Implication of sleep apnea for cardiac remodeling in patients with hypertrophic cardiomyopathy.

OBJECTIVES: Cardiac remodeling is a life-long process in hypertrophic cardiomyopathy (HCM), and if uncontrolled, would cause substantial morbidity and mortality. Sleep apnea (SA) is a common comorbidity in HCM. This study aimed to investigate the relationship between SA and cardiac remodeling in a large series of patients with HCM. METHODS: A total of 606 patients with HCM who underwent sleep evaluations at Fuwai Hospital were included. Parameters of cardiac remodeling were evaluated by echocardiographic studies. RESULTS: SA was present in 363 (59.9%) patients. Left ventricular (LV) end-diastolic diameter (P < 0.001), left atrial (LA) diameter (P = 0.024), ascending aortic diameter (P < 0.001) all increased and maximal end-diastolic wall thickness (P < 0.001) decreased with the severity of SA. After adjustment for sex, age, body mass index, hypertension, hyperlipidemia, diabetes, coronary artery disease and cigarette use, log (apnea-hypopnea index+1) was independently correlated with increasing LV end-diastolic diameter (ß = 0.729, P = 0.003) and deceasing maximal end-diastolic wall thickness (ß = -0.503, P = 0.009). Log (percentage of total sleep time spent with oxygen saturation<90% + 1) was independently correlated with increasing LV end-diastolic diameter (ß = 0.609, P = 0.004) and LA diameter (ß = 0.695, P = 0.006). Severity of SA (severe SA with odds ratio, 2.38; 95% CI, 1.20-4.70; P = 0.013), log (apnea-hypopnea index+1) (OR, 1.28; 95% CI, 1.01-1.63; P = 0.045) and log (percentage of total sleep time spent with oxygen saturation<90% + 1) (OR, 1.31; 95% CI, 1.08-1.59; P = 0.006) were also independently associated with LV enlargement. CONCLUSIONS: Severity of SA is independently associated with cardiac remodeling indicating a trend toward enlarged chamber size and thinned wall. Clinical trials are required to determine whether treatment of SA improves cardiac remodeling and long-term outcomes in patients with HCM.

A too-good-to-be-true prior to reduce shortcut reliance.

Despite their impressive performance in object recognition and other tasks under standard testing conditions, deep networks often fail to generalize to out-of-distribution (o.o.d.) samples. One cause for this shortcoming is that modern architectures tend to rely on ǣshortcutsǥ superficial features that correlate with categories without capturing deeper invariants that hold across contexts. Real-world concepts often possess a complex structure that can vary superficially across contexts, which can make the most intuitive and promising solutions in one context not generalize to others. One potential way to improve o.o.d. generalization is to assume simple solutions are unlikely to be valid across contexts and avoid them, which we refer to as the too-good-to-be-true prior. A low-capacity network (LCN) with a shallow architecture should only be able to learn surface relationships, including shortcuts. We find that LCNs can serve as shortcut detectors. Furthermore, an LCN's predictions can be used in a two-stage approach to encourage a high-capacity network (HCN) to rely on deeper invariant features that should generalize broadly. In particular, items that the LCN can master are downweighted when training the HCN. Using a modified version of the CIFAR-10 dataset in which we introduced shortcuts, we found that the two-stage LCN-HCN approach reduced reliance on shortcuts and facilitated o.o.d. generalization.

Dihydroartemisinin ameliorates the liver steatosis in metabolic associated fatty liver disease mice by attenuating the inflammation and oxidative stress and promoting autophagy.

PURPOSE: To explore the effect and potential mechanism of dihydroartemisinin (DHA) on metabolism-related fatty liver disease. METHODS: A metabolic associated fatty liver disease (MAFLD) mice model was induced with continuous supplies of high-fat diet. DHA was intraperitoneally injected into mice. The weight of mice was monitored. The concentrations of total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL), and high-density lipoprotein (HDL) in serum were detected by an automatic biochemical analyzer. The liver tissues were stained by hematoxylin and eosin and oil red O. The level of inflammation, oxidative stress, and autophagy was assessed by reverse transcription polymerase chain reaction, biochemical examination, Western blot and transmission electron microscope assays. RESULTS: DHA treatment reduced theMAFLD-enhanced the level of weight gain, the concentrations of TC, TG, LDL and malonaldehyde, while increasedthe MAFLD-decreased the concentrations of HDL and superoxide dismutase. DHA ameliorated the MAFLD-aggravated pathological changes and the number of lipid droplets. Low dose of DHA declined the MAFLD-induced the enhancement of the expression of inflammatory factor. DHA treatment increased the MAFLD-enhanced the level of autophagy related protein, while decreased the MAFLD-reduced the protein level of p62. The increased level of autophagy was confirmed by transmission electron microscope. CONCLUSIONS: DHA can improve liver steatosis in MAFLD mice by inhibiting inflammation and oxidative stress and promoting autophagy.

