Obstructive sleep apnea (OSA) is a common sleep disorder that is closely associated with ocular fundus diseases such as glaucomatous optic neuropathy, nonarteritic anterior ischemic optic neuropathy, diabetic retinopathy, central serous chorioretinopathy and retinal vein occlusion.The main mechanisms by which OSA affects fundus diseases include intermittent hypoxia, activation of sympathetic nervous system, systemic oxidative stress, and inflammatory response, but the specific mechanisms require further investigation.The therapeutic modality such as continuous positive airway pressure can alleviate the symptoms of ocular fundus diseases in the patients with OSA and reduce the risk of disease progression.Therefore, clinicians should recognize the relationship between OSA and fundus diseases, understand the impact of OSA on these diseases, and achieve early diagnosis and treatment of the OSA-associated fundus diseases to reduce the risk of severe visual impairment and blindness.

Obstructive sleep apnea (OSA) is a common sleep disorder that is closely associated with ocular fundus diseases such as glaucomatous optic neuropathy, nonarteritic anterior ischemic optic neuropathy, diabetic retinopathy, central serous chorioretinopathy and retinal vein occlusion.The main mechanisms by which OSA affects fundus diseases include intermittent hypoxia, activation of sympathetic nervous system, systemic oxidative stress, and inflammatory response, but the specific mechanisms require further investigation.The therapeutic modality such as continuous positive airway pressure can alleviate the symptoms of ocular fundus diseases in the patients with OSA and reduce the risk of disease progression.Therefore, clinicians should recognize the relationship between OSA and fundus diseases, understand the impact of OSA on these diseases, and achieve early diagnosis and treatment of the OSA-associated fundus diseases to reduce the risk of severe visual impairment and blindness.

Objective:To analyze the electrocardiographic characteristics of patients with chronic pulmonary artery stenosis (PAS), and to explore their relationship with disease severity indicators.Methods:The study was a retrospective case-series analysis. Patients with chronic PAS admitted to Gansu Provincial Hospital from January 2018 to July 2021 were enrolled. The clinical data and the results of electrocardiography, transthoracic echocardiography, right cardiac catheterization, N-terminal B-type natriuretic peptide (NT-proBNP) measurement and 6-min walking distance test of patients were analyzed. The linear regression model or logistic regression model was used to analyze the relationship between electrocardiographic characteristics and the disease severity in patients with chronic PAS.Results:Sixty-three patients aged (62.1±9.7) years including 43 females (68.3%) were enrolled in the study. Among them, 62 patients (98.4%) had (R 1+S Ⅲ)-(S Ⅰ+R Ⅲ)<1.5 mV, and no patients had V 5lead R: S ratio to V 1 lead R: S<0.04 and V 6 lead R: S ratio<0.4. There were 55 patients (87.3%), with flat or inverted T-waves in V 1, and 10 patients (15.9%) with flat or inverted T-waves in all precordial leads (V 1-V 6). There were 18 patients (28.6%) with flat or inverted T-waves in inferior leads (Ⅱ, Ⅲ, aVF). Multiple liner regression analysis showed that Max R V1, 2+Max S I, aVL-S V1 combined with the number of flat or inverted T-waves in limb leads was independently correlated with atrial area ( R2=0.290, P=0.002); R V1+S V5 was independently correlated with right ventricular area ( R2=0.257, P=0.001); R peak V 1 combined with the number of flat or inverted T waves in precordial leads was independently correlated with tricuspid annular plane systolic excursion ( R2=0.407, P<0.001); (R 1+S Ⅲ)-(S Ⅰ+R Ⅲ) combined with the number of flat or inverted T waves in precordial leads was independently correlated with NT-proBNP ( R2=0.504, P<0.001); Max R V1, 2+Max S I, aVL-S V1 were independently correlated with right atrial pressure ( R2=0.803, P=0.036); (R 1+S Ⅲ)-(S Ⅰ+R Ⅲ) were independently correlated with mean pulmonary artery pressure ( R2=0.302, P<0.001); R aVRcombined with the number of flat or inverted T-waves in precordial leads was independently correlated with cardiac index ( R2=0.173, P=0.003); (R 1+S Ⅲ)-(S Ⅰ+R Ⅲ) was independently correlated with pulmonary vascular resistance ( R2=0.173, P=0.002); R peak V 1 combined with the number of flat or inverted T-waves in precordial leads was independently correlated with mixed vein oxygen saturation ( R2=0.302, P<0.001). Conclusion:The vast majority of patients with chronic PAS have (R 1+S Ⅲ)-(S Ⅰ+R Ⅲ)<1.5 mV and flat or inverted T-wave in V 1 lead, and some characteristic electrocardiographic manifestations are correlated with indicators of disease severity.

