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Mariann R. Piano - One of the best experts on this subject based on the ideXlab platform.
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hospital and patient level characteristics associated with unplanned readmissions and in patient mortality in men and women with Alcoholic Cardiomyopathy
Journal of Studies on Alcohol and Drugs, 2021Co-Authors: Mulubrhan F Mogos, Jason L Salemi, Sanjukta Modak, Roger Zoorob, Mariann R. PianoAbstract:Objective The aims of the study were to (a) determine rates of early, late, and overall 30-day all-cause readmission for women and men with the diagnosis of Alcoholic Cardiomyopathy (ACM), (b) examine hospital- and patient-level characteristics associated with the risk of readmission and how these factors differed by sex, and (c) examine the association between sex and in-patient mortality during readmission. Method We conducted a multi-year cross-sectional analysis of adult (≥18 years) inpatient hospitalizations in the United States. Descriptive statistics including frequencies and percentages were used to describe the study population, stratified by sex. We then used Poisson regression with robust error variance estimation to estimate risk ratios (RRs) and 95% confidence intervals (CIs) that represented the associations between sex and likelihood of 30-day all-cause readmission and inpatient mortality. Results Among more than 116 million hospitalizations, there were 53,207 ACM-related hospitalizations (45,573 men and 7,634 women). Thirty-day all-cause readmission rates following an ACM-related index hospitalization were similar between men (20.3%) and women (20.5%). For men and women, cancer, hepatitis, chronic renal failure, cirrhosis, asthma, and anemia were associated with a higher risk of readmission. Although crude in-hospital mortality rates were higher among women (6.6%) than men (4.3%), there were no sex differences in mortality after adjusting for confounders (RR = 1.26, 95% CI [0.88, 1.81]). Conclusions Although men are more likely to be hospitalized for ACM, readmission risk is high (approximately 20%) and is similar in men and women following hospitalization for ACM. Hospital care transition programs that include a multidisciplinary approach are needed to help prevent these readmissions and associated morbidity and mortality.
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contemporary appraisal of sex differences in prevalence correlates and outcomes of Alcoholic Cardiomyopathy
Alcohol and Alcoholism, 2019Co-Authors: Mulubrhan F Mogos, Shane A. Phillips, Jason L Salemi, Mariann R. PianoAbstract:Aims The aims of this study were to: examine differences in Alcoholic Cardiomyopathy (ACM) prevalence, temporal trends and the distribution of socio-demographic factors and comorbidities by sex; and investigate differences in selected inpatient outcomes between women and men with ACM. Methods We used the 2002-2014 Nationwide Inpatient Sample databases. Overall and sex-specific rates of ACM were estimated across sociodemographic, clinical, and hospital characteristics. Joinpoint regression was used to estimate temporal trends (annual percent change [APC]) of ACM-related hospitalization by sex and race/ethnicity. Adjusted odds ratios (AOR) representing associations between sex and selected ACM outcomes were calculated using survey logistic regression. Results The rate of ACM among all inpatient men and women was 128 per 100,000 and 17 per 100,000 hospitalizations, respectively. Among women, the rate of ACM remained unchanged during the study period, while for men, there was 1.2% annual reduction from 2002-2010 (APC -1.3, 95% CI: -1.7, -0.8). Women with ACM were more likely than men with ACM to experience depression (AOR=2.24, 95% CI: 2.06-2.43) and anxiety (AOR=1.94, 95% CI: 1.75-2.15), while men with ACM were 21% and 24% more likely than women with ACM to experience 'any heart failure (HF)' and HF with reduced ejection fraction respectively. One in 1,471 hospitalizations were related to ACM with a male-to-female ratio of 8:1. Conclusion Individuals with ACM are at increased likelihood of adverse outcomes. Women with ACM are at increased risk of depression and anxiety, while men are at increased risk of HF.
