(Circulation. 1997;96:3430-3435.)
© 1997 American Heart Association, Inc.
Articles |
Left Ventricular Mechanics and Geometry in Patients With Congenital Complete Atrioventricular Block
From the Department of Cardiology, Children's Hospital, and the Department of Pediatrics, Harvard Medical School, Boston, Mass (S.D.C., E.P.W., P.S.G., T.G.), and the Lillie Frank Abercrombie Section of Pediatric Cardiology, Texas Children's Hospital, and the Department of Pediatrics, Baylor College of Medicine, Houston, Tex (N.J.K., R.A.F., R.J.G., R.S.).
Correspondence to Tal Geva, MD, Department of Cardiology, Children's Hospital, 300 Longwood Ave, Boston, Mass 02115. E-mail geva_t{at}a1.tch.harvard.edu
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Background Radiographic evidence of cardiomegaly is common in patients with congenital complete atrioventricular block (CCAVB). It has been speculated that left ventricular (LV) remodeling and increased stroke volume counteract the bradycardia, but the effects of slow heart rate and atrioventricular asynchrony on LV dimensions, geometry, wall stress, and function have not been examined in detail.
Methods and Results Thirty patients with CCAVB without associated congenital heart disease (mean age, 8.5±5.3 years; range, 0.2 to 20 years) were included in a cross-sectional two-institution study. Thirty-five echocardiograms were performed using standard techniques. ECG and 24-hour ECG recordings were reviewed. Seven patients did not receive a pacemaker, whereas 23 patients underwent pacemaker implantation after the echocardiogram. Compared with normal control subjects, LV volume (Z score=1.5±1.3) and LV mass (Z=1.2±1.5) were significantly increased, whereas LV mass-to-volume ratio (1.1±0.3) and geometry (short-axis diameter/length ratio=0.65±0.09) were normal. LV end-systolic stress (ESS) (a measure of afterload) was normal (Z score=0.2±2.3), whereas shortening fraction (Z=3±2.9) and velocity of circumferential fiber shortening (VCF) (Z=3±3.1) were increased. The relationship between VCF and ESS (a preload-insensitive and afterload-adjusted index of contractility) was increased (Z=2.2±2) with only small increase in preload (Z=1.02±1.1). Regression analyses showed no significant change over age in LV mass, volume, geometry, loading conditions, or systolic function. Patients who ultimately met criteria for pacemaker implantation did not differ from those who did not in terms of heart rate or LV function but did have increased LV volume (Z score=1.8±1.4 versus 0.4±0.9, P=.03) and LV mass (Z score=1.7±1.2 versus 0.2±1.7, P=.001) compared to the unpaced group.
Conclusions In most patients with CCAVB, the LV was enlarged with normal geometry and enhanced systolic function during the first two decades of life. The degree of LV dilation and enhanced function did not significantly change with age. In patients who ultimately underwent pacemaker implantation LV function did not differ from those who remained unpaced, but evidence of a slightly increased load manifested as increased end-diastolic volume and mass.
Key Words: echocardiography • systole • heart block • remodeling • ventricles
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Congenital complete AV block is a rare condition with a reported incidence between 1 in 15 000 and 1 in 25 000 live births, with most estimates at 1 in 22 000. Approximately 25% to 33% of these children will have associated heart disease.1 Survival to adulthood without pacemaker implantation has been well documented in patients with CCAVB.2–6 Several investigators have reported radiographic evidence of cardiomegaly in these patients.4,5,7 Some have postulated that the cardiomegaly may be related to LV remodeling and reorganization of myofibers to increase stroke volume and compensate for slow heart rate.8,9 Only limited information exists regarding LV adaptation to CCAVB. One report found that global LV function is normal in this population6; however, the effects of long-standing slow heart rates and AV asynchrony on LV dimensions, geometry, and function in patients with CCAVB have not been examined in detail.
