(Chest. 2005;128:628S-630S.)
© 2005
American College of Chest Physicians
Interventricular Mechanical Asynchrony Due To Right Ventricular Pressure Overload in Pulmonary Hypertension Plays an Important Role in Impaired Left Ventricular Filling*
Anton Vonk-Noordegraaf, MD, FCCP;
Johan T. Marcus, JT PhD;
C. Tji Gan, MSc;
Anco Boonstra, MD and
Pieter E. Postmus, MD, FCCP
* From the Departments of Pulmonary Medicine (Vonk-Nordegraaf and Boonstra, and Mr. Gan), and Physics and Medical Technology (Dr. Marcus), Institute for Cardiovascular Research, Vrije Universiteit Medical Centre, Amsterdam, The Netherlands.
Correspondence to: A. Vonk-Noordegraaf, MD, FCCP, University Hospital Vrije Universiteit, Department of Pulmonary Medicine, PO Box 7057, 1007 MB Amsterdam, The Netherlands; e-mail: A.Vonk{at}vumc.nl
Key Words: left ventricle • MRI • pulmonary arterial hypertension • right heart failure • right ventricle • ventricular asynchrony
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Introduction
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In severe pulmonary arterial hypertension (PAH), chronic pressure and volume overload alters right ventricle (RV) geometry (ie, hypertrophy and dilation). As a consequence, the amount of space taken by the RV in patients with PAH within the pericardium increases, causing a leftward ventricular septum bowing. This phenomenon is most markedly observed during early left ventricular (LV) diastole, impeding LV diastolic filling.1 As a consequence, LV end-diastolic volume will be reduced, altering the LV contraction function, as described by the Frank Starling mechanism.234 The aim of our study was to investigate whether a prolonged RV systolic contraction time contributes to leftward septum bowing and the hemodynamic consequences of this interventricular interaction in pulmonary hypertension.
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Materials and Methods
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Fifty-nine patients with idiopathic PAH (mean [± SD] pulmonary artery pressure, 52 ± 16 mm Hg) and 24 healthy control subjects were measured by means of MRI (1.5 T Sonata system; Siemens; Erlangen, Germany). To investigate RV and LV systolic contraction time, seven patients were measured by means of measuring myocardial tagging of the RV and LV. By means of harmonic phase strain analysis, the time from ECG R-wave trigger to peak shortening (Tpeak) was calculated as a parameter for systolic contraction duration. The principle of this technique has been described in detail recently.5
To investigate the hemodynamic consequences of LV septal bowing on diastolic filling of the LV, and its hemodynamic consequences, 52 PAH patients and 24 age-matched and sex-matched control subjects were measured. RV and LV end-diastolic volume (EDV), end-diastolic systolic volume, and LV peak filling rate were assessed by means of cine imaging. The ventricular volume ratio (VRdias), which was defined as RV EDV/(LV EDV + RV EDV) was used to determine the ventricular volumetric interactions. Flow quantification of the main pulmonary artery was part of the protocol in all patients and control subjects to assess stroke volume.
A nonparametric test was used to test the differences between the Tpeak times of the RV and LV. Single linear regression analyses were performed to assess the correlations between MRI-derived parameters within the patient group.
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Results
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For the seven patients studied with tagging, the mean Tpeak values for the RV inferior, lateral, and anterior regions were 322 ± 68, 366 ± 57, and 364 ± 53 ms, respectively. For the LV lateral region, the mean Tpeak was 266 ± 54 ms. Thus, the mean Tpeak for the RV lateral region was 100 ± 43 ms later than that for the LV lateral value (p < 0.001), and the mean Tpeak for the RV anterior region was 98 ± 38 ms later than that for the LV lateral region (p < 0.001). In comparison with the control subjects, the mean RV end-diastolic volume index was higher in the PAH patients (93 ± 23 vs 73 vs 23 mL/m2; p < 0.01), whereas the LV end-diastolic volume was reduced in the patient group (44 ± 14 vs 59 ± 9 mL/m2; p < 0.01). As a consequence, the VRdias was significantly increased in the PAH patients (0.68 ± 0.08 vs 0.56 ± 0.04; p < 0.001) and was inversely related to a decreased peak filling rate of the LV (r = 0.63; p = 0.001) and stroke volume (r = 0.61; p < 0.001). No relation was found between stroke volume on the one hand and pulmonary artery pressure or RV end-diastolic volume on the other.
