DOI:10.2214/AJR.07.2031
AJR 2008; 190:1576-1582
© American Roentgen Ray Society
Rapidly Reversible Myocardial Edema in Patients with Acromegaly: Assessment with Ultrafast T2 Mapping in a Single-Breath-Hold MRI Sequence
Hervé Gouya1,
Olivier Vignaux1,
Patrick Le Roux2,
Philippe Chanson3,
Jérome Bertherat4,
Xavier Bertagna4 and
Paul Legmann1
1 Department of Radiology, Hôpital Cochin, 27 rue du Faubourg
Saint-Jacques, 75679 Paris Cedex 14, France.
2 Global Applied Science Laboratory, GE Healthcare, Buc, France.
3 Department of Endocrinology, University Paris XI, Hôpital
Bicètre, Le Kremlin-Bicètre, France.
4 Department of Endocrinology, Université René Descartes,
Hôpital Cochin, Paris, France.
Received February 8, 2007;
accepted after revision January 2, 2008.
Address correspondence to H. Gouya
(princetgouya{at}yahoo.fr).
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Abstract
OBJECTIVE. The purpose of this study was to use a single-breath-hold
T2-mapping MRI sequence to evaluate the reversibility of myocardial edema in
patients treated for acromegaly.
SUBJECTS AND METHODS. Before and after treatment, 15 patients with
acromegaly underwent myocardial T2 mapping with an experimental
single-breath-hold black-blood fast spin-echo sequence. Myocardial T2 mapping
with both a multiple-breath-hold fast spinecho sequence and the experimental
sequence also was performed on 14 volunteers. T2 relaxation times were
calculated with a standard linear least-squares fit applied to myocardial
signal intensity. The T2 relaxation times of patients were compared with those
of volunteers and correlated with levels of serum growth hormone and
insulinlike growth factor 1. Left ventricular function and mass index were
determined with cine MRI.
RESULTS. T2 values before treatment were higher in patients (71
± 12 milliseconds) than in volunteers (55.9 ± 3.6 milliseconds)
(p = 0.0003). These T2 values in patients decreased soon after
treatment (57.6 ± 6.6 milliseconds, p = 0.0007). This
reduction correlates with successful reduction of levels of serum growth
hormone and insulinlike growth factor 1. In volunteers, myocardial T2 values
did not vary significantly between the single-breath-hold sequence and the
multiple-breath-hold fast spin-echo sequence. In patients, myocardial mass and
left ventricular function did not differ significantly before and after
treatment.
CONCLUSION. Patients with acromegaly have increased myocardial T2
values, which decrease soon after treatment, reflecting reversible myocardial
edema. T2 value is more sensitive than left ventricular mass index in the
detection of early reversal of acromegalic cardiomyopathy. These results
highlight the potential role of MRI in direct assessment of the tissular
effects of growth hormone and insulinlike growth factor 1 and in evaluation of
the efficacy of treatment.
Keywords: acromegaly • edema • MRI technique • myocardial diseases • T2 mapping
Introduction
Acromegaly is caused by excess growth hormone and is associated with
increased mortality, primarily from cardiovascular disease
[1,
2]. Growth hormone exerts its
effects on heart tissue directly and indirectly through insulinlike growth
factor 1 (IGF-1). Both growth hormone and IGF-1 receptors are present in
cardiac myocytes. A specific cardiomyopathy has been reported in acromegaly
that may be partially reversed by effective reduction of growth hormone and
IGF-1
[3-9].
Biopsy and autopsy studies have shown that interstitial fibrosis and edema are
the main histologic features of impaired myocardial function
[10-12].
Transsphenoidal surgical management of growth hormone-producing pituitary
adenoma or treatment with highly powerful drugs that block growth hormone
secretion or action can reduce growth hormone and IGF-1 plasma levels to
normal or nearly normal levels
[13-16].
The adequacy of treatment so far has relied on growth hormone and IGF-1 plasma
thresholds above which morbidity and mortality rates are higher than normal
[17-19].
These limits are highly uncertain, however, and cannot be used to assess
normal secretion of growth hormone. There is a crucial need for assessment of
the tissular effects of growth hormone and IGF-1 on myocardium rather than
reliance on measurement of plasma values of these substances.
