The sustained effects of extending cardiac rehabilitation with a six-month telemonitoring and telecoaching programme on fitness, quality of life, cardiovascular risk factors and care utilisation in CAD patients: The TeleCaRe study.

INTRODUCTION: The aim of this study was to assess the acute and sustained effects of a six-month heart-rate-based telerehabilitation programme, following the completion of cardiac rehabilitation (CR), on peak oxygen uptake (peakVO2), quality of life (QoL), cardiovascular risk factors and care utilisation in patients with coronary artery disease (CAD). METHODS: A total of 122 patients with CAD were randomised, after the completion of CR, to an intervention group with six months of telemonitoring and telecoaching (TELE) or a control group with a traditional six-month follow-up programme with monthly calls (CON). The primary outcome was peakVO2 at 12 months, to assess the sustained effects of TELE. The secondary outcomes included QoL, cardiovascular risk factors (lipid spectrum), major adverse cardiovascular events (MACE) and habitual physical activity. RESULTS: PeakVO2 increased significantly from baseline to 12 months in TELE (+2.5 mL·kg-1min-1 (95% CI 1.5-3.2)) and CON (+1.9 mL·kg-1min-1 (95% CI 1.0-2.5)), and did not differ between groups (P = 0.28). Similarly, QoL (P = 0.31), total cholesterol (P = 0.45), MACE (P = 0.86) did not differ between groups and in time. DISCUSSION: Extending CR with a heart-rate-based telerehabilitation programme did not yield additional sustainable health benefits compared with regular care with monthly telephone calls. These observations highlight that both telerehabilitation and regular care with monthly telephone calls may prevent the typically observed reductions in peakVO2 following the completion of a CR programme.Trial registration: Dutch Trial Register NL4140 (registered 6 December 2014).

Benefits of lifelong exercise training on left ventricular function after myocardial infarction.

Background Endurance exercise training induces cardio-protective effects, but athletes are not exempted from a myocardial infarction. Evidence from animal studies suggests that exercise training attenuates pathological left ventricular remodelling following myocardial infarction. We tested the hypothesis that lifelong exercise training is related to attenuated pathological left ventricular remodelling after myocardial infarction as evidenced by better left ventricular systolic function in veteran athletes compared to sedentary peers. Design This was a cross-sectional study. Methods Sixty-five males (60 ± 6 years) were included and allocated to four groups based on lifelong exercise training volumes: (a) athletes ( n = 18), (b) post-myocardial infarction athletes (athletes + myocardial infarction, n = 20), (c) sedentary controls ( n = 13), and (d) post-myocardial infarction controls (sedentary controls + myocardial infarction, n = 14). Athletes were lifelong (≥20 years) highly physically active (≥30 metabolic equivalent of task (MET)-h/week), whereas sedentary controls did not meet the exercise guidelines (<10 MET-h/week) for the past 20 years. left ventricular systolic function, diastolic function and wall strain were measured using echocardiography. Results Cardiac enzyme markers (creatine-kinase, creatinine, aspartate transaminase and lactate dehydrogenase) following myocardial infarction and infarct location did not differ between athletes + myocardial infarction and sedentary controls + myocardial infarction. Left ventricular ejection fraction was significantly higher in athletes (61% ± 4), athletes + myocardial infarction (58% ± 4) and sedentary controls (57% ± 6) compared to sedentary controls + myocardial infarction (51% ± 7; p < 0.01). Left ventricular circumferential strain was superior in athletes (-19% (-21% to -17%), athletes + myocardial infarction (-16% (-20% to -12%)), and sedentary controls (-15% (-18% to -14%) compared to sedentary controls + myocardial infarction (-13% (-15% to -8%), p < 0.01). Diastolic function parameters did not differ across groups. Conclusion These findings suggest that lifelong exercise training may preserve left ventricular systolic function and possibly attenuates or minimises the deleterious effects of pathological post-myocardial infarction left ventricular remodelling in veteran athletes.

Impact of prolonged walking exercise on cardiac structure and function in cardiac patients versus healthy controls.

BACKGROUND AND DESIGN: Previous studies have demonstrated that endurance exercise can cause an acute transient decrease in cardiac function in healthy subjects. Whether this also occurs in cardiac patients is unknown. We investigated the impact of prolonged single day and three-day walking exercise on cardiac function and cardiac biomarkers between cardiac patients and healthy controls in an observational study. METHODS: We recruited 10 cardiac patients (nine males, one female, 68 ± 5 years) and 10 age- and sex-matched healthy control subjects (nine males, one female, 68 ± 4 years) to perform 30 or 40 km of walking exercise per day for three consecutive days. Cardiac function was examined using echocardiography and cardiac biomarkers (cardiac troponin and B-type natriuretic peptide) with blood samples. Data were collected before walking and directly after walking on day 1 and day 3. RESULTS: Post-exercise early systolic tissue contraction velocity of the left ventricle (p = 0.005) and global longitudinal left ventricle strain (P = 0.026) were increased in both groups compared with baseline. Post-exercise right ventricle peak early diastolic tissue filling velocity and systolic blood pressure/left ventricle end-systolic volume ratio decreased in both groups (p = 0.043 and p = 0.028, respectively). Post-exercise cardiac troponin levels increased (p = 0.045) but did not differ across groups (p = 0.60), whereas B-type natriuretic peptide levels did not change (p = 0.43). CONCLUSION: This study suggests that stable cardiac patients are capable of performing three days of prolonged walking exercise without clinically significant acute overall deterioration in cardiac function or more pronounced increase in cardiac biomarkers compared with healthy controls.