(Circulation. 1999;100:465-467.)
© 1999 American Heart Association, Inc.
Brief Rapid Communications |
Asymmetry of Right Ventricular Enlargement in Response to Tricuspid Regurgitation
From the Division of Cardiology, Loyola University Medical Center, Maywood, Ill.
Correspondence to Eric K. Louie, MD, Professor of Medicine, Associate Director, Division of Cardiology, Loyola University Medical Center, Maywood, IL 60153.
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Abstract |
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Background—Analysis of right ventricular adaptation to tricuspid regurgitation was studied in 10 heart transplant recipients following inadvertent endomyocardial biopsy disruption of the tricuspid apparatus.
Methods and Results—Echocardiography demonstrated progressive diastolic right ventricular cavity enlargement (19.5±5.0 to 30.3±5.4 cm2, P<0.0002), with disproportionate elongation along the midminor axis (3.5±0.6 to 5.0±0.5 cm, P<0.001). As the right ventricle remodeled to more spherical (and less elliptical) proportions, the end-diastolic right ventricular midminor axis/long axis ratio increased significantly from 0.52±0.10 to 0.68±0.07, P<0.005.
Conclusions—Ventricular enlargement due to right ventricular volume overload results in disproportionate dilation along the free wall to septum minor axis.
Key Words: ventricles • regurgitation • right ventricular volume overload • tricuspid regurgitation • orthotopic heart transplantation
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Right ventricular volume overload distorts ventricular septal geometry,1 alters left ventricular filling,1 2 and impairs left ventricular systolic function.3 4 5 6 7 Inadvertent tricuspid valve trauma due to endomyocardial biopsy in heart transplant recipients results in the abrupt onset of severe tricuspid regurgitation, providing the opportunity to measure the progressive longitudinal impact of right ventricular volume overload on chamber geometry and function.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Study Population
Surveillance endomyocardial biopsy, right heart catheterization, and postprocedural echocardiography were prospectively performed during the first 4 years after cardiac transplantation in 365 patients; the study was conducted from 1984 to 1994. Review of the echocardiograms identified 54 patients in whom endomyocardial biopsy resulted in a flail tricuspid apparatus (index study). The immediately preceding echocardiogram demonstrating normal tricuspid valve anatomy (baseline study) and the succeeding echocardiograms at 6, 12, and 24 months following the index study were selected for longitudinal analysis. This study was approved by the Institutional Review Board and all patients gave informed consent for the diagnostic procedures.
Subjects were excluded from this study if they had any of the following
conditions which might independently affect ventricular
function: (1) systemic hypertension: blood pressure >160/104
mm Hg or an increase >25 mm Hg unresponsive to medication; (2)
pulmonary hypertension: systolic pulmonary
artery pressure >30 mm Hg or transpulmonary gradient
>15 mm Hg; (3) diabetes mellitus requiring pharmacological
therapy; (4) moderate to severe cardiac rejection:
endomyocardial biopsy grade 
48
requiring treatment with intravenous methyl prednisolone
and/or OKT 3 anti-thymocyte globulin; (5) allograft
coronary arteriopathy detected by annual coronary
angiography; and (6) left ventricular ejection fraction
<50% at baseline.
Ten subjects were identified who met these exclusion criteria and had technically superior echocardiograms suitable for quantitative measurements. At baseline, this study population ranged in age from 21 to 65 years (mean 46±15); 7 subjects were male.
Echocardiographic Measurements
Transthoracic echocardiograms were performed within
3 hours after endomyocardial biopsies and right
heart catheterization using standard techniques. The
transducer was positioned to maximize right ventricular
cavity area (RVA) and to include the true right ventricular
apex. End-diastolic images were selected at maximal
ventricular cavity size and end-systolic images
were selected at minimal ventricular cavity size.
Midsystole was identified by counting half the number of image frames
between end diastole and end systole. A flail tricuspid
valve was defined by9 (1) lack of normal coaptation of its
leaflets, (2) whiplike systolic prolapse of its leaflet tips
into the right atrium, and (3) erratic motion of its malcoapting
leaflet segments.
All measurements of right ventricular
geometry,10 RVA, and tricuspid annulus size11
were obtained from apical 4-chamber views of the heart through the
cardiac crux. The right ventricular long axis (L), maximal
minor axis (S1), and midminor axis (S2) dimensions are defined in
Figure 1
. Percent systolic
fractional shortening for RVA, L, S1, and S2 was calculated as
100x(end-diastolic
measurement-end-systolic
measurement)/(end-diastolic measurement). The ratio of
right ventricular minor axis dimension to L dimension was
calculated for both S1 and S2 as an index of asymmetry of right
ventricular enlargement.
