Cardiac magnetic resonance is the gold standard for evaluating the global or local myocardial function. The 3D echocardiography correlates well with cardiac magnetic resonance in measuring myocardial strain.In addition, it has the advantage of being more sensitive, easier to handle, and cheaper [6, 11]. Torrent-Guasp et al.  found that various arrangements of myocardial fibers in anatomy determine the form of myocardial movement in different directions corresponds to GLS,GRS,GCS and GAS.. Previous studies have confirmed that patients with OSA or obesity generally exhibit impaired LV diastolic function with normal LVEF values, which can reliably reflect the normal systolic function of the left ventricle. In our study we found that OSA patients' left ventricular strain was worse than the control group. Within the OSA group, the GLS of obese patients was significantly damaged compared to the non-obese patients. Consistent with the results of previous studies, the impaired LV myocardial strain observed in our study points out that though the LV ejection fraction is still normal, subclinical LV systolic insufficiency is already developing in patients with OSA. In addition, we found that the subclinical left ventricular systolic function was more significantly impaired in OSA patients who also suffered from obesity.
Studies have shown that OSA increases the risk of hypertension, arrhythmia, coronary heart disease, and heart failure. The ARIC-SHHS study showed that residents with OSA already had subclinical myocardial damage without any discernible cardiovascular and cerebrovascular diseases.Recurrent apnea and hypoxemia at night in OSA patients result in sympathetic hyperactivity and decreased parasympathetic excitability. This results in oxidative stress, systemic inflammation, and vascular endothelial dysfunction that leads to insulin resistance, abnormal lipolysis, and myocardial metabolic disorders. The significantly higher values of the biochemical parameters in the OSA group compared to the control and that of the OSA obese group compared to the non-obese measured in the present study reflect severe metabolic abnormalities and systemic inflammatory in OSA patients, particularly in those with obesity.
The OSA is also accompanied by cardiac hypertrophy and myocardial fibrosis, which are essential in myocardial remodeling. The elevated blood pressure level in patients with OSA increases the left ventricular afterload. Hypoxia and carbon dioxide retention exaggerate swings in intrathoracic pressure during the obstructive episode, which leads to an increase in return blood volume and left ventricular preload. At the molecular level, the contraction and relaxation of the heart are highly energy-dependent, 90% of which is provided by the oxidative phosphorylation in mitochondria. Intermittent hypoxia can lead to mitochondrial DNA dysfunction, mutation, or reduction, which results in cardiac insufficiency. In our study, the left ventricular strain was significantly damaged in moderate to severe OSA compared to the normal subjects. The larger the AHI, the more powerful is the strain damage. The underlying mechanism leading to cardiac insufficiency in OSA obese patients may be the aggravated oxidative stress and mitochondrial dysfunction due to apnea and hypoxemia.
In this study, the left ventricular global longitudinal strain was worse in obese OSA than non-obese OSA patients, and the higher the BMI, the more severe the damage to the left ventricular strain was. Studies have shown that the risk association between obesity and cardiovascular disease is independent of other factors like hypertension, diabetes, and hyperlipidemia, and so on. The duration and severity of obesity have been recognized as important determinants of the development of heart failure. Large-scale clinical trials and basic experiments have proved that obesity leads to left ventricular hypertrophy, left atrium volume increase, and diastolic dysfunction.. Although the left ventricular ejection fraction tends to be normal in obese patients, several speckle-tracking echocardiography studies have shown that the radial or longitudinal strain is impaired in asymptomatic obese patients, both children and adults. In the heart of obese people, there is an accumulation of intracellular triglycerides and lipids. The myocardial substrate selection due to obesity favors fatty acid oxidation, leading to lipotoxicity and myocardial dysfunction[22, 23]. The thickening of epicardial adipose tissue (EAT) leads to excessive activation of macrophages, releasing pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6. This results in activated pro-inflammatory signaling pathways that further aggravates organ dysfunction. In addition, the activation of the renin-angiotensin-aldosterone system with stimulation of the sympathetic nervous system in obese patients increases left ventricular afterload even in normotensive-obese patients, leading to cardiac remodeling and myocardial fibrosis.
Our study shows that the LV strain is associated with the degree of insulin resistance in addition to OSA and obesity. Previous studies have shown that insulin resistance is one of the major causes of myocardial injury, and both obesity and OSA can cause subclinical myocardial dysfunction by insulin resistance. The degree of OSA correlates with the severity of insulin resistance. Intermittent hypoxemia and oxidative stress in OSA patients have been critical factors leading to insulin resistance. It has been suggested that ATP synthesis in pancreatic islet β cells and inhibit insulin secretion is affected by hypoxemia. In addition, it reduces the phosphorylation of insulin receptor tyrosine kinases and thereby reduces the effects and sensitivity of the insulin receptors, resulting in insulin resistance. A high HOMA-IR index is one of the characteristics of metabolic disorders in obese patients. Insulin resistance increases cardiac toxicity by altering myocardial metabolism. The toxicity and the increased release of insulin-related growth factors activate the sympathetic and RAAS systems that result in myocardial remodeling. Studies have shown that hyperinsulinemia can further deteriorate myocardial structure in patients suffering from heart failure with preserved ejection fraction (HFpEF). In addition, insulin resistance is independently associated with impaired GLS, leading to LV hypertrophy and damaged myocardial function over time.
Various mechanisms closely related to obesity, such as insulin resistance, oxidative stress, systemic inflammation, visceral fat accumulation, and dyslipidemia, may also occur as OSA-associated manifestations. Obesity and OSAS interlink mutually and exist as complex, interleaved vicious cycles. This eventually leads to overlapping and potential effects of organ crosstalk. It is widely known that both obesity and OSAS can independently lead to cardiovascular complications. Our study further elucidates that the coexistence of obesity and OSA might have a synergistic effect on myocardial strain compared to the presence of OSA alone. In patients with OSA, if combined with obesity, the myocardial strain damage will be further exacerbated. This is also valid for obese patients sufferingfrom sleep apnea.As discussed previously, although obesity contributes to the development of cardiac insufficiency through several mechanisms, many of them also overlap with those of OSA. Obesity is also characterized by an increase in systemic blood volume and cardiac output, unlike OSA, which alters hemodynamics, increasing LV pressure and volume, and changes the strain of the myocardium. Obesity tends to coexist with OSA. And based on 3DSTE results of this study, it might be suggested that OSA and obesity have a superimposed effect on the early impairment of left ventricular systolic function. Therefore, for the treatment of OSA and improving the cardiovascular prognosis, it is crucial to focus on the treatment and the weight management of OSA patients.