7 results on '"Van Der Bruggen, Cathelijne E. E."'
Search Results
2. Right Ventricular Load and Function in Chronic Thromboembolic Pulmonary Hypertension: Differences between Proximal and Distal Chronic Thromboembolic Pulmonary Hypertension
- Author
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Ruigrok, Dieuwertje, primary, Meijboom, Lilian J., additional, Westerhof, Berend E., additional, in ’t Veld, Anna Huis, additional, van der Bruggen, Cathelijne E. E., additional, Marcus, J. Tim, additional, Nossent, Esther J., additional, Vonk Noordegraaf, Anton, additional, Symersky, Petr, additional, and Bogaard, Harm-Jan, additional
- Published
- 2019
- Full Text
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3. Pulmonary hypertension
- Author
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van der Bruggen, Cathelijne E. E., Spruijt, Onno A., Meijboom, Lilian J., Vonk Noordegraaf, Anton, Pulmonary medicine, ICaR - Heartfailure and pulmonary arterial hypertension, Radiology and nuclear medicine, and ICaR - Ischemia and repair
- Abstract
Pulmonary hypertension (PH) is a haemodynamic condition that leads to a progressive increase in pulmonary vascular resistance and mean pulmonary artery pressure. Irrespective of its aetiology, the main cause of death in PH patients is right ventricular (RV) failure. Noninvasive imaging techniques play an essential role in diagnosing PH and monitoring disease progression. This chapter provides an overview of the most important noninvasive imaging tools for assessing pulmonary pressures, RV function and monitoring.
- Published
- 2015
4. Contribution of Impaired Parasympathetic Activity to Right Ventricular Dysfunction and Pulmonary Vascular Remodeling in Pulmonary Arterial Hypertension.
- Author
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Gonçalves Bós, Denielli da Silva, Van Der Bruggen, Cathelijne E. E., Kurakula, Kondababu, Xiao-Qing Sun, Casali, Karina R., Casali, Adenauer G., Rol, Nina, Szulcek, Robert, dos Remedios, Cris, Guignabert, Christophe, Ly Tu, Dorfmüller, Peter, Humbert, Marc, Wijnker, Paul J. M., Kuster, Diederik W. D., van der Velden, Jolanda, Goumans, Marie-José, Bogaard, Harm-Jan, Vonk-Noordegraaf, Anton, and de Man, Frances S.
- Subjects
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PARASYMPATHETIC nervous system , *RIGHT ventricular hypertrophy , *VASCULAR remodeling , *PULMONARY hypertension , *LEFT heart ventricle diseases , *CHOLINESTERASE inhibitors , *PYRIDINE , *HEART ventricle diseases , *ANIMAL experimentation , *BIOLOGICAL models , *CELL culture , *COMPARATIVE studies , *ENDOTHELIUM , *HEART physiology , *RIGHT heart ventricle , *RESEARCH methodology , *MEDICAL cooperation , *PULMONARY artery , *RATS , *RESEARCH , *TISSUE culture , *EVALUATION research , *THERAPEUTICS - Abstract
Background: The beneficial effects of parasympathetic stimulation have been reported in left heart failure, but whether it would be beneficial for pulmonary arterial hypertension (PAH) remains to be explored. Here, we investigated the relationship between parasympathetic activity and right ventricular (RV) function in patients with PAH, and the potential therapeutic effects of pyridostigmine (PYR), an oral drug stimulating the parasympathetic activity through acetylcholinesterase inhibition, in experimental pulmonary hypertension (PH).Methods: Heart rate recovery after a maximal cardiopulmonary exercise test was used as a surrogate for parasympathetic activity. RV ejection fraction was assessed in 112 patients with PAH. Expression of nicotinic (α-7 nicotinic acetylcholine receptor) and muscarinic (muscarinic acetylcholine type 2 receptor) receptors, and acetylcholinesterase activity were evaluated in RV (n=11) and lungs (n=7) from patients with PAH undergoing heart/lung transplantation and