Association between engagement in exercise training and peak cardiac biomarker concentrations following ST-elevation myocardial infarction

Background: Regular exercise training is an important factor in prevention of myocardial infarction (MI). However, little is known whether exercise engagement prior to MI is related to the magnitude of post-MI cardiac biomarker concentrations and clinical outcomes. Objectives: We tested the hypothesis that exercise engagement in the week prior MI is related to lower cardiac biomarker concentrations following ST-elevated MI (STEMI). Methods We recruited hospitalised STEMI patients and assessed the amount of exercise engagement in the 7 days preceding MI onset using a validated questionnaire. Patients were classified as 'exercise' if they performed any vigorous exercise in the week prior MI, or as 'control' if they did not. Post-MI peak concentrations of high-sensitive cardiac troponin T (peak-hs-cTnT) and creatine kinase (peak-CK) were examined. We also explored whether exercise engagement prior MI is related to the clinical course (duration of hospitalisation and incidence of in-hospital, 30-day and 6-month major adverse cardiac events (reinfarction, target vessel revascularisation, cardiogenic shock or death)). Results: In total, 98 STEMI patients were included, of which 16% (n=16) was classified as 'exercise', and 84% (n=82) as 'control'. Post-MI peak-hs-cTnT and peak-CK concentrations were lower in the exercise group (941 (645-2925) ng/mL; 477 (346-1402) U/L, respectively) compared with controls (3136 (1553-4969) ng/mL, p=0.010; 1055 (596-2019) U/L, p=0.016, respectively). During follow-up, no significant differences were found between both groups. Conclusion: Engagement in exercise is associated with lower cardiac biomarker peak concentrations following STEMI. These data could provide further support for the cardiovascular health benefits of exercise training

Rapid Improvements in Physical Activity and Sedentary Behavior in Patients With Acute Myocardial Infarction Immediately Following Hospital Discharge

Background: Little is known about changes in physical activity (PA) and sedentary behavior (SB) patterns in the acute phase of a myocardial infarction (MI). We objectively assessed PA and SB during hospitalization and the first week after discharge. Methods and Results: Consecutively admitted patients hospitalized with an MI were approached to participate in this pro-spective cohort study. SB, light-intensity PA, and moderate-vigorous intensity PA were objectively assessed for 24 h/d during hospitalization and up to 7 days after discharge in 165 patients. Changes in PA and SB from the hospital to home phase were evaluated using mixed-model analyses, and outcomes were stratified for predefined subgroups based on patient character-istics. Patients (78% men) were aged 65±10 years and diagnosed with ST-segment– elevation MI (50%) or non– ST-segment– elevation MI (50%). Sedentary time was high during hospitalization (12.6 [95% CI, 11.8–13.7] h/d) but substantially decreased following transition to the home environment (−1.8 [95% CI, −2.4 to −1.3] h/d). Furthermore, the number of prolonged sedentary bouts (≥60 minutes) decreased between hospital and home (−1.6 [95% CI, −2.0 to −1.2] bouts/day). Light-intensity PA (1.1 [95% CI, 0.8–1.6] h/d) and moderate-vigorous intensity PA (0.2 [95% CI, 0.1– 0.3] h/d) were low during hospitalization but significantly increased following transition to the home environment (light-intensity PA: 1.8 [95% CI, 1.4– 2.3] h/d; moderate-vigorous intensity PA: 0.4 [95% CI, 0.3– 0.5] h/d; both P<0.001). Improvements in PA and SB were similar across groups, except for patients who underwent coronary artery bypass grafting and who did not improve their PA patterns after discharge. Conclusions: Patients with MI demonstrate high levels of SB and low PA volumes during hospitalization, which immediately improved following discharge at the patient’s home environment. Registration: URL: trialsearch.who.int/; Unique identifier: NTR7646

Neuroprotection and repair in multiple sclerosis

Multiple sclerosis (MS) is an inflammatory demyelinating disease that is considered by many people to have an autoimmune aetiology. In recent years, new data emerging from histopathology, imaging and other studies have expanded our understanding of the disease and may change the way in which it is treated. Conceptual shifts have included: first, an appreciation of the extent to which the neuron and its axon are affected in MS, and second, elucidation of how the neurobiology of axon–glial and, particularly, axon–myelin interaction may influence disease progression. In this article, we review advances in both areas, focusing on the molecular mechanisms underlying axonal loss in acute inflammation and in chronic demyelination, and discussing how the restoration of myelin sheaths via the regenerative process of remyelination might prevent axon degeneration. An understanding of these processes could lead to better strategies for the prevention and treatment of axonal loss, which will ultimately benefit patients with MS