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Statistical Methods
For the predetermined time points (index, 6, 12, and 24 months),
measurements were compared with baseline by a repeated measures
analysis of variance. Pairwise comparisons were tested with the
Scheffé correction for multiple comparisons. Data are
presented as mean±1 SD.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Hemodynamic and Clinical Parameters
Relative to baseline, there were no significant changes in body weight (64±12 versus 68±9 kg), cardiac index (2.7±0.5 versus 2.5±0.8 L · min-1 · m-2), mean systemic arterial pressure (95±8 versus 107±12 mm Hg), systolic pulmonary artery pressure (26±5 versus 22±4 mm Hg), mean pulmonary artery pressure (17±3 versus 14±3 mm Hg), or mean pulmonary artery capillary wedge pressure (10±4 versus 8±3 mm Hg) at 2-year follow-up.
Impact of Right Ventricular Volume Overload on Right
Ventricular Geometry
Tricuspid annular diameter was significantly enlarged at 24 months
relative to baseline for end-diastolic (4.0±0.5 versus
3.2±0.4 cm, P<0.01), midsystolic (3.6±0.5 versus
2.8±0.3 cm, P<0.001), and end-systolic (3.3±0.4
versus 2.5±0.3 cm, P<0.01) measurements.
End-diastolic RVA (30.3±5.4 versus 19.5±5.0
cm2, P<0.0002), and
end-systolic RVA (16.7±3.7 versus 11.0±3.2
cm2, P<0.001) were also increased
significantly at 24 months relative to baseline. The right
ventricular L dimension remained relatively unchanged over
this period (7.4±0.9 versus 6.9±0.8 cm, P=NS), whereas the
right ventricular S1 dimension increased from 4.0±0.4 to
5.1±0.7 cm (P<0.001), and the right
ventricular S2 dimension increased from 3.5±0.6 to
5.0±0.5 cm (P<0.001; Figure 2). As a result, the ratio of right
ventricular S2 to L at end diastole (0.68±0.07
versus 0.52±0.10, P<0.005) was significantly
greater at 24 months than at baseline, as were the midsystolic
(0.63±0.06 versus 0.47±0.09, P<0.005) and
end-systolic minor axis/L ratios (0.56±0.06 versus 0.42±0.11,
P<0.05).
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Impact of Right Ventricular Volume Overload and
Asymmetric Dilation of the Right Ventricle on Global and Regional
Systolic Performance
Percent systolic RVA change (RVA%) was constant
throughout the 24-month period of follow-up (RVA%: 45.1±6.9% at 24
months versus 43.8±9.2% at baseline, P=NS). Percent L
fractional shortening (L%) was preserved throughout the 24-month
period (19.6±3.1% versus 17.7±5.4%, P=NS, 24 months
versus baseline). Similarly, shortening along the minor axes (S1%:
26.0±6.3% versus 26.5±8.7%, P=NS; and S2%: 33.5±8.5%
versus 33.7±11.6%, P=NS) were unchanged comparing 24
months to baseline.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Severe tricuspid regurgitation due to the development of a flail tricuspid valve resulted in a 25% increase (P<0.01) in end-diastolic tricuspid annular diameter and a 55% (P<0.0002) increase in end-diastolic RVA at 2-year follow-up. The end-diastolic L of the right ventricle did not increase significantly compared with baseline (7% increase), whereas the S1 dimension increased 28% (P<0.001) and the S2 dimension increased 43% (P<0.001) over the same period. Thus, the right ventricle preferentially dilates in the free wall to ventricular septal axis in response to right ventricular volume overload.
Comparison to Earlier Studies
In a cross-sectional study12 comparing 10 orthotopic
heart transplant recipients with flail tricuspid valves to 62
orthotopic heart transplant recipients with normal tricuspid valves,
the magnitude of right ventricular enlargement due to right
ventricular volume overload was comparable to that found in
our longitudinal study over 2 years. Our longitudinal study builds on
these observations by demonstrating that the right
ventricular enlargement is asymmetric with preferential
dilation along the right ventricular minor axis. The
resultant distortion of ventricular septal geometry may
have important implications for our preliminary observation of
progressive depression in left ventricular ejection
fraction seen in these and other patients with severe tricuspid
regurgitation.3 4 5 6 7
Received December 22, 1998; revision received June 15, 1999; accepted June 17, 1999.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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1. Louie EK, Rich S, Levitsky S, Brundage BH. Doppler echocardiographic demonstration of the differential effects of right ventricular pressure and volume overload on left ventricular geometry and filling. J Am Coll Cardiol. 1992;19:84–90.[Abstract]
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12. Williams MJA, Lee M-Y, DiSalvo TG, Dec EN, Picard MH, Palacios IF, Semigran MJ. Biopsy induced flail tricuspid leaflet and tricuspid regurgitation following orthotopic cardiac transplantation. Am J Cardiol. 1996;77:1339–1344.In 10 heart transplant recipients whose tricuspid valves were inadvertently disrupted by endomyocardial biopsy, right ventricular end-diastolic cavity area increased from 19.5±5.0 to 30.3±5.4 cm2, P<0.0002, with disproportionate elongation along the right ventricular end-diastolic midminor axis (3.5±0.6 to 5.0±0.5 cm, P<0.001). Right ventricular volume overload results in disproportionate chamber enlargement along its free wall to septal minor axis.[Medline] [Order article via Infotrieve]
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