Objective To explore the relationship of inflammation and endothelial dysfunction with risks to cardiovascular disease （CVD）. Methods Blood pressure, body weight, body height, waist circumference and lifestyle risk ...Objective To explore the relationship of inflammation and endothelial dysfunction with risks to cardiovascular disease （CVD）. Methods Blood pressure, body weight, body height, waist circumference and lifestyle risk factors were measured and studied among 2589 participants in Inner Mongolia of China, and biomarkers of inflammation and endothelial dysfunction including high-sensitivity C-reactive protein （hsCRP）, soluble inter-cellular adhesion molecule-1 （slCAM-1）, soluble E-selectin （sE-selectin）, and angiotensin II were investigated. Results Subjects with metabolic risk factors for CVD had higher levels of hsCRP, sE-selectin and slCAM-1 than those without such risk factors （all P〈O.05）. Levels of all biomarkers positively and significantly increased with aggregation of the metabolic risk factors among the subjects （all P for trend 〈0.001）. Data from the multivariate analysis showed that participants with high levels of hsCRP [odds ratio （OR}： 1.96, 95% confidence interval （CI）： 1.52-2.53], sE-selectin （OR： 1.35, 95% Cl： 1.05-1.72）, and angiotensin II （OR： 1.81, 95% CI＂ 1.40-2.33） were more likely to develop hypertension; participants with high levels of hsCRP （OR： 2.33, 95% CI： 1.85-2.94）, sE-selectin （OR： 1.24, 95% CI： 1.00-1.54）, and slCAM-1 （OR： 1.70, 95% CI： 1.30-2.22） were more likely to develop dyslipidemia, and those with high levels of hsCRP （OR： 2.95, 95% CI： 2.27-3.83） and slCAM-I（OR： 2.80, 95% CI： 2.06-3.80） were more likely to develop hyperglycemia. Conclusion Biomarkers of inflammation and endothelial dysfunction were separately associated with relevant metabolic risk factors for CVD. And appropriate measures should be taken to control inflammation and improve endothelial function among individuals with different metabolic risk factors for CVD.展开更多
Macro and microvascular disease are the main cause of morbi-mortality in type 1 diabetes(T1DM).Although there is a clear association between endothelial dysfunction and atherosclerosis in type 2 diabetes,a cause-effec...Macro and microvascular disease are the main cause of morbi-mortality in type 1 diabetes(T1DM).Although there is a clear association between endothelial dysfunction and atherosclerosis in type 2 diabetes,a cause-effect relationship is less clear in T1 DM.Although endothelial dysfunction(ED) precedes atherosclerosis,it is not clear weather,in recent onset T1 DM,it may progress to clinical macrovascular disease.Moreover,endothelial dysfunction may either be reversed spontaneously or in response to intensive glycemic control,long-term exercise training and use of statins.Acute,long-term and post-prandial hyperglycemia as well as duration of diabetes and microalbuminuria are all conditions associated with ED in T1 DM.The pathogenesis of endothelial dysfunction is closely related to oxidative-stress.NAD(P)H oxidase over activity induces excessive superoxide production inside the mitochondrial oxidative chain of endothelial cells,thus reducing nitric oxide bioavailability and resulting in peroxynitrite formation,a potent oxidant agent.Moreover,oxidative stress also uncouples endothelial nitric oxide synthase,which becomes dysfunctional,inducing formation of superoxide.Other important mechanisms are the activation of both the polyol and protein kinase C pathways as well as the presence of advanced glycation end-products.Future studies are needed to evaluate the potential clinical applicability of endothelial dysfunction as a marker for early vascular complications in T1 DM.展开更多
