Discussion
arrhythmia, heart disease, LV myocardial, hypoxia, inflammation, OSA, Hypoxemia, hypoxemia, heart failure, endothelial dysfunction
ARRHYTHMIA, HEART DISEASE, HYPOXIA, INFLAMMATION, PATHOPHYSIOLOGY, HYPOXIC, HEART FAILURE, MYOCARDIAL DYSFUNCTION, WASTED, OXIDATIVE STRESS, CORONARY HEART DISEASE, ENDOTHELIAL DYSFUNCTION
This randomized, sham-controlled clinical trial demonstrated the association between hypoxemia severity and myocardial work using the LV P-S loop and assessed the benefits of CPAP therapy in patients with severe OSA. The key findings were as follows: (1) in patients with severe OSA, the severity of hypoxemia was more closely associated with myocardial performance than the most commonly used OSA metric, AHI; (2) CPAP treatment for 3 months improved LV myocardial performance by decreasing LV wasted work and increasing work efficacy; (3) GWW increased and GWE decreased during exercise in patients with severe OSA, and CPAP treatment reduced GWW and increased GWE in these patients.Hypoxemia leads to hypoxia, which causes endothelial dysfunction by causing oxidative stress and inflammation in endothelial cells and mitochondria by altering various intracellular moleculesAHI is the most commonly used index for diagnosis and determining OSA severity (mild: 5–14/h, moderate: 15–29/h, severe: > 30/h)Combined ventricular systolic and arterial stiffening is considered to be an important factor in the pathophysiology of heart failure with preserved ejection fractionFew studies have evaluated myocardial work during exercise stress echocardiography in healthy populations. In the healthy control individuals in these studies, GWI, GCW, and GWW increased, but there was no change in GWEThis study had some limitations. First is the innate limitation of the method  used for calculating myocardial work. Myocardial work was calculated assuming that peripheral blood pressure values were equal to central blood pressure and the myocardial strain was equal to volume change. Second, patients with structural heart disease, coronary heart disease, arrhythmia, and uncontrolled BP were excluded. It is not easy to generalize our results across all populations or clinical situations. However, we found that CPAP treatment improved LV mechanics even in patients with subclinical myocardial dysfunction. Third, since the effect of CPAP treatment was compared over a relatively short period of 3 months, the long-term effects are unknown. However, importantly, CPAP therapy improved myocardial performance, even over the short study period. Fourth, the study population was small. Thus, further studies are needed to verify the results using a greater number of patients. However, given the difficulty of conducting a randomized sham-controlled trial of CPAP on a large number of patients, the results of this study are still valuable. Finally, no comparison was made with a healthy population. Therefore, it is difficult to generalize the value of myocardial work in this study to the characteristics of patients with OSA. Nevertheless, this study is meaningful as it confirmed the correlation between the severity of hypoxemia and LV performance using myocardial work in patients with severe OSA.In conclusion, indices of hypoxic burden are more closely associated with myocardial performance than AHI in patients with severe OSA. 3-months CPAP treatment improved LV myocardial performance by decreasing LV wasted work and increasing work efficacy compared to the sham treatment.