Association of Types of Sleep Apnea and Nocturnal Hypoxemia with Atrial Fibrillation in Patients with Hypertrophic Cardiomyopathy.

BACKGROUND: Data regarding the association between sleep apnea (SA) and atrial fibrillation (AF) in hypertrophic cardiomyopathy (HCM) are still limited. We aim to investigate the association of both types of SA, obstructive sleep apnea (OSA) and central sleep apnea (CSA), and nocturnal hypoxemia with AF in HCM. METHODS: A total of 606 patients with HCM who underwent sleep evaluations were included. Logistic regression was used to assess the association between sleep disorder and AF. RESULTS: SA was presented in 363 (59.9%) patients, of whom 337 (55.6%) had OSA and 26 (4.3%) had CSA. Patients with SA were older, more often male, had a higher body mass index, and more clinical comorbidities. Prevalence of AF was higher in patients with CSA than patients with OSA and without SA (50.0% versus 24.9% and 12.8%, p < 0.001). After adjustment for age, sex, body mass index, hypertension, diabetes mellitus, cigarette use, New York Heart Association class and severity of mitral regurgitation, SA (OR, 1.79; 95% CI, 1.09-2.94) and nocturnal hypoxemia (higher tertile of percentage of total sleep time with oxygen saturation < 90% [OR, 1.81; 95% CI, 1.05-3.12] compared with lower tertile) were significantly associated with AF. The association was much stronger in the CSA group (OR, 3.98; 95% CI, 1.56-10.13) than in OSA group (OR, 1.66; 95% CI, 1.01-2.76). Similar associations were observed when analyses were restricted to persistent/permanent AF. CONCLUSION: Both types of SA and nocturnal hypoxemia were independently associated with AF. Attention should be paid to the screening of both types of SA in the management of AF in HCM.

Dihydroartemisinin ameliorates the liver steatosis in metabolic associated fatty liver disease mice by attenuating the inflammation and oxidative stress and promoting autophagy

ABSTRACT Purpose: To explore the effect and potential mechanism of dihydroartemisinin (DHA) on metabolism-related fatty liver disease. Methods: A metabolic associated fatty liver disease (MAFLD) mice model was induced with continuous supplies of high-fat diet. DHA was intraperitoneally injected into mice. The weight of mice was monitored. The concentrations of total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL), and high-density lipoprotein (HDL) in serum were detected by an automatic biochemical analyzer. The liver tissues were stained by hematoxylin and eosin and oil red O. The level of inflammation, oxidative stress, and autophagy was assessed by reverse transcription polymerase chain reaction, biochemical examination, Western blot and transmission electron microscope assays. Results: DHA treatment reduced theMAFLD-enhanced the level of weight gain, the concentrations of TC, TG, LDL and malonaldehyde, while increasedthe MAFLD-decreased the concentrations of HDL and superoxide dismutase. DHA ameliorated the MAFLD-aggravated pathological changes and the number of lipid droplets. Low dose of DHA declined the MAFLD-induced the enhancement of the expression of inflammatory factor. DHA treatment increased the MAFLD-enhanced the level of autophagy related protein, while decreased the MAFLD-reduced the protein level of p62. The increased level of autophagy was confirmed by transmission electron microscope. Conclusions: DHA can improve liver steatosis in MAFLD mice by inhibiting inflammation and oxidative stress and promoting autophagy.

Effects of Inorganic Passivators on Gas Production and Heavy Metal Passivation Performance during Anaerobic Digestion of Pig Manure and Corn Straw.

