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ABSTRACT: Arterial compliance is mainly determined by the elasticity of proximal large-conduit arteries of which the aorta is the largest contributor. Compliance forms an important part of the cardiac load and plays a role in organ (especially coronary) perfusion. To follow local changes in aortic compliance, as in aging, noninvasive determination of compliance distribution would be of great value. Our goal is to determine regional aortic compliance noninvasively in the human. In seven healthy individuals at six locations, aortic blood flow and systolic/diastolic area (ΔA) was measured with MRI. Simultaneously brachial pulse pressure (ΔP) was measured with standard cuff. With a transfer function we derived ΔP at the same aortic locations as the MRI measurements. Regional aortic compliance was calculated with two approaches, the pulse pressure method, and local area compliance (ΔA/ΔP) times segment length, called area compliance method. For comparison, pulse wave velocity (PWV) from local flows at two locations was determined, and compliance was derived from PWV. Both approaches show that compliance is largest in the proximal aorta and decreases toward the distal aorta. Similar results were found with PWV-derived compliance. Of total arterial compliance, ascending to distal arch (segments 1-3) contributes 40% (of which 15% is in head and arms), descending aorta (segments 4 and 5) 25%, and "hip, pelvic and leg arteries" 20%. Pulse pressure method includes compliance of side branches and is therefore larger than the area compliance method. Regional aortic compliance can be obtained noninvasively. Therefore, this technique allows following changes in local compliance with age and cardiovascular diseases.
Journal of Applied Physiology 08/2012; 113(8):1285-91. · 3.75 Impact Factor
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ABSTRACT: In chronic pulmonary hypertension (PH), right ventricular (RV) failure is associated with shortening of the RV free wall (RVFW) beyond pulmonary valve closure, temporarily paralleled by pronounced lengthening of the left ventricular free wall (LVFW). We hypothesized that this early-diastolic LVFW lengthening is caused by altered RVFW myofibre function and may therefore serve as a non-invasive measure of PH-induced RV (dys)function.
In 22 idiopathic pulmonary arterial hypertension (IPAH) patients, five chronic thrombo-embolic PH (CTEPH) patients, and six healthy subjects, ventricular volumes and circumferential strains were obtained using magnetic resonance imaging. RV ejection fraction (RVEF) and stroke volume index (RVSVI) were smaller in IPAH and CTEPH patients than in normals (RVEF: 32 ± 12 and 23 ± 19 vs. 59 ± 14%, respectively, both P < 0.01; RVSVI: 32 ± 9 and 23 ± 9 vs. 47 ± 6 mL/m(2), both P < 0.001). LV early-diastolic strain index (LVEDSI), defined as LVFW strain in the period between LVFW and RVFW peak shortening normalized for total systolic LVFW shortening, was larger in IPAH and CTEPH patients (0.52 ± 0.33 and 0.55 ± 0.40, both P < 0.01) than in normals (-0.03 ± 0.03). LVEDSI correlated negatively with RVEF (R = -0.74, P < 0.0001) and RVSVI (R = -0.69, P < 0.0001). Three multi-scale computer simulations of PH (all with mean pulmonary artery pressure = 55 mmHg) with complete, incomplete, and no structural adaptation of ventricular walls to local myofibre load showed that LVEDSI increased with deficiency of cardiac adaptation to PH (0.01, 0.52, and 0.84, respectively).
Early-diastolic LV lengthening reflects inadequate structural adaptation of the RVFW to increased myofibre load and is therefore a useful, non-invasive, and easily obtainable predictor of PH-induced RV dysfunction.
Cardiovascular research 08/2012; 96(2):286-95. · 5.80 Impact Factor
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ABSTRACT: Interventricular mechanical dyssynchrony is a characteristic of pulmonary hypertension. We studied the role of right ventricular (RV) wall stress in the recovery of interventricular dyssynchrony, after pulmonary endarterectomy (PEA) in chronic thromboembolic pulmonary hypertension (CTEPH).
In 13 consecutive patients with CTEPH, before and 6 months after pulmonary endarterectomy, cardiovascular magnetic resonance myocardial tagging was applied. For the left ventricular (LV) and RV free walls, the time to peak (Tpeak) of circumferential shortening (strain) was calculated. Pulmonary Artery Pressure (PAP) was measured by right heart catheterization within 48 hours of PEA. Then the RV free wall systolic wall stress was calculated by the Laplace law.
