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


   
 

Echo articles published with Irish authors:

         
   

Article title:

Alterations in Myocardial Stiffness in Elite Athletes assessed by a new Doppler Index.

Published Online First: 12 May 2008. doi:10.1136/hrt.2008.142083.

Gerard J King, Ross T Murphy, Ibraham Almuntaser, Kathleen Bennett, Emily Ho, and Angie Brown

[Abstract] [Accepted Manuscript]

Abstract:

Background. In elite athletes left ventricular morphologic changes are predicted to alter passive pressure/volume characteristics by reducing myocardial stiffness and increasing compliance.

Aim We investigated the utility of a new Doppler tissue index based on the pressure volume relation ((E/Ea)/LVEDD), which provides a measure of myocardial stiffness, and assessed its usefulness in detecting cardiac adaptation in elite rowers.

Methods Thirty-six international rowers (mean age 27±7 years,) who had trained intensively for 15-20 hours per week for more than 5 years and a control group of 30 sedentary but otherwise normal subjects (mean age 26±8 years,) were consented and enrolled into the study. The groups were similar in age and gender. Left ventricular (LV) septal and posterior wall thickness, mass, chamber size, transmitral Doppler peak early (E) and late (A) diastolic filling velocities and isovolumic relaxation times were measured. Early diastolic myocardial velocities (Ea) were averaged from 4 sites at the mitral annulus; Diastolic stiffness was assessed with the use of three indices E, Ea, and the left ventricular end diastolic diameter in diastole (LVEDD). The ratio, [(E/Ea)/LVEDD], represents a pressure/volume relationship and provides a novel index of diastolic stiffness. Rowers were further divided into 2 groups based on the presence or absence of left ventricular hypertrophy (LVH), 12mm and > 12mm.

Results There was no significant difference in Ea (4 site average) between the two groups, but there was a difference in the stiffness index, with rowers having significantly more compliant ventricles (p=0.0003). When compared with controls and adjusted for body surface area (BSA) and heart rate this difference remained statistically significant (p= 0.016). When the rowers were divided into 2 groups based on the presence or absence of LVH there was no difference in the stiffness index (p = 0.68)

Conclusions The key distinguishing feature of intense training is a reduction of myocardial stiffness despite the development of left ventricular hypertrophy.

St James Hospital, Dublin, Eire.

* To whom correspondence should be addressed. E-mail: .

Accepted 15 April 2008

 

   
         
         
   

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

Feasibility study of percutaneous transvalvular endomyocardial cryoablation for the treatment of hypertrophic obstructive cardiomyopathy.
J Invasive Cardiol. 2007 Jun;19(6):247-51.
PMID: 17541123 [PubMed - in process]

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.

 

   
         
   

Article title:  Feasibility study of percutaneous transvalvular endomyocardial cryoablation for the treatment of hypertrophic obstructive cardiomyopathy.

Abstract
Keane D, Hynes B, King G, Shiels P, Brown A.

Related Articles
  Cardiac Arrhythmia Department, St. Vincent's University Hospital, Dublin, Ireland. bghynes@hotmail.com.

BACKGROUND: Left ventricular outflow tract (LVOT) obstruction in the setting of hypertrophic cardiomyopathy (HCM) confers negative adverse outcomes. Current nonpharmacologic treatment options include surgical myectomy and percutaneous transcoronary ablation of septal hypertrophy (TASH). While TASH negates a more invasive procedure, concern remains with particular regard to the arrhythmogenic potential of the resultant myocardial scar. Percutaneous transvalvular endomyocardial septal cryoablation (PTESC) may circumvent some of these potential limitations and offer a novel treatment strategy. OBJECTIVES: The purpose of this study was to report our early experience and outcomes with percutaneous endomyocardial cryoablation of the interventricular septum in obstructive HCM. METHODS AND RESULTS: Between March 2005 and May 2006, 3 patients (2 male, 1 female) with symptomatic obstructive HCM underwent PTESC. Basal LVOT gradients measured during left heart catheterization were 70, 126 and 100 mmHg for Patients 1, 2 and 3, respectively. Using 7 Fr and 9 Fr 8 mm tip CryoCath Freezor catheters (CryoCath Technologies, Inc., Montreal, Quebec, Canada), cryothermal energy was applied to the interventricular septum under fluoroscopic guidance. A total of 20 to 32 applications of cryothermal energy were delivered, with the mean nadir temperature sustained during cryoablation being -88 degrees Celcius. Two of the 3 patients had an immediate reduction in the LVOT gradient. However, at 6 months, only 1 patient had a significant sustained reduction in LVOT gradient. No adverse events relating to the procedure were experienced. CONCLUSION: PTESC is feasible, but did not result in a significant, sustained reduction in LVOT gradient in 2 of the 3 patients in this small series of obstructive HCM patients. The technique warrants further study to improve the consistency and duration of reduction in outflow gradient.