Echocardiography is widely used to evaluate acromegalic cardiomyopathy.
This technique, however, shows only functional and morphologic modifications
in the heart (concentric left ventricular hypertrophy) induced by the tissular
effects of growth hormone and IGF-1. It does not depict structural changes in
the myocardium
[20-22].
We hypothesized that structural changes, especially edema, can be evaluated by
measurement of myocardial transverse relaxation time (T2) during MRI. This
method has been described [23,
24] for noninvasive detection
of myocardial edema in acute rejection of heart transplants. The aim of our
study was assessment of ultrafast myocardial T2 mapping with a
single-breath-hold black-blood single-shot fast spin-echo sequence for
measurement of the direct action of growth hormone and IGF-1 and for
evaluation of the efficacy of management of acromegaly.
Subjects and Methods
Patients
From March 2003 to May 2005, 15 patients with acromegaly on the basis of
clinical symptoms and laboratory data
[25,
26] were included in the
study. The study was approved by the institutional review board, and informed
consent was waived. The patients were six men and nine women with a mean age
of 50 years (range, 36-77 years). The mean duration of symptoms before
diagnosis was 103 months (range, 40-151 months). The diagnosis was made on the
basis of a growth hormone concentration greater than 5 ng/mL (10 mIU/L) or a
plasma IGF-1 concentration above the normal range for age and sex. Level of
plasma serum growth hormone was evaluated as the mean of five samples
collected during 2 hours of saline infusion. The IGF-1 level was the mean of
two measurements made on two days.
No patients had undergone previous surgery, radiation therapy, or medical
therapy with somatostatin analogues or dopamine agonists. In all cases,
acromegaly was caused by a pituitary growth hormone-secreting adenoma visible
on pituitary MRI. The adenoma was classified as microadenoma (n = 7)
if the diameter was less than 10 mm and as macroadenoma (n = 8) if
the diameter was greater than 10 mm. No patients had cardiac symptoms.
However, we carefully review ed other cardiovascular risk factors, including
hypertension (five patients) and non-insulin-dependent diabetes mellitus (five
patients). All patients underwent echocardiography. Myocardial thickness
measured on the septal and posterior left ventricular walls was normal in 11
patients. Left ventricular concentric hypertrophy (14.3 ± 1.6 mm) was
found in four patients. Left ventricular ejection fraction (68% ± 6.6%)
was normal in all patients.
Management of acromegaly consisted of transsphenoidal surgery (n =
6) or administration of somatostatin analogues either before surgery or as
long-term treatment (n = 9). During follow-up, the patients were
evaluated by measurement of growth hormone levels 6-14 days after the start of
treatment. Cardiac MRI was performed on all patients within 24 hours after
growth hormone or IGF-1 serum analysis. Short-term follow-up MRI examinations
were performed 6-15 days after treatment.
Cardiac MRI was performed on 14 volunteers (eight men, six women; mean age,
32 years) who met the following criteria: absence of clinical symptoms of
acromegaly and of biologic abnormalities suggesting acromegaly; absence of
cardiovascular disease (diabetes, hypertension, coronary artery disease);
absence of contraindications to MRI; and probable ability to undergo the
procedure. This group of volunteers constituted the control group.
MRI Protocol
Cardiac MRI was performed with a 1.5-T system (Signa Echospeed, GE
Healthcare) equipped with a 22-mT/m and 120-T/m/s gradient system with ECG
triggering and a torso phased-array coil. We developed an ultrafast T2 mapping
method consisting of a single-breath-hold half-Fourier single-shot fast
spin-echo sequence (Fig. 1A)
[27]. With the method,
n images are obtained corresponding to n effective echo
times: TEmin, TEmin + I x ESP,...,
TEmin + (n - 1)I x ESP, where ESP is the
echo space duration of the fast spin-echo sequence, TEmin is the
minimum TE, and I is the increment chosen by the user. With
single-shot acquisition of each image, n images can be acquired in
n consecutive shots if only one slice is acquired. The varying
effective TE is obtained by addition of (n - 1)I echo spaces
to the standard single-shot fast spin-echo sequence and sliding the acquired
echoes by an amount of I echo spaces between acquisitions. Although
this method unnecessarily lengthens the first acquisitions, it ensures that
the saturation contributed by the radiofrequency pulses stays constant and
that no variable longitudinal relaxation contrast enhancement is
introduced.