The incidence of type 2 diabetes mellitus is growing in epidemic proportions and has become one of the most critical public health concerns.Cardiovascular complications associated with diabetes are the leading cause o...The incidence of type 2 diabetes mellitus is growing in epidemic proportions and has become one of the most critical public health concerns.Cardiovascular complications associated with diabetes are the leading cause of morbidity and mortality.The cardiovascular diseases that accompany diabetes include angina,myocardial infarction,stroke,peripheral artery disease,and congestive heart failure.Among the various risk factors generated secondary to hyperglycemic situations,advanced glycation end products(AGEs)are one of the important targets for future diagnosis and prevention of diabetes.In the last decade,AGEs have drawn a lot of attention due to their involvement in diabetic pathophysiology.AGEs can be derived exogenously and endogenously through various pathways.These are a nonhomogeneous,chemically diverse group of compounds formed nonenzymatically by condensation between carbonyl groups of reducing sugars and free amino groups of protein,lipids,and nucleic acid.AGEs mediate their pathological effects at the cellular and extracellular levels by multiple pathways.At the cellular level,they activate signaling cascades via the receptor for AGEs and initiate a complex series of intracellular signaling resulting in reactive oxygen species generation,inflammation,cellular proliferation,and fibrosis that may possibly exacerbate the damaging effects on cardiac functions in diabetics.AGEs also cause covalent modifications and cross-linking of serum and extracellular matrix proteins;altering their structure,stability,and functions.Early diagnosis of diabetes may prevent its progression to complications and decrease its associated comorbidities.In the present review,we recapitulate the role of AGEs as a crucial mediator of hyperglycemia-mediated detrimental effects in diabetes-associated complications.Furthermore,this review presents an overview of future perspectives for new therapeutic interventions to ameliorate cardiovascular complications in diabetes.展开更多
Patients with diabetes mellitus are at high risk of developing atherosclerosis, associated with higher rates of micro and macro vascular involvement such as coronary artery disease and renal disease. The role of hyper...Patients with diabetes mellitus are at high risk of developing atherosclerosis, associated with higher rates of micro and macro vascular involvement such as coronary artery disease and renal disease. The role of hyperglycemia to induce synthesis of reactive oxygen species by the oxidation of glucose, leading to an increased production of advanced glycosylation end products, as well as inflammation and oxidative stress has been proposed as a possible mechanism in the pathogenesis of endothelial dysfunction(ED). The interaction between C-peptide- the connecting segment of pro-insulin-and nitric oxide in vasodilation is also discussed. Therefore, endothelial dysfunction has been identified as an early marker of vascular disorder in type 1 and type 2 diabetes mellitus. In some other diseases, ED has been considered an independent predictor of vascular disease, regardless of the method used. Studies have demonstrated the importance of endothelial dysfunction as an useful tool for identifying the risk of vascular complications in patients with type 1 diabetes mellitus, particularly as regards to renal impairment. The aim of this review is to clarify the prognostic value of endothelial dysfunction as a marker of vascular disease in these subjects.展开更多
The number of the circulating angiogenic cells （CACs） and colony forming units （CFUs） derived from cultured circulating mononuclear cells （MNCs） represents a laboratory surrogate for endothelial cell repair abil...The number of the circulating angiogenic cells （CACs） and colony forming units （CFUs） derived from cultured circulating mononuclear cells （MNCs） represents a laboratory surrogate for endothelial cell repair ability. The serum of men with erectile dysfunction （ED） and vascular risk factors （VRFs） showed an increased level of endothelial cell damage/dysfunction markers and reduced the numbers of CACs and CFUs derived from the cells of healthy men. We analyzed whether treating men with ED and VRFs with the selective phosphodiesterase type 5 inhibitor tadalafil improved the endothelial cell repair ability and reduced the levels of the serum markers of endothelial cell damage/dysfunction. MNCs from healthy men were cultured with 20% serum from 36 ED patients to obtain CACs and CFUs. The ED patients were evaluated before and after 4weeks of treatment with tadalafil （20 mg every other day） or with a placebo. The tadalafil treatment improved erectile function （P = 0.0028）, but had no effect on the inhibitory effects of serum from ED patients on the CACs and CFUs derived from healthy men. The levels of endothelin-1 （P = 0.011） and tissue type plasminogen activator （P = 0.005） were reduced after treatment compared to baseline and those of the placebo group, whereas no changes were observed in the E-selectin levels. The tadalafil treatment in the ED patients with VRFs resulted in only a modest effect on the laboratory measures of the endothelial cell damage/dysfunction and repair ability. The proposed beneficial effect of phosphodiesterase type 5 inhibition on vascular homeostasis requires further analysis.展开更多
