Consistency evaluation of exercise target heart rate determined by resting heart rate and anaerobic threshold in chronic heart failure patients.

PURPOSE: To evaluate the consistency on the target heart rate for exercise determined by simple target heart rate (sTHR) based on resting heart rate (HRrest) and heart rate at anaerobic threshold (HRAT) in cardiopulmonary exercise test (CPET) for patients with chronic heart failure. METHODS: This is a retrospective cohort study, in which CHF patients who underwent CPET in Tongji Hospital Cardiac Rehabilitation Center Affiliated to Tongji University from March 2007 to December 2018 were enrolled. The clinical data of the patients from the electronic medical record system, HRrest and HRAT measured by CPET were collected. Patients were further divided into subgroups according to gender, age (<60 years group and ≥ 60 years group), with or without beta-blocker therapy and subgroup of heart failure (heart failure with reduced, mid-range and preserved ejection fraction). The sTHR (HRrest plus 10, 15, 20, 25 and 30 bpm) and HRAT were all calculated in each patient. Paired t-test was used for the difference between the two methods, correlation analysis was shown by pearson analysis and intraclass correlation coefficient (ICC) was calculated for consistency test. RESULTS: A total of 547 CHF patients were enrolled, including 447 males (81.7%), aged 63 (56,69) years, with BMI of 25.2 (23.5,26.4) kg/m2 and LVEF of 45.0 (36.0, 52.0) %. The target heart rate determined by HRAT method was (93.59 ± 13.95) bpm, and its counterpart determined by HRrest plus 20 bpm (HRrest+20) was (93.16 ± 7.69) bpm. There was no significant difference between the two methods (P>0.05). However, it was statistically different between HRrest plus 10, 15, 25, 30 bpm and HRAT respectively (P<0.001). And HRrest+20 was positively correlated with HRAT (r = 0.418, P<0.001). Therefore, HRrest+20 below was regarded as sTHR. The ICC of the consistency test between sTHR and HRAT was 0.523,95%CI 0.435-0.596 (P < 0.001) in all patients (n = 547). In patients with beta-blocker therapy (n = 464), the ICC of sTHR and HRAT consistency test was 0.534,95%CI 0.441-0.612, P < 0.001; The ICC of the consistency test between sTHR and HRAT of patients without beta-blocker therapy (n = 83) was 0.407,95%CI 0.083-0.616, P < 0.05. In the sinus rhythm group (n = 466), the ICC of sTHR and HRAT consistency test was 0.527,95%CI 0.433-0.606, P < 0.001; The ICC of the consistency test between sTHR and HRAT of atrial fibrillation patients in group (n = 81) was 0.482,95%CI 0.195-0.667, P < 0.05.The ICC of the consistency test between sTHR and HRAT was 0.501,95%CI 0.338-0.623 (P < 0.001) in patients under 60 years old (n = 195); The ICC of the consistency test between sTHR and HRAT in patients ≥60 years old (n = 352) was 0.533,95%CI 0.424-0.621, P < 0.001. In the male group (n = 447), the ICC of sTHR and HRAT consistency test was 0.577,95%CI 0.491-0.649, P < 0.001; The ICC of the consistency test between sTHR and HRAT of female patients in group (n = 100) was 0.344,95%CI 0.025-0.559, P < 0.05. The ICC of sTHR and HRAT consistency test in HFrEF group (n = 170) was 0.395,95%CI 0.181-0.553, P < 0.01; The ICC values of the consistency test between sTHR and HRAT was 0.543, 95%CI 0.405-0.649 (P < 0.001) in patients with HFmrEF (n = 222); In HFpEF group (n = 155), the ICC of sTHR and HRAT consistency test was 0.620,95%CI 0.478-0.723, P < 0.001. CONCLUSION: The exercise target heart rate calculated by HRrest is consistent with that determined by HRAT in patients with CHF. For primary hospitals without CPET, exercise prescription equivalent to AT intensity for patients with CHF can be determined by HRrest. However, the target heart rate calculated by HRrest can't replace that determined by HRAT in this patient cohort completely.

Genetic analysis of DNA-damage tolerance pathways in Arabidopsis.

KEY MESSAGE: Genetic analysis revealed a two-branch DNA-damage tolerance mechanism in Arabidopsis, namely translesion DNA synthesis and error-free lesion bypass, represented by Rev3 and Rad5a-Uev1C/D, respectively. DNA-damage tolerance (DDT) is a mechanism by which cells complete replication in the presence of replication-blocking lesions. In budding yeast, DDT is achieved through Rad6-Rad18-mediated monoubiquitination of proliferating cell nuclear antigen (PCNA), which promotes translesion DNA synthesis (TLS) and is followed by Ubc13-Mms2-Rad5 mediated K63-linked PCNA polyubiquitination that promotes error-free lesion bypass. Arabidopsis and other known plant genomes contain all of the above homologous genes except RAD18, and whether plants possess an intact DDT mechanism is unclear. In this study, we created Arabidopsis UEV1 (homologous to yeast MMS2) gene mutations and obtained two sets of double mutant lines Atuev1ab and Atuev1cd. It turned out that the Atuev1cd, but not the Atuev1ab mutant, was sensitive to DNA damage. Genetic analyses revealed that AtUEV1C/D and AtRAD5a function in the same pathway, while TLS represented by AtREV3 functions in a separate pathway in response to replication-blocking lesions. Furthermore, unlike budding yeast RAD5 that also functions in the TLS pathway, AtRAD5a is not required for TLS. Observations in this study collectively establish a two-branch DDT model in plants with similarity to and difference from the yeast DDT.