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Fig. 1A —Experimental single-breath-hold sequence. Ultrafast
experimental single-breath-hold single-shot fast spin-echo MRI T2 map obtained
with generic Carr-Purcell-Meiboom-Gill sequence. Top line represents spikes in
radiofrequency pulses that are in reality selective. Next two lines depict
read gradient Gx and encoding gradient waveforms as function of time.
Phase-encoding waveform Gy(1) pertains only to first acquisition. Three
acquisitions for obtaining three effective echoes are performed in this
example. Last two acquisitions are depicted only by their encoding waveforms
Gy(2) and Gy(3), radiofrequency and read gradient being kept constant between
acquisitions. Signal acquisition periods are represented by rectangles
positioned between half-sine encoding and rewinding impulses. Principle of
proposed protocol is to shift by a certain number of echo spaces (two echo
spaces in this example) acquisition windows and encoding waveform from one
acquisition to next, increasing effective echo time by same amount of time. To
guarantee that recovery of longitudinal magnetization is not perturbed,
sufficient number of dummy echoes (four echoes in this example) with no
encoding or signal acquisition are added at end of original
Carr-Purcell-Meiboom-Gill sequence. Sequence thus is always of same length and
produces same overall action on longitudinal magnetization, ensuring images
are void of variable T1 contrast enhancement.
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After scout acquisitions in the axial and left ventricular long axes, we
acquired images of the left midventricular short axis using the experimental
sequence (single level but different TEs). The midcavity view was selected
from the region that included the entire length of the papillary muscles. Nine
echoes were thus acquired with TEs of 10-90 milliseconds (increment, 10 milli
seconds). Images had a slice thickness of 10 mm for a pixel size of 1.17
x 2.34 mm (Figs. 1B,
1C,
1D,
1E,
1F,
1G,
1H,
1I, and
1J). The other parameters were
TR, 2,000-3,000 milliseconds; trigger delay, minimum; bandwidth, 235 kHz;
effective temporal resolution, 300 milliseconds with duration of single
breath-hold of 15-22 seconds.
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Fig. 1B —Experimental single-breath-hold sequence. 35-year-old man
with acromegaly disease. Short-axis black-blood single-shot fast spin-echo MR
images with incremental TEs ranging from 10 (B) to 90 (J)
milliseconds.
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Fig. 1C —Experimental single-breath-hold sequence. 35-year-old man
with acromegaly disease. Short-axis black-blood single-shot fast spin-echo MR
images with incremental TEs ranging from 10 (B) to 90 (J)
milliseconds.
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Fig. 1D —Experimental single-breath-hold sequence. 35-year-old man
with acromegaly disease. Short-axis black-blood single-shot fast spin-echo MR
images with incremental TEs ranging from 10 (B) to 90 (J)
milliseconds.
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Fig. 1E —Experimental single-breath-hold sequence. 35-year-old man
with acromegaly disease. Short-axis black-blood single-shot fast spin-echo MR
images with incremental TEs ranging from 10 (B) to 90 (J)
milliseconds.
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Fig. 1F —Experimental single-breath-hold sequence. 35-year-old man
with acromegaly disease. Short-axis black-blood single-shot fast spin-echo MR
images with incremental TEs ranging from 10 (B) to 90 (J)
milliseconds.
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Fig. 1G —Experimental single-breath-hold sequence. 35-year-old man
with acromegaly disease. Short-axis black-blood single-shot fast spin-echo MR
images with incremental TEs ranging from 10 (B) to 90 (J)
milliseconds.
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Fig. 1H —Experimental single-breath-hold sequence. 35-year-old man
with acromegaly disease. Short-axis black-blood single-shot fast spin-echo MR
images with incremental TEs ranging from 10 (B) to 90 (J)
milliseconds.
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Fig. 1I —Experimental single-breath-hold sequence. 35-year-old man
with acromegaly disease. Short-axis black-blood single-shot fast spin-echo MR
images with incremental TEs ranging from 10 (B) to 90 (J)
milliseconds.