After PEA, the left to right free wall delay (L-R delay) in Tpeak strain decreased from 97 ± 49 ms to -4 ± 51 ms (P < 0.001), which was not different from normal reference values of -35 ± 10 ms (P = 0.18). The RV wall stress decreased significantly from 15.2 ± 6.4 kPa to 5.7 ± 3.4 kPa (P < 0.001), which was not different from normal reference values of 5.3 ± 1.39 kPa (P = 0.78). The reduction of L-R delay in Tpeak was more strongly associated with the reduction in RV wall stress (r = 0.69,P = 0.007) than with the reduction in systolic PAP (r = 0.53, P = 0.07). The reduction of L-R delay in Tpeak was not associated with estimates of the reduction in RV radius (r = 0.37,P = 0.21) or increase in RV systolic wall thickness (r = 0.19,P = 0.53).
After PEA for CTEPH, the RV and LV peak strains are resynchronized. The reduction in systolic RV wall stress plays a key role in this resynchronization.
Journal of Cardiovascular Magnetic Resonance 01/2012; 14:5. · 3.72 Impact Factor
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ABSTRACT: The purpose of this study was to examine the relationship between changes in pulmonary vascular resistance (PVR) and right ventricular ejection fraction (RVEF) and survival in patients with pulmonary arterial hypertension (PAH) under PAH-targeted therapies.
Despite the fact that medical therapies reduce PVR, the prognosis of patients with PAH is still poor. The primary cause of death is right ventricular (RV) failure. One possible explanation for this apparent paradox is the fact that a reduction in PVR is not automatically followed by an improvement in RV function.
A cohort of 110 patients with incident PAH underwent baseline right heart catheterization, cardiac magnetic resonance imaging, and 6-min walk testing. These measurements were repeated in 76 patients after 12 months of therapy.
Two patients underwent lung transplantation, 13 patients died during the first year, and 17 patients died in the subsequent follow-up of 47 months. Baseline RVEF (hazard ratio [HR]: 0.938; p = 0.001) and PVR (HR: 1.001; p = 0.031) were predictors of mortality. During the first 12 months, changes in PVR were moderately correlated with changes in RVEF (R = 0.330; p = 0.005). Changes in RVEF (HR: 0.929; p = 0.014) were associated with survival, but changes in PVR (HR: 1.000; p = 0.820) were not. In 68% of patients, PVR decreased after medical therapy. Twenty-five percent of those patients with decreased PVR showed a deterioration of RV function and had a poor prognosis.
After PAH-targeted therapy, RV function can deteriorate despite a reduction in PVR. Loss of RV function is associated with a poor outcome, irrespective of any changes in PVR.
Journal of the American College of Cardiology 12/2011; 58(24):2511-9. · 14.16 Impact Factor
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Yeun Ying Wong,
Nico Westerhof,
Gerrina Ruiter,
Mark Lubberink,
Pieter Raijmakers,
Paul Knaapen, J Tim Marcus,
Anco Boonstra,
Adriaan A Lammertsma,
Willem J van der Laarse,
Anton Vonk-Noordegraaf
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ABSTRACT: Increased afterload in idiopathic pulmonary arterial hypertension (IPAH) causes right ventricular (RV) hypertrophy and failure. Since RV remodelling occurs with alterations in RV oxygen metabolism, increasing our understanding in the factors determining RV O(2) consumption in IPAH is necessary. In the left ventricle, it is known that heart rate and systolic blood pressure are the main determinants of myocardial O(2) consumption (MVO(2)). However, the normal right heart has lower oxygen extraction and perfusion than the left myocardium, and RV energy metabolism is changed in hypertrophy. Therefore, it is not obvious that the relationsships of pressure and heart rate to MVO(2) hold for the overloaded human right heart. We hypothesize that systolic pulmonary artery pressure (PAP) and heart rate (HR) are the major determinants of RV MVO(2) in IPAH.
In 18 IPAH patients (New York Heart Association class II and III), RV MVO(2) was determined using positron emission tomography and (15)O tracers. PAP and HR were measured during right heart catheterization. RV MVO(2) was found to be related to systolic PAP (R(2) = 0.54, P < 0.001), and inversely to stroke volume (R(2) = 0.32, P = 0.015) and HR (R(2) = 0.32, P = 0.014). Relationships of MVO(2) to the rate pressure product (RPP), i.e. systolic pressure × HR, and wall stress were R(2) = 0.55, P < 0.001, and R(2) = 0.30, P = 0.020, respectively. Multiple regression of MVO(2) on HR and systolic PAP gave R(2) = 0.59, P = 0.001.