The present study was designed to evaluate LV structure and function in patients with CCAVB to determine whether bradycardia and AV asynchrony are associated with any potentially adverse effects on cardiac mechanics during the first two decades of life. The study also aimed to determine whether patients who met criteria for pacemaker implantation during the study period differed in terms of LV structure or function from those who did not.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Patients
A cross-sectional study was performed at Children's Hospital in Boston and Texas Children's Hospital in Houston. Thirty patients with CCAVB who underwent 35 echocardiograms and had no significant structural heart disease were included. Patients who had undergone pacemaker implantation before the echocardiogram were not included in this study. The following information was obtained in each patient at the time of the echocardiogram: age, sex, height, weight, and heart rate. A 15-lead ECG was evaluated for the presence of CCAVB, and the most recent 24-hour ECG was reviewed for the maximum, minimum, and average heart rates and for ectopy. Study patients were assigned into two groups based on whether they subsequently underwent pacemaker implantation. Group 1 consisted of 7 patients who did not receive a pacemaker by the time the study was concluded. Group 2 consisted of 23 patients who underwent pacemaker implantation subsequent to their echocardiographic examination. Study patients were compared with a control group of 256 children and adolescents without heart disease (age, 7 days to 19 years; 134 boys and 122 girls) who were studied at the echocardiography laboratory of Children's Hospital (Boston).10
Echocardiographic Protocol
Echocardiograms were performed with several commercially
available cardiac scanners with transducer frequency appropriate for
the patient's size and acoustic windows. Sedation with oral chloral
hydrate (70 to 100 mg/kg; maximal dose, 1 g) was used in
infants when necessary. Each study included an evaluation of cardiac
anatomy, ventricular function, and valve competence
by two-dimensional imaging, pulsed, and color Doppler mapping.
Studies were recorded on a 0.5-in (1.27-cm) super-VHS videocassette
tape for subsequent review and offline analysis.
LV length in systole (measured on the video frame showing minimal dimension) and diastole (measured on the video frame showing maximal dimension) were measured from the apical four-chamber view between the plane of the mitral valve annulus and the apical endocardium. For assessment of LV systolic function, the two-dimensionally directed M-mode tracing of the LV minor axis between the papillary muscles tips, the indirect carotid arterial pulse tracing, phonocardiogram, and ECG were simultaneously recorded on hard copy at high paper speed (100 mm/s) as described previously.11 Right arm systolic and diastolic blood pressures were recorded at the same time using a Dinamap Vital Signs Monitor 8100T (Critikon).
Data Analysis
LV Dimensions and Stress
All computer measurements were performed at Children's Hospital
in Boston by the same individual (P.S.G.). The M-mode tracing of the
endocardial borders of the interventricular septum and the
endocardial and epicardial borders of the LV posterior wall,
arterial pulse tracing, onset of Q wave on the ECG, and
first high-frequency component of the second heart sound on the
phonocardiogram were digitized using a computer-based digitizing
station with customized software.12 From the
digitized data, the following instantaneous measurements were obtained
by averaging three to six cardiac cycles: (1) LV pressure during
ejection as has been previously described and validated against
pressure measurements obtained through
catheterization,13 (2) LV
posterior wall thickness, and (3) LV internal dimensions in the
short-axis plane. End-diastolic measurements were taken at
the time of maximal LV dimension and end-systolic measurements
were taken at the time of aortic valve closure (first high-frequency
component of the second heart sound on the phonocardiogram). Because of
concerns that conventional stress calculations in the presence of
hypertrophy may misrepresent forces at the
myocardial fiber level, Mirsky14 and
Regen15 advocated the use of fiber stress instead
of mean transmural wall stress as an index of afterload. In addition to
accounting for lateral stress in the meridional and circumferential
planes, fiber stress accounts for stress in the radial
direction.15 Another concern is that in the
presence of hypertrophy and increased mass-to-volume
ration, endocardial-based indices of fiber shortening overestimate the
extent and velocity of fiber shortening in sections of the wall that
are not adjacent to the endocardium.19 Because it
is not universally agreed which of the above is the most accurate
method with which to assess afterload and fiber shortening in patients
with CCAVB, endocardial, midwall wall stress, and fiberstress indices
were calculated. (4) LV meridional wall stress (in
g/cm2) was calculated throughout ejection
according to the formula of Brodie et al.16
ESSm was measured at the onset of the aortic
component of the second heart sound on the phonocardiogram. (5)
ESSc (in g/cm2) was
calculated according to the formula of Mirsky.15
(6) Fsm was calculated according to the formula
of Regen.17 (7) ETc was
measured from the arterial pulse tracing from the onset of
upstroke to the onset of the dicrotic notch and adjusted to a heart
rate of 60 bpm by dividing the heart rate by the square root of the RR
interval on the ECG. When heart rate was 
60 bpm, no adjustments were
made. (8) SF was calculated as (end-diastolic
dimension-end-systolic dimension)/end-diastolic
dimension. (9) VCFc was calculated as SF divided
by rate-adjusted ejection time. (10) LV volume was calculated using the
modified Simpson's rule.17 Ejection fraction was
calculated as 100x(end-diastolic
volume-end-systolic volume)/end-diastolic volume.