PMID: 17541123 [PubMed - in process]

J Invasive Cardiol. 2007 Jun;19(6):247-51.
PMID: 17541123 [PubMed - in process]

 

 

   
   
 
Arola AM, Sanchez X, Murphy RT, Hasle E, Li H, Elliott PM, McKenna WJ, Towbin JA, Bowles NE.


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Abstract Mutations in PDLIM3 and MYOZ1 encoding myocyte Z line proteins are infrequently found in idiopathic dilated cardiomyopathy.
Mol Genet Metab. 2007 Apr;90(4):435-40. Epub 2007 Jan 24.
PMID: 17254821 [PubMed - in process]
 
Caforio AL, Mahon NG, Baig MK, Tona F, Murphy RT, Elliott PM, McKenna WJ.


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Abstract Prospective familial assessment in dilated cardiomyopathy: cardiac autoantibodies predict disease development in asymptomatic relatives.
Circulation. 2007 Jan 2;115(1):76-83. Epub 2006 Dec 18.
PMID: 17179019 [PubMed - indexed for MEDLINE]
 
Murphy RT, Ratliff NB, Lever HM, Kapadia SR.


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Abstract Use of percutaneous transluminal septal myocardial ablation for relief of outflow tract obstruction in cardiac amyloidosis: a novel therapeutic target.
Catheter Cardiovasc Interv. 2006 Oct;68(4):637-41.
PMID: 16969877 [PubMed - indexed for MEDLINE]
 
Hesse B, Murphy RT, Sigurdsson G, Nassif M, Greenberg NL, Gring C, Sauri D, Desai MY, Garcia MJ.


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Abstract Use of tissue Doppler imaging to guide tube current modulation in cardiac multidetector computed tomographic angiography.
Am J Cardiol. 2006 Sep 1;98(5):603-7. Epub 2006 Jul 3.
PMID: 16923444 [PubMed - indexed for MEDLINE]
 
Murphy RT, Sigurdsson G, Mulamalla S, Agler D, Popovic ZB, Starling RC, Wilkoff BL, Thomas JD, Grimm RA.


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Abstract Tissue synchronization imaging and optimal left ventricular pacing site in cardiac resynchronization therapy.
Am J Cardiol. 2006 Jun 1;97(11):1615-21. Epub 2006 Apr 7.
PMID: 16728225 [PubMed - indexed for MEDLINE]
 
Hesse B, Murphy RT, Myles J, Huang J, Sabik EM.


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Free Full Text Images in cardiovascular medicine. A left atrial appendage thrombus mimicking atrial myxoma.
Circulation. 2006 Mar 21;113(11):e456-7. No abstract available.
PMID: 16549642 [PubMed - indexed for MEDLINE]
 
Thaman R, Elliott PM, Shah JS, Mist B, Williams L, Murphy RT, McKenna WJ, Frenneaux MP.


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Abstract Reversal of inappropriate peripheral vascular responses in hypertrophic cardiomyopathy.
J Am Coll Cardiol. 2005 Sep 6;46(5):883-92.
PMID: 16139140 [PubMed - indexed for MEDLINE]
 
Mahon NG, Murphy RT, MacRae CA, Caforio AL, Elliott PM, McKenna WJ.