Systolic PAP and HR are the major determinants of RV MVO(2) in IPAH. A further increase of HR and PAP with IPAH progression suggests a compromised RV myocardial oxygen availability.
European Journal of Heart Failure 12/2011; 13(12):1290-5. · 4.90 Impact Factor
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ABSTRACT: Until now, many investigators have focused on describing right ventricular (RV) dysfunction in groups of patients with pulmonary arterial hypertension (PAH), but very few have addressed the deterioration of RV function over time. The aim of this study was to investigate time courses of RV geometric changes during the progression of RV failure.
Forty-two patients with PAH were selected who underwent right-sided heart catheterization and cardiac MRI at baseline and after 1-year follow-up. Based on the survival after this 1-year run-in period, patients were classified into two groups: survivors (26 patients; subsequent survival of > 4 years) and nonsurvivors (16 patients; subsequent survival of < 4 years). Four-chamber cine imaging was used to quantify RV longitudinal shortening (apex-base distance change), RV transverse shortening (septum-free wall distance change), and RV fractional area change (RVFAC) between end diastole and end systole.
Longitudinal shortening, transverse shortening, and RVFAC measured at the beginning of the run-in period and 1 year later were significantly higher in subsequent survivors than in nonsurvivors (P < .05). Longitudinal shortening did not change during the run-in period in either patient group. Transverse shortening and RVFAC did not change during the run-in period in subsequent survivors but did decrease in subsequent nonsurvivors (P < .05). This decrease was caused by increased leftward septal bowing.
Progressive RV failure in PAH is associated with a parallel decline in longitudinal and transverse shortening until a floor effect is reached for longitudinal shortening. A further reduction of RV function is due to progressive leftward septal displacement. Because transverse shortening incorporates both free wall and septum movements, this parameter can be used to monitor the decline in RV function in end-stage PAH.
Chest 09/2011; 141(4):935-43. · 5.25 Impact Factor
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Yeun Ying Wong,
Gerrina Ruiter,
Mark Lubberink,
Pieter G Raijmakers,
Paul Knaapen, J Tim Marcus,
Anco Boonstra,
Adriaan A Lammertsma,
Nico Westerhof,
Willem J van der Laarse,
Anton Vonk-Noordegraaf
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ABSTRACT: In idiopathic pulmonary arterial hypertension (IPAH), increased right ventricular (RV) power is required to maintain cardiac output. For this, RV O2 consumption (MVO2) must increase by augmentation of O2 supply and/or improvement of mechanical efficiency-ratio of power output to MVO2. In IPAH with overt RV failure, however, there is evidence that O2 supply (perfusion) reserve is reduced, leaving only increase in either O2 extraction or mechanical efficiency as compensatory mechanisms. We related RV mechanical efficiency to clinical and hemodynamic parameters of RV function in patients with IPAH and associated it with glucose metabolism.
The patients included were in New York Heart Association (NYHA) class II (n=8) and class III (n=8). They underwent right heart catheterization, MRI, and H2(15)O-, (15)O2-, C(15)O-, and 18FDG-PET. RV power and O2 supply were similar in both groups (NYHA class II versus class III: 0.54±0.14 versus 0.47±0.12 J/s and 0.109±0.022 versus 0.128±0.026 mL O2/min per gram, respectively). RV O2 extraction was near-significantly lower in NYHA class II compared with NYHA class III (63±17% versus 75±16%, respectively, P=0.10). As a result, MVO2 was significantly lower (0.066±0.012 versus 0.092±0.010 mL O2/min per gram, respectively, P=0.006). RV efficiency was reduced in NYHA class III (13.9±3.8%) compared with NYHA class II (27.8±7.6%, P=0.001). Septal bowing, measured by MRI, correlated with RV efficiency (r = -0.59, P=0.020). No relation was found between RV efficiency and glucose uptake rate. RV mechanical efficiency and ejection fraction were closely related (r=0.81, P<0.001).
RV failure in IPAH was associated with reduced mechanical efficiency that was partially explained by RV mechanical dysfunction but not by a metabolic shift.