LV mass was calculated as 1.05x(LV epicardial volume-LV endocardial
volume).18 (11) LVEDDmw (in
cm) was calculated as
LVEDDmw=Ded+hed,
where Ded is the LV endocardial
end-diastolic diameter and hed is the
LV end-diastolic posterior wall thickness.
LVESDmw (in cm) was calculated using the formula
of Shimizu et al.19 LV midwall shortening
fraction and midwall velocity of circumferential fiber shortening were
calculated from these end-diastolic and
end-systolic midwall dimensions. (12) Cardiac output was
calculated as the product of stroke volumexheart rate.
Contractility and Preload Indexes
The relationship between VCFc and ESS has
been previously shown to be an afterload adjusted index of
contractility that is relatively insensitive to
preload.20 The position of the relation of
VCFc to ESS for each patient was determined
relative to the previously reported distribution of this index in
normal subjects and calculated as the SVI.20 The
SVI is equal to the number of SDs from the population mean
VCFc for ESS and is expressed as Z score. In
contrast, the relationship between FS and ESS (known as SSI) is an
afterload-adjusted index of contractility sensitive to
changes in preload.11,12,20 The SSI is equal to
the number of SDs from the population mean FS for the given ESS. The
relative magnitude of VCFc compared with FS is a
measure of preload status, reflecting the fact that FS is directly
related to end-diastolic fiber length, whereas
VCFc is relatively independent of
preload.11,12,20,21 Differences between
ESS/VCFc relation and ESS/FS relation, therefore,
reflect the functional consequences of altered preload, which was
quantified as the functional preload index: FPI=SSI-SVI.
Doppler
The degree of mitral regurgitation was graded
qualitatively as trivial or none, mild, moderate, or severe on
color-Doppler flow mapping of the regurgitant jet as described
previously.22
Statistical Analysis
Data are reported as mean±SD value for each group of
measurements. To adjust for age-, body size–, and growth-related
changes in LV dimensions and mechanics,10,23 all
measurements are reported as Z scores. Z scores were computed as
follows: Z score=(measured value-mean value of normal controls)/SD of
normal control subjects. The mean Z score of the normal control group
is 0.10 To determine whether Z scores differed
from the normal population, one-factor analysis was performed
with a hypothesized difference of zero. Correlation analysis
and linear regression analysis with the least-squares method
were used to evaluate the relationship between continuous
variables. In these analyses, age was considered an
independent variable, and LV dimensions and indices of function
were considered dependent variables. Unpaired Student's
t test was used to compare paced with nonpaced patients. The
Spearman rank correlation analysis was used to correlate the
degree of mitral regurgitation with LV dimensions and
indexes of function. Data analysis was performed using a
commercially available statistical package (StatView 4.1, Abacus
Concepts, Berkeley, Calif). For all tests, a value of P<.05
was considered statistically significant.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Characteristics of Study Patients
The demographic and clinical characteristics of the study patients are summarized in Table 1
. Thirty
patients (16 male and 14 female) met the inclusion criteria for this
study and underwent 35 echocardiograms. Two patients had serial
echocardiograms. Twenty-three patients have subsequently undergone
pacemaker implantation. The indications for pacemaker implantation were
complex ventricular ectopy at rest or with exercise (n=6),
bradycardia as defined in the American Heart Association/American
College of Cardiology
guidelines24 (n=6), exercise intolerance (n=4),
syncope (n=3), LV enlargement (n=2), and pauses of >4 seconds (n=1).