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abstract 14554 contemporary appraisal of sex differences in prevalence correlates and outcomes of Alcoholic Cardiomyopathy in the united states
Circulation, 2017Co-Authors: Mulubrhan F Mogos, Jason L Salemi, Kylie D Russell, Mariann R. PianoAbstract:Introduction: Alcoholic Cardiomyopathy (ACM) is a specific heart muscle disease found in individuals with a history of long-term heavy alcohol consumption. In spite of its adverse impact, data rela...
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Alcoholic Cardiomyopathy: Pathophysiologic Insights
Cardiovascular Toxicology, 2014Co-Authors: Mariann R. Piano, Shane A. PhillipsAbstract:Alcoholic Cardiomyopathy (ACM) is a specific heart muscle disease found in individuals with a history of long-term heavy alcohol consumption. ACM is associated with a number of adverse histological, cellular, and structural changes within the myocardium. Several mechanisms are implicated in mediating the adverse effects of ethanol, including the generation of oxidative stress, apoptotic cell death, impaired mitochondrial bioenergetics/stress, derangements in fatty acid metabolism and transport, and accelerated protein catabolism. In this review, we discuss the evidence for such mechanisms and present the potential importance of drinking patterns, genetic susceptibility, nutritional factors, race, and sex. The purpose of this review is to provide a mechanistic paradigm for future research in the area of ACM.
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Alcoholic Cardiomyopathy incidence clinical characteristics and pathophysiology
Chest, 2002Co-Authors: Mariann R. PianoAbstract:In the United States, in both sexes and all races, long-term heavy alcohol consumption (of any beverage type) is the leading cause of a nonischemic, dilated Cardiomyopathy, herein referred to as Alcoholic Cardiomyopathy (ACM). ACM is a specific heart muscle disease of a known cause that occurs in two stages: an asymptomatic stage and a symptomatic stage. In general, Alcoholic patients consuming > 90 g of alcohol a day (approximately seven to eight standard drinks per day) for > 5 years are at risk for the development of asymptomatic ACM. Those who continue to drink may become symptomatic and develop signs and symptoms of heart failure. ACM is characterized by an increase in myocardial mass, dilation of the ventricles, and wall thinning. Changes in ventricular function may depend on the stage, in that asymptomatic ACM is associated with diastolic dysfunction, whereas systolic dysfunction is a common finding in symptomatic ACM patients. The pathophysiology of ACM is complex and may involve cell death (possibly due to apoptosis) and changes in many aspects of myocyte function. ACM remains an important cause of a dilated Cardiomyopathy, and in latter stages can lead to heart failure. Alcohol abstinence, as well as the use of specific heart failure pharmacotherapies, is critical in improving ventricular function and outcomes in these patients.
Bo Dong - One of the best experts on this subject based on the ideXlab platform.
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pro renin receptor is involved in myocardial damage in Alcoholic Cardiomyopathy
Alcoholism: Clinical and Experimental Research, 2019Co-Authors: Xinran Cao, Jie Xiong, Bo Dong, Shiyuan Qiao, Fan JiangAbstract:Background (Pro)renin receptor (PRR), a novel member of the renin-angiotensin system, participates in various cardiovascular diseases. However, the role of PRR in Alcoholic Cardiomyopathy (ACM), which is caused by alcohol intake and manifests as myocardial damage and cardiac dysfunction, remains unclear. Methods PRR gene silencing was achieved by transfecting recombinant adenovirus expressing anti-PRR short hairpin RNA (PRR-shRNA). In vitro, primary rat cardiac fibroblasts (CFs) were cultured with the stimulation of alcohol (200 mM), with or without PRR-shRNA and PD98059. Immunofluorescence, RT-PCR, and Western blot were used to measure the protein and messenger (mRNA) expression of PRR, fibrotic factors, and members of related signaling pathways. In vivo, Wistar rats were fed a diet containing 9% (v/v) alcohol or a normal diet for 3 months, with or without PRR-shRNA. Sirius Red staining, immunohistochemical staining, and toluidine blue staining were used to evaluate myocardial fibrosis, oxidative stress, and inflammation response. Results Alcohol markedly increased PRR mRNA and protein expression in a time- and concentration-dependent manner in CFs. The increased expression of fibrotic factors induced by alcohol was prevented by PRR-shRNA and PD98059. Moreover, PRR-shRNA decreased the phosphorylation of extracellular regulated protein kinases (ERK) 1/2 in CFs. Furthermore, PRR-shRNA decreased cardiac fibrosis, reduced oxidative stress, and alleviated inflammation response in the myocardial tissue. Conclusions Our results show that PRR-ERK1/2 signaling was involved in the development of ACM and that PRR could be a new target for the treatment of ACM.