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Fig. 1J —Experimental single-breath-hold sequence. 35-year-old man
with acromegaly disease. Short-axis black-blood single-shot fast spin-echo MR
images with incremental TEs ranging from 10 (B) to 90 (J)
milliseconds.
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Cardiac MRI was performed on the control group with the experimental
sequence and a previously described protocol consisting of a
multiple-breath-hold fast spin-echo sequence (conventional sequence) with nine
echoes of 10-90 milliseconds in a left midventricular short-axis view (level
similar to that for experimental sequence)
[23]. The parameters of the
conventional sequence were TR, more than two R-R intervals to infinity;
trigger delay, 610 milliseconds; band width, 41.7 kHz; duration of each
breath-hold, 14-19 seconds.
Functional examinations (cine MRI) were performed in both pretreatment and
posttreatment evaluations. The sequence was breath-hold shortaxis steady-state
free precession with coverage of the whole left ventricle in a single-slice
per breath-hold. The TR was adjusted to cardiac cycle/minimum TE. The slice
thickness was 10 mm, and the number of views per segment was eight.
Image Analysis
On a clinical workstation (Advantage Windows 3.2, GE Healthcare), circular
regions of interest were manually drawn along the left ventricular myocardium
by two investigators in consensus. One investigator was an experienced general
radiologist and the other a cardiac radiologist with 10 years of experience in
cardiac MRI. Six regions of interest were placed to avoid confusing signals
from the phased-array coil within the following segments according to the
standardized myocardial segmentation
[28]: midanterior (segment 7),
midanteroseptal (segment 8), midinferoseptal (segment 9), midanterolateral
(segment 12), mid inferolateral (segment 11), and midinferior (segment 10).
These regions of interest were placed on the first echo image of each sequence
(multiple-breath-hold fast spin-echo sequence for control group and
experimental sequence for both control group and patients with acromegaly) and
then automatically reproduced unchanged on eight other echo images. A total of
3,024 segments were thus analyzed.
T2 relaxation times were calculated with a standard linear least-squares
fit applied on the myocardial signal measured on the echo images and based on
the equation M(TE) = M0exp(-TE/T2) where M(TE) is the averaged
signal from regions of interest on the corresponding image (Functool software,
GE Healthcare). The values of T2 relaxation times, that is, T2 = -[TE x
logM0)/logM(TE)], measured in all segments were averaged for each patient and
each volunteer. The myocardial T2 values for patients were correlated with
serum growth hormone and IGF-1 levels and with myocardial T2 values of the
control group. Cardiac function was analyzed with dedicated software (MASS,
Medical Imaging Solutions), and parameters were normalized per square meter of
body surface area.
Statistical Analysis
Variables were expressed as mean ± SD. T2 myocardial values in
patients before and after treatment and in the control group were compared by
use of the nonparametric Mann-Whitney test. We used the nonparametric
Wilcoxon's test to compare continuous variables (myocardial T2, growth hormone
and IGF-1 serum levels, enddiastolic volume index, end-systolic volume index,
ejection fraction, and mass index) for matched groups before and after
treatment. The Spearman's correlation coefficient was calculated to analyze
the relation between myocardial T2 and decreases in serum levels of growth
hormone and IGF-1 after treatment. A value of p < 0.05 was
considered indicative of a significant difference.
Results
Table 1 shows hormone and
myocardial T2 values before and after treatment.
Hormones
Before treatment, the mean basal plasma level of growth hormone was 31.7
± 19.3 ng/mL (63.4 ± 38.6 mIU/L) and the mean plasma level of
IGF-1 was 1,045 ± 274 ng/mL. After treatment, the mean basal plasma
level of growth hormone was 3.8 ± 3.6 ng/mL (7.6 ± 7.2 mIU/L)
and the mean IGF-1 plasma level was 524 ± 214 ng/mL. The mean decrease
between pretreatment and posttreatment serum levels of growth hormone was 27.9
± 18.4 ng/mL (55.8 ± 36.8 mIU/L) and of IGF-1 was 521 ±
334 ng/mL. The differences in growth hormone and IGF-1 levels before and after
treatment were statistically significant (p = 0.0007).
