[A preliminary study on the relationship between idiopathic arrhythmia and cardiac magnetic resonance imaging defined cardiac features in patients with straight back syndrome].

Objective: To retrospectively analyze the potential correlation between cardiac magnetic resonance (CMR) imaging and clinical features and idiopathic arrhythmia in patients with straight back syndrome (SBS). Methods: Patients receiving CMR imaging examination from April 2015 to March 2016 at our department ( n =1 432) were screened, 76 patients met the diagnosis criteria of flat chest (anteroposterior diameter/transthoracic diameter (APD/TTD) ratio<0.37 at the T8 vertebra). After excluding 33 patients with structural heart disease, 43 SBS patients were divided into two groups: SBS without obvious morphological change in the heart (group A, n =19) and SBS with morphological change of the heart (group B, n =24). CMR images were analyzed, focusing the heart morphological changes induced by SBS. The clinical data were collected to comprehensively analyze the medical history, electrocardiogram and electrophysiological examination in order to observe the relationship between SBS induced heart morphological change and the arrhythmia type and origin. Results: There were 21 male patients in this cohort, mean age was (28.5±11.5) years (13-58 years). APD/TTD ratio was similar between the two groups (0.30±0.03 vs. 0.29±0.04, P >0.05). LVEF tended to be lower in group B than in group A ((47.48±12.77)%vs. (59.31±9.04)%, P >0.05) . In group B, there were 15 patients with left ventricular enlargement, 2 with left ventricular wall thickening, 5 with uncoordinated ventricular wall motion, 5 with tricuspid regurgitation, 3 with mitral regurgitation, 2 with myocardial fibrosis, 5 with increased trabecular and 16 with decreased left ventricular function. Direct compression sign of right ventricle (disappeared precordial fat tissue space, secondary right atria enlargement and tricuspid regurgitation) and left atria (with or without secondary left ventricular enlargement and mitral regurgitation) were evidenced in patients of group B. CMR revealed that the arrhythmia origin corresponded the compression site of the heart in 8 cases (42.1%) in group A and 13 cases (54.2%) in group B, not corresponded to the compression site in 6 patients (31.6%) in group A and in 7 patients (29.2%) in group B, not attributable in 5 patients (26.3%) in group A and 4 patients (16.7%) in group B. The percent of arrhythmia origin corresponded the compression site of the heart tended to be higher in group B as compared to group A ( P >0.05). Conclusion: SBS can induce changes of cardiac morphology and cardiac function. SBS induced cardiac compression is linked with the development of arrhythmias and might be one of the reasons of arrhythmias in these patients.