One patient had three indications for pacing: complex
ventricular ectopy, exercise intolerance, and bradycardia.
Seven patients remain unpaced. The age range of the entire group was
0.2 to 20 years (median, 8 years). There was no significant difference
between the ages of the paced and unpaced patients.
|
Heart Rate and Blood Pressure
The average heart rate at the time of study was 47±6 bpm, and
there was no difference between those who were subsequently paced and
those who were not. On 24-hour ECG monitoring, the average, minimum,
and maximum heart rates were not significantly different between groups
(Table 1
). When heart rate was plotted against age, there was a slight
but statistically significant inverse linear correlation
(r2=-.34, P=.04) (Fig 1A). When heart rate was adjusted to age
(expressed as Z score), it became apparent that the degree of
bradycardia relative to age-adjusted normal population is substantially
more pronounced in infancy and early childhood compared with
adolescence (Fig 1B). Pulse pressure was wide due to a relatively low
diastolic blood pressure in both groups. Compared with
unpaced patients, both peak and end-systolic pressures were
slightly increased in patients who were subsequently paced, but both
parameters were within the normal range in both groups.
|
LV Dimensions and Geometry
Overall, the LV was moderately dilated with preservation of normal
geometry. Compared with normal subjects, LV end-diastolic
volume (Z score=1.5±1.3), LV end-diastolic dimension (Z
score=1.8±1.3), and LV mass (Z=1.2±1.5) were significantly increased
(P<.0001) (Table 2), yet LV mass-to-volume ratio (1.1±0.3)
and LV geometry (LV short-axis diameter/length ratio=0.65±0.09)
remained normal. To determine whether the Z values of LV dimensions
changed with age, multiple linear regression analyses were
performed. These analyses showed that the BSA–adjusted LV
internal dimensions, volume, and mass did not significantly change
during the first two decades of life (Fig 2).
|
|
LV Mechanics
The following load-dependent indices of global LV function were
significantly increased: SF (Z score=3.0±2.9, P<.0001) and
velocity of circumferential shortening (Z score=3.0±3.1,
P<.0001). End-systolic stress was normal (Z score
0.2±2.3, P=.56). The SVI, a preload-insensitive index of
contractility (Z=2.2±2) and the SSI (Z=3.2±2.1) were
significantly increased (P<.0001) (Table 2). Preload index was only slightly
increased (Z=1.02±1.1). There were no significant differences in LV
wall stress, SVI, SSI, and preload index between measurements in the
meridional plane and the circumferential plane or between endocardial
and midwall measurements (Table 2). Cardiac index was low normal
(2.3±0.8 L · min-1 ·
m-2). To determine whether the LV function or
contractility changed with age, linear regression
analyses were performed (Fig 2). The enhanced LV
contractility index remained unchanged with age
(r2=.029, P=.3), as did the SF
(r2=.009, P=.6).
Mitral Regurgitation
In 23 of 30 patients, the degree of mitral
regurgitation was mild or less. Mild to moderate mitral
regurgitation was seen in 7 patients whose age ranged
from 3.7 to 19.8 years, with a median of 11.8 years. None of the
patients had moderate or severe mitral regurgitation.
No significant correlation was found between the degree of mitral
regurgitation and LV end-diastolic volume
(P=.46), LV end-diastolic dimension
(P=.2), or age (P=.09).
Comparison Between Paced and Unpaced Patients
The following indices of global function were increased in both
groups and did not significantly differ between groups: SF, ejection
fraction, VCFc, and SVI (Table 2). There were
also no significant differences between the groups in age or heart rate
at the time of echocardiogram. There were no differences in average
heart rate, minimum heart rate, or maximum heart rate on 24 ECG
monitoring (Table 1). Patients who were ultimately paced had
significantly increased LV mass (Z score=1.7±1.2 versus 0.2±1.7,
P=.001) and LV volume (Z score=1.8±1.4 versus 0.4±0.9,
P=.028) at the time of the echocardiogram.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The results of this study demonstrate that on average, in patients with CCAVB the LV is moderately enlarged with normal geometry, normal wall stress, and enhanced systolic function during the first two decades of life. In the patients included in this study, the degree of LV dilation and enhanced function did not significantly differ with age.