Background: Cardiovascular diseases (CVD) are the leading cause of morbidity and mortality in Western societies and are rapidly becoming a worldwide health problem. African-Americans have increased morbidity and morta...Background: Cardiovascular diseases (CVD) are the leading cause of morbidity and mortality in Western societies and are rapidly becoming a worldwide health problem. African-Americans have increased morbidity and mortality rates from CVD. Our study aimed to assess the effects of the CVD risk factors burden alone versus with diabetes mellitus in a high riskCVDpopulation. Methods: The two study groups consisted of thirty seven diabetics and thirty seven non-diabetic African-Americans aged ≥55 years without clinical atherosclerosis having similar cardiovascular risk factors (age, hypertension, hypercholesterolemia, smoking, and body mass index) except for diabetes mellitus. Brachial artery flow-mediated dilation (FMD), Nitroglycerin-mediated dilatation (NMD) and carotid intima-media thickness (IMT) were recorded in all subjects. Results: Endothelial function as assessed by the brachial artery FMD was significantly impaired in the diabetic group compared to the non-diabetic group (7.8 ± 5 vs 3.3 ± 4;p = 0.0001). There were no differences in neither Nitroglycerin-mediated dilatation (NMD) nor carotid intima-media thickness (IMT) in the diabetic and non-diabetic groups. Conclusion: The contribution of diabetes to the development of endothelial dysfunction in subjects with clustering of CVD risk factors may be early as indicated by significant functional changes preceeding structural vascular changes..展开更多
Non-alcoholic fatty liver disease(NAFLD)has emerged as a public health problem of epidemic proportions worldwide.Accumulating clinical and epidemiological evidence indicates that NAFLD is not only associated with live...Non-alcoholic fatty liver disease(NAFLD)has emerged as a public health problem of epidemic proportions worldwide.Accumulating clinical and epidemiological evidence indicates that NAFLD is not only associated with liver-related morbidity and mortality but also with an increased risk of coronary heart disease(CHD),abnormalities of cardiac function and structure(e.g.,left ventricular dysfunction and hypertrophy,and heart failure),valvular heart disease(e.g.,aortic valve sclerosis)and arrhythmias(e.g.,atrial fibrillation).Experimental evidence suggests that NAFLD itself,especially in its more severe forms,exacerbates systemic/hepatic insulin resistance,causes atherogenic dyslipidemia,and releases a variety of pro-inflammatory,pro-coagulant and pro-fibrogenic mediators that may play important roles in the pathophysiology of cardiac and arrhythmic complications.Collectively,these findings suggest that patients with NAFLD may benefit from more intensive surveillance and early treatment interventions to decrease the risk for CHD and other cardiac/arrhythmic complications.The purpose of this clinical review is to summarize the rapidly expanding body of evidence that supports a strong association between NAFLD and cardiovascular,cardiac and arrhythmic complications,to briefly examine the putative biological mechanisms underlying this association,and to discuss some of the current treatment options that may influence both NAFLD and its related cardiac and arrhythmic complications.展开更多
