Impact of Exercise-Based Cardiac Rehabilitation on the Mid-Term Outcomes of Patients After Acute Myocardial Infarction Treated With Current Acute-Phase Management and Optimal Medical Therapy.

BACKGROUND: Early reported beneficial effects of cardiac rehabilitation (CR) have recently been disputed. The present study aimed to investigate the clinical impact of CR on the mid-term outcomes of patients following ST-segment elevation myocardial infarction (STEMI) treated with currently available management. METHODS: This study reviewed 145 consecutive patients who underwent primary coronary intervention and were discharged without any disability after STEMI during 2013-2015. RESULTS: Among the patients, 66 (45.5%) completed an outpatient CR program (CR group) and 79 were their non-CR counterparts or patients who dropped out of the program (N-D group). There were no between-group differences in patient demographics and clinical profiles, including door-to-balloon times and prescriptions. A total of 27 patients developed major adverse cardiac and cerebrovascular events (MACCE) during follow-up. The MACCE-free survival rates were 88% and 76% in the CR and N-D groups, respectively (log-rank, p=0.04). Cox proportional analysis demonstrated that inclusion in the N-D group was a significant predictor of MACCEs (HR, 2.36; 95% CI, 1.07-5.74; p=0.03). In the CR group, peak oxygen consumption and ventilatory efficiency determined by cardiopulmonary exercise testing significantly improved after the program (p<0.01). CONCLUSIONS: The impact of CR on the mid-term prognosis of patients with STEMI, even in the current myocardial infarction management era, was beneficial.

Prevalence and significance of sleep disordered breathing in adolescent athletes.

Sleep disordered breathing (SDB) was more prevalent in adolescent athletes than expected, and several potential warning signs related to autonomic nerve activity appeared in SDB athletes. SDB screening may prevent associated downstream risks in the future. http://ow.ly/GQqK30nGm8r.

Potential contribution of the hepcidin-macrophage axis to plaque vulnerability in acute myocardial infarction in human.

OBJECTIVES: Hepcidin-25 serves as a key peptide in the regulation of iron homeostasis and inflammation. It remains unknown whether hepcidin-25 plays an adverse role in atherosclerotic diseases. The aim of this study was to investigate whether hepcidin-25 is involved in the pathophysiology of coronary plaque vulnerability. METHODS AND RESULTS: Serum hepcidin-25 levels were quantitatively determined by the LC-MS/MS assay system. Peripheral blood was collected from patients with acute myocardial infarction (MI, n=33) and patients with stable angina pectoris (sCAD, n=19). The levels of hepcidin-25, IL-6, and CRP were significantly higher in the patients with acute MI than in the patients with sCAD. Coronary blood was aspirated from the culprit arteries via a thrombectomy catheter in 16 of the MI patients. Serum from the aspirates contained higher levels of hepcidin-25 and IL-6 compared with the peripheral blood. In immunohistochemical staining, the macrophages of the plaques in the solid component of the aspirates were immunoreactive for hepcidin-25. To confirm the clinical observation, an in vitro study was performed using human macrophages and coronary endothelial cells. The hepcidin gene and protein were detected in the cultured macrophages but not in the endothelial cells. Hepcidin-25 exposure induced ferroportin degradation and reduced the survival rate of endothelial cells. CONCLUSIONS: The results of the present study demonstrated that circulating hepcidin-25 and IL-6 were both elevated in the acute phase of MI and that hepcidin-25 released from plaque macrophages and other cell sources contributed to the plaque instability by inducing endothelial cell death.