Myocardial T2 Relaxation Time
The mean time between the start of treatment and posttreatment MRI was 10.8
± 3.5 days. Reliable T2 relaxation time curves were obtained owing to
the six measurements with both the conventional and the single-shot sequences.
In the control group, the T2 relaxation times did not vary significantly
between the experimental single-breath-hold sequence (55.9 ± 3.6
milliseconds; range, 51-61.1 milliseconds) and the multiple-breath-hold fast
spin-echo sequence (57.2 ± 1.6 milliseconds; range, 49.6-63.5
milliseconds). Mean T2 values were 71 ± 12 milliseconds (range, 54-91
milliseconds) before treatment and 57.6 ± 6.6 milliseconds (range,
47-68 milliseconds) after treatment. This difference was statistically
significant (p = 0.0007). Myocardial T2 was significantly longer in
patients with acromegaly before treatment than in controls (p =
0.0003) without overlap. There was no significant difference between the
values for the controls (55.9 ± 3.6 milliseconds) and for the patients
after treatment (p = 0.59) (Fig.
2). In patients, the difference in absolute myocardial T2 values
before and after treatment correlated with the difference in absolute values
of serum levels of growth hormone (p = 0.022)
(Fig. 3) and IGF-1 (p
= 0.0049) (Fig. 4) before and
after treatment. No significant differences in pretreatment myocardial T2
values were observed between patients with and those without cardiovascular
disease. We also found no statistically significant difference in myocardial
T2 between patients with microadenoma and those with macroadenoma. Myocardial
T2 did not vary significantly between patients who underwent medical therapy
and those who underwent surgical intervention.
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Fig. 4 —Graph shows relation between myocardial T2 values and serum
levels of insulinlike growth factor 1 (IGF-1) for all patients before
(triangles) and after (squares) treatment. T2 = 55.2 + 0.1
IGF-1.
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Myocardial Mass and Left Ventricular Function in Patients with Acromegaly
End-diastolic volume index (p = 0.77), endsystolic volume index
(p = 0.61), and ejection fraction (p = 0.95) did not differ
significantly before and after treatment
(Table 2). Our results for left
ventricular mass index showed a moderate decrease after treatment, but the
difference was not significant compared with pretreatment values (p =
0.28).
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TABLE 2: Myocardial Mass and Left Ventricular Function in Patients with
Acromegaly and Volunteers Before and After Treatment
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Discussion
Our results show that ultrafast myocardial T2 mapping is a sensitive
approach for measuring growth hormone and IGF-1 tissular effects and for
evaluating the efficacy of treatment of patients with acromegaly. In all
patients, the myocardial T2 relaxation time was much higher than in healthy
volunteer controls. Our results also showed that increased myocardial T2
relaxation time can be lowered with effective treatment and is significantly
correlated with successful reduction of growth hormone and IGF-1 levels.
Hypersecretion of growth hormone appears to have a direct detrimental
effect on the heart and is associated with a specific cardiomyopathy that
results in structural and functional abnormalities due to interstitial
fibrosis and edema
[3-12].
It is well known that growth hormone affects water balance and that growth
hormone excess increases myocardial water content. Because T2 relaxation time
is affected by the water content of tissues, a higher than normal myocardial
T2 relaxation time would be expected
[23,
24]. In a study of
transplanted hearts, Marie et al.
[23] found that a higher than
normal T2 relaxation time determined with a black-blood MRI sequence
correlated with myocardial edema. Using this parameter, the investigators
identified most cases of moderate acute rejection detected with biopsy. In our
study, the myocardial T2 values were significantly higher in untreated
patients with acromegaly than in healthy controls. The T2 values of our
control group agreed with those in a previous study
[24] and ranged from 51 to
61.1 milliseconds.
