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  • Title: Pulse pressure amplification, pressure waveform calibration and clinical applications.
    Author: Agnoletti D, Zhang Y, Salvi P, Borghi C, Topouchian J, Safar ME, Blacher J.
    Journal: Atherosclerosis; 2012 Sep; 224(1):108-12. PubMed ID: 22832004.
    Abstract:
    Obtaining pulse pressure non-invasively from applanation tonometry requires the calibration of pressure waveform with brachial systolic and diastolic blood pressure. In the literature, several calibration methodologies are applied, and clinical studies disagree about the predictive value of central hemodynamic parameters. Our aim was to compare 4 calibration methodologies and assess the usefulness of pulse pressure amplification as an index independent of calibration. We investigated 108 subjects with tonometry in carotid, femoral, brachial, radial and dorsalis-pedis arteries; pulse pressure amplification between arterial waveforms was calculated. Four methods to calibrate the waveforms were compared: the 1/3 rule, the 40% rule, the integral of radial and brachial waveforms. Pulse pressure amplification in 5 arterial territories (carotid-femoral, carotid-brachial, carotid-radial and carotid-pedis amplifications; femoral-pedis amplification) was studied. Pulse pressure was successfully measured non-invasively at the 5 arterial sites. Pulse pressure was markedly dependent on calibration, with differences up to 18 mmHg between methods. Calculation of pulse pressure amplification eliminated effects of calibration method. Furthermore, pulse pressure amplifications in the 5 arterial sites presented a distinct pattern of clinical/biological determinants: heart rate and body height were common determinants of carotid to brachial, radial and femoral amplifications; diabetes was related to carotid to brachial amplification and pulse wave velocity to femoral to pedis amplification. In conclusion, the calibration of pulse pressure will influence results of clinical trials, but calculation of pulse pressure amplification can avoid this. We also suggest that the alteration of amplification in each arterial territory might be considered as a signal of clinical/subclinical damage.
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