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Effects of the (Pro)renin Receptor on Cardiac Remodeling and Function in a Rat Alcoholic Cardiomyopathy Model via the PRR-ERK1/2-NOX4 Pathway
Hindawi Limited, 2019Co-Authors: Xinran Cao, Yuanyuan Wang, Min Yang, Jie Xiong, Haitao Yuan, Bo DongAbstract:Alcoholic Cardiomyopathy (ACM) caused by alcohol consumption manifests mainly as by maladaptive myocardial function, which eventually leads to heart failure and causes serious public health problems. The (pro)renin receptor (PRR) is an important member of the local tissue renin-angiotensin system and plays a vital role in many cardiovascular diseases. However, the mechanism responsible for the effects of PRR on ACM remains unclear. The purpose of this study was to determine the role of PRR in myocardial fibrosis and the deterioration of cardiac function in Alcoholic Cardiomyopathy. Wistar rats were fed a liquid diet containing 9% v/v alcohol to establish an Alcoholic Cardiomyopathy model. Eight weeks later, rats were injected with 1×109v.g./100 μl of recombinant adenovirus containing EGFP (scramble-shRNA), PRR, and PRR-shRNA via the tail vein. Cardiac function was assessed by echocardiography. Cardiac histopathology was measured by Masson’s trichrome staining, immunohistochemical staining, and dihydroethidium staining. In addition, cardiac fibroblasts (CFs) were cultured to evaluate the effects of alcohol stimulation on the production of the extracellular matrix and their underlying mechanisms. Our results indicated that overexpression of PRR in rats with Alcoholic Cardiomyopathy exacerbates myocardial oxidative stress and myocardial fibrosis. Silencing of PRR expression with short hairpin RNA (shRNA) technology reversed the myocardial damage mediated by PRR. Additionally, PRR activated phosphorylation of ERK1/2 and increased NOX4-derived reactive oxygen species and collagen expression in CFs with alcohol stimulation. Administration of the ERK kinase inhibitor (PD98059) significantly reduced NOX4 protein expression and collagen production, which indicated that PRR increases collagen production primarily through the PRR-ERK1/2-NOX4 pathway in CFs. In conclusion, our study demonstrated that PRR induces myocardial fibrosis and deteriorates cardiac function through ROS from the PRR-ERK1/2-NOX4 pathway during ACM development
Ling Jing - One of the best experts on this subject based on the ideXlab platform.
