Clinical benefits of oral anticoagulants in atrial fibrillation patients with dementia: a systematic review and meta-analysis.

Background: The management of atrial fibrillation (AF) with oral anticoagulants (OAC) is generally recommended to reduce the risk of stroke. However, the decision to prescribe these medications for patients with AF and dementia remains controversial. Methods: A systematic review and meta-analysis of retrospective cohort studies were conducted. The search encompassed PubMed, Cochrane Library, Web of Science, and Embase databases from inception until May 1st, 2023, with language limited to English. Eligible studies included comparisons between exposure to OAC vs. non-OAC in the AF population with dementia or cognitive impairment. Studies that compared the effects of direct oral anticoagulants (DOAC) and vitamin-K antagonists were also included. The primary outcome was all-cause mortality, and the secondary outcomes were ischemic stroke and major bleeding. This study was registered with PROSPERO (No. CRD42023420678). Results: A total of five studies (N = 21,962 patients) met the eligibility criteria and were included in this review. The follow-up duration ranged from 1 to 4 years. Meta-analysis demonstrated that OAC treatment was associated with a lower risk of all-cause mortality in AF patients with dementia with a hazard ratio (HR) of 0.79 and a 95% confidence interval (CI) ranging from 0.68 to 0.92, compared to non-OAC treatment. No statistical differences were observed in the risk of major bleeding (HR = 1.12, 95% CI: 0.88-1.42) or ischemic stroke (HR = 0.77, 95% CI: 0.58-1.00). Three studies reported comparisons between DOAC and warfarin; however, pooled analysis was not performed due to heterogeneity. Conclusion: The use of OACs in individuals diagnosed with both AF and dementia holds the potential to reduce all-cause mortality rates, thereby improving the overall clinical prognosis within this specific population. Systematic Review Registration: https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42023420678, PROSPERO identifier, CRD42023420678.

Indole-3-propionic acid, a product of intestinal flora, inhibits the HDAC6/NOX2 signaling and relieves doxorubicin-induced cardiomyocyte damage.

The heart failure-gut hypothesis indicates that damage to intestinal mucosa leads to increased microbial translocation, resulting in alterations in metabolites entering the blood circulation. This process promotes the development of heart failure. This study aimed to reveal the involvement of indole-3-propionic acid (IPA), a microbiota-derived tryptophan metabolite, in heart failure. Human cardiomyocytes AC16 was treated with doxorubicin to induce in vitro heart failure model, the influences of IPA on the cellular viability, apoptosis, inflammation and oxidative stress were evaluated. Molecular docking and western blotting were used to initially illustrate the potential relationship between IPA and HDAC6. Through HDAC6 overexpression, its mediating role in the regulatory mechanism of IPA in the above aspects was further investigated. IPA was found to reduce the apoptosis, inflammation and oxidative stress in doxorubicin-treated cells. The visualized structure displayed that IPA bound to HDAC6 and that IPA reduced HDAC6 level. Additionally, HDAC6 overexpression reversed the regulation of IPA in the above aspects, indicating the HDAC6/NOX2 signals mediated the mechanism of IPA. Together, the present study revealed that IPA reduced oxidative stress, inflammatory response and apoptosis in cardiomyocytes via inhibiting the HDAC6/NOX2 signaling. The findings suggest that gut microbiota metabolites have potential in the treatment of heart failure.

Circulating microparticles are associated with plaque burden and cause eNOS uncoupling in patients with carotid atherosclerosis.