Circulation Heart Failure 09/2011; 4(6):700-6. · 6.29 Impact Factor
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Yeun Ying Wong,
Pieter G Raijmakers,
Paul Knaapen,
Mark Lubberink,
Gerrina Ruiter, J Tim Marcus,
Anco Boonstra,
Adriaan A Lammertsma,
Nico Westerhof,
Willem J van der Laarse,
Anton Vonk-Noordegraaf
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ABSTRACT: BackgrOUND: Impaired right ventricular (RV) myocardial blood flow (MBF) has been associated with RV dysfunction and fatal RV failure in idiopathic pulmonary hypertension during stress. MBF and O(2) extraction from myocardial capillaries (O(2) extraction fraction (OEF)) influence myocardial O(2) supply.
To determine how the baseline RV OEF affects the amount of MBF increase induced by supine exercise, the authors hypothesise that higher baseline OEF (H-OEF) results in limited O(2) extraction during exercise and that MBF must therefore be increased to obtain sufficient O(2).
In 18 patients with idiopathic pulmonary hypertension, baseline OEF, resting MBF and exercise-induced MBF at 40% of maximal cardiopulmonary exercise testing load were measured using positron emission tomography and [(15)O]O(2), [(15)O]H(2)O and [(15)O]CO.
For the whole population, exercise increased RV MBF from 0.68±0.16 to 1.13 ± 0.38 ml/min/g (p < 0.0001). The MBF exercise-to-rest ratio (reserve) was 1.7 ± 0.7. The median baseline OEF was 0.73 at which the patient population was split into H-OEF and lower baseline OEF (L-OEF). Baseline MBF values (0.61 ± 0.11 and 0.74 ± 0.17 ml/min/g, respectively) were similar, and exercise induced a significant MBF increase in both groups (p = 0.0001). However, exercise-induced increase in MBF was significantly less in the H-OEF group than in the L-OEF group (0.97 ± 0.30 and 1.30 ± 0.39 ml/min/g, respectively, p < 0.05). Moreover, H-OEF patients had lower baseline stroke volume and cardiac output than the L-OEF group (52 ± 19 ml and 4.0 ± 1.1 l/min vs 78 ± 18 ml and 5.5 ± 0.9 l/min, respectively, both p < 0.05).
H-OEF patients were hemodynamically poorer and showed a lower exercise-induced MBF increase compared to L-OEF patients, suggesting exercise-induced O(2) supply limitation.
Heart (British Cardiac Society) 08/2011; 97(24):2069-74. · 4.22 Impact Factor
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Chest 08/2011; 140(2):556-7; author reply 557-8. · 5.25 Impact Factor
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ABSTRACT: To evaluate if early onset of retrograde flow in the main pulmonary artery is a characteristic of pulmonary arterial hypertension (PAH).
Fifty-five patients with suspected pulmonary hypertension (PH) underwent right-sided heart catheterization and retrospectively ECG-gated MR phase-contrast velocity quantification in the main pulmonary artery. Pulmonary hypertension was defined by a mean pulmonary artery pressure being larger than 25 mmHg. The onset time of the retrograde flow relative to the cardiac cycle duration (Relative Onset Time = ROT) was compared with mean pulmonary artery pressure.
By the catheterization, 38 patients were identified as having PAH. The ROT for these PAH patients was significantly different from those found in the 17 non-PH subjects (0.14 ± 0.06 versus 0.37 ± 0.06, P < 0.001). The mean pulmonary artery pressure was related to the ROT (r(2) = 0.62, P < 0.001) and could be estimated from the ROT with a standard deviation of 11.7 mmHg. With a cutoff value of 0.25, the ROT distinguished PAH patients from non-PH subjects.
Early onset of retrograde flow in the main pulmonary artery is a characteristic of pulmonary arterial hypertension and is visible by standard MR phase-contrast velocity quantification.
Journal of Magnetic Resonance Imaging 06/2011; 33(6):1362-8. · 2.70 Impact Factor
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Serge A van Wolferen,
Marielle C van de Veerdonk,
Gert-Jan Mauritz,
Wouter Jacobs, J Tim Marcus,
Koen M J Marques,
Jean G F Bronzwaer,
Martijn W Heymans,
Anco Boonstra,
Pieter E Postmus,
Nico Westerhof,
Anton Vonk Noordegraaf
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ABSTRACT: Stroke volume is probably the best hemodynamic parameter because it reflects therapeutic changes and contains prognostic information in pulmonary hypertension (PH). Stroke volume directly reflects right ventricular function in response to its load, without the correction of compensatory increased heart rate as is the case for cardiac output. For this reason, stroke volume, which can be measured noninvasively, is an important hemodynamic parameter to monitor during treatment. However, the extent of change in stroke volume that constitutes a clinically significant change is unknown. The aim of this study was to determine the minimal important difference (MID) in stroke volume in PH.