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valsartan inhibits rhoa rock2 myl pathway in rat model of Alcoholic Cardiomyopathy
Experimental and Therapeutic Medicine, 2019Co-Authors: Ling Jing, Jiyi Zhao, Wen Yang, Lijun ZhouAbstract:The present study aimed to investigate variations in the Ras homolog gene family, member A (RhoA)-Rho-associated protein kinase 2 (ROCK2)-myosin light chain (MYL) pathway in a rat model of Alcoholic Cardiomyopathy (ACM) and the role of angiotensin-converting enzyme inhibitor drugs. Rat models of ACM were established via Alcoholic gavage + free access to alcohol. The structural and functional changes of the heart were analyzed by hematoxylin-eosin staining, Masson's trichrome staining, immunohistochemistry staining, western blotting and fluorescence quantitative polymerase chain reaction. A total of 16 weeks later, a decreased ejection fraction and left ventricular fractional shortening in the alcohol group compared with the control group were demonstrated resulting in an increased left ventricular end diastolic diameter. These adverse effects were ameliorated following treatment with valsartan. In addition, the alcohol group revealed a disorganized arrangement of myocardial filaments, which was improved upon treatment with valsartan. RhoA and ROCK2 protein expression significantly increased in myocardial cells in the alcohol compared with the control group. Following drug intervention with valsartan, expression of RhoA and ROCK2 proteins were inhibited in the alcohol group. Furthermore, significantly elevated RhoA and ROCK2 and decreased MYL protein and mRNA expression in the alcohol group was demonstrated compared with the control group. Administration of valsartan reversed the expression profile of RhoA, ROCK and MYL in ACM. Expression of RhoA and ROCK were elevated with downregulation of MYL resulting in heart failure. However, the angiotensin receptor antagonist diminished the expression of RhoA and ROCK and enhanced the expression of MYL. The results of the present study suggest a curative effect of valsartan in ACM.
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therapeutic effects of rapamycin on Alcoholic Cardiomyopathy
Experimental and Therapeutic Medicine, 2017Co-Authors: Chao Wang, Lili Jing, Lijun Zhou, Ling JingAbstract:The present study aimed to investigate whether rapamycin has therapeutic potential as a treatment for Alcoholic Cardiomyopathy. Rats were divided into eight groups (n=7 in each group): The control group; the alcohol group; abstinence in the first week; abstinence in the third week; abstinence in the fourth week; abstinent+rapamycin (AB-RAP) until the first week (AB-RAP 1); AB-RAP until the third week (AB-RAP 3); and AB-RAP until the fourth week (AB-RAP 4). Subsequently, echocardiography, and hematoxylin-eosin and Masson's staining were performed, followed by electron microscopy and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay. Finally, expression levels of B cell lymphoma-2, Beclin-1 and microtubule-associated protein 1A/1B-light chain 3 were detected by immunohistochemistry and western blot analysis. The levels of left ventricular end-diastolic dimension in AB-RAP 3 (7.00±0.41) and AB-RAP 4 (6.33±0.68) groups were significantly lower when compared with the alcohol group (8.01±0.30; P<0.05). Compared with the alcohol group, the apoptosis rate of left ventricular myocardial tissue in the AB+RAP 3 (37.68±2.15) and AB+RAP 4 (26.97±2.11) groups was significantly reduced (P<0.05). To conclude, rapamycin may be considered as a therapeutic tool to attenuate Alcoholic Cardiomyopathy and improve cardiac function through increasing autophagy and reducing apoptosis.
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investigation of microrna expression profiles associated with human Alcoholic Cardiomyopathy
The Cardiology, 2015Co-Authors: Ling Jing, Lijun Zhou, Chengmei Jin, Pingyan Huo, Ye Wang, Ye TianAbstract:Objectives: We aimed to investigate the differentially expressed microRNAs (miRNAs) and their target genes in human Alcoholic Cardiomyopathy (ACM). Methods: The expression levels of plasma miRNAs of 78 male ACM patients and 78 healthy men were detected by using the 6th-generation miRCURY™ LNA array (v.16.0). The prediction analysis for microarrays (PAM) method was used to identify the differentially expressed miRNAs. Target genes of the identified differentially expressed miRNAs were predicted using TargetScan 5.2 and Miranda. Gene ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to perform functional annotation and pathway enrichment analysis of target genes respectively, followed by real-time RT-PCR analysis to validate the expression changes of miRNAs. Results: Twenty-one differentially expressed miRNAs were identified. Nine differentially expressed miRNAs (hsa-miR-506, hsa-miR-1285, hsa-miR-512-3P, hsa-miR-138, hsa-miR-485-5P, hsa-miR-4262, hsa-miR-548c-3P, has-miR-548a-5P and kshv-miR-K12-1), involved in multiple functions and pathways, were selected for real-time RT-PCR confirmation. Moreover, two significantly important subpathways (neurotrophin signaling pathway and inositol phosphate metabolism) were predicted. Conclusion: The screened differentially expressed miRNAs may be involved in the development of ACM. Specific miRNAs, such as miR-138, may be considered as a new target for the early diagnosis and treatment of human ACM.