Aims: The study aimed to evaluate the correlation of different microparticle (MP) phenotypes with plaque burden and their diagnostic value and preliminarily explore the role of MPs in atherosclerosis (AS). Methods: Carotid intima-media thickness (CIMT) and maximal plaque area in 23 patients with carotid atherosclerosis (CAS) and 22 healthy subjects were measured by ultrasound. Transmission electron microscopy, nanoparticle tracking analysis and western blot were used to identify MPs. Flow cytometry assay measured absolute number of MPs, and receiver operating characteristic (ROC) analysis was used to assess the relationship between plaque burden and MPs. To study the preliminary mechanism of MPs in AS, MPs were administered to 32 male Kunming mice, which were randomly divided into control, CAS, healthy, and tetrahydrobiopterin (BH4) groups. Hematoxylin-eosin staining, immunohistochemistry staining, and Western blot were adopted to detect relevant indexes 24 h after the injection. Results: The plasma levels of CD45+ leukocyte-derived microparticle (LMP), CD11a+ LMP, CD11a+/CD45+ LMP, and CD31+/CD42b+ platelet-derived microparticle (PMP) in CAS patients were significantly higher than those in healthy subjects, and were positively correlated with the maximal plaque area. Moreover, the levels of CD11a+ LMP, CD11a+/CD45+ LMP were also positively correlated with CIMT. The area under the ROC curve of the four MPs was 0.689, 0.747, 0.741, and 0.701, respectively. Compared with healthy subjects, MPs from CAS patients resulted in a significantly lower expression of endothelial nitric oxide synthase (eNOS) dimer/monomer, and BH4 could improve eNOS uncoupling. Moreover, the level of VCAM-1 in intima in the CAS group was significantly higher than in the other three groups. Conclusion: CD11a+ LMP and CD11a+/CD45+ LMP might be potential biomarkers for CAS prediction. BH4-related eNOS uncoupling occurs in CAS patients, and circulating MPs from them lead to endothelial dysfunction through eNOS uncoupling.

Parkinson's disease protein 7 protected against oxidative stress of myocardial infarction direct through p47phox and nicotinamide adenine dinucleotide phosphate oxidase 4.

In the present study, we aimed to investigate the role and mechanism of Parkinson's disease protein 7 (Park7) in myocardial infarction (MI). The Park7 expression in the serum and tissues was down-regulated in mice with MI. Recombinant Park7 protein protected against MI-induced injury and reduced oxidative stress in mice model. Conversely, knockout Park7 increased injury of MI and promoted oxidative stress in MI mice model. In embryonic rat cardiac myoblasts H9c2 cells, over-expression of Park7 reduced reactive oxygen species (ROS)-induced oxidative stress, while down-regulation of Park7 increased ROS-induced oxidative stress. Park7 combined nicotinamide adenine dinucleotide phosphate (NADPH) oxidase cytoplasmic subunit p47phox protein had direct effect on inducing NADPH activator. The inhibition of p47phox reduced the effects of Park7 in ROS production of H2O2-treated H9c2 cells. The regulation of NADPH participated in the effects of Park7 on ROS production of in both MI mice model and H2O2-treated H9c2 cells. Our data demonstrated that Park7 protects against oxidative stress in MI model direct through p47phox and NADPH oxidase 4.

Effect of Sodium-Glucose Cotransporter 2 Inhibitors for Heart Failure With Preserved Ejection Fraction: A Systematic Review and Meta-Analysis of Randomized Clinical Trials.

Background: Heart failure with preserved ejection fraction (HFpEF) is associated with a high risk of mortality and frequent hospitalization. Sodium-glucose cotransporter 2 (SGLT2) inhibitors have favorable cardiovascular protective effect and could decrease the risk of mortality and hospitalization in patients with heart failure with reduced ejection fraction. However, the effect of SGLT2 inhibitors for HFpEF has not been well studied. Purpose: The aim of this meta-analysis is to systematically assess the effects of SGLT2 inhibitors in patients with HFpEF. Methods: MEDLINE, EMBASE, Ovid, Cochrane Library, Chinese National Knowledge Infrastructure Database, VIP database, Chinese Biomedical Database, and Wanfang Database were searched from inception to November 2021 for randomized controlled trials (RCTs) of SGLT2 inhibitors for HFpEF. Risk bias was assessed for included studies according to Cochrane handbook. The primary outcome was the composite of first hospitalization for heart failure (HHF) or cardiovascular mortality. First HHF, cardiovascular mortality, total HHF, all-cause mortality, exercise capacity, ventricular diastolic function, and adverse events were considered as secondary endpoints. PROSPERO registration: CRD42021291122. Results: A total of 12 RCTs including 10,883 patients with HFpEF (SGLT2 inhibitors group: 5,621; control group: 5,262) were included. All included RCTs were at low risk of bias. Meta-analysis showed that SGLT2 inhibitors significantly reduced the composite of first HHF or cardiovascular mortality (HR:0.78, 95% CI: [0.70, 0.87], P< 0.00001, I 2 = 0%), first HHF (HR:0.71, 95% CI: [0.62, 0.83], P < 0.00001, I 2 = 0%), total HHF (RR:0.75, 95% CI: [0.67, 0.84], P<0.00001, I 2 = 0%), E/e' (MD: -1.22, 95% CI: [-2.29, -0.15], P = 0.03, I 2 = 59%) and adverse events (RR:0.92, 95% CI: [0.88, 0.97], P = 0.001, I 2 = 0%). No statistical differences were found in terms of cardiovascular mortality, all-cause mortality, NT-proBNP, BNP and 6-min walk test distance. Conclusion: SGLT2 inhibitors significantly improve cardiovascular outcomes with a lower risk of serious adverse events in patients with HFpEF. However, these findings require careful recommendation due to the small number of RCTs at present. More multi-center, randomized, double-blind, placebo-controlled trials are needed. Systematic Review Registration: [https://www.crd.york.ac.Uk/prospero/], identifier [CRD42021291122].