Non-alcoholic fatty liver disease(NAFLD)has emerged as the commonest cause of chronic liver disease worldwide in recent years.With time,our understanding of NAFLD has evolved from an isolated liver condition to a syst...Non-alcoholic fatty liver disease(NAFLD)has emerged as the commonest cause of chronic liver disease worldwide in recent years.With time,our understanding of NAFLD has evolved from an isolated liver condition to a systemic disease with significant manifestations beyond the liver.Amongst them,cardiovascular diseases(CVDs)are the most important and clinically relevant.Recent research supports a strong independent link between NALFD and CVD beyond the shared risk factors and pathophysiology.Female sex hormones are well known to not only protect against CVD in pre-menopausal females,but also contribute to improved adipose tissue function and preventing its systemic deposition.Recent research highlights the increased risk of major adverse cardiovascular-cerebral events(MACCE)amongst male with NAFLD compared to females.Further,racial variation was observed in MACCE outcomes in NAFLD,with excess mortality in the Native Americans and Asian Pacific Islanders compared to the other races.展开更多
Background:Research on fetal congenital heart defect(CHD)mostly focuses on etiology and mechanisms.However,studies on maternal complications or pathophysiology are limited.Our objective was to determine whether vascul...Background:Research on fetal congenital heart defect(CHD)mostly focuses on etiology and mechanisms.However,studies on maternal complications or pathophysiology are limited.Our objective was to determine whether vascular dysfunction exists in pregnant women carrying a fetus with congenital heart defects.Methods:We conducted a case-control study.27 cases of pregnant women carrying a fetus with major CHD admitted to our hospital for delivery between April 2021 and August 2022 were selected.Every case was matched with about 2 pregnant complication-free controls without fetal abnormalities.The proangiogenic and anti-angiogenic factors and pregnancy outcomes were compared.Results:The proangiogenic factors include vascular endothelial growth factor(VEGF)and placental growth factor(PlGF).The anti-angiogenic factors involve soluble fms-like tyrosine kinase 1(sFlt-1)and soluble endoglin(sEng).No differences were found in maternal plasma concentrations of PlGF,VEGF,and sFlt-1 between case-control groups when analyzed at 36 weeks≤gestational age(GA)<39 weeks and 39 weeks≤GA≤41 weeks.The concentrations of sEng in maternal plasma in the fetal CHD group were significantly higher than those in the control group:0.60(0.77)vs.0.32(0.26)ng/ml at 36 weeks≤GA<39 weeks,p=0.001 and 0.75(0.55)vs.0.28(0.27)ng/ml at 39 weeks≤GA≤41 weeks,p<0.001.Conclusion:Vascular dysfunction exists in pregnant women with fetal congenital heart defects,manifesting significantly elevated sEng concentration at delivery.展开更多
Emerging data highlights the heightened risk of atherosclerotic cardiovascular diseases(ASCVD)in patients with chronic inflammatory disorders,particularly those afflicted with inflammatory bowel disease(IBD).This revi...Emerging data highlights the heightened risk of atherosclerotic cardiovascular diseases(ASCVD)in patients with chronic inflammatory disorders,particularly those afflicted with inflammatory bowel disease(IBD).This review delves into the epidemiological connections between IBD and ASCVD,elucidating potential underlying mechanisms.Furthermore,it discusses the impact of current IBD treatments on cardiovascular risk.Additionally,the cardiovascular adverse effects of novel small molecule drugs used in moderate-to-severe IBD are investigated,drawing parallels with observations in patients with rheumatoid arthritis.This article aims to comprehensively evaluate the existing evidence supporting these associations.To achieve this,we conducted a meticulous search of PubMed,spanning from inception to August 2023,using a carefully selected set of keywords.The search encompassed topics related to IBD,such as Crohn’s disease and ulcerative colitis,as well as ASCVD,including coronary artery disease,cardiovascular disease,atrial fibrillation,heart failure,conduction abnormalities,heart blocks,and premature coronary artery disease.This review encompasses various types of literature,including retrospective and prospective cohort studies,clinical trials,meta-analyses,and relevant guidelines,with the objective of providing a comprehensive overview of this critical intersection of inflammatory bowel disease and cardiovascular health.展开更多