One hundred eleven patients were evaluated at baseline and after 1 year of follow-up with a 6-min walk test (6MWT) and cardiac MRI. Using the anchor-based method with 6MWT as the anchor, and the distribution-based method, the MID of stroke volume change could be determined.
After 1 year of treatment, there was, on average, a significant increase in stroke volume and 6MWT. The change in stroke volume was related to the change in 6MWT. Using the anchor-based method, an MID of 10 mL in stroke volume was calculated. The distribution-based method resulted in an MID of 8 to 12 mL.
Both methods showed that a 10-mL change in stroke volume during follow-up should be considered as clinically relevant. This value can be used to interpret changes in stroke volume during clinical follow-up in PH.
Chest 05/2011; 139(5):1003-9. · 5.25 Impact Factor
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ABSTRACT: Pulmonary artery (PA) dilatation is one of the consequences of pulmonary arterial hypertension (PAH) and is used for noninvasive detection. However, it is unclear how the size of the PA behaves over time and whether it is related to pressure changes. The aim of this study was to evaluate PA size during follow-up in treated patients with PAH and whether it reflects pulmonary vascular hemodynamics.
Fifty-one patients with PAH who underwent at least two right-sided heart catheterizations (RHCs) together with cardiac MRI (CMR) were included in this study. Another 18 patients who had normal pressure at RHC were included for comparison at baseline. From RHC, we derived PA pressures and cardiac output. From the CMR images we derived PA diameter (PAD) and the ratio of the PAD and ascending aorta diameter.
The PAD was significantly larger in patients with PAH than in patients without PAH (P < .001). A ratio of the PAD and ascending aorta diameter > 1 had a positive predictive value of 92% for PAH. Mean follow-up time was 942 days, and there was a significant dilatation during this period (P < .001). The change of the PAD did not correlate with the changes in pressure or cardiac output. A moderate correlation with follow-up time was found (r = 0.56; P < .001).
A dilatated PA is useful for identifying patients with PAH. However, during patient follow-up, progressive dilatation of the PA is independent of the change in PA pressure and cardiac output and might become independent from hemodynamics.
Chest 12/2010; 138(6):1395-401. · 5.25 Impact Factor
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ABSTRACT: Pulmonary hypertension (PH) is characterized by increased arterial load requiring more right ventricular (RV) hydraulic power to sustain adequate forward blood flow. Power can be separated into a mean and oscillatory part. The former is associated with mean and the latter with pulsatile blood flow and pressure. Because mean power provides for net blood flow, the ratio of oscillatory to total power (oscillatory power fraction) preferably should be small. It is unknown whether this is the case in pulmonary arterial hypertension (PAH).
To derive components of power generated by the right ventricle in PAH.
Thirty-five patients with idiopathic PAH (IPAH) and 14 subjects without PH were included. The patients were divided in two groups, "moderate" and "high," based on pulmonary artery (PA) pressure. PA pressures were obtained by right heart catheterization and PA flows by magnetic resonance imaging. Total hydraulic power (Power(total)) was calculated as the integral product of pressure and flow. Mean hydraulic power (Power(mean)) was calculated as mean pulmonary artery pressure times mean flow. Their difference is oscillatory power (Power(oscill)). Total hydraulic power in subjects without PH compared with moderate and high IPAH was 0.29 ± 0.10 W (n = 14), 0.52 ± 0.14 W (n = 17), and 0.73 ± 0.24 W (n = 18), respectively. The oscillatory power fraction is approximately 23% and not different between groups.
In this study, oscillatory power fraction is constant at 23% in non-PH and IPAH, implying that a considerable amount of power is not used for forward flow, making the RV less efficient with respect to its arterial load. Our findings emphasize the need to develop new therapy strategies to optimize RV power output in PAH.
American Journal of Respiratory and Critical Care Medicine 11/2010; 182(10):1315-20. · 11.08 Impact Factor
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ABSTRACT: In pulmonary arterial hypertension (PAH) a prolonged time interval between pulmonary valve closure and tricuspid valve opening is found. This period is interpreted as prolonged right ventricular (RV) relaxation, and thus a reflection of diastolic dysfunction. This concept recently has been questioned, since it was shown that RV contraction continues after pulmonary valve closure causing a post-systolic contraction period.