Efficacy and safety of Wuling capsule for insomnia disorder: a systematic review and meta-analysis of randomized controlled trials.

OBJECTIVES: Wuling capsule has been used in treatment of insomnia disorder in China for decades, but the reported treatment efficacy of different studies was not consistent. This study intended to evaluate the efficacy and safety of Wuling capsule for insomnia disorder, so as to provide evidence for clinical application. METHODS: Eight databases (MEDLINE, EMBASE, Ovid, Cochrane Library, Chinese National Knowledge Infrastructure, VIP information database, Chinese Biomedical Database and Wanfang) were searched from inception to September 14, 2021. Randomized controlled trials (RCTs) comparing Wuling capsule with controls in adults with insomnia disorder were eligible. The primary outcome was sleep quality assessed by Pittsburgh Sleep Quality Index (PSQI), and the secondary outcomes were severity of insomnia disorder measured by Sleep Dysfunction Rating Scale (SDRS) and adverse events. This study was conducted according to the Cochrane Handbook for Systematic Reviews of Interventions version 5.1.0. RESULTS: Nineteen RCTs with a total of 1850 participants were included. In terms of sleep quality assessed by PSQI, Wuling capsule significantly lowered PSQI score (MD: -1.92, 95% CI: [-2.34, -1.50], P < 0.00001, I2 = 95%) compared to controls, and the effect of Wuling capsule was significantly better than control no matter when Wuling capsule as monotherapy (MD: -1.71, 95% CI: [-2.33, -1.09], P < 0.00001, I2 = 97%) or as adjunctive therapy (MD: -2.10, 95% CI: [-2.66, -1.55], P < 0.00001, I2 = 90%). Wuling capsule was more effective for the treatment duration lasted 8 weeks (MD: -2.57, 95% CI: [-3.52, -1.62], P < 0.00001, I2 = 93%) than 4 weeks (MD: -1.68, 95% CI: [-2.13, -1.22], P < 0.00001, I2 = 95%). In terms of severity of insomnia disorder measured by SDRS, Wuling capsule significantly reduced SDRS score (MD: -4.21, 95% CI: [-4.95, -3.46], P < 0.00001, I2 = 0%) compared to benzodiazepines. Wuling capsule significantly reduced adverse events compared to controls (RR: 0.47, 95% CI: [0.34, 0.65], P < 0.00001, I2 = 43%). CONCLUSION: Wuling capsule can safely and effectively improve sleep quality in patients with insomnia disorder. However, these findings require careful recommendation due to the high heterogeneity and high risk of bias in the included trials. Clinical trials with higher quality designs are needed.

Effect of Sodium Tanshinone IIA Sulfonate Injection on Blood Lipid in Patients With Coronary Heart Disease: A Systematic Review and Meta-Analysis of Randomized Clinical Trials.

