Pub Date : 2002-05-01DOI: 10.1111/J.1527-5299.2002.00300.X
A. Zafari, D. Harrison
{"title":"Free radicals in heart failure: therapeutic targets for old and new drugs.","authors":"A. Zafari, D. Harrison","doi":"10.1111/J.1527-5299.2002.00300.X","DOIUrl":"https://doi.org/10.1111/J.1527-5299.2002.00300.X","url":null,"abstract":"","PeriodicalId":10536,"journal":{"name":"Congestive heart failure","volume":"24 1","pages":"129-30"},"PeriodicalIF":0.0,"publicationDate":"2002-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84389582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-05-01DOI: 10.1111/J.1527-5299.2002.00939.X
D. Sica
Doxazosin remains a commonly used antihypertensive medication, although its use has been tainted by recent findings from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). ALLHAT was a large, simple trial, designed in a fashion to closely mimic clinical practice as it occurs in high-risk hypertensive patients aged 55 years or older. Its goals were to determine whether the incidence of the primary outcome--a composite of fatal coronary heart disease and nonfatal myocardial infarction--differed between treatment with a diuretic (chlorthalidone) (12.5-25.0 mg/day) and treatment with each of three other types of antihypertensive drugs-a calcium-channel blocker (amlodipine), an angiotensin-converting enzyme inhibitor (lisinopril), and a peripheral alpha-adrenergic blocker (doxazosin) (2-8 mg/day). Doxazosin was recently withdrawn from this trial after an interim analysis showed the secondary end point of combined cardiovascular disease to be 25% greater in patients on doxazosin than in those assigned to treatment with chlorthalidone. This finding was largely driven by congestive heart failure. The practicing clinician should not abandon doxazosin completely because of the ALLHAT findings, although these findings are indisputably important. These results represent an interim analysis and their application to clinical practice needs to occur carefully. A valued member of our therapeutic armamentarium need not be laid entirely to rest; rather, doxazosin should now be viewed as a secondary or tertiary antihypertensive therapy pending a more complete review of the ALLHAT data.
{"title":"Doxazosin and congestive heart failure.","authors":"D. Sica","doi":"10.1111/J.1527-5299.2002.00939.X","DOIUrl":"https://doi.org/10.1111/J.1527-5299.2002.00939.X","url":null,"abstract":"Doxazosin remains a commonly used antihypertensive medication, although its use has been tainted by recent findings from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). ALLHAT was a large, simple trial, designed in a fashion to closely mimic clinical practice as it occurs in high-risk hypertensive patients aged 55 years or older. Its goals were to determine whether the incidence of the primary outcome--a composite of fatal coronary heart disease and nonfatal myocardial infarction--differed between treatment with a diuretic (chlorthalidone) (12.5-25.0 mg/day) and treatment with each of three other types of antihypertensive drugs-a calcium-channel blocker (amlodipine), an angiotensin-converting enzyme inhibitor (lisinopril), and a peripheral alpha-adrenergic blocker (doxazosin) (2-8 mg/day). Doxazosin was recently withdrawn from this trial after an interim analysis showed the secondary end point of combined cardiovascular disease to be 25% greater in patients on doxazosin than in those assigned to treatment with chlorthalidone. This finding was largely driven by congestive heart failure. The practicing clinician should not abandon doxazosin completely because of the ALLHAT findings, although these findings are indisputably important. These results represent an interim analysis and their application to clinical practice needs to occur carefully. A valued member of our therapeutic armamentarium need not be laid entirely to rest; rather, doxazosin should now be viewed as a secondary or tertiary antihypertensive therapy pending a more complete review of the ALLHAT data.","PeriodicalId":10536,"journal":{"name":"Congestive heart failure","volume":"29 1","pages":"178-84"},"PeriodicalIF":0.0,"publicationDate":"2002-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86810770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-05-01DOI: 10.1111/J.1527-5299.2002.00718.X
W. Book
Despite advances in therapy, congestive heart failure is a major public health problem with a high mortality and morbidity. The benefits of β blockers in slowing disease progression and decreasing mortality have recently been shown in large clinical trials. Oxidative stress contributes to disease progression in both post-myocardial reperfusion injury and dilated cardiomyopathy. Several medications are known to have antioxidant effects, including some angiotensin-converting enzyme inhibitors. Carvedilol is a non-selective β blocker with antioxidant properties approved for use in congestive heart failure.