Acromegaly treatment has two goals: to eliminate the local threat of a
pituitary tumor and to reduce or suppress the increased morbidity and
mortality associated with chronic excess of growth hormone and IGF-1. The
latter goal can be met more easily with highly powerful drugs that can block
growth hormone secretion (somatostatin analogues and dopamine agonists) or
action (growth hormone antagonists)
[13-17,
29]. As do those of previous
studies [8,
30,
31], our results imply that
structural myocardial changes, especially edema, are partially or totally
reversible with successful treatment with either surgery or short-term medical
therapy. We found that myocardial T2 values normalize soon after treatment (10
days for seven patients). Previous studies
[8,
9,
11,
15,
16,
30,
32] have shown that the
clinical status of some patients with cardiac acromegaly improves when therapy
for acromegaly is started. Except for those in one report
[30], however, no data are
available about immediate improvement. In that study, changes in cardiac
status with treatment and serial echocardiographic measurements revealed a
reduction (
12%) in increased left ventricular mass index. Morphologic
cardiac changes appeared to occur reasonably quickly, within 8 days. No
changes were observed in patients with normal left ventricular mass. The rapid
reduction in left ventricular mass strongly supports the hypothesis that real
myocardial edema is reversed with successful treatment. Regression in the
relative increase in myocyte size associated with concentric thickening of the
ventricular walls also may explain the reduction in left ventricular mass in
midterm and long-term follow-up
[29,
32].
Our findings showed that myocardial T2 values decreased in all patients
with no correlation with the simultaneous echocardiographic diagnosis of left
ventricular hypertrophy before treatment. A more interesting finding was that
enddiastolic volume index, end-systolic volume index, and ejection fraction
did not differ significantly before and after treatment. These results
corroborated the hypothesis that functionally the main early consequence of
structural and morphologic heart changes in patients with acromegaly is
impaired left ventricular diastolic function, not systolic function
[33]. Moreover, in contrast to
findings in a previous study
[30], left ventricular mass
index exhibited a modest but not significant decrease after treat ment. These
preliminary results suggest that cardiac MRI with T2 mapping significantly
improves the diagnostic performance of detection of early resolution of
acromegalic cardiomyopathy.
Our study showed the feasibility of mapping myocardial T2 relaxation time
with a single-breath-hold MRI sequence. The T2 relaxation times were measured
with an experimental single-shot fast spin-echo sequence with 10 echoes with
the addition of echo spaces to the standard single-shot fast spinecho sequence
and incremental changes in the encoding lobe amplitude of each echo space. The
sequence used is a generic Carr-Purcell-Meiboom-Gill (CPMG) sequence
(Fig. 1A), such as rapid
acquisition with relaxation enhancement, fast spin-echo, and turbo spin-echo.
The radiofrequency selection in the top line is represented symbolically by
hard pulses, and a 90° flip pulse is followed by a regular train of
refocusing pulses. The next two lines depict the read and encoding gradient
waveforms as a function of time pertaining to the first acquisition. The
signal acquisition periods are visualized by the small rectangles between the
ogival encoding and rewinding waveforms. One or several dummy echoes are
generally accommodated in the CPMG sequence to allow the pseudosteady state to
become established. Figure 1A
shows one such dummy echo followed by 10 echoes with encoding and signal
acquisition. After the normal CPMG sequence, four echoes without encoding or
signal acquisition have been added. In the proposed protocol, the same slice
is acquired several times to obtain different effective echo times. In this
example, three acquisitions for obtaining three effective echoes are
performed. Because only the encoding waveform is modified between
acquisitions, only the encoding waveforms Gy(2) and Gy(3) are depicted for the
two last lines. To obtain a variable effective echo time without perturbing
the dynamic, a certain number of dummy echoes with no encoding or signal
acquisition are added at the end of the original CPMG sequence. The result can
be verified on the encoding waveform Gy(1) of the first acquisition, in which
four dummy echoes have been added to the 10 original echoes.
We developed an ultrafast T2 mapping sequence for single-breath-hold
acquisitions that minimizes respiratory artifacts. The shorter acquisitions
times also allow the unchanged relaxation time required for T2 mapping. The
heart rate did not change during the single-breath-hold acquisition, whereas
it can vary during multiple-breath-hold acquisitions. Blurring was observed
but was minimized by phase-encoding steps that allow correct delimitation of
both epicardial and endocardial borders of the myocardium. Unlike the
conventional sequence, our breath-hold technique avoids shifting of the
regions of interest among several breath holds.