Pulmonary vein stenosis (PVS) is an extremely rare and lethal disease caused by multiple etiologies. PVS has a bimodal distribution in the population, affecting children and adults. Congenital PVS is the usual PVS type in children, which sometimes develops after cardiothoracic surgery. Acquired PVS, in turn, is the most common PVS type in adults. A review of the relevant literature has shown that PVS after radiofrequency ablation of atrial fibrillation is the most common, as well as that caused by compression of proliferative fibrous tissues or tumor in the mediastinum (eg, PVS caused by fibrosing mediastinitis, lung tumors, metastases, etc). This article provides a comprehensive review of PVS in terms of embryology and anatomy, etiology and triggers, classification, clinical symptoms and signs, treatment, and prognosis, intending to promote the understanding and treatment of this disease.

Chronic pulmonary artery stenosis (CPAS) is characterized by a reduction or complete obstruction of the cross-sectional area of the pulmonary artery owing to various causes. The condition exhibits similar pathophysiological progress, leading to pulmonary hypertension (PH), reduced physical endurance, right heart failure, and death. Although CPAS is often regarded as a subgroup of PH, it can manifest independently for an extended duration before the onset of PH and can significantly impact patient quality of life. It may therefore be more appropriate to consider PH as pathophysiological progression of CPAS, thereby recognizing CPAS as a distinct disease entity.

Pulmonary vein stenosis (PVS) is an extremely rare and lethal disease caused by multiple etiologies. PVS has a bimodal distribution in the population, affecting children and adults. Congenital PVS is the usual PVS type in children, which sometimes develops after cardiothoracic surgery. Acquired PVS, in turn, is the most common PVS type in adults. A review of the relevant literature has shown that PVS after radiofrequency ablation of atrial fibrillation is the most common, as well as that caused by compression of proliferative fibrous tissues or tumor in the mediastinum (eg, PVS caused by fibrosing mediastinitis, lung tumors, metastases, etc). This article provides a comprehensive review of PVS in terms of embryology and anatomy, etiology and triggers, classification, clinical symptoms and signs, treatment, and prognosis, intending to promote the understanding and treatment of this disease.

Chronic pulmonary artery stenosis (CPAS) is characterized by a reduction or complete obstruction of the cross-sectional area of the pulmonary artery owing to various causes. The condition exhibits similar pathophysiological progress, leading to pulmonary hypertension (PH), reduced physical endurance, right heart failure, and death. Although CPAS is often regarded as a subgroup of PH, it can manifest independently for an extended duration before the onset of PH and can significantly impact patient quality of life. It may therefore be more appropriate to consider PH as pathophysiological progression of CPAS, thereby recognizing CPAS as a distinct disease entity.

