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Ventriculo-atrial gradient due to first degree atrio-ventricular block: a case report.
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PMID:  16091145     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Isolated, asymptomatic first degree AV block with narrow QRS has not prognostic significance and is not usually treated with pacemaker implantation. In some cases, yet, loss of AV synchrony because of a marked prolongation of the PR interval may cause important hemodynamic alterations, with subsequent symptoms of heart failure. Indeed, AV synchrony is crucial when atrial systole, the "atrial kick", contributes in a major way to left ventricular filling, as in case of reduced left ventricular compliance because of aging or concomitant structural heart disease. CASE PRESENTATION: We performed a trans-septal left atrium catheterization aimed at evaluating the entity of a mitral valve stenosis in a 72-year-old woman with a marked first-degree AV block, a known moderate aortic stenosis and NYHA class III symptoms of functional deterioration. We occurred in a deep alteration in cardiac hemodynamics consisting in an end-diastolic ventriculo-atrial gradient without any evidence of mitral stenosis. The patient had a substantial improvement in echocardiographic parameters and in her symptoms of heart failure after permanent pacemaker implantation with physiological AV delay. CONCLUSION: We conclude that if a marked first degree AV block is associated to instrumental signs or symptoms of heart failure, the restoration of an optimal AV synchrony, achieved with dual-chamber pacing, may represent a reasonable therapeutic option leading to a consequent clinical improvement.
Authors:
Giuseppe Ando'; Francesco Versaci
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Publication Detail:
Type:  Case Reports; Journal Article; Research Support, Non-U.S. Gov't     Date:  2005-08-09
Journal Detail:
Title:  BMC cardiovascular disorders     Volume:  5     ISSN:  1471-2261     ISO Abbreviation:  BMC Cardiovasc Disord     Publication Date:  2005  
Date Detail:
Created Date:  2005-09-08     Completed Date:  2006-11-30     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  100968539     Medline TA:  BMC Cardiovasc Disord     Country:  England    
Other Details:
Languages:  eng     Pagination:  23     Citation Subset:  IM    
Affiliation:
Department of Cardiac Surgery, Tor Vergata University of Rome, Italy. giuseppe.ando@tiscali.it
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MeSH Terms
Descriptor/Qualifier:
Aged
Aortic Valve Stenosis / physiopathology,  therapy
Cardiac Output, Low / physiopathology,  therapy
Female
Heart Block / physiopathology,  therapy*
Heart Catheterization
Hemodynamics
Humans
Pacemaker, Artificial*
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Full Text
Journal Information
Journal ID (nlm-ta): BMC Cardiovasc Disord
ISSN: 1471-2261
Publisher: BioMed Central, London
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Copyright ? 2005 Ando' and Versaci; licensee BioMed Central Ltd.
open-access: This is an Open Access article distributed under the terms of the Creative Commons Attribution License (), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Received Day: 25 Month: 2 Year: 2005
Accepted Day: 9 Month: 8 Year: 2005
collection publication date: Year: 2005
Electronic publication date: Day: 9 Month: 8 Year: 2005
Volume: 5First Page: 23 Last Page: 23
ID: 1199590
Publisher Id: 1471-2261-5-23
PubMed Id: 16091145
DOI: 10.1186/1471-2261-5-23

Ventriculo-atrial gradient due to first degree atrio-ventricular block: a case report
Giuseppe Ando'1 Email: giuseppe.ando@tiscali.it
Francesco Versaci1 Email: francescoversaci@yahoo.it
1Cardiac Catheterization Laboratory, Department of Cardiac Surgery, Tor Vergata University of Rome, Italy

Background

Loss of atrio-ventricular (AV) synchrony due to first-degree AV block may cause important hemodynamic alterations, with subsequent decrease in cardiac output and symptoms of heart failure. Indeed, AV synchrony is crucial when atrial systole contributes in a major way to left ventricular (LV) filling, as in case of reduced LV compliance because of aging or concomitant structural heart disease. We present the case of a patient with first degree AV block, associated with aortic valve disease, who received an evident clinical benefit by sequential pacing despite having refused aortic valve replacement as a first-line therapeutic option.