The treatment of livestock manure caused by the expansion of the breeding industry in China has attracted wide attention. Heavy metals in pig manure can pollute soil and water and even transfer to crops, posing harm to humans through the food chain. In this study, corn straw was selected as the additive and introduced into the anaerobic digestion. Sepiolite (SE), ferric oxide (Fe2O3), attapulgite (AT) and ferric sulfate (FeSO4) were used as passivators to compare the effects of these inorganic passivators on gas production and passivation of heavy metals during the process of the anaerobic digestion. When the dry mass ratio of pig manure to straw is 8:2, the gas production efficiency is optimal. SE, AT and ferric sulfate have a much stronger ability to improve gas production performance than Fe2O3. The total gas production increased by 10.34%, 6.62% and 4.56%, and the average methane production concentration increased by 0.7%, 0.3% and 0.4%, respectively. The influence of SE, AT and ferric sulfate on the passivation of heavy metals is much better than Fe2O3, and the fractions in biological effective forms of Cu and Zn reduced by 41.87 and 19.32%, respectively. The anaerobic digestion of mixed materials is conducive to the gas production and the passivation of heavy metals. Therefore, SE, AT and ferric sulfate are selected as composite passivators, and the optimal ratio of inorganic composite passivators i: AT 7.5 g/L, ferric sulfate 5 g/L and SE 7.5 g/L, according to the results of orthogonal experiments. This study can provide a theoretical basis for the safe application of biogas fertilizers.

MicroRNA-122-5p Inhibition Improves Inflammation and Oxidative Stress Damage in Dietary-Induced Non-alcoholic Fatty Liver Disease Through Targeting FOXO3.

Misregulated microRNA network has been emerging as the main regulator in non-alcoholic fatty liver disease (NAFLD). The deregulation of miR-122-5p is associated with the liver disease. However, the specific role and molecular mechanism of miR-122-5p in NAFLD remain unclear. In this study, we have reported that the high-fat diet (HFD) or palmitic acid (PA) significantly upregulated the hepatic miR-122-5p expression in vivo and in vitro. Inhibition of miR-122-5p suppressed accumulation-induced inflammation of lipids and oxidative stress damage in PA-treated L02 cells and HFD-induced fatty liver. The effect of the miR-122-5p inhibitor on NAFLD did not depend on insulin resistance-mediated PI3K/AKT/mammalian target of rapamycin (mTOR) signaling pathway but rather on the upregulation of its downstream FOXO3. Subsequently, we validated that miR-122-5p directly binds to the predicted 3'-UTR of FOXO3 to inhibit its gene expression. Conversely, silencing FOXO3 abolished the hepatic benefits of miR-122-5p inhibition to obese mice by decreasing the activity of antioxidant enzymes of superoxide dismutase (SOD). This study provides a novel finding that FOXO3 was the target gene of miR-122-5p to attenuate inflammatory response and oxidative stress damage in dietary-induced NAFLD. Our study provided evidence to reveal the physiological role of miR-122-5p in dietary-induced NAFLD.

Profile and outcomes of patients with mediastinal hematoma after cardiac catheterization: A retrospective analysis.

OBJECTIVE: To provide a comprehensive introduction of mediastinal hematoma. BACKGROUND: Mediastinal hematoma is a rare complication that is usually not considered in the differential diagnosis of chest pain after cardiac catheterization. METHODS: From January 1, 2006, to December 31, 2013, at Fuwai Hospital, 126,265 patients underwent coronary angiography (CAG); 121,215 of them underwent CAG via the radial artery. Ultimately, 10 patients with mediastinal hematoma due to cardiac catheterization were included. Patients' clinical characteristics, diagnosis, treatment, and prognosis were retrospectively analyzed. RESULTS: The incidences of mediastinal hematoma in cardiac catheterization and transradial cardiac catheterization were 0.79‱ and 0.74‱, respectively. A super slide hydrophilic guidewire was used in all 10 patients with mediastinal hematoma. These patients felt chest pain and dyspnea during/after the procedure, and computed tomography (CT) was used to diagnose mediastinal hematoma. Among them, two patients had a neck hematoma. The post-procedural hemoglobin level decreased substantially in all patients. Antiplatelet therapy was discontinued for 8-20 days in three patients without stents implanted, and then only oral aspirin was prescribed. Aspirin was transiently discontinued for 2 days in one patient undergoing percutaneous coronary intervention. The others continued taking dual antiplatelet drugs. Two patients received blood transfusion. There was no case of stent thrombosis, and surgery was not indicated for any patient. No complication was observed after discharge during the 9.0 ± 2.5-year follow-up. CONCLUSION: CT should be performed as early as possible in patients with suspected mediastinal hematoma. The prognosis of mediastinal hematoma is usually good with early diagnosis and suitable therapy.

