Ambulatory arterial stiffness index is not a stiffness parameter but a ventriculo-arterial coupling factor.
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Biomedical subjects
Publications and source records attributed to Jan-Willem Lankhaar.
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Right ventricular (RV) afterload is commonly defined as pulmonary vascular resistance, but this does not reflect the afterload to pulsatile flow. The purpose of this study was to quantify RV afterload more completely in patients with and without pulmonary hypertension (PH) using a three-element windkessel model. The model consists of peripheral resistance (R), pulmonary arterial compliance (C), and characteristic impedance (Z). Using pulmonary artery pressure from right-heart catheterization and pulmonary artery flow from MRI velocity quantification, we estimated the windkessel parameters in patients with chronic thromboembolic PH (CTEPH; n = 10) and idiopathic pulmonary arterial hypertension (IPAH; n = 9). Patients suspected of PH but in whom PH was not found served as controls (NONPH; n = 10). R and Z were significantly lower and C significantly higher in the NONPH group than in both the CTEPH and IPAH groups (P < 0.001). R and Z were significantly lower in the CTEPH group than in the IPAH group (P < 0.05). The parameters R and C of all patients obeyed the relationship C = 0.75/R (R(2) = 0.77), equivalent to a similar RC time in all patients. Mean pulmonary artery pressure P and C fitted well to C = 69.7/P (i.e., similar pressure dependence in all patients). Our results show that differences in RV afterload among groups with different forms of PH can be quantified with a windkessel model. Furthermore, the data suggest that the RC time and the elastic properties of the large pulmonary arteries remain unchanged in PH.
The aim of this study was to investigate the contribution of direct right-to-left ventricular interaction to left ventricular filling and stroke volume in 46 patients with pulmonary arterial hypertension (PAH) and 18 control subjects. Stroke volume, right and left ventricular volumes, left ventricular filling rate, and interventricular septum curvature were measured by magnetic resonance imaging and left atrial filling by transesophageal echocardiography. Stroke volume, left ventricular end-diastolic volume, and left ventricular peak filling rate were decreased in PAH patients compared with control subjects: 28 +/- 13 vs. 41 +/- 10 ml/m(2) (P < 0.001), 46 +/- 14 vs. 61 +/- 14 ml/m(2) (P < 0.001), and 216 +/- 90 vs. 541 +/- 248 ml/s (P < 0.001), respectively. Among PAH patients, stroke volume did not correlate to right ventricular end-diastolic volume or mean pulmonary arterial pressure but did correlate to left ventricular end-diastolic volume (r = 0.62, P < 0.001). Leftward interventricular septum curvature was correlated to left ventricular filling rate (r = 0.64, P < 0.001) and left ventricular end-diastolic volume (r = 0.65, P < 0.001). In contrast, left atrial filling was normal and not correlated to left ventricular end-diastolic volume. In PAH patients, ventricular interaction mediated by the interventricular septum impairs left ventricular filling, contributing to decreased stroke volume.
PURPOSE: To investigate whether an existing method for correction of phase offset errors in phase-contrast velocity quantification is applicable for assessment of main pulmonary artery flow with an MR scanner equipped with a high-power gradient system. MATERIALS AND METHODS: The correction method consists of fitting a surface through the time average of stationary pixels of velocity-encoded phase images, and subtracting this surface from the velocity images. Pixels are regarded as stationary if their time standard deviation falls into the lowest percentile. Flow was measured in the main pulmonary artery of 15 subjects. Each measurement was repeated on a stationary phantom. The phase offset error in the phantom was used as a reference. Correction was applied with varying polynomial surface orders (0-5) and stationarity percentiles (5-50%). The optimal surface order and stationarity percentile were determined by comparing the fitted surface with the phantom. RESULTS: Using a first-order surface and a (noncritical) 25% percentile, the correction method significantly reduced the phase offset error from 1.1 to 0.35 cm/second (RMS), which is equivalent to a reduction from 11% to 3.3% of mean volume flow. Phase error correction strongly affected stroke volume (range -11 to 26%). CONCLUSION: The method significantly reduces phase offset errors in pulmonary artery flow.
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