Background: Lipid-lowering therapy is very important in secondary prevention of coronary heart disease (CHD). In many clinical trials, it has been found that Sodium Tanshinone IIA Sulfonate Injection (STS) have a lipid-lowering effect while reducing major cardiovascular events in patients with CHD. However, up to now, there is no system review on the effectiveness and safety of STS affecting blood lipids. Purpose: The aim of this review is to systematically assess the effects of STS on blood lipid levels in patients with CHD. Methods: Until Mar 2021, five databases (PubMed, EMBASE, Cochrane Library, China National Knowledge Infrastructure, and Wanfang Database) were searched for randomized controlled trials (RCTs) about STS treating patients with CHD. Risk bias was assessed for included studies according to Cochrane handbook. The primary outcome was total cholesterol (TC). The secondary outcomes were triglycerides (TG), low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c), and adverse events (AEs). Results: A total of 27 trials including 2,445 CHD patients met the eligibility criteria. Most trials had high risks in random sequence generation, allocation concealment, blinding of patients and personal, blinding of outcome assessment. Meta-analysis showed that STS significantly reduced plasma TC levels [MD = -1.34 mmol/l 95% CI (-1.59, -1.09), p < 0.00001, I 2 = 98%], TG levels [MD = -0.49 mmol/l 95% CI (-0.62, -0.35), p < 0.00001, I 2 = 97%], LDL-c levels [MD = -0.68 mmol/l (-0.80, -0.57), p < 0.00001, I 2 = 96%], increased HDL-c levels [MD = 0.26 mmol/l (0.15, 0.37), p < 0.00001, I 2 = 97%], without increasing the incidence of AEs [RR = 1.27 95% CI (0.72, 2.27), p = 0.94, I 2 = 0%] in patients with CHD. Conclusion: STS can safely and effectively reduce plasma TC, TG and LDL-c levels in patients with CHD, and improve plasma HDL-c levels. However, these findings require careful recommendation due to the low overall quality of RCTs at present. More multi-center, randomized, double-blind, placebo-controlled trials which are designed follow the CONSORT 2010 guideline are needed.

Exercise and Circulating Microparticles in Healthy Subjects.

This study aimed to explore the relationship between exercise and circulating microparticles (CMPs). PubMed, Web of Science, Embase, and the Cochrane Library databases were searched until August 13, 2020, using the terms "exercise" and "cell-derived microparticles." The Cochrane tool of risk of bias and the Methodological Index for Non-Randomized Studies were used to grade the studies. Twenty-six studies that met criteria were included in this review, including one before-after self-control study, 2 cohort studies, 4 randomized control trials, 5 case-control studies, and 14 descriptive studies. The studies were divided into a single bout and long-term exercise. The types of MPs contained endothelium-derived microparticles (EMPs), leukocyte-derived microparticles (LMPs), platelet-derived microparticles (PMPs), and erythrocyte-derived microparticles (ErMPs). This first systematic review found that the levels of CMPs continued to increase after a single bout of exercise in untrained subjects and were lower in trained subjects. PMPs expressed a transient increase after a single bout of exercise, and the proportion and duration of PMPs increment reduced in long-term exercise. Most studies showed a decline in LMPs in trained subjects after a single bout and long-term exercise, and variable changes were found in EMPs and ErMPs after exercise. A single bout of exercise drives the vessels exposed to high shear stress that promotes the formation of CMPs. However, the decline in CMPs in trained subjects may be attributed to the fact that they have a better ability to adapt to changes in hemodynamics and cellular function during exercise.

Therapeutic Effect of Platinum Nanoparticles on Atherosclerosis Research Model Based on Microfluidics and Determination of Injury.

The atherosclerosis (AS) microenvironment plays an important role in pathogenicity, including blood flow and blood pressure, high cholesterol, high blood sugar, angiotensin II, tumor necrosis factor, and the like. The AS microfluidic model was established, and the fluid shear stress and cyclic stretching were set to 5.07 Pa and 1.17 Hz to simulate normal blood flow, respectively. The effects of different biochemical environments on endothelial cells (ECs) and cardiomyocytes were analyzed. The results confirmed that different biochemical environments had significant damage to ECs and cardiomyocytes. Subsequently, the further effect of ECs on cardiomyocytes in AS microenvironment was studied, and the results proved that ECs caused further damage to cardiomyocytes under AS biochemical factors. We used Pt nanoparticles (Pt NPs) to study the anti-AS efficiency. The results showed that the addition of Pt NPs played a particular role in the AS treatment of ECs in the AS microenvironment, and the protection for myocardial cells was achieved.

Effects and mechanisms of glucose-insulin-potassium on post-procedural myocardial injury after percutaneous coronary intervention.