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chronic alcohol intake induced oxidative stress and apoptosis role of cyp2e1 and calpain 1 in Alcoholic Cardiomyopathy
Molecular and Cellular Biochemistry, 2012Co-Authors: Ling Jing, Chengmei Jin, Fengmin Zhang, Lin Yuan, Ying Sang, Lijun ZhouAbstract:Cytochrome P-450 2E1 CYP2E1 induction has been linked to oxidative stress in a number of experimental models. The aim of this study was to investigate the relationship between CYP2E1 activity and markers of oxidative stress and cardiac cell apoptosis during the development of Alcoholic Cardiomyopathy (ACM). Changes in left ventricular morphology were evaluated in 4 groups of chronically instrumented dogs (control; alcohol-receiving; and alcohol-receiving plus treatment with either valsartan or carnitine) after 6 months of treatment. CYP2E1 and calpain-1 protein expression were determined by Western blotting, and apoptosis evaluated by TUNEL and immunohistochemistry. Malonyl dialdehyde levels were assessed as a marker of oxidative stress, while superoxide dismutase and glutathione peroxidase levels were evaluated as markers of antioxidant defense mechanisms. Expression of CYP2E1 was increased in the alcohol-receiving group compared with controls (P<0.05) and was associated with oxidative stress. Similarly, expression of Bad and calpain-1 protein was increased after chronic alcohol exposure, while Bcl-xL protein expression remained at a low level. Bad and calpain-1 protein expressions were significantly inhibited by treatment with valsartan or carnitine, while expression of Bcl-xL protein was increased (P<0.05). Collectively, our results indicate a possibly significant role for CYP2E1 in the oxidative stress associated with chronic alcoholism. The resulting increase in oxidative stress is accompanied by cellular apoptosis and may ultimately contribute to tissue remodeling and ACM. Importantly, these alcohol-induced effects may be abrogated by means such as angiotensin 1 receptor blockade or carnitine supplementation.
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tenascin x facilitates myocardial fibrosis and cardiac remodeling through transforming growth factor β1 and peroxisome proliferator activated receptor γ in Alcoholic Cardiomyopathy
Chinese Medical Journal, 2011Co-Authors: Ling Jing, Lijun Zhou, Fengmin Zhang, Ying SangAbstract:BACKGROUND Tenascin-x, an extracellular matrix glycoprotein exclusively expressed in fibroblasts, can mediate fibrosis in the presence of collagen. Therefore, we have investigated its potential role in facilitating myocardial fibrosis and cardiac remodeling via the transforming growth factor-β1 and peroxisome proliferator-activated receptor γ (TGFβ(1)-PPARγ) pathway in Alcoholic Cardiomyopathy (ACM). METHODS Experimental animals were divided into control (group A) and tenascin-x knock-out groups (group B) receiving alcohol. Six months post treatment, cardiac ejections fraction (EF), fractional shortening (FS), left ventricle end-diastole internal diameter (LVEDd) and collagen column fraction (CVF) were observed. Tenascin-x, smad-3, TGFβ(1), smad-7 and PPARγ protein expression levels were detected by Western blotting. RESULTS Six months post treatment, EF and FS values were higher in group B than in group A (P < 0.05 and P < 0.01, respectively), while LVEDd and CVF were lower in group B (P < 0.05 and P < 0.01, respectively). Tenascin-x, smad-3 and TGFβ(1) protein expression levels were higher in group A, while smad-7 and PPARγ levels were lower than in group B (P < 0.01), as measured by immunohistochemistry and Western blotting. Tenascin-x protein expression was negatively correlated with EF, FS, smad-7 and PPARγ, and positively correlated with LVEDd, CVF, smad-3, and TGFβ(1) (P < 0.001). CONCLUSION Tenascin-x is an initiator of myocardial fibrosis and ACM development via upregulation of TGFβ(1) and downregulation of PPARγ.