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Free Full Text Echocardiographic evaluation in asymptomatic relatives of patients with dilated cardiomyopathy reveals preclinical disease.
Ann Intern Med. 2005 Jul 19;143(2):108-15.
PMID: 16027452 [PubMed - indexed for MEDLINE]
 
Murphy RT, Starling RC.


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Abstract Genetics and cardiomyopathy: where are we now?
Cleve Clin J Med. 2005 Jun;72(6):465-6, 469-70, 472-3 passim. Review.
PMID: 16018289 [PubMed - indexed for MEDLINE]
 
Murphy RT, Garcia MJ.


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Abstract Role of Echocardiography in Diagnosis and Management of Endocarditis.
Curr Infect Dis Rep. 2005 Jul;7(4):257-263.
PMID: 15963326 [PubMed - as supplied by publisher]
 
Thaman R, Gimeno JR, Murphy RT, Kubo T, Sachdev B, Mogensen J, Elliott PM, McKenna WJ.


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Free Full Text Prevalence and clinical significance of systolic impairment in hypertrophic cardiomyopathy.
Heart. 2005 Jul;91(7):920-5.
PMID: 15958362 [PubMed - indexed for MEDLINE]
 
Murphy RT, Mogensen J, McGarry K, Bahl A, Evans A, Osman E, Syrris P, Gorman G, Farrell M, Holton JL, Hanna MG, Hughes S, Elliott PM, Macrae CA, McKenna WJ.


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Abstract Adenosine monophosphate-activated protein kinase disease mimicks hypertrophic cardiomyopathy and Wolff-Parkinson-White syndrome: natural history.
J Am Coll Cardiol. 2005 Mar 15;45(6):922-30.
PMID: 15766830 [PubMed - indexed for MEDLINE]
 
Murphy RT, Thaman R, Blanes JG, Ward D, Sevdalis E, Papra E, Kiotsekolglou A, Tome MT, Pellerin D, McKenna WJ, Elliott PM.


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Free Full Text Natural history and familial characteristics of isolated left ventricular non-compaction.
Eur Heart J. 2005 Jan;26(2):187-92. Epub 2004 Nov 30.
PMID: 15618076 [PubMed - indexed for MEDLINE]
 
Mogensen J, Murphy RT, Kubo T, Bahl A, Moon JC, Klausen IC, Elliott PM, McKenna WJ.


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Abstract Frequency and clinical expression of cardiac troponin I mutations in 748 consecutive families with hypertrophic cardiomyopathy.
J Am Coll Cardiol. 2004 Dec 21;44(12):2315-25.
PMID: 15607392 [PubMed - indexed for MEDLINE]
 
Mogensen J, Murphy RT, Shaw T, Bahl A, Redwood C, Watkins H, Burke M, Elliott PM, McKenna WJ.


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Abstract Severe disease expression of cardiac troponin C and T mutations in patients with idiopathic dilated cardiomyopathy.
J Am Coll Cardiol. 2004 Nov 16;44(10):2033-40.
PMID: 15542288 [PubMed - indexed for MEDLINE]
 
Thaman R, Gimeno JR, Reith S, Esteban MT, Limongelli G, Murphy RT, Mist B, McKenna WJ, Elliott PM.


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Abstract Progressive left ventricular remodeling in patients with hypertrophic cardiomyopathy and severe left ventricular hypertrophy.
J Am Coll Cardiol. 2004 Jul 21;44(2):398-405.
PMID: 15261938 [PubMed - indexed for MEDLINE]

 

   
   
 
Ho E, Foley DP, Brown A.


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Abstract Aortic hypoplasia and right ventricular outflow tract obstruction in a young man with uncontrolled hypertension.
J Am Soc Echocardiogr. 2005 Aug;18(8):883.
PMID: 16084344 [PubMed - indexed for MEDLINE]

 

   
         
         
         
         
 
   
 
 
 
 
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