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A simplified substitute for heart rate (HR) at the anaerobic threshold (AT), i.e., resting HR plus 30 beats per minute or a percentage of predicted maximum HR, is used as a way to determine exercise intensity without cardiopulmonary exercise testing (CPX) data. However, difficulties arise when using this method in subacute myocardial infarction (MI...
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Context 1
... cardiopulmonary exercise testing; LVEF, left ventricular ejection fraction; Max CK-MB, maximum value of serum creatine kinase-myocardial band; MI, myocardial infarction. Table 2 summarizes the data obtained during CPX. None of the patients showed ischemic ST changes or experienced chest pain or serious arrhythmias during CPX. ...Similar publications
Cardiopulmonary exercise testing (CPET) is the standard of objective assessment of functional status prior to consideration for adult liver transplantation (LT) in UK. Suboptimal CPET results are associated with poorer outcomes and decreased 90-day survival. 1,2 Little is currently known regarding predicting longer term survival, complications and...
Citations
... Committees of the American Heart Association (AHA) and American College of Cardiology (ACC) recommend 150 minutes of moderate-intensity or 75 minutes of high-intensity aerobic exercise per week [11]. Exercise rehabilitation programs significantly improve the clinical prognosis of CHD patients after percutaneous coronary intervention (PCI) [12][13][14]. In addition to a single statin treatment, the combination of aerobic exercise and statin therapy is thought to be more effective for lowering plasma lipid and glucose levels and improving prognosis and quality of life in patients with CHD [15]. ...
Recent research has confirmed that moderate-intensity exercise affects the gut microbiome composition and improves cardiac function in an animal model after myocardial infarction (MI). However, few studies have investigated the effects of exercise on glucose and lipid metabolism in patients with coronary heart disease (CHD) receiving a statin treatment and successful percutaneous coronary intervention (PCI). Meanwhile, since statin therapy may lead to the risk of an increase in blood glucose level in CHD patients, we hypothesized that moderate-intensity exercise may be helpful for regulating glucose-lipid metabolism and stabilizing the blood glucose level in CHD patients. Therefore, to confirm our conjecture, we conducted a clinical retrospective study and animal experiment, respectively. The clinical study involved a total of 501 statin-treated patients with CHD after PCI. According to the study protocol, patients were divided into the following three groups: a non-exercise group, exercise at the recommended standard group, and exercise not at the recommended standard group. We found that qualified moderate-intensity exercise decreased blood glucose and lipid levels at follow-up at a mean of 2.2 years, and the incidence of new-onset diabetes showed a downward trend compared with the non-exercise and exercise not at the recommended standard groups. Furthermore, we used a high-fat rat model to explore an additional mechanism of the beneficial effects of exercise-based management on glucose-lipid metabolism apart from the known mechanism. We used 16S rRNA high-throughput sequencing technology to analyze the changes induced by exercise in the composition of intestinal flora in experimental rats. We found that rats that exercised with or without statin administration had lower plasma glucose and lipid levels and that these parameters were higher in the control and statin-treated rats that did not exercise. These results were consistent with the human study. The results from high-throughput sequencing of the intestinal flora of rats showed, to the best of our knowledge, that exercise leads to an increased relative abundance of Akkermansia muciniphila, which contributes to improved glucose and lipid metabolism. Based on our current results, we suggest that moderate-intensity exercise can improve glucose and lipid metabolism and prevent statin treatment-related side effects, such as hyperglycemia, in patients after PCI. Exercise could facilitate the applicability of statins for lower lipid levels. Exercise training also provides additional benefits, such as alteration of the gut microbiota, which contributes to improved glucose and lipid metabolism.
... Although both α β-blockers and β1-blockers are frequently prescribed for MI patients due to their effectiveness, [12][13][14] our previous studies suggested that only β1-blockers strongly decrease HR response during incremental CPX in MI patients. 15,16 Thus, we hypothesized that it would be possible to predict HR AT with a new formula that includes β1-blockers as a predictor variable. The aim of the present study was to create a new formula to accurately predict HR AT that considers the effects of β-blockers in MI patients and to validate the accuracy of the new formula. ...
... 27 Accordingly, low BMI was considered a predictor of lower HR AT in the present study . Regarding β1-blocker treatment, we reported that β1-blockers independently decrease HR response during incremental CPX in MI patients, 15,16 and multiple regression analysis revealed that β1-blockers were a significant predictor of lower HR AT in the present study. Resting HR and SBP were also significant predictors of higher HR AT in the present study, as high resting HR and SBP were shown to be associated with an increase in sympathetic nervous system activity. ...
Purpose:
It is recommended that patients with myocardial infarction (MI) be prescribed exercise by target heart rate (HR) at the anaerobic threshold (AT) via cardiopulmonary exercise testing (CPX). Although percent HR reserve using predicted HRmax (%HRRpred) is used to prescribe exercise if CPX or an exercise test cannot be performed, %HRRpred is especially difficult to use when patients take β-blockers. We devised a new formula to predict HR at AT (HRAT) that considers β-blocker effects in MI patients and validated its accuracy.
Methods:
The new formula was created using the data of 196 MI patients in our hospital (derivation sample), and its accuracy was assessed using the data of 71 MI patients in other hospitals (validation sample). All patients underwent CPX 1 mo after MI onset, and resting HR, resting systolic blood pressure (SBP), and HRAT were measured during CPX.
Results:
The results of multiple regression analysis in the derivation sample gave the following formula (R2 = 0.605, P < .001): predicted HRAT = 2.035 × (≥65 yr:-1, <65 yr:1) + 3.648 × (body mass index <18.5 kg/m2:-1, body mass index ≥18.5 kg/m2:1) + 4.284 × (β1-blocker(+):-1, β1-blocker(-):1) + 0.734 × (HRrest) + 0.078 × (SBPrest) + 36.812. This formula consists entirely of predictors that can be obtained at rest. HRAT and predicted HRAT with the new formula were not significantly different in the validation sample (mean absolute error: 5.5 ± 4.1 bpm).
Conclusions:
The accuracy of the new formula appeared to be favorable. This new formula may be a practical method for exercise prescription in MI patients, regardless of their β-blocker treatment status, if CPX is unavailable.