The Costs and Benefits of Goal-Directed Attention in Deep Convolutional Neural Networks.

People deploy top-down, goal-directed attention to accomplish tasks, such as finding lost keys. By tuning the visual system to relevant information sources, object recognition can become more efficient (a benefit) and more biased toward the target (a potential cost). Motivated by selective attention in categorisation models, we developed a goal-directed attention mechanism that can process naturalistic (photographic) stimuli. Our attention mechanism can be incorporated into any existing deep convolutional neural networks (DCNNs). The processing stages in DCNNs have been related to ventral visual stream. In that light, our attentional mechanism incorporates top-down influences from prefrontal cortex (PFC) to support goal-directed behaviour. Akin to how attention weights in categorisation models warp representational spaces, we introduce a layer of attention weights to the mid-level of a DCNN that amplify or attenuate activity to further a goal. We evaluated the attentional mechanism using photographic stimuli, varying the attentional target. We found that increasing goal-directed attention has benefits (increasing hit rates) and costs (increasing false alarm rates). At a moderate level, attention improves sensitivity (i.e. increases d ' ) at only a moderate increase in bias for tasks involving standard images, blended images and natural adversarial images chosen to fool DCNNs. These results suggest that goal-directed attention can reconfigure general-purpose DCNNs to better suit the current task goal, much like PFC modulates activity along the ventral stream. In addition to being more parsimonious and brain consistent, the mid-level attention approach performed better than a standard machine learning approach for transfer learning, namely retraining the final network layer to accommodate the new task.

[Two types of exercise-induced abnormal blood pressure response in hypertrophic cardiomyopathy].

Objective: Insufcient exercise blood pressure response(blunted ABPR) and lower blood pressure during the recovery period (LBP)after exercise are common abnormalities in patients with hypertrophic cardiomyopathy (HCM). The purpose of this study was to analyze the related factors of these two types of abnormal blood pressure response in HCM patients and their relationship with cardiopulmonary function. Methods: A total of 219 consecutive HCM patients who underwent CPET in Fuwai hospital were recruited from April 1, 2018 to Jan 31, 2020 with a complete clinical assessment, including electrocardiography, HOLTER, rest echocardiography and cardiac MRI. One hundred and eleven healthy age- and gender-matched volunteers enrolled as control group. Results: The incidences of blunted ABPR and LBP in HCM patients were much higher than normal control group (8.7% vs 1.8%, P=0.016; 6.8% vs 0.0%, P=0.003, respectively). In HCM group, patients with blunted ABPR combined more coronary artery disease (CAD) (P=0.029), pulmonary hypertension (PH) (P=0.002) and atrial fibrillation/flutter (P=0.036) compared with patients without blunted ABPR. Compared with HCM patients without LBP, the patients with LBP had higher rest left ventricular outflow tract (LVOT) gradient (P=0.017) and left ventricular ejection fraction (P=0.043), more incidence of LVOT obstructive (P=0.015) and systolic anterior motion (P=0.022). After Logistic regression analysis, CAD and PH were independent factor of blunted ABPR, while LBP was only independently associated with rest LVOT gradient. Blunted ABPR was associated with lower Peak VO2, peak heart rate and hear rate reserve, and higher NT-proBNP (P=0.019), VE/VO2 (P=0.000). LBP was not associated with any index of cardiopulmonary function. Conclusion: The incidences of blunted ABPR and LBP in HCM patients were much higher than normal control group. In HCM patients, CAD and PH were independent determinants of blunted ABPR, while LBP was only independently associated with rest LVOT gradient. Patients with blunted ABPR had lower cardiopulmonary function, but LBP was not associated cardiopulmonary function.

Clinical predictors of the presence of obstructive sleep apnea in patients with hypertrophic cardiomyopathy.

