ABSTRACT
BACKGROUND: Secundum atrial septal defect (ASD) closure leads to electrical and mechanical remodeling that occurs early after shunt disappearance. The relationship between electromechanical remodeling using electrocardiogram (ECG) and cardiac magnetic resonance (CMR) after percutaneous and surgical closure has not yet been recorded in prospective studies. OBJECTIVE: We thought to study right atrium (RA) and right ventricle (RV) changes by CMR 3 months after transcatheter and surgical closure and their comparison with electrical remodeling by ECG. RESULTS: We prospectively evaluated 30 consecutive adult patients with isolated secundum ASD who were referred for (transcatheter and surgical) ASD closure. There was significant reduction in all of the electrical parameters within the same group as compared to the baseline values, except P wave dispersion (Pd). (P max was 97.33 ± 16.67 (pre closure) to 76 ± 15.49 (post closure) in the device group and 97.33 ± 12.79 (preclosure) to 73.33 ± 16.32 (post closure) in the surgical group, QRS complex was 104 ± 18.82 (preclosure) to 80 ± 18.51 (post closure) in the device group and 106.67 ± 14.47 (preclosure) to 86.67 ± 17.99 (post closure) in the surgical group. QTc maximum was 478.53 ± 36.79 (preclosure) to 412.53 ± 38.03 (post closure) in the device group and 470.53 ± 65.70 (preclosure) to 405.93 ± 63.08 (post closure) in the surgical group, and QTc dispersion was 70.33 ± 24.04 (preclosure) to 60.26 ± 28.56 (post closure) in the device group and 80.73 ± 30.38 (preclosure) to 60.27 ± 28.57 (post closure) in the surgical group).There was no significant difference between two groups indicating that transcatheter and surgical closure had led to equivalent value of electrical remodeling. In CMR study, we measured RA maximal volume and right ventricle end diastolic volume (RVEDV), RA maximal volume decreased significantly as compared to the base line values post closure in both groups (P value < 0.001). The reduction in RA max volume was more in the transcatheter closure group; however, this difference was not statistically significant when compared with the surgical arm (P value = 0.5).RVEDV decreased significantly in both groups as compared to the baseline values (P value < 0.001). Transcatheter closure resulted in more significant reduction in the RVEDV than the surgical closure (P value = 0.03). CONCLUSION: Our study showed early significant electromechanical reverse remodeling in most of the study parameters from the baseline values after ASD closure. We found no significant differences in all of the electrical and RA mechanical remodeling parameters with significantly better mechanical remodeling of RV in the device group.
ABSTRACT
This study aimed to assess serum irisin level in myocardial infarction (MI) with or without heart failure (HF) and the possible relation between irisin and cardiac markers, tumor necrosis factor-α (TNF-α) and lipid profile. Eighty-six subjects were included (33 patients had MI, 33 patients had MI with HF, and 20 controls). Body mass index (BMI), waist/hip ratio (WHR), systolic and diastolic blood pressure (SBP and DBP), heart rate, and left ventricular ejection fraction (LVEF) were measured. Blood samples were withdrawn on admission for measuring irisin, cardiac markers, TNF-α, total cholesterol (TC), triglycerides (TGs), low-density lipoprotein-cholesterol concentration (LDL-C), and high-density lipoprotein-cholesterol concentration (HDL-C). Patients with MI and HF had reduced serum irisin, LVEF, and HDL-C and higher levels of BMI, WHR, SBP, DBP, troponin-I, creatine kinase-MB (CK-MB), TNF-α, TC, TGs, and LDL-C compared with control. Negative correlations were observed between irisin and BMI, WHR, SBP, DBP, troponin-I, CK-MB, TNF-α, TC, TGs, and LDL-C. However, positive association was noticed between irisin and LVEF and HDL-C. Irisin might be a useful biomarker in diagnosis of MI with or without HF. It could have anti-inflammatory and hypolipidemic effects. Further studies are needed to elucidate the role of irisin as a promising prophylactic or therapeutic agent in cardiovascular diseases.