Our results show that patients with acromegaly have rapidly reversible
abnormally increased myocardial T2 values as assessed with an ultrafast
single-breath-hold single-shot fast spin-echo MRI sequence. This effect is
probably due to myocardial edema, as suggested in previous histologic reports
[7,
10-12].
Our findings highlight the challenge of noninvasive visualization of reversal
of myocardial involvement in treated patients. T2 mapping is more sensitive
than assessment of left ventricular mass index and significantly improves the
diagnostic performance of detection of early resolution of acromegalic
cardiomyopathy. Further studies are needed to correlate the reversal of
cardiomyopathy with diastolic function as the main echocardiographic feature
of this condition.
Acknowledgments
We are grateful to Stephane Silvera and Thierry Plantier for helping with
the statistical analysis.
References
- Bengtsson BA, Eden S, Ernest I, Oden A, Sjögren B.
Epidemiology and long-term survival in acromegaly: a study of 166 cases
diagnosed between 1955 and 1984. Acta Med Scand1988; 223:327
-335[Medline]
- Orme SM, McNally RJ, Cartwright RA, Belchetz PE. Mortality and
cancer incidence in acromegaly: a retrospective cohort study. J
Clin Endocrinol Metab 1998;83
: 2730-2734[Abstract/Free Full Text]
- Ciulla M, Arosio M, Barelli MV, et al. Blood pressure-independent
cardiac hypertrophy in acromegalic patients. J
Hypertens 1999; 17:1965
-1969[CrossRef][Medline]
- Fazio S, Cittadini A, Cuocolo A, et al. Impaired cardiac
performance is a distinct feature of un-complicated acromegaly. J
Clin Endocrinol Metab 1994;79
: 441-446[Abstract]
- Lombardi G, Colao A, Ferone D. Effect of growth hormone on cardiac
function. Horm Res 1997;48
: 38-42[CrossRef][Medline]
- Lombardi G, Colao A, Marzullo P, et al. Is growth hormone bad for
your heart? Cardiovascular impact of GH deficiency and of acromegaly.
J Endocrinol 1997;155
: S33-S37[CrossRef][Medline]
- Lopez-Velasco R, Escobar-Morreale HF, Vega B, et al. Cardiac
involvement in acromegaly: specific myocardiopathy or consequence of systemic
hypertension? J Clin Endocrinol Metab1997; 82:1047
-1053[Abstract/Free Full Text]
- Colao A, Cuocolo A, Marzullo P, et al. Is the acromegalic
cardiomyopathy reversible? Effect of 5-year normalization of growth hormone
and insuline-like growth factor I levels on cardiac performance. J
Clin Endocrinol Metab 2001;86
: 1551-1557[Abstract/Free Full Text]
- Vianna CB, Vieira ML, Mady C, et al. Treatment of acromegaly
improves myocardial abnormalities. Am Heart J2002; 143:873
-876[CrossRef][Medline]
- Frustaci A, Chimenti C, Setoguchi M, et al. Cell death in
acromegalic cardiomyopathy. Circulation1999; 99:1426
-1434[Abstract/Free Full Text]
- Nishiki M, Murakami Y, Sohmiya M, et al. Histopathological
improvement of acromegalic cardiomyopathy by intermittent subcutaneous
infusion of octreotide. Endocr J 1997;44
: 655-660[Medline]
- Lie JT. Pathology of the heart in acromegaly: anatomic findings in
27 autopsied patients. Am Heart J 1980;100
: 41-52[CrossRef][Medline]
- Melmed S, Jackson I, Kleinberg D, Klibanski A. Current treatment
guidelines for acromegaly. J Clin Endocrinol Metab1998; 83:2646
-2652[Abstract/Free Full Text]
- Melmed S, Casanueva F, Cavagnini F, et al. Consensus statement:
medical management of acromegaly. Eur J Endocrinol2005; 153:737
-740[Abstract/Free Full Text]
- Merola B, Cittadini A, Colao A, et al. Chronic treatment with the
somatostatin analog octreotide improves cardiac abnormalities in acromegaly.
