In this prospective cohort of 123 patients who underwent OPCABG, the prevalence of OSA was 42.3%. AHI, the criteria for severity of OSA, has limitations in predicting the prognosis of OPCABG. Hs-CRP level was closely related to the severity of OSA, and it independently correlated with POAF, duration of hospitalization and hospital cost.
OSA is closely related to CHD. A study showed that the prevalence of CHD in patients with OSA was 16.2% and that of patients without OSA was 5.4% ; in a population with suspected CHD, the proportion of patients with moderate-severe OSA was 24%, four times higher than the prevalence in the normal population . In the present study, we found that the proportion of patients with moderate-severe OSA was significantly higher than that of the previous study. Patients undergoing OPCABG with severe coronary artery disease were included in this study, which potentially indicated that OSA was a substantial risk factor for CHD.
CABG is the standard of care for patients with extensive CHD. Few studies showed that OSA might affect the prognosis of patients undergoing CABG. Uchôa et al. found that OSA significantly increased the long-term incidence of MACCEs (follow-up time of 4.5 years), revascularization rate, the proportion of angina attacks, and AF incidence in patients with CABG; however, there was no significant effect on the 30-day prognosis after CABG . Another study found that AHI was an independent risk factor for increased duration of hospitalization and postoperative circulatory fluctuation in patients with CABG . In contrast, we found no significant difference in postoperative indicators between the moderate-severe OSA and absent-mild OSA groups. The possible reason for the discrepancy was that all patients included in our study underwent OPCABG, avoiding the effects of extracorporeal circulation, shortening the postoperative recovery cycle, which in turn reduced the short-term effect of OSA.
Evidence to identify the effect of OSA on the prognosis of OPCABG only using OSA classification is insufficient. OSA may affect the clinical outcome of CABG by influencing other indicators. For example, our previous study found that OSA might further affect the perioperative indicators such as the cardiac function . In addition, biomarkers related to OSA and CHD may also be examined to predict more accurately the effect of OSA on CABG.
CRP is an acute phase reaction protein. Repeated hypoxia and inadequate ventilation in OSA could trigger oxidative stress and systemic inflammatory response, which could in turn enhance the synthesis and release of CRP . Shamsuzzaman et al. showed that CRP has a significant linear correlation with AHI and is an independent influencing factor for OSA severity . Moreover, inflammatory responses play key roles in the development of atherosclerosis. CRP, the product and mediator of inflammatory responses in atherosclerosis, is an important marker of endothelial dysfunction. Elevated CRP levels have been shown to be an independent risk factor for diseases such as myocardial infarction, peripheral vascular disease, and stroke . Han et al. found that high CRP levels related to acute renal function injury, all-cause death, duration of hospitalization, and ICU stay after CABG .
Compared with the CRP, Hs-CRP extends the detection linear range from 3–200 to 0.005–0.10 mg/L, thereby making the determination of low-concentration CRP more accurate. Moreover, Hs-CRP has a long half-life, with no diurnal difference and no sex- or age-dependence and has a higher value in predicting the prognosis of cardiovascular and cerebrovascular diseases . Previous studies have shown a relationship between Hs-CRP levels and OSA, nevertheless, these results are controversial because of obesity and various confounding factors . In our study, we found that the Hs-CRP level was significantly increased in the moderate-severe OSA group, and there were significant correlations between Hs-CRP level and severity of OSA after adjusting sex, age, and BMI.
Hs-CRP plays an important role in predicting the prognosis of cardiovascular disease; nevertheless, only one report on the early effect of Hs-CRP on OPCABG has been conducted . In the present study, we found that elevated Hs-CRP levels were significantly associated with increased AF incidence and duration of hospitalization. Our results also demonstrated that AF incidence, duration of hospitalization, and hospital costs were significantly higher in the elevated Hs-CRP group than in the normal group after OPCABG. Further regression analysis showed that Hs-CRP level was an independent risk factor for POAF and was independently correlated with the duration of hospitalization and hospital cost.
In addition, stability of respiratory regulation is an important factor in determining OSA severity . Compared with the normal population, patients with OSA had significantly reduced respiratory center responses to low PO2 and high PCO2 during sleep, and the respiratory center response of some patients was also suppressed during wakefulness. Moreover, patients with OSA have long durations of apnea at night with short intervals. While hyperventilation occurs at the end of an apneic event, it is insufficient to clear the accumulated CO2, thereby resulting in hypercapnia or even type II respiratory failure. In this study, we found that the periods of apnea were significantly longer and the PCO2 level was significantly higher in the moderate-severe OSA group than in the absent-mild OSA group when awake. Further study involving the change in PCO2 and internal environment is needed.
In this sudy, the preoperative LVEF of patients with moderate-severe OSA was significantly lower than that of patients with absent-mild OSA. Previous studies also found that LVEF was independently related to moderate-severe OSA. The main mechanisms by which OSA affects cardiac function may be as follows [19, 20]: first, each respiratory obstruction event could result in an intrathoracic negative pressure of 60–70 cm H2O, and hypoxia could cause pulmonary vasoconstriction, resulting in preload and afterload imbalance between the left and right ventricles; subsequently, myocardial oxygen consumption increases and myocardial ischemia occurs, which in turn alters cardiac function; second, the long-term repeated fluctuation of intrathoracic pressure could increase intraglomerular pressure variability, leading to impaired cardiac function; and finally, sympathetic hyperactivity affects all-day cardiopulmonary hemodynamics. In addition, hypopharyngeal edema due to decreased cardiac function could also promote the development of OSA.
CPAP remains the standard of care for patients with OSA, and evidence has revealed that it is correlated with a reduced inflammatory response . Studies have confirmed that CPAP might result in decreased risk of repeat revascularization and cardiac death of patients with OSA after percutaneous coronary intervention (PCI) [22, 23]. However, we know little about the role of CPAP in improving prognosis of CABG. In consideration of our previous clinical practice, patient compliance and timing of CPAP treatment after CABG might be the key to curative effects. Additional trials evaluating the effects of CPAP in patients with OSA who underwent CABG are warranted.
Our study has the following limitations: first, it is a single-center study with a limited sample size; the results need to be validated using multi-center, large-sample studies. Second, we were unable to use polysomnography (PSG), which appears to offer a more accurate evaluation of OSA than does PG. In addition, PG may underestimate the OSA severity. PSG requires patients to sleep at the sleep center for more than 8 h. The sleep center in our hospital has not been provided with urgent response equipment and medical teams for patients with heart disease. All of our patients had severe coronary artery disease and were consequently at a high risk of emergent cardiac events. Therefore, we decided to use a portable PG monitor so that we could keep our patients in the cardiac surgery department for the assessment of OSA. Finally, we only analyzed Hs-CRP levels at one time point; thus, it remains unclear as to whether Hs-CRP level has the same predictive value at other time points.