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* From the Departments of Clinical Physics and Informatics (Drs. Marcus and Heethaar), Pulmonary Medicine (Drs. Vonk Noordegraaf, Roeleveld, Postmus, and Boonstra), and Cardiology (Dr. Van Rossum), ICaR-VU, University Hospital Vrije Universiteit, Amsterdam, The Netherlands.
Correspondence to: J. Tim Marcus, PhD, Department of Clinical Physics and Informatics, University Hospital, Vrije Universiteit, PO Box 7057, Boelelaan 1117, 1007 MB Amsterdam, The Netherlands; e-mail: jt.marcus{at}azvu.nl
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Abstract |
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Methods: In 12 patients (9 women; age range, 30 to 56 years), the diagnosis of PPH had been established by catheterization (mean ± SD pulmonary artery pressure [PAP] was 56 ± 8 mm Hg). With breath-hold cine MRI, a series of short-axis images was acquired covering the whole left ventricle (LV) and right ventricle (RV). The curvature, defined as 1 divided by the radius of curvature in centimeters, was calculated for the septum and the LV free wall in early diastole. Leftward ventricular septal bowing (LVSB) is denoted by a negative curvature. For the LV and the RV, the end-diastolic volume (EDV), stroke volume (SV), and volumetric filling rate were calculated. The control subjects were all healthy (n = 14; 11 women; age range, 20 to 57 years).
Results: In the patients, LVSB was quantified in early diastole by the septal curvature of - 0.14 ± 0.07 cm-1, and the septal to free-wall curvature ratio of - 0.42 ± 0.21. LV EDV and LV SV correlated negatively with diastolic PAP (p = 0.004 and p = 0.04, respectively). In patients vs control subjects, RV SV was reduced (52 ± 12 mL vs 82 ± 11 mL, p < 0.0001); LV peak filling rate was smaller (2.2 ± 0.7 EDV/s vs 3.3 ± 0.5 EDV/s, p < 0.001); LV EDV was smaller (81 ± 23 mL vs 117 ± 19 mL, p = 0.001); and LV SV was smaller (49 ± 18 mL vs 83 ± 13 mL, p < 0.0001).
Conclusion: In PPH, RV pressure overload leads to LVSB and reduced RV output. By decreased blood delivery, LV filling is reduced, which results in decreased LV SV by the Frank-Starling mechanism.
Key Words: diastole • heart failure • hypertension • pulmonary • pulmonary heart disease • ventricles
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Introduction |
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Different therapeutic options are under investigation.2 It is essential to monitor each patient’s response to therapeutic intervention at an early stage.3 The choice of therapy, dosage, and duration can then be tailored to the patient. To enable this monitoring of therapy efficacy, it is desirable to measure the signs of pulmonary hypertension (PH) noninvasively.
These signs of PH include increased steepness of the main pulmonary artery (MPA) flow curve,4 leftward ventricular septum bowing (LVSB), reduced RV output, and decreased left ventricle (LV) filling and LV output.3 5 6 In PPH, the ventricular geometry is disturbed; therefore, volume estimations of the RV and LV are hard to obtain from single-plane acquisitions. With MRI, the ventricular volumes can be measured independent of any geometric assumption, as done earlier with spin-echo MRI.5 With gradient-echo cine MRI, the septal motion and the RV and LV volumes can now be quantified as a function of time.
In this study, the signs of PH are quantified by gradient-echo cine MRI, with focus on ventricular septal motion, RV output, and LV filling. The MRI-derived indicators of PH will be related to the PAP measurements. The mechanisms by which the loss of cardiac output can be explained will be explored.
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Materials and Methods |
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Clinical Data
PAP and RV pressure were measured by standard right-heart
catheterization, and given as systolic, diastolic, and mean values. The
responsiveness to short-term vasodilator infusion was tested by
simultaneous invasive PAP measures. No patient responded to this acute
vasodilator testing. All patients but one received continuous IV
prostacyclin treatment. In all patients, the ECG showed sinus rhythm
without any bundle-branch block. Clinical status was New York Heart
Association class 3 or class 4.
MRI Acquisition
The MRI acquisition method was described earlier7
and was approved by the institutional review committee. Part of the
protocol was magnetic resonance flow quantification in the MPA. The
scanner was a Siemens 1.5 T "Vision" (Siemens; Medical Systems;
Erlangen, Germany) with temporal resolution of 40 ms for cine
imaging. Additional long-axis cine images were acquired through the LV
outflow tract.