LV Mechanics and Geometry
Previous studies of patients with CCAVB have speculated that these
patients maintain their cardiac output by increasing their stroke
volume.1,9 The increased stroke volume was
postulated to be secondary to the increased time for
diastolic filling, which resulted in increased
end-diastolic volume with stretching of myocardial fibers
and facilitation of myocardial
contractility.9 In the
present study, the increased LV end-diastolic volume
was accompanied by a parallel increase in LV mass, thereby preserving
normal LV wall stress. Normal LV geometry, expressed as the ratio
between short-axis diameter and LV length, was also preserved. This
observation contrasts with findings in patients in whom a volume load
is acquired as a result of valve regurgitation or a
shunt lesion. In patients with severe mitral or aortic valve
regurgitation, the change in shape of the LV from an
ellipsoid bullet-shaped to a globular geometry is associated with
deterioration of systolic performance and
contractility.25–27
In the patients with CCAVB evaluated in this study, enhanced systolic function appears primarily related to increased contractility without evidence of significantly altered loading conditions. There was evidence of marginally but not significantly elevated preload (afterload-adjusted fractional shortening was only slightly more elevated than afterload-adjusted velocity of circumferential fiber shortening) and normal afterload. The failure of a prolonged diastolic filling period in these subjects to result in a substantial increase in preload, considered as end-diastolic fiber stretch, is not surprising given the normal myocardial response to chronic volume load. Elevated diastolic stress normally elicits myocardial hypertrophy and remodeling with addition of fibers in series until stress is normalized.26,27 Because of this, persistent elevation of diastolic stress is an indication of inadequate hypertrophy and would not be expected in well-compensated hypertrophy with an appropriate mass-to-volume ratio as was found in these patients. These findings are in contrast to those in physiological hypertrophy in athletes,12 where reduced afterload is the primary factor responsible for elevated systolic function, without evidence of enhanced contractility. The etiology of the enhanced contractility in these patients is not known. Evidence of persistent elevation in contractility has been described in young patients with congenital chronic pressure overload hypertrophy secondary to coarctation of the aorta28 but has not been described in volume overload lesions. The enhanced contractility found in patients with CCAVB cannot be explained by an artifact caused by the use of endocardial indices because the results of midwall indices were essentially the same as the endocardial indices. The agreement between these indices is expected in light of the normal LV mass-to-volume ratio found in these patients.
Although the majority of patients in this cohort had enhanced LV function, there were 2 patients whose function was depressed (fractional shortening, 26% and 28%). Others have reported patients with depressed LV function and cardiomyopathy despite the implantation of dual-chambered pacemakers in the neonatal period.29 It appears from the data presented by Moak et al29 that whatever causes these patients to have depressed function is not reversible with the institution of pacing. One could speculate that either there is more immunopathological damage to the heart, as Michaelsson et al30 suggested to be the cause for those with mitral regurgitation, or that the etiology of CCAVB in the subgroup of patients with depressed LV function is different from that of patients with normal function. In one reported case of a neonate with CCAVB, severe LV dysfunction was attributed to associated myocarditis.31 The etiology of depressed LV function in one of the 2 patients in our study is attributed to mitochondrial disease and is unknown in the other patient.
Mitral Regurgitation
Concerns that the development of mitral
regurgitation would be a complication of long-term
CCAVB without pacing were addressed by Michaelsson et
al,30 who reported a 16% incidence in adults
with CCAVB; these patients had slower ventricular rates and
the mitral regurgitation was postulated to result from
overdistention of the heart. In the present study, mitral
regurgitation was seen by color-coded Doppler in
77% of patients, with greater than mild regurgitation
in 23%, and was first noted in patients as young as 4 years. However,
the degree of mitral regurgitation did not correlate
with heart rate, LV function, LV end-diastolic volume, or
short-axis LV end-diastolic dimension. Because of the
cross-sectional nature of this study, it is not possible to determine
whether the degree of mitral regurgitation is
progressive or is alleviated by pacemaker placement. In the study by
Michaelsson et al,30 only 1 patient had
resolution of his mitral regurgitation with pacemaker
placement; however, this intervention occurred relatively late in the
natural history of the disease.
