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. 2021 Aug 2;16(8):e0255561.
doi: 10.1371/journal.pone.0255561. eCollection 2021.

The effect of left ventricular contractility on arterial hemodynamics: A model-based investigation

Stamatia Pagoulatou  1 , Dionysios Adamopoulos  2 , Georgios Rovas  1 , Vasiliki Bikia  1 , Nikolaos Stergiopulos  1
Affiliations

The effect of left ventricular contractility on arterial hemodynamics: A model-based investigation

Stamatia Pagoulatou et al. PLoS One. .

Abstract

Ventricular-arterial coupling is a major determinant of cardiovascular performance, however, there are still inherent difficulties in distinguishing ventricular from vascular effects on arterial pulse phenotypes. In the present study, we employed an extensive mathematical model of the cardiovascular system to investigate how sole changes in cardiac contractility might affect hemodynamics. We simulated two physiologically relevant cases of high and low contractility by altering the end-systolic elastance, Ees, (3 versus 1 mmHg/mL) under constant cardiac output and afterload, and subsequently performed pulse wave analysis and wave separation. The aortic forward pressure wave component was steeper for high Ees, which led to the change of the total pressure waveform from the characteristic Type A phenotype to Type C, and the decrease in augmentation index, AIx (-2.4% versus +18.1%). Additionally, the increase in Ees caused the pulse pressure amplification from the aorta to the radial artery to rise drastically (1.86 versus 1.39). Our results show that an increase in cardiac contractility alone, with no concomitant change in arterial properties, alters the shape of the forward pressure wave, which, consequently, changes central and peripheral pulse phenotypes. Indices based on the pressure waveform, like AIx, cannot be assumed to reflect only arterial properties.

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Intraventricular pressure-volume loops for two scenarios of high (Ees = 3 mmHg/mL, Vd = −2 mL—green curve) and low (Ees = 1 mmHg/mL, Vd = −60 mL—red curve) LV contractility with a maintained stroke volume.
Note that for the low Ees scenario an increase in preload was needed in order to restore stroke volume. The dashed lines represent the respective linear ESPVRs.
Fig 2
Fig 2. Aortic pulse wave analysis for the characteristic Type A and Type C phenotypes.
SBP: systolic blood pressure, PP: pulse pressure, DBP: diastolic blood pressure, cAP: central augmentation pressure, AIx: augmentation index.
Fig 3
Fig 3. Effect of LV contractility on central hemodynamics.
(A) LV and aortic pressure as a function of time. (B) Characteristic Type C and Type A aortic pressure phenotypes reproduced by high and low contractility, respectively. (C) Aortic flow. (D) Forward and backward travelling pressure waves. Note that the forward peak occurs significantly earlier in the high contractility simulation, while the amplitudes of the forward and backward pressure waves are left unchanged.
Fig 4
Fig 4. Central and peripheral arterial pressure for the two cases of LV contractility.
Note the rise in the radial systolic pressure as well as in the pulse pressure amplification when Ees is higher; in this case, pAIx is significantly lower.
See this image and copyright information in PMC

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Grants and funding

The author(s) received no specific funding for this work.
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