The bidirectional relationship between periodontitis and type 2 diabetes mellitus has been well-established.However,the underlying molecular mechanisms remain unclear.Diabetic retinopathy(DR)is an important complicati...The bidirectional relationship between periodontitis and type 2 diabetes mellitus has been well-established.However,the underlying molecular mechanisms remain unclear.Diabetic retinopathy(DR)is an important complication of diabetes,but there are few studies on the relationship between DR and periodontitis,especially on the intrinsic inflammatory pathway mechanism.This article reviews the latest clinical data on how diabetes promotes susceptibility to periodontitis from the epidemiological and molecular perspectives,with a special focus on the key roles of systemic inflammation and endothelial dysfunction in the interplay between DR and periodontitis.Comprehension of the intertwined pathogenesis of DR and periodontitis can better guide the development of comprehensive management strategies for glycemic control and periodontal health,with the aim of mitigating the progression of DR and enhancing overall well-being.展开更多
基金supported by the National Natural Science Foundation of China (Grant Nos.30471484 and 30972531)Project of the Priority Academic Program Development of Jiangsu Higher Education Institutions
文摘Objective To explore the relationship of inflammation and endothelial dysfunction with risks to cardiovascular disease （CVD）. Methods Blood pressure, body weight, body height, waist circumference and lifestyle risk factors were measured and studied among 2589 participants in Inner Mongolia of China, and biomarkers of inflammation and endothelial dysfunction including high-sensitivity C-reactive protein （hsCRP）, soluble inter-cellular adhesion molecule-1 （slCAM-1）, soluble E-selectin （sE-selectin）, and angiotensin II were investigated. Results Subjects with metabolic risk factors for CVD had higher levels of hsCRP, sE-selectin and slCAM-1 than those without such risk factors （all P〈O.05）. Levels of all biomarkers positively and significantly increased with aggregation of the metabolic risk factors among the subjects （all P for trend 〈0.001）. Data from the multivariate analysis showed that participants with high levels of hsCRP [odds ratio （OR}： 1.96, 95% confidence interval （CI）： 1.52-2.53], sE-selectin （OR： 1.35, 95% Cl： 1.05-1.72）, and angiotensin II （OR： 1.81, 95% CI＂ 1.40-2.33） were more likely to develop hypertension; participants with high levels of hsCRP （OR： 2.33, 95% CI： 1.85-2.94）, sE-selectin （OR： 1.24, 95% CI： 1.00-1.54）, and slCAM-1 （OR： 1.70, 95% CI： 1.30-2.22） were more likely to develop dyslipidemia, and those with high levels of hsCRP （OR： 2.95, 95% CI： 2.27-3.83） and slCAM-I（OR： 2.80, 95% CI： 2.06-3.80） were more likely to develop hyperglycemia. Conclusion Biomarkers of inflammation and endothelial dysfunction were separately associated with relevant metabolic risk factors for CVD. And appropriate measures should be taken to control inflammation and improve endothelial function among individuals with different metabolic risk factors for CVD.
文摘Macro and microvascular disease are the main cause of morbi-mortality in type 1 diabetes(T1DM).Although there is a clear association between endothelial dysfunction and atherosclerosis in type 2 diabetes,a cause-effect relationship is less clear in T1 DM.Although endothelial dysfunction(ED) precedes atherosclerosis,it is not clear weather,in recent onset T1 DM,it may progress to clinical macrovascular disease.Moreover,endothelial dysfunction may either be reversed spontaneously or in response to intensive glycemic control,long-term exercise training and use of statins.Acute,long-term and post-prandial hyperglycemia as well as duration of diabetes and microalbuminuria are all conditions associated with ED in T1 DM.The pathogenesis of endothelial dysfunction is closely related to oxidative-stress.NAD(P)H oxidase over activity induces excessive superoxide production inside the mitochondrial oxidative chain of endothelial cells,thus reducing nitric oxide bioavailability and resulting in peroxynitrite formation,a potent oxidant agent.Moreover,oxidative stress also uncouples endothelial nitric oxide synthase,which becomes dysfunctional,inducing formation of superoxide.Other important mechanisms are the activation of both the polyol and protein kinase C pathways as well as the presence of advanced glycation end-products.Future studies are needed to evaluate the potential clinical applicability of endothelial dysfunction as a marker for early vascular complications in T1 DM.