{"title":"Carvedilol: A Nonselective β Blocking Agent With Antioxidant Properties","authors":"W. Book","doi":"10.1111/J.1527-5299.2002.00718.X","DOIUrl":"https://doi.org/10.1111/J.1527-5299.2002.00718.X","url":null,"abstract":"Despite advances in therapy, congestive heart failure is a major public health problem with a high mortality and morbidity. The benefits of β blockers in slowing disease progression and decreasing mortality have recently been shown in large clinical trials. Oxidative stress contributes to disease progression in both post-myocardial reperfusion injury and dilated cardiomyopathy. Several medications are known to have antioxidant effects, including some angiotensin-converting enzyme inhibitors. Carvedilol is a non-selective β blocker with antioxidant properties approved for use in congestive heart failure.","PeriodicalId":10536,"journal":{"name":"Congestive heart failure","volume":"15 1","pages":"173-190"},"PeriodicalIF":0.0,"publicationDate":"2002-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77208562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-05-01DOI: 10.1111/J.1527-5299.2002.00941.X
H. Ventura
{"title":"H istorical V ignettes in H eart F ailure","authors":"H. Ventura","doi":"10.1111/J.1527-5299.2002.00941.X","DOIUrl":"https://doi.org/10.1111/J.1527-5299.2002.00941.X","url":null,"abstract":"","PeriodicalId":10536,"journal":{"name":"Congestive heart failure","volume":"10 1","pages":"111-111"},"PeriodicalIF":0.0,"publicationDate":"2002-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79759472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-05-01DOI: 10.1111/J.1527-5299.2002.00715.X
C. Searles
Chronic heart failure is associated with pathophysiologic alterations in myocardial and vascular function. Accompanying these changes are increased oxidative stress and modulation of the nitric oxide pathway. The role of the nitric oxide(.) pathway in heart failure and the effect of its interaction with reactive oxygen species are complex, with diverse pathophysiologic implications in both the heart and the peripheral vasculature. This review discusses current information regarding the nitric oxide(.) pathway in heart failure and its relationship with increased oxidative stress.
{"title":"The nitric oxide pathway and oxidative stress in heart failure.","authors":"C. Searles","doi":"10.1111/J.1527-5299.2002.00715.X","DOIUrl":"https://doi.org/10.1111/J.1527-5299.2002.00715.X","url":null,"abstract":"Chronic heart failure is associated with pathophysiologic alterations in myocardial and vascular function. Accompanying these changes are increased oxidative stress and modulation of the nitric oxide pathway. The role of the nitric oxide(.) pathway in heart failure and the effect of its interaction with reactive oxygen species are complex, with diverse pathophysiologic implications in both the heart and the peripheral vasculature. This review discusses current information regarding the nitric oxide(.) pathway in heart failure and its relationship with increased oxidative stress.","PeriodicalId":10536,"journal":{"name":"Congestive heart failure","volume":"30 1","pages":"142-7, 155"},"PeriodicalIF":0.0,"publicationDate":"2002-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83728916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-05-01DOI: 10.1111/J.1527-5299.2002.00719.X
F. F. Alameddine, A. Zafari
Heart failure results from various known cardiovascular diseases, such as coronary artery disease, or can be the result of an idiopathic dilated cardiomyopathy. It is of utmost importance for diagnostic, preventive, and therapeutic purposes to understand the cellular events that trigger the cascade of functional and structural changes that result in the development and progression of heart failure. Progress in unraveling the genetic background in both ischemic and nonischemic cardiomyopathies has been slow compared with that for monogenic diseases, such as some forms of hypertrophic cardiomyopathy or familial dilated cardiomyopathies. It is likely that susceptibility to and risk of progression of heart failure are both influenced by many genes acting in concert or independently. Among the diverse subcellular mechanisms implicated in the pathogenesis and progression of heart failure, reactive oxygen species play a major role. The search for genetic polymorphisms in clinical association studies in order to identify genotypes susceptible to develop and affect the progression to heart failure has been the focus of many investigations over the past several years. In this review, the authors summarize the current data in support of the role of various polymorphisms of genes related to oxidative stress in the susceptibility to develop heart failure, and its progression.
