Quantitative Assessment of CMR T1 Mapping on the Interventional Effects of Wenlü Pingji Granule on Myocardial Fibrosis and Atrial Fibrillation
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Graphical Abstract
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Abstract
OBJECTIVE To observe the quantitative assessment of cardiac magnetic resonance longitudinal relaxation time (CMR T1 mapping) on the interventional effect of Wenlü Pingji Granule on patients with atrial fibrillation (deficiency of both qi and yin) in terms of left ventricular myocardial fibrosis. METHODS 43 patients with atrial fibrillation with deficiency of qi and yin syndrome who met the inclusion criteria from March 2017 to November 2019, including 17 cases of persistent atrial fibrillation and 26 cases of paroxysmal atrial fibrillation. They were randomly divided into western medicine control group (20 cases) and Chinese medicine group (23 cases) applied with Wenlü Pingji Granule. The treatment and observation period was 24 weeks. The left ventricular myocardial fibrosis after treatment was quantitatively assessed by CMR T1 mapping imaging. ELISA was applied to detect serum interleukin 18 (IL-18), tumor necrosis factor-α (TNF-α), superoxide dismutase (SOD), malondialdehyde (MDA), liver kinase B1 (LKB1) levels and fibrosis indicator matrix metalloproteinase-2 (MMP-2), pre-collagen amino terminal peptide Ⅲ (PⅢ NP) so as to assess the changes of upstream oxidative inflammation-related factors in atrial fibrillation fibrosis. RESULTS The number of recurrence frequency and rate of atrial fibrillation in patients with paroxysmal atrial fibrillation in the Chinese medicine group were lower than those in the control group (P<0.05). The T1 value and ECV were significantly decreased (P<0.01), serum MMP-2, PⅢ NP, IL-18, TNF-α and MDA levels were significantly decreased (P<0.01) and SOD and LKB1 levels were significantly increased (P<0.01) after treatment in the Chinese medicine group, which were better than those in the western medicine control group (P<0.01). CONCLUSION Wenlü Pingji Granule can keep Sinus rhythm maintenance and reduce recurrence in patients with paroxysmal atrial fibrillation, as well as inhibit myocardial fibrosis in atrial fibrillation patients with deficiency of qi and yin syndrome. The mechanism may be related to the inhibition of the upstream oxidative inflammatory cascade.
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