J Clin Endocrinol Metab 1993;77
: 790-793[Abstract]
- Legrand V, Beckers A, Pham VT, Demoulin JC, Stevenaert A. Dramatic
improvement of severe dilated cardiomyopathy in an acromegalic patient after
treatment with octreotide and trans-sphenoidal surgery. Eur Heart
J 1994; 15:1286
-1289[Abstract/Free Full Text]
- Melmed S. Acromegaly. N Engl J Med1990; 322:966
-977[Medline]
- Rajasoorya C, Holdaway IM, Wrightson P, Scott DJ, Ibbertson HK.
Determinants of clinical outcome and survival in acromegaly. Clin
Endocrinol 1994; 41:95
-102[Medline]
- Davies PH, Stewart SE, Lancranjan L, Sheppard MC, Stewart PM.
Long-term therapy with long-acting octreotide (Sandostatin-LAR) for the
management of acromegaly. Clin Endocrinol1998; 48:311
-316[CrossRef][Medline]
- Fazio S, Cittadini A, Sabatini D, et al. Evidence for biventricular
involvement in acromegaly: a Doppler echocardiographic study. Eur
Heart J 1993; 14:26
-33[Abstract/Free Full Text]
- Galanti G, Cappelli B, Diricatti G, Mininni S, Vono MC, Gensini GF.
Systolic and diastolic cardiac function in acromegaly: an echocardiographic
study. Ann Ital Med Int 1996;11
: 27-32[Medline]
- Terzolo M, Avonto L, Matrella C, et al. Doppler echocardiographic
patterns in patients with acromegaly. J Endocrinol
Invest 1995; 18:613
-620[Medline]
- Marie PY, Angioi M, Carteaux JP, et al. Detection and prediction of
acute heart transplant rejection with the myocardial T2 determination provided
by a black-blood magnetic resonance imaging sequence. J Am Coll
Cardiol 2001; 37:825
-831[Abstract/Free Full Text]
- Lund G, Morin RL, Olivari MT, Ring WS. Serial myocardial T2
relaxation time measurements in normal subjects and heart transplant
recipients. J Heart Transplant 1988;7
: 274-279[Medline]
- Lim EM, Pullan P. Biochemical assessment and long-term monitoring
in patients with acromegaly: statement from a joint consensus conference of
the Growth Hormone Research Society and the Pituitary Society. Clin
Biochem Rev 2005; 26:41
-43[Medline]
- Doga M, Bonadonna S, Gola M, Nuzzo M, Giustina A. Diagnostic and
therapeutic consensus on acromegaly. J Endocrinol
Invest 2005; 28:56
-60[Medline]
- Vignaux O, Augui J, Coste J, et al. Comparison of single-shot fast
spin-echo and conventional spinecho sequences for MR imaging of the heart:
initial experience. Radiology 2001;219
: 545-550[Abstract/Free Full Text]
- Cerqueira MD, Weissman NJ, Dilsizian V, et al. Standardized
myocardial segmentation and nomenclature for tomographic imaging of the heart:
a statement for healthcare professionals from the Cardiac Imaging Committee of
the Council on Clinical Cardiology of the American Heart Association.
Circulation 2002;105
: 539-542[Free Full Text]
- Newmann CB, Melmed S, George A, et al. Octreotide as primary
therapy for acromegaly. J Clin Endocrinol Metab1998; 83:3031
-3033[Free Full Text]
- Lim MJ, Barkan AL, Buda AJ. Rapid reduction of left ventricular
hypertrophy in acromegaly after suppression of growth hormone hypersecretion.
Ann Intern Med 1992;117
: 719-726[Abstract/Free Full Text]
- Weber KT, Brilla CG. Pathological hypertrophy and cardiac
interstitium. Circulation 1991;83
: 1849-1865[Abstract/Free Full Text]
- Colao A, Marzullo P, Cuocolo A, et al. Reversal of acromegalic
cardiomyopathy in young but not in middle-aged after 12 months of treatment
with the depot long-acting somatostatin analogue octreotide. Clin
Endocrinol 2003; 58:169
-176[CrossRef][Medline]
- Ozbey N, Oncül A, Bugra Z, et al. Acromegalic cardiomyopathy:
evaluation of the left ventricular diastolic function in the subclinical
stage. J Endocrinol Invest 1997;20
: 305-311[Medline]
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Abstract
Introduction