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Discussion
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These results show that in PAH, there is a significant interventricular asynchrony due to a prolonged RV systolic contraction time in comparison to the LV. This is probably caused by a decrease of electrical conductivity over the RV, a high prestretch of the RV myocardial fibers, and the large force these fibers must generate to shorten. This ventricular asynchrony impedes LV diastolic filling, causing a lowered LV end-diastolic volume.
Underfilling of the LV can be explained in two ways. First, LV septal bowing impedes early LV filling, leading to a reduced end-diastolic LV volume, which will lead to a reduced stroke volume that is explained by the Frank Starling mechanism. Second, decreased RV function due to elevated afterload leads to a decrease in stroke volume and thus to a decrease in LV diastolic filling and end-diastolic volume. Although both mechanisms cannot be separated from each other in this study, the direct relationship between LV EDV and VRdias with stroke volume in the absence of any significant relationship between RV EDV or pulmonary artery pressure supports the idea that diastolic ventricular interaction is the major factor impairing stroke volume. These results are in line with those of animal studies, showing that the reduction of stroke volume was not primarily caused by RV failure but by the failure of the LV to fill adequately due to direct diastolic ventricular interaction.34 In their study, opening the pericardium facilitated LV filling leading to an increase of LV end-diastolic volume and consequently, output, providing further evidence that the detrimental effects of RV pressure overload are primarily caused by the failure of the LV to fill. Since a relationship exists between pericardial pressure and right atrial pressure, and right atrial pressure is increased in patients with severe PAH, the process of direct diastolic interaction will be facilitated in end-stage disease.
From these results, we concluded that interventricular asynchrony due to a prolonged RV contraction is one of the main mechanisms of LV septal bowing leading to underfilling of the LV in patients with PAH. Cardiac dysfunction in patients with PAH should thus be understood as a complex interventricular interaction instead of RV function solely.
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Footnotes
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Abbreviations: EDV = end-diastolic volume; LV = left ventricle, ventricular; PAH = pulmonary arterial hypertension; RV = right ventricle, ventricular; Tpeak = ECG R-wave trigger to peak shortening; Vrdias = ventricular volume ratio
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References
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- Marcus, JT, Vonk Noordegraaf, A, Roeleveld, RJ, et al (2001) Impaired left ventricular filling due to right ventricular pressure overload in primary pulmonary hypertension: noninvasive monitoring using MRI. Chest 119,1761-1765[Abstract/Free Full Text]
- Belenkie, I, Dani, R, Smith, ER, et al Effects of volume loading during experimental acute pulmonary embolism. Circulation 1989;80,178-188[Abstract/Free Full Text]
- Baker, AE, Dani, R, Smith, ER, et al Quantitative assessment of independent contributions of pericardium and septum to direct ventricular interaction. Am J Physiol 1989;275,H476-H483
- Belenkie, I, Sas, R, Mitchell, J, et al Opening the pericardium during pulmonary artery constriction improves cardiac function. J Appl Physiol 2004;96,917-922[Abstract/Free Full Text]
- Zwanenburg, JJ, Gotte, MJ, Kuijer, JP, et al Timing of cardiac contraction in humans mapped by high-temporal-resolution MRI tagging: early onset and late peak of shortening in lateral wall. Am J Physiol Heart Circ Physiol 2004;286,H1872-H1880[Abstract/Free Full Text]
- Tyberg, JV, Taichman, GC, Smith, ER, et al The relationship between pericardial pressure and right atrial pressure: an intraoperative study. Circulation 1986;73,428-432[Abstract/Free Full Text]
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Introduction
Materials and Methods
2 images (below), at trigger delays of 242 ms (left) and 382 ms (right) in a patient with PAH. Increased darkness in the