Influence of Pacemaker Requirement
Patients who ultimately underwent pacemaker implantation did not
differ from those who did not with respect to age or sex. Although the
average and minimum heart rates measured from 24-hour ECG were slightly
lower in patients who were eventually paced, these differences did not
reach statistical significance. Most measurements of LV mechanics were
similar in the two groups. The groups did not significantly differ from
each other in terms of LV geometry, SF, and SVI. Those who underwent
pacemaker placement had significantly increased LV mass and volume,
which is consistent with the findings of Sholler and
Walsh,32 whose symptomatic patients
had cardiac enlargement on chest radiograms and ECG. This finding,
however, may represent a selection bias because LV enlargement
was considered an indication for pacemaker in 2 patients. There was no
apparent relationship between changes in LV mechanics and indication
for pacemaker placement based on the data in the present study. Of
note, this patient population had a marginal cardiac index at rest
(Table 2), which may have contributed to the exercise intolerance
reported by some patients and was the indication for pacemaker
placement in 5 patients. In addition, LV dysfunction was not the reason
for pacemaker implantation in the majority of patients who ultimately
had a device implanted. In this study, we could not determine the
optimal time for pacemaker placement or address the potential long-term
benefits of pacing. The dilemma regarding optimal timing and patient
selection for pacemaker implantation in children and adolescents with
CCAVB was discussed elsewhere.33
Study Limitations
Because of the rarity of CCAVB, the study design was cross
sectional. This limitation precludes inference regarding the natural
history of patients with CCAVB. In the 2 patients who were followed
longitudinally over 15 years by echocardiograms, the longitudinal data
followed the trend of the cross-sectional cohort.
Conclusions
In most patients with congenital AV block, the LV is moderately
enlarged with normal geometry and enhanced systolic function
during the first two decades of life. The degree of LV dilation and
enhanced function did not significantly change with age. In patients
who ultimately underwent pacemaker implantation, LV function did not
differ from those who remained unpaced but had evidence of a slightly
increased load manifested as increased end-diastolic volume
and mass.
|
Selected Abbreviations and Acronyms |
|---|
|
|
Acknowledgments |
|---|
We thank Emily Flynn-McIntosh for artwork.
|
Footnotes |
|---|
Guest editor for this article was David J. Sahn, MD, Portland, Ore.
Received June 5, 1997; revision received July 25, 1997; accepted August 1, 1997.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
-
Ross BA. Atrioventricular block.
In Garson A Jr, Bricker JT, McNamara DG, eds. The Science and
Practice of Pediatric Cardiology. Philadelphia,
Pa: Lea & Febiger; 1990:1803.
-
Michaelsson M, Engle MA. Congenital complete heart
block: an international study of the natural history. Cardiovasc
Clin. 1972;4:86–101.
-
Campbell M, Emanuel R. Six cases of congenital
complete heart block followed for 34–40 years. Br Heart
J. 1967;29:577–587.
[Free Full Text]
-
Nakamura FF, Nadas AS. Complete heart block in infants
and children. N Engl J Med. 1964;270:1261–1268.
-
Esscher EB. Congenital complete heart block in
adolescence and adult life: a follow-up study. Eur Heart
J. 1981;2:281–288.
[Abstract/Free Full Text]
-
Cecconi M, Renzi R, Bettuzzi MG, Colonna P, Cuccaroni
G, Ricciotti R, Pozzato E, Berrettini U, Sgarbi E, Sparvieri F.
Blocco atrioventricolare completo congenito isolato: esperienza a lungo
termine in 38 pazienti. G Ital Cardiol. 1993;23:39–53.[Medline]
[Order article via Infotrieve]
-
Molthan ME, Miller RA, Hastreiter AR, Paul MH.