Lijun Zhou - One of the best experts on this subject based on the ideXlab platform.
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valsartan inhibits rhoa rock2 myl pathway in rat model of Alcoholic Cardiomyopathy
Experimental and Therapeutic Medicine, 2019Co-Authors: Ling Jing, Jiyi Zhao, Wen Yang, Lijun ZhouAbstract:The present study aimed to investigate variations in the Ras homolog gene family, member A (RhoA)-Rho-associated protein kinase 2 (ROCK2)-myosin light chain (MYL) pathway in a rat model of Alcoholic Cardiomyopathy (ACM) and the role of angiotensin-converting enzyme inhibitor drugs. Rat models of ACM were established via Alcoholic gavage + free access to alcohol. The structural and functional changes of the heart were analyzed by hematoxylin-eosin staining, Masson's trichrome staining, immunohistochemistry staining, western blotting and fluorescence quantitative polymerase chain reaction. A total of 16 weeks later, a decreased ejection fraction and left ventricular fractional shortening in the alcohol group compared with the control group were demonstrated resulting in an increased left ventricular end diastolic diameter. These adverse effects were ameliorated following treatment with valsartan. In addition, the alcohol group revealed a disorganized arrangement of myocardial filaments, which was improved upon treatment with valsartan. RhoA and ROCK2 protein expression significantly increased in myocardial cells in the alcohol compared with the control group. Following drug intervention with valsartan, expression of RhoA and ROCK2 proteins were inhibited in the alcohol group. Furthermore, significantly elevated RhoA and ROCK2 and decreased MYL protein and mRNA expression in the alcohol group was demonstrated compared with the control group. Administration of valsartan reversed the expression profile of RhoA, ROCK and MYL in ACM. Expression of RhoA and ROCK were elevated with downregulation of MYL resulting in heart failure. However, the angiotensin receptor antagonist diminished the expression of RhoA and ROCK and enhanced the expression of MYL. The results of the present study suggest a curative effect of valsartan in ACM.
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therapeutic effects of rapamycin on Alcoholic Cardiomyopathy
Experimental and Therapeutic Medicine, 2017Co-Authors: Chao Wang, Lili Jing, Lijun Zhou, Ling JingAbstract:The present study aimed to investigate whether rapamycin has therapeutic potential as a treatment for Alcoholic Cardiomyopathy. Rats were divided into eight groups (n=7 in each group): The control group; the alcohol group; abstinence in the first week; abstinence in the third week; abstinence in the fourth week; abstinent+rapamycin (AB-RAP) until the first week (AB-RAP 1); AB-RAP until the third week (AB-RAP 3); and AB-RAP until the fourth week (AB-RAP 4). Subsequently, echocardiography, and hematoxylin-eosin and Masson's staining were performed, followed by electron microscopy and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay. Finally, expression levels of B cell lymphoma-2, Beclin-1 and microtubule-associated protein 1A/1B-light chain 3 were detected by immunohistochemistry and western blot analysis. The levels of left ventricular end-diastolic dimension in AB-RAP 3 (7.00±0.41) and AB-RAP 4 (6.33±0.68) groups were significantly lower when compared with the alcohol group (8.01±0.30; P<0.05). Compared with the alcohol group, the apoptosis rate of left ventricular myocardial tissue in the AB+RAP 3 (37.68±2.15) and AB+RAP 4 (26.97±2.11) groups was significantly reduced (P<0.05). To conclude, rapamycin may be considered as a therapeutic tool to attenuate Alcoholic Cardiomyopathy and improve cardiac function through increasing autophagy and reducing apoptosis.