OBJECTIVE: To evaluate the effects and mechanisms of glucose-insulin-potassium (GIK) on post-procedural myocardial injury (PMI) after percutaneous coronary intervention (PCI). METHODS: A total of 200 non-diabetic patients with documented coronary heart disease (CHD) were divided into the Group GIK and Group G, with 100 patients in each group. Patients in Group G were given intravenous infusion of glucose solution 2 hours before PCI. As compared, patients in Group GIK were given GIK. RESULTS: Both post-procedural creatine phosphokinase isoenzyme MB (CK-MB; 62.1 ± 47.8 vs. 48.8 ± 52.6 U/L, P = 0.007) and cTnI (0.68 ± 0.83 vs. 0.19 ± 0.24 ng/mL, P < 0.001) in Group GIK were significantly higher than those in Group G. In Group G, 9.0% and 4.0% of patients had post-procedural increases in CK-MB 1-3 times and > 3 times, which were significantly lower than those in Group GIK (14.0% and 7.0%, respectively; all P values < 0.01); 13.0% and 7.0% of patients had post-procedural increases in cTnI 1-3 times and > 3 times, which were also significantly lower than those in Group GIK (21.0% and 13.0%, respectively; all P < 0.001). Pre-procedural (10.2 ± 4.5 vs. 5.1 ± 6.3, P < 0.001) and post-procedural rapid blood glucose (RBG) levels (8.9 ± 3.9 vs. 5.3 ± 5.6, P < 0.001) in Group G were higher than those in Group GIK. In adjusted logistic models, usage of GIK (compared with glucose solution) remained significantly and independently associated with higher risk of post-procedural increases in both CK-MB and cTnI levels > 3 times. Furthermore, pre-procedural RBG levels < 5.0mmol/L were significantly associated with higher risk of post-procedural increases in both CK-MB and cTnI levels. CONCLUSIONS: In non-diabetic patients with CHD, the administration of GIK may increase the risk of PMI due to hypoglycemia induced by GIK.

Regulation of lipoprotein-associated phospholipase A2 silencing on myocardial fibrosis in mice with coronary atherosclerosis.

To explore the regulation of PLA2G7 silencing on myocardial fibrosis in mice with coronary atherosclerosis, we established model of atherosclerosis using ApoE knockout mice, and set up a normal group. The successfully modeled mice were assigned into the following three groups: PLA2G7 silencing (shRNA) group, negative control (NC) group and blank group. Peripheral blood and myocardial tissue of each group of mice were harvested. The expressions of serum total cholesterol, triglyceride, low density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) in mice were determine using Elisa, and the atherosclerosis index was calculated. The pathological changes of myocardial tissue were observed after HE staining. The collagen volume fraction in myocardium was determined with the use of Masson staining. The expression of PLA2G7 in myocardial tissue as well as myocardial fibrosis markers C-reactive protein, interleukin-6 and intercellular adhesion molecule-1 in each group were detected by qRT-PCR and Western blot. The area of thoracic aorta injury was detected after oil red O staining. Compared with the normal group, the levels of total cholesterol, triglyceride and LDL-C were increased, HDL-C levels were decreased, and atherosclerosis index was increased in the PLA2G7 shRNA group, NC group and blank group (all P < 0.05). The pathological state of myocardial tissue in the other three groups (except for the normal group) was obvious, but the PLA2G7 shRNA group showed certain improvement as compared with the blank group and the NC group (all P < 0.05). Compared with the NC group, the PLA2G7 shRNA group had significantly decreased collagen volume fraction, myocardial fibrosis and area of thoracic aorta injury (all P < 0.05). In conclusion, PLA2G7 silencing can improve the myocardial fibrosis in mice with coronary atherosclerosis, and PLA2G7 is expected to be a potential target for coronary atherosclerosis.

The serum anion gap is associated with disease severity and all-cause mortality in coronary artery disease.