compared with tissue obtained from controls. In addition, we investigated the effects of PYR (40 mg/kg per day) in experimental PH. PH was induced in male rats by SU5416 (25 mg/kg subcutaneously) injection followed by 4 weeks of hypoxia. In a subgroup, sympathetic/parasympathetic modulation was assessed by power spectral analysis. At week 6, PH status was confirmed by echocardiography, and rats were randomly assigned to vehicle or treatment (both n=12). At the end of the study, echocardiography was repeated, with additional RV pressure-volume measurements, along with lung, RV histological, and protein analyses.Results: Patients with PAH with lower RV ejection fraction (<41%) had a significantly reduced heart rate recovery in comparison with patients with higher RV ejection fraction. In PAH RV samples, α-7 nicotinic acetylcholine receptor was increased and acetylcholinesterase activity was reduced versus controls. No difference in muscarinic acetylcholine type 2 receptor expression was observed. Chronic PYR treatment in PH rats normalized the cardiovascular autonomic function, demonstrated by an increase in parasympathetic activity and baroreflex sensitivity. PYR improved survival, increased RV contractility, and reduced RV stiffness, RV hypertrophy, RV fibrosis, RV inflammation, and RV α-7 nicotinic acetylcholine receptor and muscarinic acetylcholine type 2 receptor expression, as well. Furthermore, PYR reduced pulmonary vascular resistance, RV afterload, and pulmonary vascular remodeling, which was associated with reduced local and systemic inflammation.Conclusions: RV dysfunction is associated with reduced systemic parasympathetic activity in patients with PAH, with an inadequate adaptive response of the cholinergic system in the RV. Enhancing parasympathetic activity by PYR improved survival, RV function, and pulmonary vascular remodeling in experimental PH. [ABSTRACT FROM AUTHOR]- Published
- 2018
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5. RV pressure overload: from hypertrophy to failure.
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van der Bruggen, Cathelijne E. E., Tedford, Ryan J., Louis Handoko, Martin, van der Velden, Jolanda, and de Man, Frances S.
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RIGHT heart ventricle , *PULMONARY hypertension treatment , *RIGHT ventricular hypertrophy , *RIGHT heart ventricle diseases , *CARDIAC hypertrophy , *HEART failure treatment - Abstract
In pulmonary arterial hypertension (PAH), right ventricular (RV) adaptation is essential to overcome the chronic increases in RV pressure overload. Ultimately, RV compensatory mechanisms are not sufficient and patients succumb to RV failure. The processes underlying the transition of RV adaptation to RV failure are not well understood. In this review, we propose that important insights in RV adaptation processes can be obtained by comparing different etiologies of PAH, namely patients with PAH secondary to Eisenmenger syndrome, patients with PAH secondary to systemic sclerosis and patients where no cause is identified: idiopathic PAH. Although the amount of RV afterload does not differ between these patient groups, their prognosis is distinctly different. We will show that an adaptive RV phenotype, as is observed in Eisenmenger patients, coincides with RV hypertrophy, increased RV contractility, low RV fibrosis and low RV diastolic stiffness. Whereas a phenotype of RV failure, as is observed in patients with PAH-secondary to systemic sclerosis, is characterized by impaired contractile reserve, RV fibrosis and RV diastolic stiffness. [ABSTRACT FROM AUTHOR]
- Published
- 2017
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6. Bisoprolol therapy does not reduce right ventricular sympathetic activity in pulmonary arterial hypertension patients.