Obstructive sleep apnea (OSA) is much common and associated with worse clinical outcomes in patients with hypertrophic cardiomyopathy (HCM), however, the diagnosis of OSA in HCM is still insufficient. We aim to investigate the clinical predictors of OSA in a large series of patients with HCM. A total of 589 patients with HCM who underwent sleep evaluations were retrospectively enrolled. Data from clinical characteristics and polysomnography studies were recorded. OSA was present in 346 patients (58.7%). Patients who had OSA were older, more likely to be male and had more clinical comorbidities such as hypertension, atrial fibrillation and cardiac remodeling. Multivariate logistic analyses showed that male, age, body mass index, hypertension and left ventricular outflow tract obstruction were significant factors associated with OSA. The area under the ROC curve (AUC) was 0.78 (95% CI 0.74-0.82; P < 0.001). These factors were also able to identify moderate to severe OSA with an AUC of 0.77 (95% CI 0.73-0.81; P < 0.001). These findings suggest that identifying HCM patients with high risk for OSA is feasible using characteristics from clinical practices and clinicians should have no hesitate to conduct sleep test in these patients.

Association Between Obstructive Sleep Apnea and Metabolic Abnormalities in Patients With Hypertrophic Cardiomyopathy.

OBJECTIVES: Metabolic abnormalities have been associated with long-term cardiac mortality in patients with hypertrophic cardiomyopathy (HCM). Obstructive sleep apnea (OSA) is a risk factor for metabolic abnormalities in general populations, but association between OSA and metabolic abnormalities in HCM is still undefined. This study aimed to investigate the relationship between OSA and metabolic dysfunction in a large series of patients with HCM. METHODS: A total of 587 patients with HCM who underwent sleep evaluations at Fuwai Hospital were included. Data from clinical characteristics, polysomnography studies, and metabolic measurements were collected. RESULTS: OSA was present in 344 patients (58.6%). Patients with OSA were older, more often male, and had more clinical comorbidities. Body mass index, blood pressure, fasting glucose, and triglycerides all increased (all P < 0.001) and high-density lipoprotein cholesterol decreased (P = 0.046) with the severity of OSA. In multivariate analysis, moderate to severe OSA and Log (apnea-hypopnea index + 1) were independently associated with obesity (odds ratio [OR], 2.42; 95% CI, 1.48-3.95 and OR, 1.60; 95% CI, 1.31-1.95), elevated blood pressure (OR, 1.99; 95% CI, 1.42-3.26 and OR, 1.31; 95% CI, 1.08-1.60), and elevated triglycerides (OR, 1.71; 95% CI, 1.05-2.78 and OR, 1.24; 95% CI, 1.02-1.51 but not elevated fasting glucose (OR, 0.88; 95% CI, 0.50-1.52 and OR, 1.02; 95% CI, 0.82-1.28) or reduced high-density lipoprotein cholesterol (OR, 1.30; 95% CI, 0.83-2.04 and OR, 1.06; 95% CI, 0.89-1.27). CONCLUSIONS: Severity of OSA is independently associated with some profiles of metabolic abnormalities. Clinical trials are required to determine whether OSA treatment improves metabolic abnormalities and long-term outcomes in patients with HCM.

Impacts of smoking status on the clinical outcomes of coronary non-target lesions in patients with coronary heart disease: a single-center angiographic study.

BACKGROUND: Coronary atherosclerotic plaque could go through rapid progression and induce adverse cardiac events. This study aimed to evaluate the impacts of smoking status on clinical outcomes of coronary non-target lesions. METHODS: Consecutive patients with coronary heart disease who underwent two serial coronary angiographies were included. All coronary non-target lesions were recorded at first coronary angiography and analyzed using quantitative coronary angiography at both procedures. Patients were grouped into non-smokers, quitters, and smokers according to their smoking status. Clinical outcomes including rapid lesion progression, lesion re-vascularization, and myocardial infarction were recorded at second coronary angiography. Multivariable Cox regression analysis was used to investigate the association between smoking status and clinical outcomes. RESULTS: A total of 1255 patients and 1670 lesions were included. Smokers were younger and more likely to be male compared with non-smokers. Increase in percent diameter stenosis was significantly lower (2.7 [0.6, 7.1] % vs. 3.5 [0.9, 8.9]%) and 3.4 [1.1, 7.7]%, P = 0.020) in quitters than those in smokers and non-smokers. Quitters tended to have a decreased incidence of rapid lesions progression (15.8% [76/482] vs. 21.6% [74/342] and 20.6% [89/431], P = 0.062), lesion re-vascularization (13.1% [63/482] vs. 15.5% [53/432] and 15.5% [67/431], P = 0.448), lesion-related myocardial infarction (0.8% [4/482] vs. 2.6% [9/342] and 1.4% [6/431], P = 0.110) and all-cause myocardial infarction (1.9% [9/482] vs. 4.1% [14/342] and 2.3% [10/431], P = 0.128) compared with smokers and non-smokers. In multivariable analysis, smoking status was not an independent predictor for rapid lesion progression, lesion re-vascularization, and lesion-related myocardial infarction except that a higher risk of all-cause myocardial infarction was observed in smokers than non-smokers (hazards ratio: 3.00, 95% confidence interval: 1.04-8.62, P = 0.042). CONCLUSION: Smoking cessation mitigates the increase in percent diameter stenosis of coronary non-target lesions, meanwhile, smokers are associated with increased risk for all-cause myocardial infarction compared with non-smokers.

