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Multiparametric cardiovascular magnetic resonance characterisation of myocardial inflammation in patients with rheumatic heart disease
Author(s)
Samuels, Petronella
Date Issued
2020
Type
Thesis
Publisher
Cape Peninsula University of Technology
Abstract
INTRODUCTION: Rheumatic heart disease (RHD) is the major sequel of acute rheumatic fever (ARF) and occurs in approximately 60% of the cases. Globally, RHD is the most common acquired cardiovascular disease, affecting more than 15 million people per year, causing approximately 233,000 deaths. RHD remains a significant cause of heart failure in low- and middle-income countries, including sub-Saharan Africa, contributing to considerable morbidity and mortality, often affecting young economically active members of society.
OBJECTIVE: The aim of the study was to document the extent of myocardial fibrosis in subjects with RHD, in order to determine the degree of altered myocardial tissue characteristics using a multiparametric cardiovascular magnetic resonance (CMR) approach; assess left ventricular (LV) function and strain, and to assess focal and diffuse myocardial fibrosis in subjects with RHD.
METHODOLOGY: Enrolled subjects with a confirmed diagnosis of RHD, and age- and sex-matched healthy controls underwent CMR using a 3T Siemens Skyra (Erlangen, Germany) scanner. CMR parameters included steady-state-free-precession (SSFP) cine, cine tagging, T1-weighted imaging, T2 short Tau inversion-recovery (STIR), native T1 mapping (Modified-Look-Locker inversion recovery), T2 mapping and late gadolinium enhancement (LGE) imaging and extracellular volume (ECV) estimation.
RESULTS: Forty-four (44) subjects (mean age 42.8 ± 13.8 years; female 63.6%) with a confirmed diagnosis of RHD, and 30 age- and sex-matched healthy controls (mean age 38.87 ± 12.31 years; female 53.3%) were enrolled in the study. RHD subjects showed an increased indexed LV end-diastolic, end-systolic, and stroke volume and mass, compared to controls (p = 0.001). LV ejection fraction (LVEF) was reduced in the RHD cohort compared to controls (44.0 ± 13.26% versus 56.9 ± 5.19%, p < 0.001). There was significant left atrial dilatation in RHD subjects compared to controls (41.37 ± 11.84 mm versus 21.77 ± 3.13 mm, p < 0.001). Increased indexed RV end-diastolic, end-systolic and stroke volumes were found. RV ejection fraction was significantly lower in RHD subjects compared to controls (41.07 ± 16.19% versus 53.60 ± 7.46%, p < 0.001). Valvular lesions most commonly observed were mixed mitral valve disease (27%) and mixed mitral and aortic valve disease (43%). Native T1 values were elevated in RHD subjects compared to controls (1279.98 ± 54.14 ms versus 1212.85 ± 33.34 ms, p = 0.004). T2 mapping values to assess oedema were normal, in both RHD subjects and controls (39.26 ± 2.92 versus 38.72 ± 2.19, p = 0.32); relative T2 STIR imaging parameters were 1.31 ± 0.34 versus 1.48 ± 0.22, p = 0.02.
Late gadolinium enhancement (LGE) was evident in all 44 (100%) RHD subjects, with linear (26%), patchy (36%) and diffuse (38%) patterns of enhancement. ECV values were elevated in RHD subjects compared to controls (0.36 ± 0.05 versus 0.28 ± 0.01 %, p < 0.001). Linear regression analysis showed moderate negative correlation between native T1 and peak diastolic circumferential strain rate (R = -0.412, p = 0.001) and strong correlation between ECV and peak diastolic circumferential strain rates (R = -0.43, p = 0.00).
CONCLUSION: This study showed a high prevalence of fibrosis throughout the myocardium in all RHD subjects, irrespective of valvular pathology. Increased native T1 and ECV indicate increased myocardial fibrosis. Normal signal intensity ratio on T2-weighted oedema imaging (STIR) and T2 values indicated absence of active inflammation in advanced, chronic RHD. These data, showing a high fibrotic burden, may provide an explanation for increased mortality in RHD as excess myocardial fibrosis has been strongly linked with mortality in other disease contexts.
OBJECTIVE: The aim of the study was to document the extent of myocardial fibrosis in subjects with RHD, in order to determine the degree of altered myocardial tissue characteristics using a multiparametric cardiovascular magnetic resonance (CMR) approach; assess left ventricular (LV) function and strain, and to assess focal and diffuse myocardial fibrosis in subjects with RHD.
METHODOLOGY: Enrolled subjects with a confirmed diagnosis of RHD, and age- and sex-matched healthy controls underwent CMR using a 3T Siemens Skyra (Erlangen, Germany) scanner. CMR parameters included steady-state-free-precession (SSFP) cine, cine tagging, T1-weighted imaging, T2 short Tau inversion-recovery (STIR), native T1 mapping (Modified-Look-Locker inversion recovery), T2 mapping and late gadolinium enhancement (LGE) imaging and extracellular volume (ECV) estimation.
RESULTS: Forty-four (44) subjects (mean age 42.8 ± 13.8 years; female 63.6%) with a confirmed diagnosis of RHD, and 30 age- and sex-matched healthy controls (mean age 38.87 ± 12.31 years; female 53.3%) were enrolled in the study. RHD subjects showed an increased indexed LV end-diastolic, end-systolic, and stroke volume and mass, compared to controls (p = 0.001). LV ejection fraction (LVEF) was reduced in the RHD cohort compared to controls (44.0 ± 13.26% versus 56.9 ± 5.19%, p < 0.001). There was significant left atrial dilatation in RHD subjects compared to controls (41.37 ± 11.84 mm versus 21.77 ± 3.13 mm, p < 0.001). Increased indexed RV end-diastolic, end-systolic and stroke volumes were found. RV ejection fraction was significantly lower in RHD subjects compared to controls (41.07 ± 16.19% versus 53.60 ± 7.46%, p < 0.001). Valvular lesions most commonly observed were mixed mitral valve disease (27%) and mixed mitral and aortic valve disease (43%). Native T1 values were elevated in RHD subjects compared to controls (1279.98 ± 54.14 ms versus 1212.85 ± 33.34 ms, p = 0.004). T2 mapping values to assess oedema were normal, in both RHD subjects and controls (39.26 ± 2.92 versus 38.72 ± 2.19, p = 0.32); relative T2 STIR imaging parameters were 1.31 ± 0.34 versus 1.48 ± 0.22, p = 0.02.
Late gadolinium enhancement (LGE) was evident in all 44 (100%) RHD subjects, with linear (26%), patchy (36%) and diffuse (38%) patterns of enhancement. ECV values were elevated in RHD subjects compared to controls (0.36 ± 0.05 versus 0.28 ± 0.01 %, p < 0.001). Linear regression analysis showed moderate negative correlation between native T1 and peak diastolic circumferential strain rate (R = -0.412, p = 0.001) and strong correlation between ECV and peak diastolic circumferential strain rates (R = -0.43, p = 0.00).
CONCLUSION: This study showed a high prevalence of fibrosis throughout the myocardium in all RHD subjects, irrespective of valvular pathology. Increased native T1 and ECV indicate increased myocardial fibrosis. Normal signal intensity ratio on T2-weighted oedema imaging (STIR) and T2 values indicated absence of active inflammation in advanced, chronic RHD. These data, showing a high fibrotic burden, may provide an explanation for increased mortality in RHD as excess myocardial fibrosis has been strongly linked with mortality in other disease contexts.
Additional information
Thesis (MSc (Radiography))--Cape Peninsula University of Technology, 2020
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