文摘The incidence of type 2 diabetes mellitus is growing in epidemic proportions and has become one of the most critical public health concerns.Cardiovascular complications associated with diabetes are the leading cause of morbidity and mortality.The cardiovascular diseases that accompany diabetes include angina,myocardial infarction,stroke,peripheral artery disease,and congestive heart failure.Among the various risk factors generated secondary to hyperglycemic situations,advanced glycation end products(AGEs)are one of the important targets for future diagnosis and prevention of diabetes.In the last decade,AGEs have drawn a lot of attention due to their involvement in diabetic pathophysiology.AGEs can be derived exogenously and endogenously through various pathways.These are a nonhomogeneous,chemically diverse group of compounds formed nonenzymatically by condensation between carbonyl groups of reducing sugars and free amino groups of protein,lipids,and nucleic acid.AGEs mediate their pathological effects at the cellular and extracellular levels by multiple pathways.At the cellular level,they activate signaling cascades via the receptor for AGEs and initiate a complex series of intracellular signaling resulting in reactive oxygen species generation,inflammation,cellular proliferation,and fibrosis that may possibly exacerbate the damaging effects on cardiac functions in diabetics.AGEs also cause covalent modifications and cross-linking of serum and extracellular matrix proteins;altering their structure,stability,and functions.Early diagnosis of diabetes may prevent its progression to complications and decrease its associated comorbidities.In the present review,we recapitulate the role of AGEs as a crucial mediator of hyperglycemia-mediated detrimental effects in diabetes-associated complications.Furthermore,this review presents an overview of future perspectives for new therapeutic interventions to ameliorate cardiovascular complications in diabetes.
文摘Patients with diabetes mellitus are at high risk of developing atherosclerosis, associated with higher rates of micro and macro vascular involvement such as coronary artery disease and renal disease. The role of hyperglycemia to induce synthesis of reactive oxygen species by the oxidation of glucose, leading to an increased production of advanced glycosylation end products, as well as inflammation and oxidative stress has been proposed as a possible mechanism in the pathogenesis of endothelial dysfunction(ED). The interaction between C-peptide- the connecting segment of pro-insulin-and nitric oxide in vasodilation is also discussed. Therefore, endothelial dysfunction has been identified as an early marker of vascular disorder in type 1 and type 2 diabetes mellitus. In some other diseases, ED has been considered an independent predictor of vascular disease, regardless of the method used. Studies have demonstrated the importance of endothelial dysfunction as an useful tool for identifying the risk of vascular complications in patients with type 1 diabetes mellitus, particularly as regards to renal impairment. The aim of this review is to clarify the prognostic value of endothelial dysfunction as a marker of vascular disease in these subjects.
文摘The number of the circulating angiogenic cells （CACs） and colony forming units （CFUs） derived from cultured circulating mononuclear cells （MNCs） represents a laboratory surrogate for endothelial cell repair ability. The serum of men with erectile dysfunction （ED） and vascular risk factors （VRFs） showed an increased level of endothelial cell damage/dysfunction markers and reduced the numbers of CACs and CFUs derived from the cells of healthy men. We analyzed whether treating men with ED and VRFs with the selective phosphodiesterase type 5 inhibitor tadalafil improved the endothelial cell repair ability and reduced the levels of the serum markers of endothelial cell damage/dysfunction. MNCs from healthy men were cultured with 20% serum from 36 ED patients to obtain CACs and CFUs. The ED patients were evaluated before and after 4weeks of treatment with tadalafil （20 mg every other day） or with a placebo. The tadalafil treatment improved erectile function （P = 0.0028）, but had no effect on the inhibitory effects of serum from ED patients on the CACs and CFUs derived from healthy men. The levels of endothelin-1 （P = 0.011） and tissue type plasminogen activator （P = 0.005） were reduced after treatment compared to baseline and those of the placebo group, whereas no changes were observed in the E-selectin levels. The tadalafil treatment in the ED patients with VRFs resulted in only a modest effect on the laboratory measures of the endothelial cell damage/dysfunction and repair ability. The proposed beneficial effect of phosphodiesterase type 5 inhibition on vascular homeostasis requires further analysis.