Implication of Apnea-Hypopnea Index, a Measure of Obstructive Sleep Apnea Severity, for Atrial Fibrillation in Patients With Hypertrophic Cardiomyopathy.

Background Obstructive sleep apnea (OSA) is common and independently associated with atrial fibrillation (AF) in patients with hypertrophic cardiomyopathy (HCM). This study aimed to investigate the relationship between apnea-hypopnea index (AHI), a measure of OSA severity, and prevalence of AF in a large series of patients with HCM. Methods and Results A total of 555 patients with HCM who underwent sleep evaluations were retrospectively included. Data from polysomnography studies, echocardiography, and baseline clinical characteristics were collected. OSA was present in 327 patients (58.9%). Patients with OSA or higher AHI quartiles were older, more often male, had a higher body mass index, and more clinical comorbidities. The prevalence of AF increased in patients with OSA (23.9% versus 13.6%, P=0.003) or across AHI quartiles (9.4%, 17.3%, 26.6%, and 25.2%, respectively; P for trend <0.001). After adjustment for age, sex, body mass index, New York Heart Association class, left atrial diameter, hypertension, oxygen desaturation index, and obstructive HCM, highest AHI quartile (odds ratio, 4.42; 95% CI, 1.35-14.52 [P=0.014]) or moderate to severe OSA (odds ratio, 3.03; 95% CI, 1.28-7.20 [P=0.012]) but not presence of OSA (odds ratio, 1.58; 95% CI, 0.84-2.97 [P=0.153]) were significantly associated with AF. Higher AHI levels were also factors associated with persistent or permanent AF (highest AHI quartile with odds ratio, 10.96; 95% CI, 1.07-111.85). Conclusions Severity of AHI level is independently associated with AF in patients with HCM. Clinical trials are required to determine the benefits of OSA treatment on AF in patients with HCM.

The relationship between ß1 -adrenergic and M2 -muscarinic receptor autoantibodies and hypertrophic cardiomyopathy.

NEW FINDINGS: What is the central question of this study? The concentrations of ß1 -adrenergic receptor and M2 -muscarinic receptor autoantibodies in hypertrophic cardiomyopathy (HCM) patients and the relationship between the cardiac autoantibodies and clinical manifestations of HCM have rarely been reported. What is the main finding and its importance? We found that the concentrations of the two autoantibodies in HCM patients were significantly higher than those in control subjects. Furthermore, we found that the concentrations of the two autoantibodies could reflect myocardial injury and diastolic dysfunction in HCM patients to some extent and might be involved in the occurrence of arrhythmia. These findings might be valuable in exploration of the mechanisms of occurrence and progression of HCM. ABSTRACT: Increasing attention is being given to the role of immunological mechanisms in the development of heart failure. The purpose of this study was to investigate the concentration of serum ß1 -adrenergic receptor autoantibody (ß1 -AAb) and M2 -muscarinic receptor autoantibody (M2 -AAb) in patients with hypertrophic cardiomyopathy (HCM), and the relationship between ß1 -AAb, M2 -AAb and clinical indices. One hundred and thirty-four patients with HCM were recruited consecutively into the HCM group. Forty healthy subjects were assigned as the normal controls (NCs). Serum samples were collected to measure the concentrations of ß1 -AAb and M2 -AAb by enzyme-linked immunosorbent assay. The clinical data of HCM patients were collected. The serum concentrations of ß1 -AAb and M2 -AAb of HCM patients were significantly higher than those of NCs. In HCM patients, those with a left atrial diameter ≥50 mm or moderate-to-severe mitral regurgitation had significantly higher concentrations of the two autoantibodies. Patients with a history of syncope had higher concentrations of ß1 -AAb. Female patients and patients with a family history of sudden cardiac death or atrial fibrillation had higher concentrations of M2 -AAb. Maximal wall thickness, interventricular septum thickness and resting left ventricular outflow tract gradient were positively correlated with log ß1 -AAb or log M2 -AAb in HCM patients. In conclusion, the serum concentrations of ß1 -AAb and M2 -AAb of HCM patients were significantly higher than those of NCs. Being female, syncope, a family history of sudden death, atrial fibrillation, left atrial diameter ≥50 mm, moderate-to-severe mitral regurgitation, maximal wall thickness, interventricular septum thickness and resting left ventricular outflow tract gradient may affect the concentrations of the two autoantibodies.