{"title":"Genetic polymorphisms and oxidative stress in heart failure.","authors":"F. F. Alameddine, A. Zafari","doi":"10.1111/J.1527-5299.2002.00719.X","DOIUrl":"https://doi.org/10.1111/J.1527-5299.2002.00719.X","url":null,"abstract":"Heart failure results from various known cardiovascular diseases, such as coronary artery disease, or can be the result of an idiopathic dilated cardiomyopathy. It is of utmost importance for diagnostic, preventive, and therapeutic purposes to understand the cellular events that trigger the cascade of functional and structural changes that result in the development and progression of heart failure. Progress in unraveling the genetic background in both ischemic and nonischemic cardiomyopathies has been slow compared with that for monogenic diseases, such as some forms of hypertrophic cardiomyopathy or familial dilated cardiomyopathies. It is likely that susceptibility to and risk of progression of heart failure are both influenced by many genes acting in concert or independently. Among the diverse subcellular mechanisms implicated in the pathogenesis and progression of heart failure, reactive oxygen species play a major role. The search for genetic polymorphisms in clinical association studies in order to identify genotypes susceptible to develop and affect the progression to heart failure has been the focus of many investigations over the past several years. In this review, the authors summarize the current data in support of the role of various polymorphisms of genes related to oxidative stress in the susceptibility to develop heart failure, and its progression.","PeriodicalId":10536,"journal":{"name":"Congestive heart failure","volume":"11 1","pages":"157-64, 172"},"PeriodicalIF":0.0,"publicationDate":"2002-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81995493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-05-01DOI: 10.1111/J.1527-5299.2002.00717.X
D. Sorescu, K. Griendling
Reactive oxygen species (ROS) released acutely in large amounts have been traditionally implicated in the cell death associated with myocardial infarction or reperfusion injury. These ROS can be released from the cardiac myocyte mitochondria, xanthine oxidase, and the phagocytic nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase. Interestingly, the chronic release of ROS has been recently linked to the development of left ventricular hypertrophy and heart failure progression. The chronic release of ROS appears to derive from the nonphagocytic NAD(P)H oxidase and mitochondria. Experimental data are accumulating suggesting that the release of ROS is required for the normal, physiologic activity of cardiac cells, but abnormal activation of the nonphagocytic NAD(P)H oxidase in response to neurohormones (angiotensin II, norepinephrine, tumor necrosis factor-a) has been shown to contribute to cardiac myocyte hypertrophy. Furthermore, the fibrosis, collagen deposition, and metalloproteinase activation involved in the remodeling of the failing myocardium are dependent on ROS released during the phenotypic transformation of fibroblasts to myofibroblasts associated with progression of end-stage heart failure. Future studies are necessary to identify the sources, mechanisms of activation of NAD(P)H oxidases, and downstream signaling targets implicated in the progression of chronic heart failure.
{"title":"Reactive oxygen species, mitochondria, and NAD(P)H oxidases in the development and progression of heart failure.","authors":"D. Sorescu, K. Griendling","doi":"10.1111/J.1527-5299.2002.00717.X","DOIUrl":"https://doi.org/10.1111/J.1527-5299.2002.00717.X","url":null,"abstract":"Reactive oxygen species (ROS) released acutely in large amounts have been traditionally implicated in the cell death associated with myocardial infarction or reperfusion injury. These ROS can be released from the cardiac myocyte mitochondria, xanthine oxidase, and the phagocytic nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase. Interestingly, the chronic release of ROS has been recently linked to the development of left ventricular hypertrophy and heart failure progression. The chronic release of ROS appears to derive from the nonphagocytic NAD(P)H oxidase and mitochondria. Experimental data are accumulating suggesting that the release of ROS is required for the normal, physiologic activity of cardiac cells, but abnormal activation of the nonphagocytic NAD(P)H oxidase in response to neurohormones (angiotensin II, norepinephrine, tumor necrosis factor-a) has been shown to contribute to cardiac myocyte hypertrophy. Furthermore, the fibrosis, collagen deposition, and metalloproteinase activation involved in the remodeling of the failing myocardium are dependent on ROS released during the phenotypic transformation of fibroblasts to myofibroblasts associated with progression of end-stage heart failure. Future studies are necessary to identify the sources, mechanisms of activation of NAD(P)H oxidases, and downstream signaling targets implicated in the progression of chronic heart failure.","PeriodicalId":10536,"journal":{"name":"Congestive heart failure","volume":"19 1","pages":"132-40"},"PeriodicalIF":0.0,"publicationDate":"2002-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76782702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-05-01DOI: 10.1111/J.1527-5299.2002.00942.X
A. Berman, Theresa Roca, P. Uber, M. Mehra
Hypoplastic left heart syndrome is a complex conglomerate of congenital cardiac abnormalities encountered in early life. Heart failure compensation and survival are intricately dependent on maintenance of ductal patency and avoidance of hyperoxic ventilation. While medical therapy is woefully inadequate, the staged Norwood procedure or cardiac transplantation remain the better options for treatment. Critically dependent on surgical outcomes, 5-year survival appears better with cardiac transplantation.
