Interventricular Septal Configuration at MR Imaging and Pulmonary Arterial Pressure in Pulmonary Hypertension

Roeleveld, R.J.; Marcus, J. Tim; Faes, T.J.C.; Gan, C. Tji-Joong; Boonstra, Anco; Postmus, Pieter E.; Vonk‐Noordegraaf, Anton

doi:10.1148/radiol.2343040151

Cited by 186 publications

(134 citation statements)

References 19 publications

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“…Although the current clinical selection criteria for resynchronisation therapy (wide QRS complex on ECG) sub-optimally predict clinical benefit for the individual LHF patient, resynchronisation therapy has been shown to significantly reduce morbidity and mortality, and is now a well-established treatment modality in LHF [14,15]. Ventricular dyssynchrony is often also observed in progressive stages of PAH-induced right heart failure [80,81]. Mechanical interventricular dyssynchrony in PAH (which is clinically easily recognised by the paradoxical bulging of the interventricular septum) is associated with impaired RV systolic function.…”

Section: Cardiac Resynchronisation Therapymentioning

confidence: 99%

Perspectives on novel therapeutic strategies for right heart failure in pulmonary arterial hypertension: lessons from the left heart

Handoko

Man

Allaart³

et al. 2010

Eur Respir Rev

111

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Right heart function is the main determinant of prognosis in pulmonary arterial hypertension (PAH). At present, no treatments are currently available that directly target the right ventricle, as we will demonstrate in this article.Meta-analysis of clinical trials in PAH revealed that current PAH medication seems to have limited cardiac-specific effects when analysed by the pump-function graph. Driven by the hypothesis that ''left'' and right heart failure might share important underlying pathophysiological mechanisms, we evaluated the clinical potential of left heart failure (LHF) therapies for PAH, based on currently available literature.As in LHF, the sympathetic nervous system and the renin-angiotension-aldosterone system are highly activated in PAH. From LHF we know that intervening in this process, e.g. by angiotensinconverting enzyme inhibition or b-blockade, is beneficial in the long run. Therefore, these medications could be also beneficial in PAH. Furthermore, the incidence of sudden cardiac death in PAH could be reduced by implantable cardioverter-defibrillators. Finally, pilot studies have demonstrated that interventricular dyssynchrony, present at end-stage PAH, responded favourably to cardiac resynchronisation therapy as well.In conclusion, therapies for LHF might be relevant for PAH. However, before they can be implemented in PAH management, safety and efficacy should be evaluated first in well-designed clinical trials.

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Section: Cardiac Resynchronisation Therapymentioning

confidence: 99%

Perspectives on novel therapeutic strategies for right heart failure in pulmonary arterial hypertension: lessons from the left heart

Handoko

Man

Allaart³

et al. 2010

Eur Respir Rev

111

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“…Estimation of changes in pulmonary artery pressure with MRI In order to measure any possible effect of sildenafil on pulmonary artery pressure (Ppa) the acceleration time/ejection time ratio [18] and the left ventricular septal bowing (LVSB) [19] were measured. The acceleration time is the time from onset of forward flow to the moment of maximum flow velocity in the main pulmonary artery, as measured by velocity-encoded cine MRI.…”

Section: Measurement Of Exercise-induced Sv Response By Mrimentioning

confidence: 99%

Sildenafil treatment in COPD does not affect stroke volume or exercise capacity

et al. 2007

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In chronic obstructive pulmonary disease (COPD) patients, stroke volume response to exercise is impaired. The aim of the present study was to investigate whether 3 months of sildenafil treatment improves stroke volume and, if so, whether this improvement is related to the pulmonary artery pressure and translated into an improved exercise capacity.A total of 15 stable COPD patients (Global Initiative for Chronic Obstructive Lung Disease stage II-IV) underwent right heart catheterisation at rest and during exercise. Stroke volume was assessed by magnetic resonance imaging (MRI) at rest and during submaximal exercise in the supine position and compared with eight age-matched controls. Additionally, a cardiopulmonary exercise test and a 6-min walking distance test were performed. Exercise tests and MRI were repeated after 12 weeks of oral therapy with 50 mg sildenafil three times daily.Stroke volume in COPD patients was significantly lower than in healthy controls (62¡12 versus 81¡22 mL at rest and 70¡15 versus 101¡28 mL during exercise). Pulmonary hypertension (PH) was diagnosed in nine patients and was absent in six. Treatment with sildenafil had no effect on stroke volume or exercise capacity. Although the stroke volume was lower in COPD patients with associated PH in comparison with non-PH patients, there was no difference in treatment response between both groups.In the present group of 15 chronic obstructive pulmonary disease patients, a reduced stroke volume was found at rest and during exercise. Neither stroke volume nor exercise capacity were improved by 3 months of sildenafil therapy.

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“…Temporal resolution is better with CMR imaging [33], without the need for ionising radiation or intravenous contrast [34]. As a result, CMR has emerged over recent years as the gold standard for detailed study of the right ventricle [9,[35][36][37], and has become an established modality for the physiological assessment of PH patients in cross-sectional studies [31,[38][39][40], longitudinal follow-up studies [41] and clinical trials of therapy [16]. EBCT, in contrast, is not routinely used to assess PH patients.…”

Section: )mentioning

confidence: 99%

NT-proBNP can be used to detect right ventricular systolic dysfunction in pulmonary hypertension

Blyth¹,

Groenning²,

Mark³

et al. 2006

Eur Respir J

104

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Right ventricular systolic dysfunction (RVSD) at baseline (pre-treatment) predicts early death in patients with pulmonary hypertension (PH). However, RVSD can only be detected reliably by prohibitively invasive or expensive techniques. N-terminal B-type natriuretic peptide concentration ([NT-proBNP]) correlates with RV function in PH; however, an [NT-proBNP] threshold that indicates RVSD in individual patients has not previously been determined.Twenty-five patients with PH (pulmonary arterial hypertension (n519) or chronic thromboembolic PH (n56)) underwent cardiovascular magnetic resonance (CMR) imaging and NT-proBNP measurement at baseline. [NT-proBNP] was correlated against RV dimensions and ejection fraction (RVEF) measured directly by CMR imaging. The ability of NT-proBNP to detect RVSD (defined as a CMR-derived RVEF .2 SDs below control values) was tested and predictors of [NTproBNP] identified.[NT-proBNP] correlated negatively with RVEF. RVSD was present in nine out of 25 patients. An [NT-proBNP] threshold of 1,685 pg?mL -1 was sensitive (100%) and specific (94%) in detecting RVSD. RVEF and RV mass index independently predicted [NT-proBNP].In pulmonary hypertension, a baseline N-terminal B-type natriuretic peptide concentration of .1,685 ng?L -1 suggests right ventricular systolic dysfunction, and thus an increased risk of early death. N-terminal B-type natriuretic peptide could prove useful as an objective, noninvasive means of identifying patients with pulmonary hypertension who have right ventricular systolic dysfunction at presentation.

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Interventricular Septal Configuration at MR Imaging and Pulmonary Arterial Pressure in Pulmonary Hypertension

Abstract: In 37 patients with pulmonary hypertension, systolic PAP higher than 67 mm Hg may be expected when leftward curvature is observed.

Cited by 186 publications

References 19 publications

Perspectives on novel therapeutic strategies for right heart failure in pulmonary arterial hypertension: lessons from the left heart

Perspectives on novel therapeutic strategies for right heart failure in pulmonary arterial hypertension: lessons from the left heart

Sildenafil treatment in COPD does not affect stroke volume or exercise capacity

NT-proBNP can be used to detect right ventricular systolic dysfunction in pulmonary hypertension

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