Long-term outcomes of percutaneous coronary intervention in grafts and native vessels in coronary artery bypass grafting patients with diabetes mellitus.

BACKGROUND: Atherosclerosis in diabetic patients progresses fast. Evidence on how to choose target vessels of percutaneous coronary interventions (PCIs) in diabetic patients post-coronary artery bypass graft (post-CABG) is insufficient. METHODS: One hundred and fifty-seven patients with diabetes and previous CABG, who underwent PCI of either a graft vessel (GV) (n=44) or a native vessel (NV) (n=113) in the National Center for Cardiovascular Disease, China, were studied. In-hospital and long-term clinical outcomes were compared between the groups. RESULTS: Diabetic patients with prior CABG had more PCI to native arteries, but the proportion of grafts PCI increased as time went on. Both groups had similar baseline characteristics. Group GV patients compared with group NV had more totally occluded NVs, less totally occluded grafts and more in-stent restenosis. However, there was no difference in in-hospital mortality and long-term incidence of major adverse cardiac event (MACE), cardiac death, nonfatal myocardial infarction (MI), or revascularization. Multivariate logistic regression analysis showed that PCI success [hazard ratio (HR), 11.488; 95% confidence interval (CI), 1.135-116.303; P<0.05] was independent predictor of MACE. CONCLUSIONS: It suggested similar long-term clinical outcomes after PCI in GV or NV in prior CABG patients with diabetes. Thus, the vessel with higher estimated PCI success rate should be prioritized by operators.

Titin-Truncating Variants Increase the Risk of Cardiovascular Death in Patients With Hypertrophic Cardiomyopathy.

BACKGROUND: Titin-truncating variants (TTNtv) have been detected in a variety of cardiomyopathies and represent the most common cause of dilated cardiomyopathy. However, their significance in hypertrophic cardiomyopathy (HCM) is still unclear. METHODS: The titin gene (TTN) was sequenced for truncating variants in a cohort of 529 Chinese patients with HCM and 307 healthy controls. Baseline and follow-up clinical data (for 4.7 ± 3.2 years) from these patients were obtained. RESULTS: We identified 13 and 8 TTNtv in patients with HCM (13 of 529 [2.5%]) and controls (8 of 307 [2.6%]), respectively. The prevalence of TTNtv in patients with HCM and in healthy controls was comparable (P = 0.895). There were no significant differences in baseline characteristics between patients with and those without TTNtv. However, during follow-up, patients with TTNtv (3 of 13 [23.1%]) were more likely to experience cardiovascular death compared with those without TTNtv (39 of 516 [7.6%]) [adjusted hazard ratio, 6.88; 95% confidence interval, 2.04-23.20; P = 0.002). CONCLUSIONS: Our study suggests that TTNtv might be a genetic modifier of HCM and confer an increased risk for cardiovascular death.

Prognostic Significance of Plasma High-Sensitivity C-Reactive Protein in Patients With Hypertrophic Cardiomyopathy.

