The Load of Pulmonary Hypertension

Vonk Noordegraaf, A. [Promotor]Boonstra, A. [Copromotor

Abnormal Pulmonary Artery Stiffness in Pulmonary Arterial Hypertension: In Vivo Study with Intravascular Ultrasound

BACKGROUND: There is increasing recognition that pulmonary artery stiffness is an important determinant of right ventricular (RV) afterload in pulmonary arterial hypertension (PAH). We used intravascular ultrasound (IVUS) to evaluate the mechanical properties of the elastic pulmonary arteries (PA) in subjects with PAH, and assessed the effects of PAH-specific therapy on indices of arterial stiffness. METHOD: Using IVUS and simultaneous right heart catheterisation, 20 pulmonary segments in 8 PAH subjects and 12 pulmonary segments in 8 controls were studied to determine their compliance, distensibility, elastic modulus and stiffness index β. PAH subjects underwent repeat IVUS examinations after 6-months of bosentan therapy. RESULTS: AT BASELINE, PAH SUBJECTS DEMONSTRATED GREATER STIFFNESS IN ALL MEASURED INDICES COMPARED TO CONTROLS: compliance (1.50±0.11×10(-2) mm(2/)mmHg vs 4.49±0.43×10(-2) mm(2/)mmHg, p<0.0001), distensibility (0.32±0.03%/mmHg vs 1.18±0.13%/mmHg, p<0.0001), elastic modulus (720±64 mmHg vs 198±19 mmHg, p<0.0001), and stiffness index β (15.0±1.4 vs 11.0±0.7, p = 0.046). Strong inverse exponential associations existed between mean pulmonary artery pressure and compliance (r(2) = 0.82, p<0.0001), and also between mean PAP and distensibility (r(2) = 0.79, p = 0.002). Bosentan therapy, for 6-months, was not associated with any significant changes in all indices of PA stiffness. CONCLUSION: Increased stiffness occurs in the proximal elastic PA in patients with PAH and contributes to the pathogenesis RV failure. Bosentan therapy may not be effective at improving PA stiffness

A history of auditing: The changing audit process in Britain from the nineteenth century to the present day

The anatomical differences between the pulmonary and systemic arterial system are the main cause of the difference in distribution of compliance. In the pulmonary arterial system compliance is distributed over the entire arterial system, and stands at the basis of the constancy of the RC-time. This distribution depends on the number of peripheral vessels, which is ∼8–10 times more in the pulmonary system than the systemic tree. In the systemic arterial tree the compliance is mainly located in the aorta (80% of total compliance in thoracic-abdominal aorta). The constant RC-time in the pulmonary bed results in proportionality of systolic and diastolic pressure with mean pressure and, in turn, in the constant ratio of oscillatory and mean power

Left subclavian artery revascularization as part of thoracic stent grafting

Contains fulltext : 153269.pdf (publisher's version ) (Closed access)OBJECTIVES: Intentional covering of the left subclavian artery (LSA) as part of thoracic endovascular aortic repair (TEVAR) can cause (posterior) strokes or left arm malperfusion. LSA revascularization can be done as prophylaxis against, or as treatment of, these complications. We report our experience with the surgical technique, indications and the results of LSA revascularization. METHODS: Between 2000 and 2013, 51 patients of 444 patients who were treated by TEVAR, had LSA revascularization. All elective patients had a preoperative work-up with magnetic resonance angiography to evaluate the circle of Willis. In all, surgical access was through a left supraclavicular incision only. RESULTS: The majority (90%) had prophylactic LSA revascularization because of incomplete circle of Willis and or dominant left vertebral artery (LVA) (n=29), patent left internal mammary artery (n=1), prevention spinal cord ischaemia (SCI) (n=2), prevention left arm ischaemia due to small LVA (n=2) and LVA origin in arch (n=1). Fourteen percent had secondary revascularization, either immediate because of malperfusion of the left arm (n=2) or late after TEVAR because of persisting left arm claudication (n=5). In 12 patients, the following early complications were observed: re-exploration for bleeding, n=1; left recurrent nerve paralysis, n=2; left phrenic nerve paralysis, n=1; left sympathetic chain neuropraxia, resulting in Horner's syndrome, n=3; Chyle duct lesions, resulting in persistent Chyle leakage, n=3. Neither strokes nor SCI was observed. One patient experienced occlusion of the bypass at 6 months. CONCLUSIONS: The present study shows that the procedure of LSA revascularization as part of TEVAR is safe with low morbidity consisting of mainly (transient) nerve palsy

Thoracic aorta stent grafting through transapical access.

Item does not contain fulltextBACKGROUND: To describe the transapical approach for thoracic endovascular aortic repair (TEVAR). METHODS: Three patients, 2 elective and 1 emergent, with thoracic aorta aneurysm are described with vascular or direct aortic inaccessible access, who underwent TEVAR through transapical access. The technique is described in detail emphasizing the usefulness of the through-and-through guidewire, rapid pacing, and transesophageal echocardiography guidance. RESULTS: All patients were technical successfully treated with TEVAR through transapical access. The emergent patient, however, died due to multiorgan failure. CONCLUSIONS: Our early experience shows that the transapical approach for TEVAR procedures is feasible in experienced hands. The selection of the patient and careful planning based on imaging are of paramount importance and should lead to the most suitable access site tailored to the need of the individual patient.1 februari 201

RC time constant of single lung equals that of both lungs together: a study in chronic thromboembolic pulmonary hypertension

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 vasculatur