- Author
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Rijnierse MT, Groeneveldt JA, van Campen JSJA, de Boer K, van der Bruggen CEE, Harms HJ, Raijmakers PG, Lammertsma AA, Knaapen P, Bogaard HJ, Westerhof BE, Vonk Noordegraaf A, Allaart CP, and de Man FS
- Abstract
Right ventricular (RV) function and autonomic dysfunction are important determinants of morbidity and mortality in patients with pulmonary arterial hypertension (PAH). Although successful in animal studies, effects of beta-blocker therapy on RV function in clinical trials were disappointing. To understand this discrepancy, we studied whether beta-blocker therapy changes RV sympathetic activity. Idiopathic PAH (IPAH) patients received beta-blocker therapy (uptitrated to a maximal tolerated dose) and underwent cardiac magnetic resonance imaging, right heart catheterization, and a [
11 C]-hydroxyephedrine positron emission tomography ([11 C]HED PET) scan at baseline to determine, respectively, RV ejection fraction (RVEF), RV pressures, and sympathetic activity. [11 C]HED, a norepinephrine analogue, allows determination of sympathetic innervation of the RV. [11 C]HED retention index reflects norepinephrine transporter activity. As a consequence of excessive catecholamine levels in the synaptic cleft, this transporter may be downregulated. Therefore, low [11 C]HED retention index indicates high sympathetic activity. 13 IPAH patients underwent [11 C]HED PET scans at baseline and after bisoprolol treatment. Although heart rate was reduced, systemic modulation of autonomic activity by bisoprolol did not affect local RV sympathetic nerve activity, RV function, or RV wall tension. In PAH patients, RV [11 C]HED retention index was lower compared to LV tracer uptake (p<0.01) and was related to systolic wall tension (R2 = 0.4731, p<0.01) and RV function (R2 = 0.44, p = 0.01). In RV failure, the tolerated dosage of bisoprolol did not result in an improvement of RV function nor in a reduction in RV sympathetic activity., (© The Author(s) 2020.)- Published
- 2020
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7. Bisoprolol in idiopathic pulmonary arterial hypertension: an explorative study.
- Author
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van Campen JS, de Boer K, van de Veerdonk MC, van der Bruggen CE, Allaart CP, Raijmakers PG, Heymans MW, Marcus JT, Harms HJ, Handoko ML, de Man FS, Vonk Noordegraaf A, and Bogaard HJ
- Subjects
- Adult, Aged, Cross-Over Studies, Double-Blind Method, Exercise, Female, Heart Failure complications, Hemodynamics, Humans, Male, Middle Aged, Prognosis, Prospective Studies, Ventricular Function, Left, Ventricular Function, Right, Walking, Antihypertensive Agents therapeutic use, Bisoprolol therapeutic use, Familial Primary Pulmonary Hypertension drug therapy
- Abstract
While beta-blockers are considered contraindicated in pulmonary arterial hypertension (PAH), the prognostic significance of sympathetic nervous system over-activity suggests a potential benefit of beta-blocker therapy. The aim of this randomised, placebo-controlled, crossover, single centre study was to determine the effects of bisoprolol on right ventricular ejection fraction (RVEF) in idiopathic PAH (iPAH) patients. Additional efficacy and safety parameters were explored.Patients with optimally treated, stable iPAH (New York Heart Association functional class II/III) were randomised to placebo or bisoprolol. Imaging and functional measurements were performed at baseline, crossover and end of study.18 iPAH patients were included, because inclusion faltered before enrolment of the targeted 25 patients. 17 patients completed 6 months of bisoprolol, 15 tolerated bisoprolol, one patient required intravenous diuretics. Bisoprolol was associated with a lower heart rate (17 beats per minute, p=0.0001) but RVEF remained unchanged. A drop in cardiac index (0.5 L·min(-1)·m(-2), p=0.015) was observed, along with a trend towards a decreased 6-min walking distance (6MWD).Although careful up-titration of bisoprolol was tolerated by most patients and resulted in a decreased heart rate, no benefit of bisoprolol in iPAH was demonstrated. Decreases in cardiac index and 6MWD suggest a deteriorated cardiac function. The results do not favour the use of bisoprolol in iPAH patients., (Copyright ©ERS 2016.)
- Published
- 2016
- Full Text
- View/download PDF
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