Case presentation

A 72-year-old woman was referred to our Catheterization Laboratory for an invasive re-evaluation of her NYHA class III heart failure symptoms. Three months before she had received, at a different Institution, the echocardiographic diagnosis of moderate aortic and apparently trivial mitral stenosis, despite severe valve calcification, with mild LV hypertrophy (wall thickness was 13 mm) and good systolic function. A pharmacological regimen, consisting in enalapril and furosemide, both 20 mg a day, had been established; despite medical therapy she kept complaining of effort dyspnea. ECG (figure 1) had revealed a first degree AV block, PR interval measuring 290 milliseconds, with normal QRS duration.

She underwent left and right cardiac catheterization with trans-septal access to the left atrium. Coronary arteries and regional LV systolic function were angiographically normal. LV ejection fraction was 0.65, cardiac index was 2.6 L/min/m2 and aortic and pulmonary systolic pressure were 130 and 38 mmHg, respectively. Aortic stenosis was confirmed to be moderate (the ventricle-to-aorta gradient was 50 mmHg at catheter pullback and aortic valve area was calculated to be 1.0 cm2). At fluoroscopy the mitral annulus was heavily calcified, but there was no hemodynamic evidence of mitral stenosis. With the trans-septal technique, moreover, we demonstrated (figure 2) that atrial contraction prematurely occurred soon after mitral valve opening, as shown on the left atrial tracing by the a wave (corresponding to atrial systole) falling very close to the preceding y wave (corresponding to early-diastolic unloading of the atrium into the ventricle). The high and prominent v wave consequently represented marked pressure elevation and reduced compliance of both left atrium and ventricle. Furthermore, LV filling pressure was as increased by the preceding atrial contraction as to cause a 6-mmHg end-diastolic ventriculo-atrial gradient that was evident, at the time of the R wave on the ECG, between the x wave (corresponding to the atrial relaxation not followed by a properly timed ventricular contraction) and the LV pressure tracing.

We discussed with the patient the therapeutic options [1]: she preferred to defer aortic valve replacement, whereas accepted to undergo permanent pacing. We performed an echocardiographic evaluation of systolic and diastolic function before pacemaker implantation (Table 1). Of note, the functional deterioration could be explained by the evidence of a grade II diastolic dysfunction[2]: transmitral flow was showing a high-velocity (150 cm/s) single filling wave with a deceleration time of 155 ms. Dual-chamber pacemaker implantation with optimal restoration of AV synchrony (programmed AV delay 150 ms) resulted in clinical improvement up to NYHA class II on the same medications. Since both sinus node function and atrial sensing were satisfying, ventricular pacing was triggered by P wave with a QRS duration of 120 ms [3-5]. The echocardiographic evaluation 2 days after pacemaker implantation showed a reduction of both diastolic dysfunction[2] to grade I (pattern of abnormal relaxation with an E/A ratio of 0.6) and pulmonary artery systolic pressure to 28 mmHg, whereas cardiac output appeared to be slightly improved (Table 1) despite the depletive effect of furosemide could have kept the systolic performance lower than expected in such a hypertrophied, non-enlarged left ventricle with aortic stenosis. The patient is now under close echocardiographic monitoring for the optimal timing of aortic valve replacement.


Conclusion

Isolated, asymptomatic first degree AV block with narrow QRS has not prognostic significance[6] and is not usually treated with pacemaker implantation in clinical practice. Yet, a hemodynamic condition similar to that of pacemaker syndrome [7-10] may occur when a marked first-degree AV block compromises the physiological sequence of events in the cardiac cycle[11]. Indeed, either, with longer PR intervals atrial, contraction takes place during the preceding ventricular systole against closed AV valves[7,10] or, with less long PR intervals, it falls during the early or the mid ventricular diastole, shortening the diastolic period itself and creating an abnormal ventriculo-atrial gradient[11], as in the present case, possibly leading to reversal diastolic AV flow, provided that LV pressure is higher than atrial one during atrial relaxation[9,12,13]. Anyway, the hemodynamic consequences are an increase in pulmonary capillary wedge pressure and a related decrease in cardiac output. Such changes, indeed, are especially harmful both in case of LV systolic[9,14-16] and diastolic (as in the present case) dysfunction and may be, at least in part, antagonized with permanent pacemaker implantation[17,18]. Thus, a properly timed atrial contraction, the "atrial kick", is necessary for optimal LV systolic function by increasing LV end-diastolic pressure while maintaining a low mean left atrial pressure[11].