文摘Background: Cardiovascular diseases (CVD) are the leading cause of morbidity and mortality in Western societies and are rapidly becoming a worldwide health problem. African-Americans have increased morbidity and mortality rates from CVD. Our study aimed to assess the effects of the CVD risk factors burden alone versus with diabetes mellitus in a high riskCVDpopulation. Methods: The two study groups consisted of thirty seven diabetics and thirty seven non-diabetic African-Americans aged ≥55 years without clinical atherosclerosis having similar cardiovascular risk factors (age, hypertension, hypercholesterolemia, smoking, and body mass index) except for diabetes mellitus. Brachial artery flow-mediated dilation (FMD), Nitroglycerin-mediated dilatation (NMD) and carotid intima-media thickness (IMT) were recorded in all subjects. Results: Endothelial function as assessed by the brachial artery FMD was significantly impaired in the diabetic group compared to the non-diabetic group (7.8 ± 5 vs 3.3 ± 4;p = 0.0001). There were no differences in neither Nitroglycerin-mediated dilatation (NMD) nor carotid intima-media thickness (IMT) in the diabetic and non-diabetic groups. Conclusion: The contribution of diabetes to the development of endothelial dysfunction in subjects with clustering of CVD risk factors may be early as indicated by significant functional changes preceeding structural vascular changes..
基金Supported by(in part)the Southampton National Institute for Health Research Biomedical Research Centre(Byrne CD)grants from the School of Medicine of the Verona University(Targher GT)
文摘Non-alcoholic fatty liver disease(NAFLD)has emerged as a public health problem of epidemic proportions worldwide.Accumulating clinical and epidemiological evidence indicates that NAFLD is not only associated with liver-related morbidity and mortality but also with an increased risk of coronary heart disease(CHD),abnormalities of cardiac function and structure(e.g.,left ventricular dysfunction and hypertrophy,and heart failure),valvular heart disease(e.g.,aortic valve sclerosis)and arrhythmias(e.g.,atrial fibrillation).Experimental evidence suggests that NAFLD itself,especially in its more severe forms,exacerbates systemic/hepatic insulin resistance,causes atherogenic dyslipidemia,and releases a variety of pro-inflammatory,pro-coagulant and pro-fibrogenic mediators that may play important roles in the pathophysiology of cardiac and arrhythmic complications.Collectively,these findings suggest that patients with NAFLD may benefit from more intensive surveillance and early treatment interventions to decrease the risk for CHD and other cardiac/arrhythmic complications.The purpose of this clinical review is to summarize the rapidly expanding body of evidence that supports a strong association between NAFLD and cardiovascular,cardiac and arrhythmic complications,to briefly examine the putative biological mechanisms underlying this association,and to discuss some of the current treatment options that may influence both NAFLD and its related cardiac and arrhythmic complications.
文摘Non-alcoholic fatty liver disease(NAFLD)has emerged as the commonest cause of chronic liver disease worldwide in recent years.With time,our understanding of NAFLD has evolved from an isolated liver condition to a systemic disease with significant manifestations beyond the liver.Amongst them,cardiovascular diseases(CVDs)are the most important and clinically relevant.Recent research supports a strong independent link between NALFD and CVD beyond the shared risk factors and pathophysiology.Female sex hormones are well known to not only protect against CVD in pre-menopausal females,but also contribute to improved adipose tissue function and preventing its systemic deposition.Recent research highlights the increased risk of major adverse cardiovascular-cerebral events(MACCE)amongst male with NAFLD compared to females.Further,racial variation was observed in MACCE outcomes in NAFLD,with excess mortality in the Native Americans and Asian Pacific Islanders compared to the other races.