Congenital heart block with fatal Adams-Stokes attacks in childhood.
Pediatrics. 1962;30:32–41.
[Abstract/Free Full Text]
-
Manno BV, Hakki A, Eshaghpour E, Iskandrian AS. Left
ventricular function at rest and during exercise in
congenital complete heart block: a radionuclide angiographic
evaluation. Am J Cardiol. 1983;52:92–94.[Medline]
[Order article via Infotrieve]
-
Scarpelli EM, Rudolph AM. The
hemodynamics of congenital heart block. Prog
Cardiovasc Dis. 1964;6:327–342.
-
Colan SD, Parness IA, Spevak PJ, Sanders SP.
Developmental modulation of myocardial mechanics: age- and
growth-related alterations in afterload and
contractility. J Am Coll Cardiol. 1992;19:19–29.[Medline]
[Order article via Infotrieve]
-
Colan SD, Sanders SP, Ingelfinger JR, Harmon W. Left
ventricular mechanics and contractile state in children and
young adults with end stage renal disease: effect of dialysis and renal
transplantation. J Am Coll Cardiol. 1987;10:1085–1094.[Abstract]
-
Colan SD, Sanders SP, Borow KM. Physiologic
hypertrophy: effect on left ventricular
systolic mechanics in athletes. J Am Coll
Cardiol. 1987;9:776–783.[Abstract]
-
Borow KM, Newburger JW. Noninvasive estimation of
central aortic pressure using the oscillometric method for analyzing
systemic artery pulsatile blood flow: comparative study of indirect
systolic, diastolic, and mean brachial artery
pressure with simultaneous direct ascending aortic pressure
measurements. Am Heart J. 1982;103:879–886.[Medline]
[Order article via Infotrieve]
-
Mirsky I. Review of various theories for evaluation of
left ventricular wall stress. In Mirsky I, Chiston DN,
Sander J, eds. Cardiac Mechanics:
Physiological, Chemical and Mathematical
Considerations. New York, NY: Wiley; 1974:381–409.
-
Regen DM. Calculation of left ventricular
wall stress. Circ Res. 1990;67:245–252.
[Abstract/Free Full Text]
-
Brodie BR, McLaurin LP, Grossman W. Combined
hemodynamically-ultrasonic method for studying left
ventricular wall stress: comparison with angiography.
Am J Cardiol. 1976;37:864–870.[Medline]
[Order article via Infotrieve]
-
Silverman NH, Ports TA, Snider AR, Schiller NB,
Carlsson E, Heilborn DC. Determination of left ventricular
volume in children: echocardiographic and angiographic
comparisons. Circulation. 1980;62:548–557.
[Free Full Text]
-
Reichek N, Helak J, Plappert T, St John Sutton M, Weber
KT. Anatomic validation of left ventricular mass estimates
from clinical two-dimensional echocardiography:
initial results. Circulation. 1983;67:348–352.
[Abstract/Free Full Text]
-
Shimizu G, Zile MR, Blaustein AS, Gaasch WH. Left
ventricular chamber filling and midwall fiber lengthening
in patients with left ventricular hypertrophy:
overestimation of fiber velocities by conventional midwall
measurements. Circulation. 1985;71:266–272.
[Abstract/Free Full Text]
-
Colan SD, Borow KM, Neumann A. Left
ventricular end systolic wall stress-velocity of
fiber shortening relation: a load-independent index of myocardial
contractility. J Am Coll Cardiol. 1984;4:715–724.[Abstract]
-
Nixon JV, Murray RG, Leonard PD, Mitchell JH, Blomqvist
CG. Effect of large variations in preload on left
ventricular performance characteristics in normal
subjects. Circulation. 1982;65:698–703.
[Free Full Text]
-
Sanders SP. Echocardiography. In
Long WA, ed. Fetal and Neonatal Cardiology.