OBJECTIVE: To evaluate the associations between the serum anion gap (AG) with the severity and prognosis of coronary artery disease (CAD). METHODS: We measured serum electrolytes in 18,115 CAD patients indicated by coronary angiography. The serum AG was calculated according to the equation: AG = Na+[(mmol/L) + K+ (mmol/L)] - [Cl- (mmol/L) + HCO3- (mmol/L)]. RESULTS: A total of 4510 (24.9%) participants had their AG levels greater than 16 mmol/L. The serum AG was independently associated with measures of CAD severity, including more severe clinical types of CAD (P < 0.001) and worse cardiac function (P = 0.004). Patients in the 4th quartile of serum AG (≥ 15.92 mmol/L) had a 5.171-fold increased risk of 30 days all-cause death (P < 0.001). This association was robust, even after adjustment for age, sex, evaluated glomerular filtration rate [hazard ratio (HR): 4.861, 95% confidence interval (CI): 2.150-10.993, P < 0.001], clinical diagnosis, severity of coronary artery stenosis, cardiac function grades, and other confounders (HR: 3.318, 95% CI: 1.76-2.27, P = 0.009). CONCLUSION: In this large population-based study, our findings reveal a high percentage of increased serum AG in CAD. Higher AG is associated with more severe clinical types of CAD and worse cardiac function. Furthermore, the increased serum AG is an independent, significant, and strong predictor of all-cause mortality. These findings support a role for the serum AG in the risk-stratification of CAD.

The Impact of Different Plasma Glucose Levels on Heart Rate in Experimental Rats With Acute Myocardial Infarction.

BACKGROUND: The aim of the study was to evaluate the impact of different plasma glucose levels on heart rate (HR) in experimental rats with acute myocardial infarction (AMI). METHODS: One hundred and twenty-one male Wistar rats were randomly divided into AMI group (n = 70) and sham-operation group (n = 51). Both groups had low, normal and high glucose levels, respectively. In the former group, hypertonic glucose was injected into the rats to make their blood glucose levels above 16 mmol/L and insulin below 3.3 mmol/L; then, the left anterior descending artery was ligated. In the later group, the models of different blood glucose levels were the same as the former ones, but false operations, thread without ligating, were given to the rats. Electrocardiogram and troponin I (TnI) confirmed that the models were prepared successfully. Electrocardiogram expression of AMI was the formation of Q-wave in over three adjacent leads and abnormal elevation of TnI. RESULTS: The HR of the rats in the hypoglycemic group is higher than that of the hyperglycemic group and normal blood glucose group before AMI (P < 0.05). The HR of the hyperglycemic rats is higher than that of the hypoglycemic group and normal blood glucose group after AMI (P < 0.05). In the hypoglycemic group, the HR of the rats who suffered from AMI was lower than that of the rats of the sham group (P < 0.05). CONCLUSION: Hypoglycemia allows faster HR and the HR in the rats with hyperglycemia is higher than that in the rats with hypoglycemia among the AMI rats.

Mutation and clinical relevance in a large cohort of unrelated Chinese patients with hypertrophic cardiomyopathy / 中华心血管病杂志

<p><b>OBJECTIVE</b>To explore the genetic basis and phenotypic correlation with disease severity in a large cohort of Chinese patients with hypertrophic cardiomyopathy (HCM).</p><p><b>METHODS</b>A total of 179 unrelated Chinese HCM patients admitted to our department from 2002 to 2011 were enrolled in this study. Direct gene sequencing of β-myosin heavy chain (MYH7), myosin binding protein-C ( MYBPC3), and cardiac troponin T (TNNT2) were performed and clinical data were obtained in these patients.</p><p><b>RESULTS</b>A total of 34 mutations were identified in 40 patients (22.3%), 79.4% (27/34) mutations occurred only once and a possible hot spot, A26 in MYH7, was found. Distribution of mutations was 52.9% (18/34) (MYBPC3), 35.3% (12/34) ( MYH7) and 11.8% (4/34) (TNNT2) respectively. Double mutations were identified in 2.2% (4/179) patients. Genotype-positive patients were associated with an earlier symptom onset, severer left ventricular hypertrophy, a higher incidence of syncope, and were more likely to have positive family history of HCM or sudden cardiac death (SCD) , and were more likely to progress into heart failure (24.2% vs. 5.0%, P = 0.002) and at a higher risk of SCD (9.1% vs. 0, P = 0.009) during the 6.5-year follow-up. No statistical difference in any clinical parameters and outcomes was found between patients carrying MYBPC3 and MYH7 mutations. Double mutations were associated with malignant clinical progression in this cohort. Different phenotype severity could be seen in HCM patients with same genotype (e. g. MYH7-1736T, TNNT2-R92W).</p><p><b>CONCLUSION</b>MYBPC3 is the most predominant gene mutation in this HCM cohort. The presence of a sarcomere mutation in patients with HCM is associated with poor clinical outcome, although no specific genes or mutations can exactly predict the severity of clinical phenotypes.</p>

Association of dysglycemia and all-cause mortality across the spectrum of coronary artery disease.