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investigation of microrna expression profiles associated with human Alcoholic Cardiomyopathy
The Cardiology, 2015Co-Authors: Ling Jing, Lijun Zhou, Chengmei Jin, Pingyan Huo, Ye Wang, Ye TianAbstract:Objectives: We aimed to investigate the differentially expressed microRNAs (miRNAs) and their target genes in human Alcoholic Cardiomyopathy (ACM). Methods: The expression levels of plasma miRNAs of 78 male ACM patients and 78 healthy men were detected by using the 6th-generation miRCURY™ LNA array (v.16.0). The prediction analysis for microarrays (PAM) method was used to identify the differentially expressed miRNAs. Target genes of the identified differentially expressed miRNAs were predicted using TargetScan 5.2 and Miranda. Gene ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to perform functional annotation and pathway enrichment analysis of target genes respectively, followed by real-time RT-PCR analysis to validate the expression changes of miRNAs. Results: Twenty-one differentially expressed miRNAs were identified. Nine differentially expressed miRNAs (hsa-miR-506, hsa-miR-1285, hsa-miR-512-3P, hsa-miR-138, hsa-miR-485-5P, hsa-miR-4262, hsa-miR-548c-3P, has-miR-548a-5P and kshv-miR-K12-1), involved in multiple functions and pathways, were selected for real-time RT-PCR confirmation. Moreover, two significantly important subpathways (neurotrophin signaling pathway and inositol phosphate metabolism) were predicted. Conclusion: The screened differentially expressed miRNAs may be involved in the development of ACM. Specific miRNAs, such as miR-138, may be considered as a new target for the early diagnosis and treatment of human ACM.
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chronic alcohol intake induced oxidative stress and apoptosis role of cyp2e1 and calpain 1 in Alcoholic Cardiomyopathy
Molecular and Cellular Biochemistry, 2012Co-Authors: Ling Jing, Chengmei Jin, Fengmin Zhang, Lin Yuan, Ying Sang, Lijun ZhouAbstract:Cytochrome P-450 2E1 CYP2E1 induction has been linked to oxidative stress in a number of experimental models. The aim of this study was to investigate the relationship between CYP2E1 activity and markers of oxidative stress and cardiac cell apoptosis during the development of Alcoholic Cardiomyopathy (ACM). Changes in left ventricular morphology were evaluated in 4 groups of chronically instrumented dogs (control; alcohol-receiving; and alcohol-receiving plus treatment with either valsartan or carnitine) after 6 months of treatment. CYP2E1 and calpain-1 protein expression were determined by Western blotting, and apoptosis evaluated by TUNEL and immunohistochemistry. Malonyl dialdehyde levels were assessed as a marker of oxidative stress, while superoxide dismutase and glutathione peroxidase levels were evaluated as markers of antioxidant defense mechanisms. Expression of CYP2E1 was increased in the alcohol-receiving group compared with controls (P<0.05) and was associated with oxidative stress. Similarly, expression of Bad and calpain-1 protein was increased after chronic alcohol exposure, while Bcl-xL protein expression remained at a low level. Bad and calpain-1 protein expressions were significantly inhibited by treatment with valsartan or carnitine, while expression of Bcl-xL protein was increased (P<0.05). Collectively, our results indicate a possibly significant role for CYP2E1 in the oxidative stress associated with chronic alcoholism. The resulting increase in oxidative stress is accompanied by cellular apoptosis and may ultimately contribute to tissue remodeling and ACM. Importantly, these alcohol-induced effects may be abrogated by means such as angiotensin 1 receptor blockade or carnitine supplementation.
