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J. Cardiovasc. Pharmacol. · Feb 2008
Towards new indices of arterial stiffness using systolic pulse contour analysis: a theoretical point of view.
- Denis Chemla, Karsten Plamann, and Alain Nitenberg.
- Université Paris Sud, Equipe d'Accueil EA4046, Service de Physiologie-APHP, Le Kremlin-Bicêtre, France. denis.chemla@bct.aphp.fr
- J. Cardiovasc. Pharmacol. 2008 Feb 1;51(2):111-7.
AbstractTotal arterial stiffness plays a contributory role throughout aging and in numerous cardiovascular diseases, including hypertension. Aortic stiffening is responsible for an increased characteristic impedance (ie, the impedance to the left ventricular pulsatile flow), thus increasing the forward pressure-wave amplitude that contributes to pulse pressure elevation. Aortic stiffening also increases pulse wave velocity, and this results in anticipated and enhanced wave reflections, further augmenting central pulse pressure. Unfortunately, there is no simple time-domain estimate of characteristic impedance. Furthermore, recent guidelines have reviewed the limitations of diastolic pulse contour analysis to estimate arterial stiffness in the time domain. The present theoretical article proposes that systolic pulse contour analysis may provide new, simple time-domain indices quantifying pulsatile load in resting humans. Our proposal was mainly based on 2 simple, validated assumptions: (1) a linear aortic pressure-flow relationship in early systole and (2) a triangular aortic flow wave during systole. This allowed us to describe new time-domain estimates of characteristic impedance, pulsatile load (waveguide ratio), total arterial compliance, and total arterial stiffness. It is demonstrated that total arterial stiffness may be estimated by the following formula: [(Pi - DAP) x ST] / (SV x Deltat), where Pi is the aortic pressure at the inflection point (peak forward pressure wave), DAP is diastolic aortic pressure, ST is systolic ejection time, SV is stroke volume, and Deltat is the time-to-Pi. A mathematical relationship among time intervals and indices of pulsatile load is demonstrated, and the clinical implications are discussed in terms of cardiovascular risk and stroke volume prediction.
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