OBJECTIVE: To assess the association between fasting plasma glucose (FPG) and all-cause mortality across the spectrum of coronary artery disease (CAD). PATIENTS AND METHODS: The study included 18,999 patients during a study period of April 1, 2004, through October 31, 2010. The primary end points were in-hospital and follow-up all-cause mortality. According to the quartiles of FPG levels, patients were categorized into 4 groups: quartile 1, less than 5.1 mmol/L; quartile 2, 5.1 to less than 5.9 mmol/L; quartile 3, 5.9 to less than 7.5 mmol/L; and quartile 4, 7.5 mmol/L or greater. The conversion factor for units of plasma glucose is 1.00 mmol/L equals 18 mg/dL. Presented as mg/dL, the 4 quartile ranges of plasma glucose concentrations used in our data analysis are ≤90.0 mg/dL, 90.1-106.0 mg/dL, 106.1 mg/dL-135.0 mg/dL and ≥135.1 mg/dL. Quartile 1 was recognized as the lower glycemic group, quartiles 2 and 3 as the normoglycemic groups, and quartile 4 as the higher glycemic group. RESULTS: In patients with acute myocardial infarction, all-cause mortality for the dysglycemic groups was higher than for the normoglycemic groups: in-hospital mortality for quartiles 1, 2, 3, and 4 was 1.0%, 0.9%, 0.2%, and 1.5%, respectively (P=.001); follow-up mortality for quartiles 1, 2, 3, and 4 was 1.7%, 0.9%, 0.3%, and 1.8%, respectively (P<.001). In patients with stable CAD, no significant differences in mortality were found among groups. However, in patients with unstable angina pectoris, the normoglycemic groups had lower follow-up mortality and roughly equal in-hospital mortality compared with the dysglycemic groups. After adjusting for confounding factors, this observation persisted. CONCLUSION: The association between lower FPG level and mortality differed across the spectrum of CAD. In patients with acute myocardial infarction, there was a U-shaped relationship. In patients with stable CAD or unstable angina pectoris, mildly to moderately decreasing FPG level was associated with neither higher nor lower all-cause mortality.

[Comparative study of gene mutation between Chinese patients with familial and sporadic hypertrophic cardiomyopathy].

OBJECTIVE: To compare the gene mutation between Chinese patients with familial and sporadic hypertrophic cardiomyopathy (HCM). METHODS: Peripheral blood samples were collected from 36 patients with familial HCM (FHCM) and 50 patients with sporadic HCM (SHCM), all un-related and from different provinces of China. PCR was used to amplify the 26 protein-coding axons of beta-myosin heavy chain (MYH7), 16 exons for cardiac troponin T (TNNT2), and 38 exons for cardiac myosin-binding protein C (MYBPC3). The amplified products were sequenced and compared with the standard sequence in the genBank so as to determine the potential mutation sites. RESULTS: (1) 13 of the 36 FHCM patients (36.1%) harbored 3 different mutations in MYH7 gene: Arg663His in exon18, Glu924Lys in exon 23, and Ile736Thr in exon 20. Of the 50 SHCM patients, only 1 (2%) harbored MYH7 gene missence mutation: Ile736Thr located in exon 20. (2) TNNT2 was not identified in all SHCM patients and FHCM patients. (3) MYBPC3 was not identified in all SHCM patients. Four FHCM patients harbored 2 different mutations: Arg502Trp in exon 18 and Arg346fs in exon 13 respectively. CONCLUSION: MYH7 and MYBPC3 may be the dominant disease-causing genes in Chinese familial HCM patients; however the mutation rate of MYH7 and MYBPC3 genes is significantly lower in the SHCM patients compared with the FHCM patients. TNNT2 seems not the predominant disease-causing gene in all Chinese patients with HCM.