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MRI assessment of aortic flow in patients with pulmonary arterial hypertension in response to exercise
BACKGROUND: While primarily a right heart disease, pulmonary arterial hypertension (PAH) can impact left heart function and aortic flow through a shifted interventricular septum from right ventricular pressure overload and reduced left ventricular preload, among other mechanisms. In this study, we u...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6303959/ https://www.ncbi.nlm.nih.gov/pubmed/30577768 http://dx.doi.org/10.1186/s12880-018-0298-9 |
Sumario: | BACKGROUND: While primarily a right heart disease, pulmonary arterial hypertension (PAH) can impact left heart function and aortic flow through a shifted interventricular septum from right ventricular pressure overload and reduced left ventricular preload, among other mechanisms. In this study, we used phase contrast (PC) MRI and a modest exercise challenge to examine the effects of PAH on systemic circulation. While exercise challenges are typically performed with ultrasound in the clinic, MRI exercise studies allow for more reproducible image alignment, more accurate flow quantification, and improved tissue contrast. METHODS: Six PAH patients and fifteen healthy controls (8 older age-matched, 7 younger) exercised in the magnet bore with an MRI-compatible exercise device that allowed for scanning immediately following cessation of exercise. PC scans were performed in the ascending aorta during a breath hold immediately after modest exercise to non-invasively measure stroke volume (SV), cardiac output (CO), aortic peak systolic flow (PSF), and aortic wall stiffness via relative area change (RAC). RESULTS: Images following exercise showed mild blurring, but were high enough quality to allow for segmentation of the aorta. While SV was approximately 30% lower in PAH patients (SV(PAH,rest) = 67 ± 16 mL; SV(PAH,stress) = 90 ± 42 mL) than age-matched controls (SV(,older,rest) = 93 ± 16 mL; SV(older,stress) = 133 ± 40 mL) at both rest and following exercise, CO was similar for both groups following exercise (CO(PAH,stress) = 10.8 ± 5.7 L/min; CO(older,stress) = 11.8 ± 5.0 L/min). This was achieved through a compensatory increase in heart rate in the PAH subjects (74% increase as compared to 29% in age-matched controls). The PAH subjects also demonstrated reduced aortic peak systolic flow relative to the healthy controls (PSF(PAH),(rest) = 309 ± 52 mL/s; PSF(older),(rest) = 416 ± 114 mL/s; PSF(PAH),(stress) = 388 ± 113 mL/s; PSF(older),(stress) = 462 ± 176 mL/s). PAH patients and older controls demonstrated stiffer aortic walls when compared to younger controls (RAC(PAH,rest) = 0.15 ± 0.05; RAC(older,rest) = 0.17 ± 0.05; RAC(young,rest) = 0.28 ± 0.08). CONCLUSIONS: PC MRI following a modest exercise challenge was capable of detecting differences in left heart dynamics likely induced from PAH. These results demonstrated that PAH can have a significant influence on systemic flow, even when the patient has no prior left heart disease. Image quantification following exercise could likely be improved in future studies through the implementation of free-breathing or real-time MRI acquisitions. TRIAL REGISTRATION: Retrospectively registered on 02/26/2018 (TRN:NCT03523910). |
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