MRI Postprocessing
Flow and Volumes:
The MPA flow curve was characterized by
the upslope,4
7
defined as the quotient of acceleration
time divided by ejection time (AT/ET). From the stack of parallel
short-axis cine images, the RV and LV volumes were calculated for each
temporal frame in the cardiac cycle, using the MR Analytical Software
System (Leiden University Medical Center; Leiden, The
Netherlands). The end-diastolic volume (EDV), end-systolic volume
(ESV), and stroke volume (SV) were calculated. The peak LV filling rate
was expressed as LV EDV per second.
MRI Postprocessing
Septal Curvature:
The septal curvature was evaluated for the
short-axis image plane at about midventricular level (at least one
papillary muscle visible). The cine time frame was in early diastole,
ie, the first temporal frame after systole in which
filling of the RV was manifest (for this frame, the delay after the
R-wave trigger was in the range from 320 to 400 ms). Septal bowing was
quantified by the curvature (defined as 1 divided by the radius of
curvature in centimeters), as calculated by entering septal image
coordinates (midwall) into an analytical fitting routine. To account
for different heart sizes, septal curvature was also expressed as a
relative number with respect to the free-wall curvature: the
septal/free-wall curvature ratio.8
Positive values of this
curvature ratio denote rightward septal bowing (as is physiologic), and
negative values denote LVSB.
Statistics
The MRI-derived parameters were tested in the patients vs the
control group by unpaired-samples t testing (equal variances
not assumed). In the patients, the relation between MRI-derived
parameters and PAP values was tested by simple linear regression.
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The relations between the PAP values and the MRI-derived cardiac parameters are given in Figure 2 . The correlations of septal curvature with systolic PAP, diastolic PAP, mean PAP, RV EDV, RV SV, and RV EF were not significant (NS).
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MRI Parameters of PH
The smaller AT/ET ratio in the pulmonary artery flow is compatible
with earlier studies: PH leads to a steeper upslope of the pulmonary
artery flow, which is related to larger pulmonary vascular
resistance.4
The septal curvature was rightward in systole and leftward in early diastole. We hypothesize the following: during systole, pressure in the LV overrules the pressure in the RV, and thus the septum is pushed away from the LV center. This is supported by the value of the systolic RV pressure (75 ± 17 mm Hg), which is still below the systolic LV pressure. During early diastole, the LV pressure drops to near zero to enable rapid LV filling. Now the pressure in the RV prevails, pushing the septum away from the RV center. This explains why the LVSB sign is most manifest in early diastole.
This mechanism has been documented in an animal study of RV pressure overload by pulmonary artery constriction, in which a linear relation was observed between the septal curvature and the transseptal pressure gradient. The septum bowed to the left (negative curvature) when the RV pressure exceeded the LV pressure by > 5 mm Hg.10
Impaired LV Filling
In PPH, the increased pulmonary vascular resistance limits the RV
stroke volume, and thus limits automatically the volume available for
LV filling. LVSB reduces the LV volume in early diastole, and thereby
might present a secondary, additive mechanism that further impairs the
LV-filling process just in the most important phase of rapid filling.
The resulting impaired LV filling interferes with LV pump function: the
LV blood volume is reduced, and also the contractile force of the
LV myocardial muscle fibers is reduced due to the Frank-Starling law.
The observations of LVSB and LV-filling impairment have potential implications. If a patient shows a high degree of LVSB, this indicates a high transseptal pressure gradient with RV pressure exceeding LV pressure in diastole.10 Then, nonselective vasodilatory medication may be contraindicated, because systemic vasodilation might trigger a fatal drop in systemic BP.3 Further validation is required.
Relation Between MRI Parameters and PAP Values
The significant negative correlations of LV EDV and SV vs
diastolic PAP and mean PAP support the concept of impaired LV diastolic
filling due to PPH. The correlation of the AT/ET ratio vs systolic PAP
is consistent with the presentation of AT/ET ratio as an indicator of
systolic pulmonary arterial resistance.
Study Limitations
The study was small and therefore should be considered
preliminary, requiring a larger prospective study of test performance
characteristics as compared to Doppler echocardiography findings.
As yet, the correlations between septal curvature, and PAP values and RV parameters were not significant. We presume that this is caused by a confounding factor, being the degree of RV wall hypertrophy that was very different between patients, with RV wall thickness ranging between 5.3 mm and 10.9 mm at midlevel. If a patient has PPH for a longer time, then marked thickening of the RV wall and septum will develop. A very thick septum will show less leftward bowing, in spite of very high PAP and impaired RV and LV function. Thus, the value of the leftward septal curvature is probably also influenced by the degree of hypertrophy, while the sign of leftward septal bowing is consistent in all patients.
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Footnotes |
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Received for publication August 31, 2000. Accepted for publication November 30, 2000.
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