We conclude that if a marked first degree AV block is associated to instrumental signs or symptoms of heart failure, the restoration of an optimal AV synchrony, achieved by dual-chamber pacing and despite permanent right ventricular stimulation[4,5], may represent a reasonable therapeutic option leading to a consequent clinical improvement.


Abbreviations

AV: atrio-ventricular

LV: left ventricular

NYHA: New York Heart Association


Competing interests

The author(s) declare that they have no competing interests.


Authors' contributions

FV and GA carried out the catheterization procedure. FV coordinated the clinical management of the patient whereas GA prepared, edited and reviewed the manuscript. Both authors read and approved the final draft of the manuscript.


Pre-publication history

The pre-publication history for this paper can be accessed here:


Acknowledgements

GA has been admitted to the PhD course in "Cardiovascular Imaging" at the University of Messina, Italy and has received a Grant by the Italian Society of Cardiology for a Fellowship in Interventional Cardiology at the Department of Cardiac Surgery of the Tor Vergata University of Rome, Italy.

Written consent was obtained from the patient for the publication of this case report.


References
Carabello BA. Evaluation and management of patients with aortic stenosisCirculation 2002;105:1746–1750. [pmid: 11956110] [doi: 10.1161/01.CIR.0000015343.76143.13]
Galderisi M. Diastolic dysfunction and diastolic heart failure: diagnostic, prognostic and therapeutic aspectsCardiovasc Ultrasound 2005;3:9. [pmid: 15807887] [doi: 10.1186/1476-7120-3-9]
Rediker DE,Eagle KA,Homma S,Gillam LD,Harthorne JW. Clinical and hemodynamic comparison of VVI versus DDD pacing in patients with DDD pacemakersAm J Cardiol 1988;61:323–329. [pmid: 3341209] [doi: 10.1016/0002-9149(88)90938-1]
Leclercq C,Gras D,Le Helloco A,Nicol L,Mabo P,Daubert C. Hemodynamic importance of preserving the normal sequence of ventricular activation in permanent cardiac pacingAm Heart J 1995;129:1133–1141. [pmid: 7754944] [doi: 10.1016/0002-8703(95)90394-1]
Maurer DE,Naegeli B,Straumann E,Bertel O,Frielingsdorf J. Quality of life and exercise capacity in patients with prolonged PQ interval and dual chamber pacemakers: a randomized comparison of permanent ventricular stimulation vs intrinsic AV conductionEuropace 2003;5:411–417. [pmid: 14753640] [doi: 10.1016/S1099-5129(03)00087-4]
Mymin D,Mathewson FA,Tate RB,Manfreda J. The natural history of primary first-degree atrioventricular heart blockN Engl J Med 1986;315:1183–1187. [pmid: 3762641]
Kim YH,O'Nunain S,Trouton T,Sosa-Suarez G,Levine RA,Garan H,Ruskin JN. Pseudo-pacemaker syndrome following inadvertent fast pathway ablation for atrioventricular nodal reentrant tachycardiaJ Cardiovasc Electrophysiol 1993;4:178–182. [pmid: 8269289]
Prech M,Grygier M,Mitkowski P,Stanek K,Skorupski W,Moszynska B,Zerbe F,Cieslinski A. Effect of restoration of AV synchrony on stroke volume, exercise capacity, and quality-of-life: can we predict the beneficial effect of a pacemaker upgrade?Pacing Clin Electrophysiol 2001;24:302–307. [pmid: 11310298] [doi: 10.1046/j.1460-9592.2001.t01-1-00302.x]
de Gregorio C,Recupero A,Cento D,Coglitore S. [Reversal left diastolic ventriculo-atrial flow induced by asynchronism in a patient with dilated cardiopathy and VVI pacemaker]G Ital Cardiol 1999;29:81–85. [pmid: 9987053]
