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SUMMARYAims: The aim of this study was to investigate the effects of spironolactone on left ventricular (LV) remodeling in patients with preserved LV function following acute myocardial infarction (AMI). Methods and Results: Successfully revascularized patients (n = 186) with acute ST elevation MI (STEMI) were included in the study. Patients were randomly divided into three groups, each of which was administered a different dose of spironolactone (12.5, 25 mg, or none). Echocardiography was performed within the first 3 days and at 6 months after MI. Echocardiography control was performed on 160 patients at a 6-month follow-up. The median left ventricular ejection fraction (LVEF) increased significantly in all groups, but no significant difference was observed between groups (P = 0.13). At the end of the sixth month, the myocardial performance index (MPI) had improved in each of the three groups, but no significant difference was found between groups (F = 2.00, P = 0.15). The mean LV peak systolic velocities (S m ) increased only in the control group during the follow-up period, but there is no significant difference between groups (F = 1.79, P = 0.18). The left ventricular end-systolic volume index (LVESVI) and the left ventricular end-diastolic volume index (LVEDVI) did not change significantly compared with the basal values between groups (F = 0.05, P = 0.81 and F = 1.03, P = 0.31, respectively). Conclusion: In conclusion, spironolactone dosages of up to 25 mg do not augment optimal medical treatment for LV remodeling in patients with preserved cardiac functions after AMI.

The aim of this study is to investigate the presence of limitations in the shoulder range of motion (ROM) or the loss of upper extremity function on the affected side in patients with cardiac implantable electronic devices (CIEDs) with respect to the implantation time. Forty-nine patients (30 men and 19 women), mean age 64.84±11.18 years, who had been living with a CIED for less than 3 months were included in the short-term recipient (STR) group and 127 patients (85 men and 42 women), mean age 64.91±14.70 years, and with the device for longer than 3 months were included in the long-term recipients group. Shoulder ROMs were measured using a digital goniometer. The other arm was used as the control. The Constant-Murler Score, Shoulder Pain Disability Index, and Shoulder Disability Questionnaire were used to assess the functional status. Limitations of ROM for flexion, abduction, and internal rotation were found to be significantly lower in the arm on the side of CIED compared with the control arm. Significant differences in shoulder flexion, abduction, and external rotation in STRs were found compared with long-term recipient (P<0.05). However, the functional comparison of groups by the Constant-Murler Score was not significant. A low to moderate amount of shoulder disability measured by Shoulder Pain Disability Index and Shoulder Disability Questionnaire was found in patients with CIEDs, which was more prominent in STRs (P<0.05). Pain, association of CIED with pectoral muscles, a possible subtle ongoing capsular pathology, and avoidance behaviors of patients to minimize the risk of lead dislodgement might be related to restriction of motion and function in the shoulder joint in patients with CIEDs.

Background: Heart rate (HR) reduction is associated with improved outcomes in patients with heart failure (HF) and biomarkers can be a valuable diagnostic tool in HF management. The primary aim of our study was to evaluate the short-term (6 months) effect of ivabradine on N-terminal pro B-type natriuretic peptide (NT-proBNP), CA-125, and cystatin-C values in systolic HF outpatients, and secondary aim was to determine the relationship between baseline HR and the and , and cystatin-C were taken at baseline and at the end of a 6-month follow-up in both groups. Results: There was a significant decrease in NYHA class in the ivabradine group (2.67 ± ± 0.47 vs. 1.85 ± 0.61, p < 0.001). When ivabradine and control groups were compared, a significant difference was also found in NHYA class 6 months later (p = 0.013). A significant decrease was found in HR in the ivabradine and control groups (84.10 ± 8.76 vs. 68.36 ± ± 8.32 bpm, p = 0.001; 84.51 ± 10 vs. 80.40 ± 8.3 p < 0.001),353.02 ± 1,453.77 vs. 717.81 ± 834.76 pg/mL, p < 0.001) in the ivabradine group. When ivabradine and control groups were compared after 6 months, a significant decrease was found in all HF parameters (respectively;. Creatinine level was significantly decreased and glomerular filtration rate (GFR) was significantly increased in the ivabradine group (1.02 ± 0.26 vs. 0.86 ± 0.17, creatinine: p = 0.001; 79.26 Cardiology Journal 2015, Vol. 22, No. 5, 501-509 DOI: 10.5603/CJ.a2015.0012 Copyright © 2015 Via Medica ISSN 1897 , and cystatin-C may prove to be useful in biomarker panels evaluating ivabradine therapy response in HF patients. (Cardiol J 2015; 22, 5: 501-509) bpm, p = 0.001). When both groups were compared, a significant difference was also found in HR after 6 months (p = 0.001). A significant decrease was found in cystatin-C (2.10 ± 0.73 vs. 1.50 ± 0.44 mg/L, p < 0.001),