dos pulse in the AF group ( Fig. 3 , Table 3 ). O2 pulse trend ratio was calculated by O2 pulse at Peak/O2 pulse at AT, and AF patients were divided into two groups according to O2 pulse trend ratio (median = 1.1). High O2 pulse trend (high-O2p trend) had the O2 pulse trend ratio > 1.1, whereas low O2 pulse trend (low-O2p trend) had the O2 pulse trend ratio < 1.1. In the low-O2p trend group, the HR at Rest was comparatively low compared with the high-O2p trend group. HR change from Rest to Peak (HR reserve) was significantly higher in the low-O2p trend group as compared with that of high-O2p trend group. In contrast, the O2 pulse was comparatively increased below the Rc level in the low-O2p trend group, whereas, above the Rc level, there was no increase in the O2 pulse in the low-O2p trend group. In the high-O2p trend group, the increase in the O2 pulse was somewhat low below the Rc level compared with that of the low-O2p trend group, whereas the O2 pulse at peak in the high-O2p trend group exceeded that in the low-O2p trend group. From these results, blunted increase in relative O2 pulse in the AF group was associated with HR increase during exercise.
Changes in the newest Hour, VO2/kilogram, and you may cousin O2 heartbeat inside AF people immediately following split up into several groups according to O2 heartbeat trend proportion.
AF, atrial fibrillation; cSR, heart rate-matched controls with sinus rhythm; HR, heart rate; VO2, oxygen uptake; Rest, average of 4 min of rest; Wu; average of 3–4 min after exercise commenced; AT, anaerobic threshold; RC, respiratory compensation point; Peak, exercise peak.
Characteristics of AF patients after they were divided into two groups according to O2 pulse trend ratio calculated by O2 pulse at Peak/O2 pulse at AT (median = 1.1).
N, number of patients; AF, atrial fibrillation; BMI, body mass index; CAD, coronary artery disease; RAS, renin–angiotensin system; Rest, average of 4 min of rest; AT, anaerobic threshold; Peak, exercise peak; VO2, oxygen uptake; %AT; percent-predicted VO2/kg at AT; %Peak; percent-predicted VO2/kg at Peak; VE/VCO2 slope; the minute ventilation/carbon dioxide production relation slope; HRR, heart rate reserve; %HRR, percentage of heart rate reserve; Hb, hemoglobin; BNP, brain natriuretic peptide; LVEF, left ventricular ejection fraction; LVDd, left ventricular end-diastolic diameter; LVDs, left ventricular end-systolic diameter; LAD, left atrial dimension; RVSP, right ventricular systolic pressure. Data are presented as the mean ± SD or number of patients.
We compared the contributions of the HR change (from Rest to Peak/from Rest to AT/from AT to Peak) during exercise on the value of O2 pulse trend ratio (= O2 pulse at Peak/O2 pulse at AT) between the AF and cSR groups ( Fig. 4 ). There was a significant inverse-correlation between the HR change and the O2 pulse trend ratio in AF patients, whereas the association was comparatively weak in the cSR group. These inverse correlations between O2 pulse trend ratio and the HR change from Rest to Peak as well as those from AT to Peak were significantly different by Z-score analysis between AF and cSR groups.
Correlative relationships between the O2 pulse trend ratio (O2 pulse at Peak/O2 pulse at AT) and HR change from Rest to Peak, Rest to AT and AT to Peak.
The exercise capacity of AF patients is greatly affected by the HR response. In the present study, we identified HR-matched controls with SR who had a similar HR trend to AF patients during exercise and, we demonstrated that the value of VO2/kg is significantly lower in AF patients above the AT level. This study ultimately suggests that exercise impairment in the setting of AF is developed above the exercise level of the AT point after standardization of HR [14,15]. The results of this study show that adverse effects on the hemodynamics due to AF become apparent with a load exceeding the AT level. Regarding the hemodynamic derangement of AF, rhythm irregularity and loss of atrial contribution to LV filling impair cardiac output in AF patients . Exercise capacities in AF patients have been shown to be impaired by multiple pathways, such as endothelial dysfunction or neurohumoral factors [16,17]. In addition, hemodynamic effects derived from AF change according to the exercise level.