Cardiac contractility is a key factor in determining pulse pressure and its peripheral amplification

Figures

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  Figure 1. In vivo data showing relationships between the systolic index of contractility (dP/dt, left panels) or arterial compliance (right panels) and (top) central pulse pressure (PP), (middle) peripheral PP, and (bottom) PP amplification in the normotensive cohort receiving rising dose infusions of dobutamine (DB) and noradrenaline (NA) (see text for details). Pearson correlation coefficients (R) are provided for dP/dt and Spearman correlation coefficients (rs) are given for compliance. For a better interpretation of the figure, the reader is referred to the coloured web version of this article.

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  Figure 2. In silico data showing relationships between the systolic index of contractility (dP/dt, left panels) or arterial compliance (right panels) and (top) central pulse pressure (PP), (middle) peripheral PP, and (bottom) PP amplification. Pearson correlation coefficients (R) are provided for dP/dt and Spearman correlation coefficients (rs) are given for compliance.

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  Figure 3. In vivo data showing variations in (A) aortic peak flow (PF), (B) rate of increase in early-systolic aortic flow (ΔQ/ΔtES), and (C) rate of decrease in late-systolic aortic flow (ΔQ/ΔtLS) with increasing contractility (light-red line, dP/dt < 489 mmHg/s; red line, 489 < dP/dt < 740 mmHg/s; dark-red line, dP/dt > 740 mmHg/s) and compliance (light-blue line, C < 1.5 ml/mmHg; blue line, 1.5 < C < 2.3 ml/mmHg; dark-blue line, C > 2.3 ml/mmHg) in the normotensive cohort. All measures are shown as means ± SD. Asterisks indicate a significant difference between the first and third groups. For a better interpretation of the figure, the reader is referred to the coloured web version of this article.

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  Figure 4. In silico data showing aortic flow (left), aortic pressure (centre), and radial pressure (right) waveforms with increasing cardiac contractility (top) and decreasing arterial compliance (bottom) in the 45–year–old virtual subject from baseline (solid lines; dashed and dotted lines indicated variations from baseline). Increasing contractility raised the peak aortic flow (PF) (A), first systolic shoulder in central pressure (P1) (B), and peripheral systolic blood pressure (pSBP) (C). Decreasing compliance increased the peak or second shoulder in central pressure (P2) (E) and the second peak or shoulder in the peripheral systolic blood pressure (pSBP2) (F), without affecting the peak aortic flow (D). For a better interpretation of the figure, the reader is referred to the coloured web version of this article.

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  Figure 5. In vivo data showing variations in (A) central pulse pressure (PP), (B) peripheral PP, and (C) PP amplification with increasing contractility (light-red, dP/dt < 489 mmHg/s; red, 489 < dP/dt < 740 mmHg/s; dark-red, dP/dt > 740 mmHg/s) and compliance (light-blue, C < 1.5 ml/mmHg; blue, 1.5 < C < 2.3 ml/mmHg; dark-blue, C > 2.3 ml/mmHg) in the normotensive cohort. All measures are shown as means ± SD. Asterisks indicate a significant difference between the first and third groups. For a better interpretation of the figure, the reader is referred to the coloured web version of this article.

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  Figure 6. The relationship between peak emission (γpeak, top) or reflection (RCpeak, bottom) coefficients and central pulse pressure (PP). Left: normotensive cohort receiving rising dose infusions of dobutamine (DB) and noradrenaline (NA). Centre: hypertensive cohort. Right: increasing cardiac contractility (red dots) or decreasing arterial compliance (blue dots) from baseline in the 45–year–old virtual subject. Pearson correlation coefficients (R) are provided. For a better interpretation of the figure, the reader is referred to the coloured web version of this article.