The present study analyzed the relationship between AHR and in-hospital mortality in patients with AECOPD and RF admitted to a hospital ward. AHR was found to be independently associated with in-hospital mortality. Furthermore, a non-linear relationship was observed in restricted cubic spline analysis of the association between AHR and in-hospital mortality in our study population, indicating an inflection point at approximately 100 beats/min. For AHR ≥ 100 beats/min, we found that each 1 beat/min increase in AHR corresponded with an increase in risk for in-hospital death by 10%. In addition, there were no significant differences of survival among the patients with heart rate < 100 beats/min.
Many studies have shown that increased resting heart rate is a major risk factor for cardiovascular disease [20, 21] and is associated with cardiovascular and all-cause mortality[22–24]. It has been reported that there are more cardiovascular events in patients with non-ST-segment elevation acute coronary syndrome at a high heart rate[25]. A study showed that a heart rate ≥ 120 beats/min risk factors associated with in-hospital death from coronavirus disease 2019[26]. Heart rate is an independent predictor of in-hospital death in patients with intermediate- to high-risk acute pulmonary embolism [27]. Therefore, heart rate has been confirmed as an important determinant of adverse events in patients with cardiovascular disease [28]. Chen et al. indicated that an AHR > 90 beats/min was an independent predictor of short-and long-term mortality in patients with acute aortic dissection [29]. Okuno et al. found that AHR was a determinant of the effectiveness of beta-blockers in patients with acute myocardial infarction[30]; however, the association between AHR and in-hospital mortality of patients with combined AECOPD and RF was unclear.
AECOPD considerably affects disease progression, worsens pulmonary function, increases the risk for further exacerbation and death, and impairs quality of life[31, 32]. Studies have reported that the in-hospital mortality rate for AECOPD is 4.8–10.4% [33]. Morasert et al. indicated that respiratory failure on admission was a prognostic indicator of in-hospital mortality in patients with AECOPD [34]. Simultaneously, patients may have a negative impact on the short term survival, who had an obvious respiratory failure [35]. Many studies have probed the risk factors associated with mortality in patients with AECOPD, to date, it is known that RR, BUN, blood gas analysis (Hb, PCO2), ALB are inflammation-related indicators, are important prognostic factors for mortality in these patients[36], and our results are consistent with these results. Combined with clinical practice, we hypothesize that AHR may be associated with in-hospital mortality in patients with AECOPD and RF, although no relevant study has focused on the association between them. The present study investigated the association between AHR and in-hospital mortality in AECOPD patients with RF who were admitted to hospital and found a significant association. An AHR of 100 beats/min was identified through a two-piecewise linear regression model; as such, results of this study may be helpful for respiratory physicians to select appropriate medical and interventional measures according to AHR.
The exact mechanisms underlying the relationship between AHR and clinical outcomes in AECOPD patients with RF are not well known, although potential explanations include the following. Sympathy-vagal imbalance, with autonomic dysfunction in COPD, may be the main factor for elevated heart rate [37]. Rapid heart rate may be a risk marker of autonomic imbalance, which may directly promote myocardial ischemia or heighten the potential for arrhythmias or sudden death [38]. Particulate matter in polluted air and cigarette smoke have been reported to be associated with autonomic dysfunction [39, 40]. Furthermore, nicotine in cigarette smoke can increase sympathetic activity[41]. Another reason for autonomic dysfunction could be chronic hypoxemia. Simultaneously, autonomic dysfunction has been associated with arrhythmia and sudden cardiac death [42]. Compensation for elevated heart rate may be caused by the mechanical effects of obstruction and hyperinflation on cardiac filling, which may be an important factor [43, 44].
Our study had several strengths. The data demonstrated that AHR may be used as an easily obtained risk marker to predict the prognosis of patients with AECOPD and RF. Furthermore, AHR is a convenient indicator for identifying high-risk AECOPD in patients with RF and can help physicians assess the state of illness.
However, the present study also had some limitations, the first of which was its retrospective design and that we could not obtain all baseline characteristics. Second, we could not assess whether the excluded patients had an impact on the results of this study. We did not collect data regarding other factors associated with AECOPD/RF mortality, including lung function, long-term oxygen treatment, and body mass index. We also did not collect data regarding the use of β-blocker(s), which may affect heart rate. Third, our investigation was a single-center study, and the sample size was small; therefore, we cannot rule out the possibility of selection bias. Finally, heart rates in these patients were evaluated only on admission, and no dynamic analyses of the association between heart rates over time and patients with AECOPD/RF were performed. As such, future studies should be designed to address these limitations in an effort to validate and expand on our results.