Objective: To evaluate the feasibility and safety percutaneous pulmonary vein intervention in patients with severe pulmonary vein stenosis (PVS) caused by fibrosing mediastinitis(FM). Methods: This retrospective analysis included 5 FM patients (2 male, 3 female, 54-77 years old) confirmed by clinical presentation and chest computed tomography (CT) scan from January to June 2018 who were from Gansu Provincial Hospital and Shanghai Chest Hospital. CT pulmonary angiography (CTPA) further revealed severe PVS caused by fibrotic tissue compression in mediastinum. After selective pulmonary vein angiography, gradually balloon angioplasty was used to expand the pulmonary vein and then stents were implanted in the pre-dilated stenotic pulmonary veins. Evaluation of therapeutic effect was made at 6 months after the procedure. Results: All of 11 serious compression PVS were treated with stent implantation (diameter: 7-10 mm, length: 17-27 mm). After stenting, degree of pulmonary vein stenosis decreased from (83±16)% to (12±4)% (P<0.01). The minimal diameter of the stenotic pulmonary vein was significantly increased from (0.8±0.5)mm to (7.5±0.8)mm (P<0.01). Trans-stenotic gradient decreased from (27.0±15.1)mmHg (1 mmHg=0.133 kPa) to (2.50±0.58)mmHg (P<0.05). Mean pulmonary pressure measured by cardiac catheter decreased from (45.0±9.0)mmHg to (38.7±8.4)mmHg (P<0.05). One patient experienced cardiac arrest due to vagal nerve reflex during big sizing balloon stent dilation and recovered after cardiopulmonary resuscitation. There were no other serious procedure related complications. During the follow-up, severe stenosis at end of proximal stent was evidenced in 1 patient due to fibrotic compression, and another patient developed in-stent thrombosis due to discontinuation of prescribed anticoagulant. Conclusion Percutaneous intervention for severe pulmonary vein stenosis caused by FM is feasible and safe, and can improve hemodynamic caused by the compression of mediastinal vascular structures in these carefully selected patients.

Objective To evaluate the feasibility and safety percutaneous pulmonary vein intervention in patients with severe pulmonary vein stenosis (PVS) caused by fibrosing mediastinitis(FM). Methods This retrospective analysis included 5 FM patients (2 male, 3 female, 54-77 years old) confirmed by clinical presentation and chest computed tomography (CT) scan from January to June 2018 who were from Gansu Provincial Hospital and Shanghai Chest Hospital. CT pulmonary angiography (CTPA) further revealed severe PVS caused by fibrotic tissue compression in mediastinum. After selective pulmonary vein angiography, gradually balloon angioplasty was used to expand the pulmonary vein and then stents were implanted in the pre?dilated stenotic pulmonary veins. Evaluation of therapeutic effect was made at 6 months after the procedure. Results All of 11 serious compression PVS were treated with stent implantation (diameter: 7-10 mm, length: 17-27 mm). After stenting, degree of pulmonary vein stenosis decreased from (83 ± 16)% to (12 ± 4)% (P<0.01). The minimal diameter of the stenotic pulmonary vein was significantly increased from (0.8±0.5)mm to (7.5±0.8)mm (P<0.01). Trans?stenotic gradient decreased from (27.0±15.1) mmHg (1 mmHg=0.133 kPa) to (2.50±0.58)mmHg (P<0.05). Mean pulmonary pressure measured by cardiac catheter decreased from (45.0 ± 9.0)mmHg to (38.7 ± 8.4)mmHg (P<0.05). One patient experienced cardiac arrest due to vagal nerve reflex during big sizing balloon stent dilation and recovered after cardiopulmonary resuscitation. There were no other serious procedure related complications. During the follow?up, severe stenosis at end of proximal stent was evidenced in 1 patient due to fibrotic compression, and another patient developed in?stent thrombosis due to discontinuation of prescribed anticoagulant. Conclusion Percutaneous intervention for severe pulmonary vein stenosis caused by FM is feasible and safe, and can improve hemodynamic caused by the compression of mediastinal vascular structures in these carefully selected patients.