BACKGROUND: Elevated high-sensitivity C-reactive protein (hsCRP) has been associated with increased risks of adverse outcomes of various cardiovascular diseases. The relationship between hsCRP and the prognosis of hypertrophic cardiomyopathy remains to be evaluated. METHODS AND RESULTS: The study used an observational cohort methodology. A total of 490 patients were enrolled in the Fuwai Hospital from 2001 to 2011 and were followed for 3.7±2.0 years. According to the risk category of hsCRP, subjects in the high hsCRP group (>3.0 mg/L) had a higher risk of developing adverse events than the low hsCRP group (<1.0 mg/L): cardiovascular death (adjusted hazard ratios[HR] 5.41, 95% CI 1.96-14.93, P=0.001), all-cause mortality (adjusted HR 4.78, 95% CI 1.99-11.47, P<0.001), sudden cardiac death (adjusted HR 11.29, 95% CI 1.38-92.20, P=0.024), and heart failure-related death (adjusted HR 4.38, 95% CI 1.15-16.60, P=0.030). Similarly, the continuous variable of hsCRP was also an independent predictor for adverse outcomes: cardiovascular death (adjusted HR 1.15, 95% CI 1.06-1.25, P=0.001), all-cause mortality (adjusted HR 1.17, 95% CI 1.09-1.26, P<0.001), sudden cardiac death (adjusted HR 1.20, 95% CI 1.06-1.36, P=0.003), and heart failure-related death (adjusted HR 1.15, 95% CI 1.02-1.30, P=0.020). CONCLUSIONS: Our results indicate that elevated plasma hsCRP is associated with increased risk for adverse outcomes in patients with hypertrophic cardiomyopathy.

Abnormalities of myocardial perfusion and glucose metabolism in patients with isolated left ventricular non-compaction.

BACKGROUND: The prevalence of myocardial perfusion and glucose metabolic abnormalities and their significance in patients with isolated left ventricular non-compaction (ILVNC) have not been well investigated. METHODS: Seventeen ILVNC patients who underwent cardiac magnetic resonance (CMR) and (99m)Tc-sestamibi SPECT/fluorine-18 deoxyglucose ((18)F-FDG) PET imaging were included. Left ventricular non-compaction, regional wall motion abnormalities, left ventricular ejection fraction (LVEF), and delayed enhancement (DE) were estimated using CMR. Myocardial perfusion and metabolism were evaluated with SPECT/PET. RESULTS: Ninety-five (32.9%) segments were considered non-compacted. DE was present in 52 (18.0%) segments and 10 (58.8%) patients. The rate of occurrence of DE was significantly higher in compacted segments than in non-compacted segments (22.7% vs 8.4%, P = .003). Myocardial perfusion abnormalities were present in 92 (31.8%) segments, of which 66 were perfusion/metabolism match and 26 were perfusion/metabolism mismatch. The rate of occurrence of perfusion abnormality was similar between compacted and non-compacted segments (32.0% vs 31.6%, P = .948), but it was significantly higher in segments with DE than in those without DE (51.9% vs 27.4%, P = .001). None of the imaging features alone (non-compaction, DE, perfusion abnormalities, match or mismatch) showed significant correlations with LVEF (all P > .05). CONCLUSION: In the current study, myocardial perfusion/metabolism mismatch and match were observed in both non-compacted and compacted myocardium in ILVNC patients. Further research is warranted to determine their pathologic and clinical significance.

Poly(9,9'-diheylfluorene carbazole) functionalized with reduced graphene oxide: convenient synthesis using nitrogen-based nucleophiles and potential applications in optical limiting.

Covalently functionalized reduced graphene oxide (RGO) sheet was prepared by treating nitrogen-centered anions generated from poly(9,9'-diheylfluorene carbazole) (PCF) with GO. The resultant hybrids with different chemical behavior were separated by centrifugation. The covalent modification was fully characterized by IR spectroscopy, UV/Vis spectroscopy, thermogravimetric analysis (TGA), Raman spectroscopy, TEM, and SEM. It was found that RGO-PCF-s, the soluble part, was split into small platelets with a size of about 200 nm, and the hydrophobic polymer PCF became hydrophilic after wrapping by RGO. The content of RGO in RGO-PCF-s was about 11.9%, and the hybrid material showed good dispersion stability in water. Besides, RGO-PCF-i, the insoluble part, with larger size, displayed excellent optical-limiting response, in which both nonlinear absorption and nonlinear scattering play important roles. As nitrogen-centered anions are an important type of intermediates in chemistry, this one-step "grafting-to" strategy could be used to obtain RGO-based materials with different applications.