[A retrospective controlled study on the treatment effect of distraction osteogenesis and maxillomandibular advancement for severe obstructive sleep apnea hypopnea syndrome patients].

Objective: To compare the treatment effect of distraction osteogenesis (DO) and maxillomandibular advancement (MMA) for severe obstructive sleep apnea hypopnea syndrome (OSAHS) patients and to guide clinical decisions about treatment of OSAHS. Methods: Thirty-seven OSAHS patients which accepted maxillomandibular advancement (MMA) or distraction osteogenesis (DO) in Stomatological Hospital of the Department of Maxillofacial Trauma and Orthognathic Surgery, School of Stomatology, The Forth Military Medical University from June 2017 to June 2019 were collected. Their preoperative and postoperative data of cephalometry, polysomnography (PSG), Pittsburgh sleep quality index (PSQI) and Epworth sleepiness scale (ESS) scores were collected and analyzed. With propensity score matching method, the treatment effect of MMA and DO was analyzed and compared. Results: According to the statistics of MMA group, only AHI was correlated with operative successful rate and cure rate. With the increase of AHI, the treatment effect of MMA on OSAHS patients gradually decreased. The cut-off point of AHI as a predictor of MMA treatment failure was 78.2 n/h. All the matched cases were severe OSAHS patients. Statistical analysis showed that the mandibular elongation of DO patients[(24.00±4.39) mm] was significantly more than that of MMA group [(11.20±1.37) mm] (t=-6.11, P<0.001), the improvement of PSG index [including lowest oxygen saturation (LSpO2), longest apnea (LA) and longest hypopnea (LH)] in DO group [LSpO2=(93.40±1.82)%; LA=(18.28±8.32) s; LH=(61.84±32.94) s] was significantly higher than that in the MMA group [LSpO2=(86.00±4.06)%, LA=(64.08±21.78) s, LH=(172.40±30.70) s](t=-3.72, P=0.005; t=4.39, P=0.003; t=5.49, P=0.004). The PSQI and the ESS scores of DO group (PSQI=4.20±0.83; ESS=3.40±1.52) were also significantly better than that of MMA group (PSQI=8.80±2.39, ESS=9.40±2.88)(t=4.07, P=0.001; t=4.12, P=0.002). Conclusions: For severe OSAHS patients, the objective and subjective indicators of DO treatment group showed a better therapeutic effect than that of MMA.

Physical training alters the pathogenesis of pacing-induced heart failure through endothelium-mediated mechanisms in awake dogs.

BACKGROUND: Beneficial effects of exercise training on cardiovascular function in chronic heart failure (CHF) have been suggested previously, but the underlying mechanisms are unknown. We tested whether daily exercise training improves systemic hemodynamics and preserves endothelium-mediated vasodilator function during development of heart failure. METHODS AND RESULTS: Fifteen dogs were surgically instrumented for hemodynamic measurements. One group of dogs underwent 4 weeks of cardiac pacing (210 bpm for 3 weeks and 240 bpm during week 4), and another group underwent pacing plus daily exercise training (4.4+/-0.3 km/h, 2 h/d). Pacing-alone dogs developed CHF characterized by typical hemodynamic abnormalities, blunted endothelium-mediated vasodilator function in coronary and femoral circulations, and decreased gene expression of endothelial constitutive nitric oxide synthase (ECNOS, normalized to GAPDH expression; normal, 1.15+/-0.31 versus CHF, 0.29+/-0.08, P<.05). Exercise training preserved normal hemodynamics at rest, endothelium-mediated vasodilator function, and gene expression of ECNOS (0.72+/-0.16 versus normal, P=NS). Inhibition of NO synthesis (nitro-L-arginine) in exercise-trained dogs abolished the preserved endothelium-mediated vasodilation of epicardial coronary arteries and elevated left ventricular end-diastolic pressure (7.7+/-0.3 to 19+/-3.4 mm Hg, P<.05), suggesting that the preservation of resting hemodynamics was in large part due to preserved endothelial function concealing the underlying CHF state. CONCLUSIONS: Long-term exercise training altered the natural history of heart failure due to rapid cardiac pacing. One of the underlying mechanisms is through the preservation of endothelial vasodilator function.

Relationship between left ventricular end-diastolic compliance and abnormal Doppler mitral filling in patients with coronary artery disease.

Left ventricular end-diastolic compliance (LVEDC) and transmitral flow velocities were measured in 19 patients with coronary artery disease associated with hypertension and 10 normal subjects by LV catheterization and pulsed-Doppler echocardiography. LVEDC was much lower in the patient than in the normal subjects (P less than 0.01). The data showed that abnormal Doppler diastolic function such as elevated late diastolic peak flow velocity (PVA) and decreased LVEDC occurred in the patients at the same time. In addition, the negative correlation of PVA with LVEDC observed in normal controls but not in patients suggested that in patients with impaired diastolic filling, factors other than the decreased LVEDC itself must also participate in the development of diastolic dysfunction.

[Characteristics of left ventricular diastolic function in patients with hypertension].

Left ventricular (LV) diastolic filling was examined by Doppler echocardiography in 239 patients with essential hypertension and 100 normal subjects. The Doppler study showed an inverse correlation between age and early diastolic peak velocity (PVE, r-0.201, P less than 0.05) [and a positive correlation between age and late diastolic peak velocity (PVA, r = 0.202, P less than 0.05) in normal subjects. Isovolumic relaxation time and late diastolic filling time were prolonged, PVA, A/E and Ai elevated, PVE, E/A and Ei/Ai as well as total filling time decreased in patients with hypertension as compared with the values found in the normal subjects (P less than 0.05 to 0.01). The results showed definite impairement of LV diastolic function in hypertensive patients. PVA correlated positively with systolic blood pressure (r = 0.68, P less than 0.01) and modestly with left atrial dimension in the hypertensives. No significant differences were found in FS and EF between the two study populations, indicating that LV filling abnormalities may occur early in patients with hypertension, even at a time when systolic performance has not yet been affected.