Objective To approach the mechanisms and myocardial protective effect of Qishen Yiqi dropping pills on rats with myocardial infarction. Methods Sixty clean healthy male Sprague-Dawley (SD) rats were randomly divided into sham operation group, model group and observation group (each n = 20). The rat model of acute myocardial infarction (AMI) was established by ligation of left anterior descent (LAD) branch of coronary artery. After modeling, the rats in observation group were given 0.135 g/kg of Qishen Yiqi dropping pills, and sham operation group and model group were administered the same amount of normal saline, once a day for consecutive 28 days. At the end of treatment, the levels of serum inflammatory factors of leukotriene B4 (LTB4), prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) were measured by enzyme linked immunosorbent assay (ELISA); the changes of the indexes of hemodynamic [left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), the maximal rate of increase/decrease in left ventricular pressure (±dp/dt max)], the ratio of the heart weight/body weight, and the ratio of the left ventricular weight/heart weight (LVW/HW), the myocardial infarction area, myocardial histopathological changes were observed in the three groups; myocardial tissues inflammatory related factors [the mRNA and protein expressions of cytosolic phospholipase A2 (cPLA2), cyclooxygenase-2 (COX-2), 5-lipoxygenase (5-LOX)], and the expression levels of transforming growth factor-β (TGF-β)/Smads signal transduction pathway related protein (TGF-β1, Smad2/3, Collagen Ⅰ, Collagen Ⅲ ) and cell apoptosis related factors (Bcl-2, Bax) protein were measured. Results Compared with the sham operation group, levels of serum inflammatory factors, the index of LVEDP, the ratio of the heart weight/body weight, LVW/HW, myocardial infarction area, the mRNA and protein expression levels of inflammatory factors in myocardium, the expression levels of TGF-β/Smads signal transduction pathway related protein and the cell apoptosis related factors protein in model group were all significantly elevated, while LVSP and ±dp/dt max were obviously decreased in model group. Compared with the model group, the levels of inflammatory factor in serum [LTB4 (ng/L): 370.11±46.98 vs. 633.23±83.37, PGE2 (ng/L):48.75±26.35 vs. 131.25±29.75, TNF-α (μg/L): 177.28±22.65 vs. 248.47±16.21, IL-6 (μg/L): 493.22±165.99 vs. 638.41±191.66], LVEDP [mmHg (1 mmHg = 0.133 kPa): -2.03±2.98 vs. 7.03±1.39], the ratio of the heart weight/body weight [(6.53±0.11)% vs. (7.14±0.24)%], LVW/HW (0.26±0.01 vs. 0.32±0.02), myocardial infarction area [(27.21±2.87)% vs. (44.98±1.52)%], mRNA and protein expression of myocardial inflammatory factors, the expression of TGF-β/Smads signal transduction pathway related protein, and the protein expression of Bax were all significantly decreased in observation group (all P < 0.05), LVSP (mmHg: 129.01±11.93 vs. 108.11±12.69), the +dp/dt max (mmHg/s: 3101.3±378.6 vs. 2105.3±245.9), the -dp/dt max (mmHg/s: 2612.4±249.7 vs. 1654.4±188.1), while the protein expression of Bcl-2 in observation group were obviously increased (all P < 0.05). It was demonstrated by hematoxylin-eosin (HE) staining that there were no obvious pathological changes in the sham operation group; obvious infiltration of inflammatory factors in myocardium was shown in model group; pathological changes in the observation group were significantly improved as compared with those in the model group. It was shown by Masson staining that there were slight hyperplasia of myocardial fibers and no obvious pathological changes in the sham operation group. Severe collagen hyperplasia was found in model group, and the degree of fibrosis in the observation group was significantly improved. Conclusions Qishen Yiqi dropping pills can reduce the degree of myocardial fibrosis and inhibit the ventricular remodeling via TGF-β/Smads signal transduction pathway. The dropping pills can also suppress the release of inflammatory factors by reducing cPLA2 to decrease the inflammatory response and inhibit apoptosis and alleviate myocardial injury by up-regulating the expression of Bcl-2 and down-regulating the expression of Bax.