Clinical Implications of Non-Invasive Measurement of Central Aortic Blood Pressure

2010 ◽  
Vol 8 (6) ◽  
pp. 747-752 ◽  
Author(s):  
Mariusz Stepien ◽  
Maciej Banach ◽  
Piotr Jankowski ◽  
Jacek Rysz
Author(s):  
Zahra Ghasemi ◽  
Chang-Sei Kim ◽  
Eric Ginsberg ◽  
John Duell ◽  
Anuj Gupta ◽  
...  

This paper presents a model-based system identification approach to estimation of central aortic blood pressure waveform from non-invasive cuff pressure oscillation signals. First, we developed a mathematical model that can reproduce the relationship between central aortic blood pressure waveform and non-invasive cuff pressure oscillation signals at diametric locations by combining models to represent wave propagation in the artery, arterial pressure-volume relationship, and mechanics of the occlusive cuff. Second, we formulated the problem of estimating central aortic blood pressure waveform from non-invasive cuff pressure oscillation signals into a system identification problem. Third, we showed the proof-of-concept of the approach using simulated central aortic blood pressure waveform and cuff pressure oscillation signals. Finally, we illustrated the feasibility of the approach using central aortic blood pressure waveform and cuff pressure oscillation signals collected from a human subject. We showed that the proposed approach could estimate central aortic blood pressure waveform with accuracy: the root-mean-squared error associated with the central aortic blood pressure waveform was 1.7 mmHg (amounting to 1.6 % of the underlying mean blood pressure) while the errors associated with central aortic systolic and pulse pressures were −0.4 mmHg and −1.5 mmHg (amounting to −0.3 % and −1.4 % of the underlying mean blood pressure).


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Bernard I. Levy ◽  
Jean-Guillaume Dillinger ◽  
Patrick Henry ◽  
Damien Logeart ◽  
Stephane Manzo Silberman ◽  
...  

Background: Treatment of hypertensive patients with beta-blockers reduces heart rate (HR) and increases central blood pressure, implying that the decrease in HR could explain reported increases in cardiovascular risk with beta-blocker. This analysis from a randomized, double-blind study explores whether HR reduction with the I f inhibitor ivabradine had an impact on central blood pressure and coronary perfusion. Methods and results: We included 12 normotensive patients with stable CAD, HR ≥70 bpm (sinus rhythm), and stable background beta-blocker therapy. Patients received ivabradine 7.5 mg bid or matched placebo for two 3-week periods with a crossover design and evaluation by aplanation tonometry. Treatment with ivabradine was associated with a significant reduction in resting HR after 3 weeks versus no change with placebo (-15.8±7.7 versus +0.3±5.8 bpm, p=0.0010). There was no relevant between-group difference in change in central aortic SBP (-4.0±9.6 versus +2.4±12.0 mm Hg, p=0.13) or augmentation index (-0.8±10.0% versus +0.3±7.6%, p=0.87). Treatment with ivabradine was associated with prolongation of diastolic perfusion time by 41% from baseline to 3 weeks (+215.6±105.3 versus -3.0±55.8 ms with placebo, p=0.0005) (Figure) and with a pronounced increase in an index of myocardial viability (Buckberg index, +39.3±27.6% versus -2.5±13.5% with placebo, p=0.0015). There were no safety issues during the study. Conclusion: Heart rate reduction with ivabradine does not modify central aortic blood pressure and is associated with a marked prolongation of diastolic perfusion time and an improvement in myocardial perfusion.


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