Philadelphia, Pa: WB Saunders; 1990:301–326:
-
Gutgesell HP, Rembold CM. Growth of the human heart
relative to body surface area. Am J Cardiol. 1990;65:662–668.[Medline]
[Order article via Infotrieve]
-
Dreifus LS, Fisch C, Griffin JC, Gillette PC, Mason JW,
Parsonnet. Guidelines for implantation of cardiac pacemakers and
antiarrhythmia devices: a report of the American College of
Cardiology/American Heart Association Task Force on
Assessment of Diagnostic and Therapeutic
Cardiovascular Procedures (Committee on Pacemaker
Implantation). Circulation. 1991;84:455–467.
[Free Full Text]
-
Sluysmans T, Sanders SP, van der Velde M, Matitiau A,
Parness IA, Spevak PJ, Mayer JE, Colan SD. Natural history and patterns
of recovery of contractile function in single left ventricle after
Fontan operation. Circulation. 1992;86:1753–1761.
[Abstract/Free Full Text]
-
Mehmel HC, Mazzoni S, Krayenbuehl HP.
Contractility of the hypertrophied human left ventricle
in chronic pressure and volume overload. Am Heart J. 1975;90:236–240.[Medline]
[Order article via Infotrieve]
-
Ross J Jr. Adaptation of the left ventricle to chronic
volume overload. Circ Res. 1974;34(suppl II):II-64-II-70.
-
Kimball TR, Reynolds JM, Mays WA, Khoury P, Claytor RP,
Daniels SR. Persistent hyperdynamic cardiovascular
state at rest and during exercise in children after successful repair
of coarctation of the aorta. J Am Coll Cardiol. 1994;24:194–200.[Abstract]
-
Moak J, Barron K, Hougen T, Cohen M, Friedman R, Perez
M, Buyon J. Congenital heart block: new observations. Pacing Clin
Electrophysiol. 1996;19:613.
-
Michaelsson M, Jonzon A, Reisenfeld T. Isolated
congenital complete atrioventricular block in adult
life: a prospective study. Circulation. 1995;92:442–449.
[Abstract/Free Full Text]
-
Ferrazzini G, Fasnacht M, Arbenz U, Seger R, Biedermann
R, Simma B, Uehlinger J, Dangel P, Fanconi S. Neonatal lupus
erythematosus with congenital heart block and
severe heart failure due to myocarditis and endocarditis of the mitral
valve. Intens Care Med. 1996;22:464–466.[Medline]
[Order article via Infotrieve]
-
Sholler GF, Walsh EP. Congenital complete heart block
in patients without anatomic cardiac defects. Am Heart
J. 1989;118:1193–1198.[Medline]
[Order article via Infotrieve]
-
Friedman RA. Congenital AV block: pace me now or pace
me later. Circulation. 1995;92:283–285.
[Free Full Text]
This article has been cited by other articles:
 |
|
 |
|
  O. L. Nelson, C. T. Robbins, Y. Wu, and H. Granzier Titin isoform switching is a major cardiac adaptive response in hibernating grizzly bears Am J Physiol Heart Circ Physiol, July 1, 2008; 295(1): H366 - H371. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Balmer, M. Fasnacht, M. Rahn, L. Molinari, and U. Bauersfeld Long-term follow up of children with congenital complete atrioventricular block and the impact of pacemaker therapy Europace, January 1, 2002; 4(4): 345 - 349. [Abstract] [PDF]
|
|
|
|
 |
|
 F. E. A. Udink ten Cate, J. M. P. J. Breur, M. I. Cohen, N. Boramanand, L. Kapusta, J. E. Crosson, J. I. Brenner, L. J. Lubbers, A. H. Friedman, V. L. Vetter, et al. Dilated cardiomyopathy in isolated congenital complete atrioventricular block: early and long-term risk in children J. Am. Coll. Cardiol., March 15, 2001; 37(4): 1129 - 1134. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. S. Rivera, T. R. Kimball, W. W. Bailey, S. A. Witt, P. R. Khoury, and S. R. Daniels Effect of veno-venous ultrafiltration on myocardial performance immediately after cardiac surgery in children: A prospective randomized study J. Am. Coll. Cardiol., September 1, 1998; 32(3): 766 - 772. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||