基金supported by grants from the Guangzhou Municipal Science and Technology Bureau(Nos.202102080466,202201011423,202206010049,2023B03J0596,2023B03J1254,2023B03J1255)Department of Science and Technology of Guangdong Province(Nos.2020B1111170011,2023A1515012501)+1 种基金the Natural Science Foundation of Guangdong Province(Nos.2023A1515010801,2021A1515011445)the National Natural Science Foundation of China(Nos.82100371,81903287).
文摘Background:Research on fetal congenital heart defect(CHD)mostly focuses on etiology and mechanisms.However,studies on maternal complications or pathophysiology are limited.Our objective was to determine whether vascular dysfunction exists in pregnant women carrying a fetus with congenital heart defects.Methods:We conducted a case-control study.27 cases of pregnant women carrying a fetus with major CHD admitted to our hospital for delivery between April 2021 and August 2022 were selected.Every case was matched with about 2 pregnant complication-free controls without fetal abnormalities.The proangiogenic and anti-angiogenic factors and pregnancy outcomes were compared.Results:The proangiogenic factors include vascular endothelial growth factor(VEGF)and placental growth factor(PlGF).The anti-angiogenic factors involve soluble fms-like tyrosine kinase 1(sFlt-1)and soluble endoglin(sEng).No differences were found in maternal plasma concentrations of PlGF,VEGF,and sFlt-1 between case-control groups when analyzed at 36 weeks≤gestational age(GA)<39 weeks and 39 weeks≤GA≤41 weeks.The concentrations of sEng in maternal plasma in the fetal CHD group were significantly higher than those in the control group:0.60(0.77)vs.0.32(0.26)ng/ml at 36 weeks≤GA<39 weeks,p=0.001 and 0.75(0.55)vs.0.28(0.27)ng/ml at 39 weeks≤GA≤41 weeks,p<0.001.Conclusion:Vascular dysfunction exists in pregnant women with fetal congenital heart defects,manifesting significantly elevated sEng concentration at delivery.
文摘Emerging data highlights the heightened risk of atherosclerotic cardiovascular diseases(ASCVD)in patients with chronic inflammatory disorders,particularly those afflicted with inflammatory bowel disease(IBD).This review delves into the epidemiological connections between IBD and ASCVD,elucidating potential underlying mechanisms.Furthermore,it discusses the impact of current IBD treatments on cardiovascular risk.Additionally,the cardiovascular adverse effects of novel small molecule drugs used in moderate-to-severe IBD are investigated,drawing parallels with observations in patients with rheumatoid arthritis.This article aims to comprehensively evaluate the existing evidence supporting these associations.To achieve this,we conducted a meticulous search of PubMed,spanning from inception to August 2023,using a carefully selected set of keywords.The search encompassed topics related to IBD,such as Crohn’s disease and ulcerative colitis,as well as ASCVD,including coronary artery disease,cardiovascular disease,atrial fibrillation,heart failure,conduction abnormalities,heart blocks,and premature coronary artery disease.This review encompasses various types of literature,including retrospective and prospective cohort studies,clinical trials,meta-analyses,and relevant guidelines,with the objective of providing a comprehensive overview of this critical intersection of inflammatory bowel disease and cardiovascular health.
基金Supported by the Zhejiang Medical Technology Project,No.2022RC009National Natural Science Foundation of China,No.81900692.
文摘The bidirectional relationship between periodontitis and type 2 diabetes mellitus has been well-established.However,the underlying molecular mechanisms remain unclear.Diabetic retinopathy(DR)is an important complication of diabetes,but there are few studies on the relationship between DR and periodontitis,especially on the intrinsic inflammatory pathway mechanism.This article reviews the latest clinical data on how diabetes promotes susceptibility to periodontitis from the epidemiological and molecular perspectives,with a special focus on the key roles of systemic inflammation and endothelial dysfunction in the interplay between DR and periodontitis.Comprehension of the intertwined pathogenesis of DR and periodontitis can better guide the development of comprehensive management strategies for glycemic control and periodontal health,with the aim of mitigating the progression of DR and enhancing overall well-being.