To investigate in PAH whether the increased RV post-systolic isovolumic period is caused by either an additional post-systolic contraction period, or an increased relaxation period (diastolic dysfunction).
23 patients with PAH (mean pulmonary arterial pressure 54 ± 12 mm Hg), and 18 healthy subjects were studied using cardiac MRI. In a RV two-chamber view, times of pulmonary valve closure (T(PVC)) and tricuspid valve opening (T(TVO)) were measured, defining the total post-systolic isovolumic period. Time to peak of RV free wall contraction (T(peak)RV) was determined with myocardial tagging. Post-systolic contraction and relaxation periods were defined as the time intervals between T(PVC) and T(peak)RV and between T(peak)RV and T(TVO), respectively. These periods were normalised to an RR interval.
The total post-systolic isovolumic period was longer in patients than in healthy subjects (0.15 ± 0.04 vs 0.04 ± 0.02, p < 0.001), but the relaxation period was not different (0.06 ± 0.02 vs 0.05 ± 0.02, p = 0.09). The post-systolic contraction period in patients was strongly related to the total post-systolic isovolumic period (y = 0.98x-0.05; r = 0.89, p < 0.001), and was associated with disease severity.
In PAH, the prolonged post-systolic isovolumic period is caused by an additional post-systolic contraction period, rather than by an increased relaxation period.
Heart (British Cardiac Society) 10/2010; 97(6):473-8. · 4.22 Impact Factor
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ABSTRACT: Longitudinal wall motion of the right ventricle (RV), generally quantified as tricuspid annular systolic excursion (TAPSE), has been well studied in pulmonary hypertension (PH). In contrast, transverse wall motion has been examined less. Therefore, the aim of this study was to evaluate regional RV transverse wall motion in PH, and its relation to global RV pump function, quantified as RV ejection fraction (RVEF).
In 101 PH patients and 29 control subjects cardiovascular magnetic resonance was performed. From four-chamber cine imaging, RV transverse motion was quantified as the change of the septum-free-wall (SF) distance between end-diastole and end-systole at seven levels along an apex-to-base axis. For each level, regional absolute and fractional transverse distance change (SFD and fractional-SFD) were computed and related to RVEF. Longitudinal measures, including TAPSE and fractional tricuspid-annulus-apex distance change (fractional-TAAD) were evaluated for comparison.
Transverse wall motion was significantly reduced at all levels compared to control subjects (p < 0.001). For all levels, fractional-SFD and SFD were related to RVEF, with the strongest relation at mid RV (R(2) = 0.70, p < 0.001 and R(2) = 0.62, p < 0.001). For TAPSE and fractional-TAAD, weaker relations with RVEF were found (R(2) = 0.21, p < 0.001 and R(2) = 0.27, p < 0.001).
Regional transverse wall movements provide important information of RV function in PH. Compared to longitudinal motion, transverse motion at mid RV reveals a significantly stronger relationship with RVEF and thereby might be a better predictor for RV function.
Journal of Cardiovascular Magnetic Resonance 01/2010; 12:35. · 3.72 Impact Factor
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ABSTRACT: Normal left ventricular (LV) torsion is caused by opposite basal and apical rotation. Opposite rotation can be lost in heart failure, but might be restored by pacing; therefore, the predictive value of the loss of opposite base-apex rotation in heart failure patients for the response to cardiac resynchronization therapy (CRT) was studied.
In 34 CRT candidates and 12 controls, basal and apical LV rotations were calculated using magnetic resonance image tagging. Loss of opposite rotation was quantified by the correlation between both rotation curves: a negative correlation indicates normal, opposite rotation and a positive correlation indicates that base and apex rotate in the same direction. In patients, LV pressure was measured invasively during biventricular stimulation. Acute response to CRT was defined by >10% increase in dP/dt(max) relative to baseline. LV volume was determined at baseline and 8 months follow-up using echocardiography. The base-apex rotation correlation (BARC) was significantly higher in acute responders (n=22) than in nonresponders (n=12) and controls (0.64+/-0.51, -0.23+/-0.67, and -0.68+/-0.22, respectively; P=.001). The sensitivity and specificity for prediction of acute response were 82% and 83%, respectively, at a cutoff value of 0.5. At follow-up, volumes could be analyzed in 18 patients. In the group with BARC >0.5, end-diastolic volume decreased by 7% (NS), end-systolic volume by 16%, and ejection fraction increased by 28% (both P=.02), whereas in the group with BARC <0.5, no significant changes were observed.