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tenascin x facilitates myocardial fibrosis and cardiac remodeling through transforming growth factor β1 and peroxisome proliferator activated receptor γ in Alcoholic Cardiomyopathy
Chinese Medical Journal, 2011Co-Authors: Ling Jing, Lijun Zhou, Fengmin Zhang, Ying SangAbstract:BACKGROUND Tenascin-x, an extracellular matrix glycoprotein exclusively expressed in fibroblasts, can mediate fibrosis in the presence of collagen. Therefore, we have investigated its potential role in facilitating myocardial fibrosis and cardiac remodeling via the transforming growth factor-β1 and peroxisome proliferator-activated receptor γ (TGFβ(1)-PPARγ) pathway in Alcoholic Cardiomyopathy (ACM). METHODS Experimental animals were divided into control (group A) and tenascin-x knock-out groups (group B) receiving alcohol. Six months post treatment, cardiac ejections fraction (EF), fractional shortening (FS), left ventricle end-diastole internal diameter (LVEDd) and collagen column fraction (CVF) were observed. Tenascin-x, smad-3, TGFβ(1), smad-7 and PPARγ protein expression levels were detected by Western blotting. RESULTS Six months post treatment, EF and FS values were higher in group B than in group A (P < 0.05 and P < 0.01, respectively), while LVEDd and CVF were lower in group B (P < 0.05 and P < 0.01, respectively). Tenascin-x, smad-3 and TGFβ(1) protein expression levels were higher in group A, while smad-7 and PPARγ levels were lower than in group B (P < 0.01), as measured by immunohistochemistry and Western blotting. Tenascin-x protein expression was negatively correlated with EF, FS, smad-7 and PPARγ, and positively correlated with LVEDd, CVF, smad-3, and TGFβ(1) (P < 0.001). CONCLUSION Tenascin-x is an initiator of myocardial fibrosis and ACM development via upregulation of TGFβ(1) and downregulation of PPARγ.
Arshad Jahangir - One of the best experts on this subject based on the ideXlab platform.
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Burden of arrhythmia and electrophysiologic procedures in Alcoholic Cardiomyopathy hospitalizations.
International journal of cardiology, 2020Co-Authors: Samian Sulaiman, Nazdar Yousef, Mina M. Benjamin, Sakthi Sundararajan, Romina Wingert, Michael Wingert, Asim A. Mohammed, Arshad JahangirAbstract:Abstract Background Limited national US data are available regarding the prevalence of and trends in different arrhythmias and the use of electrophysiological procedures in patients with Alcoholic Cardiomyopathy. Methods This was a cross-sectional study that used the Nationwide Inpatient Sample database (2007–2014). Hospitalizations of adults with Alcoholic CMP were identified with the ICD-9 code (425.5). CAD and other causes of Cardiomyopathy were excluded. Chi-square test, t-test, mixed-effect logistic regression and quantile regression were used. Results Among 75,430 hospitalizations, 48% had arrhythmias. Individuals with a co-diagnosis of arrhythmia tended to be older (56.9 vs 53.2-year-old) and male (89.5% vs 81.9%). The most prevalent arrhythmias were atrial fibrillation/flutter (31.5%), followed by ventricular tachycardia (7.9%). The prevalence of arrhythmias increased from 44% to 50% (2007–2014) (p Conclusion Arrhythmias were reported in 48% of hospitalizations. There was an increasing burden of arrhythmias secondary to increasing atrial fibrillation. Excluding cardiac arrest, arrhythmias were not associated with increased in-hospital mortality but were associated with longer hospital stays and higher total charges.
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abstract 17175 trendsin Alcoholic Cardiomyopathy hospitalizations and in hospital mortality and comorbidity united states 2005 2014
Circulation, 2018Co-Authors: Samian Sulaiman, Nazdar Yousef, Arshad Jahangir, Vijayadershan Muppidi, Addis Asfaw, Muhammad Shahreyar, Romina WingertAbstract:Background: Yearly trends and prevalence of Alcoholic Cardiomyopathy (ACMP) hospitalizations and its associated in-hospital mortality, arrhythmia, complications and outcomes are not well studied on...