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Publications

Links to relevant publications by members of the Irish Cardiac Echo Group.


   
 

Echocardiography articles published from Ireland:

 

         
   

Article title: Myocardial stiffness and the timing difference between tissue Doppler imaging Ea and peak mitral valve opening can distinguish physiological hypertrophy in athletes from hypertrophic cardiomyopathy, 15 November 2005
King G, Foley JB, Royse CF, Yastrebov K, Hussey M, Boyle G, Bennet K, Cosgrave J, Crean P, Walsh M
pages 423-429
Abstract | Full Text | PDF (529 KB) 

Corresponding author: Dr. G. King. 
First author: Dr. G. King
Cardiology Department, St James Hospital, Dublin 8, Ireland.

Reference: YEUJE906 

Journal title: European Journal of Echocardiography 
volume 7, issue 6, on pages 423-429, cover date December 2006.

   
         
         
   


Article title: Research: Early diastolic filling dynamics in diastolic dysfunction
Gerard J King, Jerome B Foley, Faisal Almane, Peter A Crean, Michael J Walsh
Cardiovascular Ultrasound 2003, 1:9 (25 July 2003)
[Abstract]
[Full Text] [PDF] [PubMed] [Related articles]

   
         
         
   

Article title:  Transventricular pressure-velocity wave propagation in diastole: adherence to the Moens-Korteweg equation.

1:

Brennan EG, O'Hare NJ, Walsh MJ.

Related Articles, Links

Abstract

Physiol Meas. 1998 Feb;19(1):117-23.
PMID: 9522393 [PubMed - indexed for MEDLINE]

Department of Cardiology, St James's Hospital, Dublin, Ireland.

In the latter half of the diastolic phase of the cardiac cycle, the left atrium contracts and generates a pressure-velocity wave which enters the left ventricle. The wave moves through the inflow tract of the ventricle, reflects off the apex and heads towards the aortic valve. The time taken for the pressure-velocity wave to propagate through the ventricle, referred to as the A-Ar interval, may be measured using pulsed Doppler echocardiography and occurs in the range 20-80 ms. It has been shown previously that there is a significant negative linear correlation between the A-Ar interval and the passive elastic modulus of the ventricular wall (r = -0.782, p < 0.001). This relationship may be explained by modelling the left ventricle as a folded-over elastic tube through which the pressure-velocity wave is propagated according to the principles of the Moens-Korteweg equation.

   
   

Article title:  Correlation of end-diastolic pressure and myocardial elasticity with the transit time of the left atrial pressure wave (A-Ar interval).

 

Brennan EG, O'Hare NJ, Walsh MJ.

Related Articles, Links

Abstract

J Am Soc Echocardiogr. 1997 May;10(4):293-9.
PMID: 9168350 [PubMed - indexed for MEDLINE]

Department of Cardiology, St. James Hospital, Dublin, Ireland.

Contraction of the left atrium in diastole generates a pressure wave that moves along the postero-lateral wall of the left ventricle (LV), rebounds off the LV apex, and is then directed toward the outflow tract. The movement of this atrial pressure wave may be detected with pulsed Doppler echocardiography by placing a sample volume in the LV outflow tract. The resulting spectral profile shows the initial. A velocity wave and also the Ar velocity wave, which is caused by the atrial pressure wave rebounding off the LV apex. The transit time from the inflow tract to the outflow tract of the atrial pressure wave (A-Ar interval) may be determined from the time axis of the spectral profile by measuring the peak-to-peak separation of the A and Ar, velocity waves. It occurs in the range 25 to 80 milliseconds. The primary determinant of the A-Ar interval is the elasticity of the LV myocardium. We correlated ventricular elasticity with the A-Ar interval in 47 patients and found a significant negative linear correlation (r = -0.782, p < 0.001). Because the pressure in a viscoelastic conduit such as the LV is determined by the elasticity of the ventricular wall, we correlated end-diastolic pressure with the A-Ar interval and again showed a significant negative linear correlation (r = -0.701, p < 0.001). The A-Ar interval is an easily measured noninvasive index of the diastolic function of the LV that reflects its intrinsic elasticity and end-diastolic pressure. It is therefore a quantitative measurement of LV wall stiffness and end-diastolic pressure.

 

   
         
         
 
   
 
 
 
 
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