{"title":"Neonatal congenital heart disease and \"complex\" heart failure.","authors":"A. Berman, Theresa Roca, P. Uber, M. Mehra","doi":"10.1111/J.1527-5299.2002.00942.X","DOIUrl":"https://doi.org/10.1111/J.1527-5299.2002.00942.X","url":null,"abstract":"Hypoplastic left heart syndrome is a complex conglomerate of congenital cardiac abnormalities encountered in early life. Heart failure compensation and survival are intricately dependent on maintenance of ductal patency and avoidance of hyperoxic ventilation. While medical therapy is woefully inadequate, the staged Norwood procedure or cardiac transplantation remain the better options for treatment. Critically dependent on surgical outcomes, 5-year survival appears better with cardiac transplantation.","PeriodicalId":10536,"journal":{"name":"Congestive heart failure","volume":"98 1","pages":"188-90"},"PeriodicalIF":0.0,"publicationDate":"2002-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83648789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-05-01DOI: 10.1111/J.1527-5299.2002.00714.X
R. Sharma, M. Davidoff
The clinical syndrome of congestive heart failure (CHF) is characterized by abnormalities of left ventricular function and neurohormonal regulation, which are accompanied by effort intolerance, fluid retention, and decreased longevity. While an increased sympathetic tone and an activated renin-angiotensin system may contribute to the reduced vasodilatory capacity in patients with CHF, the important role of the endothelium in coordinating tissue perfusion has now been recognized. CHF is associated with endothelial dysfunction, as demonstrated by impaired endothelium-mediated vasodilation. Endothelial dysfunction in patients with CHF is a critical component in the systemic vasoconstriction and reduced peripheral perfusion that characterizes these patients. Endothelial regulation of vascular tone is mediated mainly by nitric oxide. Increased oxidative stress in patients with CHF is likely caused by decreased bioavailability of nitric oxide due to reduced expression of endothelial nitric oxide synthase and increased generation of reactive oxygen species. These react with nitric oxide in the setting of decreased antioxidant defenses that would normally clear these radicals, culminating in attenuated endothelium-dependent vasodilation in patients with CHF. Therapies that improve endothelial function have been shown to improve exercise tolerance and outcomes in patients with CHF. Endothelial dysfunction is thus an important target for future therapy in patients with CHF.
{"title":"Oxidative stress and endothelial dysfunction in heart failure.","authors":"R. Sharma, M. Davidoff","doi":"10.1111/J.1527-5299.2002.00714.X","DOIUrl":"https://doi.org/10.1111/J.1527-5299.2002.00714.X","url":null,"abstract":"The clinical syndrome of congestive heart failure (CHF) is characterized by abnormalities of left ventricular function and neurohormonal regulation, which are accompanied by effort intolerance, fluid retention, and decreased longevity. While an increased sympathetic tone and an activated renin-angiotensin system may contribute to the reduced vasodilatory capacity in patients with CHF, the important role of the endothelium in coordinating tissue perfusion has now been recognized. CHF is associated with endothelial dysfunction, as demonstrated by impaired endothelium-mediated vasodilation. Endothelial dysfunction in patients with CHF is a critical component in the systemic vasoconstriction and reduced peripheral perfusion that characterizes these patients. Endothelial regulation of vascular tone is mediated mainly by nitric oxide. Increased oxidative stress in patients with CHF is likely caused by decreased bioavailability of nitric oxide due to reduced expression of endothelial nitric oxide synthase and increased generation of reactive oxygen species. These react with nitric oxide in the setting of decreased antioxidant defenses that would normally clear these radicals, culminating in attenuated endothelium-dependent vasodilation in patients with CHF. Therapies that improve endothelial function have been shown to improve exercise tolerance and outcomes in patients with CHF. Endothelial dysfunction is thus an important target for future therapy in patients with CHF.","PeriodicalId":10536,"journal":{"name":"Congestive heart failure","volume":"44 1","pages":"165-72"},"PeriodicalIF":0.0,"publicationDate":"2002-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72905010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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