The loss of opposite base-apex rotation in patients eligible for CRT is an excellent predictor of acute response and is associated with LV reverse remodeling.
Journal of cardiac failure 10/2009; 15(8):717-25. · 3.25 Impact Factor
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ABSTRACT: The product of resistance, R, and compliance, C (RC time), of the entire pulmonary circulation is constant. It is unknown if this constancy holds for individual lungs. We determined R and C in individual lungs in chronic thromboembolic pulmonary hypertension (CTEPH) patients where resistances differ between both lungs. Also, the contribution of the proximal pulmonary arteries (PA) to total lung compliance was assessed. Patients (n=23) were referred for the evaluation of CTEPH. Pressure was measured by right heart catheterization and flows in the main, left, and right PA by magnetic resonance imaging. Total, left, and right lung resistances were calculated as mean pressure divided by mean flow. Total, left, and right lung compliances were assessed by the pulse pressure method. Proximal compliances were derived from cross-sectional area change DeltaA and systolic-diastolic pressure difference DeltaP (DeltaA/DeltaP) in main, left, and right PA, multiplied by vessel length. The lung with the lowest blood flow was defined "low flow" (LF), the contralateral lung "high flow" (HF). Total resistance was 0.57+/-0.28 mmHg.s(-1).ml(-1), and resistances of LF and HF lungs were 1.57+/-0.2 vs. 1.00+/-0.1 mmHg.s(-1).ml(-1), respectively, P<0.0001. Total compliance was 1.22+/-1.1 ml/mmHg, and compliances of LF and HF lung were 0.47+/-0.11 and 0.62+/-0.12 ml/mmHg, respectively, P=0.01. Total RC time was 0.49+/-0.2 s, and RC times for the LF and HF lung were 0.45+/-0.2 and 0.45+/-0.1 s, respectively, not different. Proximal arterial compliance, given by the sum of main, right, and left PA compliances, was only 19% of total lung compliance. The RC time of a single lung equals that of both lungs together, and pulmonary arterial compliance comes largely from the distal vasculature.
AJP Heart and Circulatory Physiology 10/2009; 297(6):H2154-60. · 3.71 Impact Factor
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ABSTRACT: To compare left ventricular (LV) torsion represented as the circumferential-longitudinal (CL) shear angle between 2D and 3D quantification, using cardiovascular magnetic resonance (CMR).
CMR tagging was performed in six healthy volunteers. From this, LV torsion was calculated using a 2D and a 3D method. The cross-correlation between both methods was evaluated and comparisons were made using Bland-Altman analysis.
The cross-correlation between the curves was r2 = 0.97 +/- 0.02. No significant time-delay was observed between the curves. Bland-Altman analysis revealed a significant positive linear relationship between the difference and the average value of both analysis methods, with the 2D results showing larger values than the 3D. The difference between both methods can be explained by the definition of the 2D method.
LV torsion represented as CL shear quantified by the 2D and 3D analysis methods are strongly related. Therefore, it is suggested to use the faster 2D method for torsion calculation.
Journal of Cardiovascular Magnetic Resonance 05/2009; 11:8. · 3.72 Impact Factor
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The American journal of cardiology 04/2009; 103(6):894-5. · 3.58 Impact Factor
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ABSTRACT: The aim of our study was to describe the efficacy of addition of intravenous or subscutaneous prostanoids in idiopathic pulmonary arterial hypertension (PAH) patients deteriorating on bosentan or on bosentan-sildenafil.
PAH treatment at our hospital is standardized with first-line oral therapy in New York Heart Association class III patients followed by addition of prostanoids on clinical worsening.
Mean improvement in 6-minute walk distance after 4 months of prostanoids was 86 m (p < 0.01) in the bosentan group versus 41 m (p < 0.05) in the bosentan-sildenafil group, and these improvements persisted at long-term follow-up.
From these results we conclude that addition of subcutaneous or intravenous prostanoids can be efficacious in PAH deteriorating on oral therapy.
The Journal of heart and lung transplantation: the official publication of the International Society for Heart Transplantation 04/2009; 28(3):280-4. · 3.54 Impact Factor