Ellenbogen KA,Thames MD,Mohanty PK. New insights into pacemaker syndrome gained from hemodynamic, humoral and vascular responses during ventriculo-atrial pacingAm J Cardiol 1990;65:53–59. [pmid: 1967200] [doi: 10.1016/0002-9149(90)90025-V]
Nishimura RA,Hayes DL,Holmes DRJ,Tajik AJ. Mechanism of hemodynamic improvement by dual-chamber pacing for severe left ventricular dysfunction: an acute Doppler and catheterization hemodynamic studyJ Am Coll Cardiol 1995;25:281–288. [pmid: 7829778] [doi: 10.1016/0735-1097(94)00419-Q]
Panidis IP,Ross J,Munley B,Nestico P,Mintz GS. Diastolic mitral regurgitation in patients with atrioventricular conduction abnormalities: a common finding by Doppler echocardiographyJ Am Coll Cardiol 1986;7:768–774. [pmid: 3958334]
Schnittger I,Appleton CP,Hatle LK,Popp RL. Diastolic mitral and tricuspid regurgitation by Doppler echocardiography in patients with atrioventricular block: new insight into the mechanism of atrioventricular valve closureJ Am Coll Cardiol 1988;11:83–88. [pmid: 3335709]
Reiter MJ,Hindman MC. Hemodynamic effects of acute atrioventricular sequential pacing in patients with left ventricular dysfunctionAm J Cardiol 1982;49:687–692. [pmid: 7064819] [doi: 10.1016/0002-9149(82)91947-6]
Brecker SJ,Xiao HB,Sparrow J,Gibson DG. Effects of dual-chamber pacing with short atrioventricular delay in dilated cardiomyopathyLancet 1992;340:1308–1312. [pmid: 1360034] [doi: 10.1016/0140-6736(92)92492-X]
Auricchio A,Sommariva L,Salo RW,Scafuri A,Chiariello L. Improvement of cardiac function in patients with severe congestive heart failure and coronary artery disease by dual chamber pacing with shortened AV delayPacing Clin Electrophysiol 1993;16:2034–2043. [pmid: 7694250]
Hochleitner M,Hortnagl H,Hortnagl H,Fridrich L,Gschnitzer F. Long-term efficacy of physiologic dual-chamber pacing in the treatment of end-stage idiopathic dilated cardiomyopathyAm J Cardiol 1992;70:1320–1325. [pmid: 1442585] [doi: 10.1016/0002-9149(92)90769-U]
Auricchio A,Klein H. Dual-chamber pacing in dilated cardiomyopathy: insufficient sample size, heterogeneous population and inappropriate end point may lead to erroneous conclusionsJ Am Coll Cardiol 1996;27:1548–1549. [pmid: 8626973] [doi: 10.1016/S0735-1097(96)90107-2]

Figures

[Figure ID: F1]
Figure 1 

12-lead ECG showing first degree Atrio-Ventricular block. Paper speed is 25 mm/s and scale is 10 mm/mV.



[Figure ID: F2]
Figure 2 

Hemodynamic tracing showing left atrium and ventricle pressures. Capital letters represent ECG waves, whereas small letters represent left atrium waves (see text for details). Scale is 40 mmHg and paper speed is 100 mm/s.



Tables
[TableWrap ID: T1] Table 1 

Echocardiographic parameters in basal conditions and 2 days after pacemaker implantation.


Basal 2 days after implantation
LV ED diameter (mm) 41 43
LV ES diameter (mm) 26 26
LV ED volume (ml) 111 123
LV ES volume (ml) 43 43
LV Ejection Fraction (%) 61 65
LV mass (g) 195 197
LVOT VTI (cm) 23 25.5
Stroke volume (ml) 57 64
Cardiac output (L/min) 4.3 4.5
Cardiac index (L/min/m2) 2.6 2.7
Pulmonary artery systolic pressure (mmHg) 38 28

LV, left ventricular. ED, end-diastolic. ES, end-systolic. LVOT VTI, velocity-time integral measured at the left ventricular outflow tract. Body surface area is 1,65 m2.



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