Cardiovascular magnetic resonance-determined left ventricular myocardium impairment is associated with C-reactive protein and ST2 in patients with paroxysmal atrial fibrillation.

BACKGROUND: Myocardial strain assessed with cardiovascular magnetic resonance (CMR) feature tracking can detect early left ventricular (LV) myocardial deformation quantitatively in patients with a variety of cardiovascular diseases, but this method has not yet been applied to quantify myocardial strain in patients with atrial fibrillation (AF) and no coexistent cardiovascular disease, i.e., the early stage of AF. This study sought to compare LV myocardial strain and T1 mapping indices in AF patients and healthy subjects, and to investigate the associations of a portfolio of inflammation, cardiac remodeling and fibrosis biomarkers with LV myocardial strain and T1 mapping indices in AF patients with no coexistent cardiovascular disease.
METHODS: The study consisted of 80 patients with paroxysmal AF patients and no coexistent cardiovascular disease and 20 age- and sex-matched healthy controls. Left atrial volume (LAV), LV myocardial strain and native T1 were assessed with CMR, and compared between the AF patients and healthy subjects. Biomarkers of C-reactive protein (CRP), transforming growth factor beta-1 (TGF-β1), collagen III N-terminal propeptide (PIIINP), and soluble suppression of tumorigenicity 2 (sST2) were obtained with blood tests, and compared between the AF patients and healthy controls. Associations of these biomarkers with those CMR-measured parameters were analyzed for the AF patients.
RESULTS: For the CMR-measured parameters, the AF patients showed significantly larger LAV and LV end-systolic volume, and higher native T1 than the healthy controls (max P = 0.027). The absolute values of the LV peak systolic circumferential strain and its rate as well as the LV diastolic circumferential strain rate were all significantly reduced in the AF patients (all P < 0.001). For the biomarkers, the AF patients showed significantly larger CRP (an inflammation biomarker) and sST2 (a myocardium stiffness biomarker) than the controls (max P = 0.007). In the AF patients, the five CMR-measured parameters of LAV, three LV strain indices and native T1 were all significantly associated with these two biomarkers of CRP and sST2 (max P = 0.020).
CONCLUSIONS: In patients with paroxysmal AF and no coexistent cardiovascular disease, LAV enlargement and LV myocardium abnormalities were detected by CMR, and these abnormalities were associated with biomarkers that reflect inflammation and myocardial stiffness.