ventricle developing an aneurysm), solid circles (initial aneurysm size expressed as a ratio of the S2 and S1 sections from 10-90 to 50-50); solid squares (mildly decreased distensibilty of section S2), white squares (severely decreased distensibilty of section S2), solid triangles (mild systolic insufficiency of section S1), white triangles (severe systolic insufficiency of section S1).