Intravascular ultrasound of the elastic pulmonary arteries: A new approach for the evaluation of primary pulmonary hypertension

Department of Cardiology, Hospital Universitari Vall d'Hebron, Barcelona, Spain.
Heart (British Cardiac Society) (Impact Factor: 5.6). 04/2003; 89(3):311-5. DOI: 10.1136/heart.89.3.311
Source: PubMed


To assess the structural and functional characteristics of pulmonary arteries by intravascular ultrasound (IVUS) in the setting of primary pulmonary hypertension, and to correlate the ultrasound findings with haemodynamic variables and mortality at follow up.
Prospective observational study.
University hospital (tertiary referral centre).
20 consecutive patients with primary pulmonary hypertension (16 female; mean (SD) age, 39 (14) years).
Cardiac catheterisation and simultaneous IVUS of pulmonary artery branches at baseline and after infusion of epoprostenol.
33 pulmonary arteries with a mean diameter of 3.91 (0.80) mm were imaged, and wall thickening was observed in all cases, 64% being eccentric. Mean wall thickness was 0.37 (0.13) mm, percentage wall area 31.0 (9.3)%, pulsatility 14.6 (4.8)%, and pulmonary/elastic strain index 449 (174) mm Hg. No correlation was observed between IVUS findings and haemodynamic variables. Epoprostenol infusion increased pulsatility by 53% and decreased the pulmonary/elastic strain index by 41% (p = 0.0001), irrespective of haemodynamic changes. At 18 (12) months follow up, nine patients had died. A reduced pulsatility and an increased pulmonary/elastic strain index were associated with increased mortality at follow up (12.0 (4.4)% v 16.4 (4.4)%, p = 0.03; 369 (67) v 546 (216) mm Hg, p = 0.02).
IVUS demonstrated pulmonary artery wall abnormalities in all patients with primary pulmonary hypertension, mostly eccentric. The severity of the changes did not correlate with haemodynamic variables, and epoprostenol improved pulmonary vessel stiffness. There was an association between impaired pulmonary artery functional state as determined by IVUS and mortality at follow up.

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Available from: Joaquim Majó, Feb 25, 2014
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    • "Rodes-Cabau et al. [72] IPAH 20 RHC with IVUS Reduced pulsatility in PH, with reduced pulsatility predictive of future mortality. Epoprostenol infusion increased pulsatility by 53%. "
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    ABSTRACT: COPD is the second most common cause of pulmonary hypertension, and is a common complication of severe COPD with significant implications for both quality of life and mortality. However, the use of a rigid diagnostic threshold of a mean pulmonary arterial pressure (mPAP) of ≥25mHg when considering the impact of the pulmonary vasculature on symptoms and disease is misleading. Even minimal exertion causes oxygen desaturation and elevations in mPAP, with right ventricular hypertrophy and dilatation present in patients with mild to moderate COPD with pressures below the threshold for diagnosis of pulmonary hypertension. This has significant implications, with right ventricular dysfunction associated with poorer exercise capability and increased mortality independent of pulmonary function tests. The compliance of the pulmonary artery (PA) is a key component in decoupling the right ventricle from the pulmonary bed, allowing the right ventricle to work at maximum efficiency and protecting the microcirculation from large pressure gradients. PA stiffness increases with the severity of COPD, and correlates well with the presence of exercise induced pulmonary hypertension. A curvilinear relationship exists between PA distensibility and mPAP and pulmonary vascular resistance (PVR) with marked loss of distensibility before a rapid rise in mPAP and PVR occurs with resultant right ventricular failure. This combination of features suggests PA stiffness as a promising biomarker for early detection of pulmonary vascular disease, and to play a role in right ventricular failure in COPD. Early detection would open this up as a potential therapeutic target before end stage arterial remodelling occurs. Copyright © 2015. Published by Elsevier Ltd.
    Respiratory medicine 06/2015; 54. DOI:10.1016/j.rmed.2015.06.005 · 3.09 Impact Factor
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    • "IVUS examination was performed with an Eagle Eye Gold catheter 20 MHz, 3.5 F (Volcano Corporation, USA) with an axial resolution of 200 μm and an automatic pullback of 0.5 mm/s. The images were obtained from a segmental PA of the inferior lobe (elastic PA between 2–3 mm) [16-18] and stored in digital form. Both diastolic and systolic cross-sectional areas of the studied segment were analyzed off-line by two observers unaware of clinical and hemodynamic findings. "
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    ABSTRACT: Exercise capacity is impaired in pulmonary arterial hypertension (PAH). We hypothesized that cardiovascular reserve abnormalities would be associated with impaired hemodynamic response to pharmacological stress and worse outcome in PAH. Eighteen PAH patients (p) group 1 NYHA class II/III and ten controls underwent simultaneous right cardiac catheterization and intravascular ultrasound at rest and during low dose-dobutamine (10 mcg/kg/min) with trendelenburg (DST). We estimated cardiac output (CO), pulmonary vascular resistance (PVR) and capacitance (PC), and PA elastic modulus (EM). We concomitantly measured tricuspid annular plane systolic excursion (TAPSE), RV myocardial peak systolic velocity (Sm) and isovolumic myocardial acceleration (IVA) in PAH patients. Based on the rounded mean + 2 SD of the increase in mPAP in our healthy control group during DST (2.8 + 1.8 mm Hg), PAH p were divided into two groups according to mean PA pressure (mPAP) response during DST, 1: DeltamPAP >5 mm Hg and 2: DeltamPAP <=5 mm Hg. Cardiovascular reserve was estimated as the change (delta, Delta) during DST compared with rest, including DeltamPAP with respect to DeltaCO (DeltamPAP/DeltaCO). All patients were prospectively followed up for 2 years. PAH p showed significant lower heart rate and CO increase than controls during DST, with a significant mPAP and pulse PAP increase and higher DeltamPAP/DeltaCO (p < 0.05). Neither hemodynamic, IVUS and echocardiographic data were different between both PAH groups at rest. In group 1, DST caused a higher DeltaEM, DeltamPAP/DeltaCO, DeltaPVR, and DeltaTAPSE than group 2, with a lower IVA increase and a negative DeltaSV (p < 0.05). TAPSE correlated with mPAP and RVP (p < 0.05) and, IVA and Sm correlated with CO (p < 0.05). DeltaEM correlated with DeltamPAP and DeltaIVA with DeltaCO (p < 0.05). There were two deaths/pulmonary transplantations in group 1 and one death in group 2 during the follow-up (p > 0.05). Pulmonary vascular reserve and RV systolic reserve are significantly impaired in patients with PAH. The lower recruitable cardiovascular reserve is significantly related to a worse hemodynamic response to DST and it could be associated with a poor clinical outcome.
    BMC Pulmonary Medicine 04/2014; 14(1):69. DOI:10.1186/1471-2466-14-69 · 2.40 Impact Factor
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    • "IVUSp was estimated as: ((systolic area–diastolic area) / diastolic area) × 100; ((sA–dA) / dA) × 100 (Fig. 1), and PA stiffness was assessed as the elastic modulus (E: dA × Pp / (sA–dA)) [10] [17] "
    Dataset: Paper-2013

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