Pub Date : 2002-09-01DOI: 10.1111/J.1527-5299.2002.00303.X
B. Greenberg, Denise D. Herman
{"title":"Neurohormonal Blockade in the Treatment of Heart Failure: Where Do We Go From Here?","authors":"B. Greenberg, Denise D. Herman","doi":"10.1111/J.1527-5299.2002.00303.X","DOIUrl":"https://doi.org/10.1111/J.1527-5299.2002.00303.X","url":null,"abstract":"","PeriodicalId":10536,"journal":{"name":"Congestive heart failure","volume":"24 1","pages":"245-245"},"PeriodicalIF":0.0,"publicationDate":"2002-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88331124","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 : 2002-07-01DOI: 10.1111/J.1527-5299.2002.00292.X
J. Müller-Ehmsen, L. Kedes, R. Schwinger, R. Kloner
Cell transplantation is a novel experimental strategy to treat heart disease, such as myocardial infarction and heart failure. Its beneficial effects may include active contribution of transplanted cells to contractile function, passive improvement of the mechanics of the heart, induction of neoangiogenesis or other indirect influences on the biology of the heart. Several cell types have been used for cardiac cell transplantation including cardiac cells from fetal or newborn animals and cardiac muscle cell lines, skeletal myoblasts and skeletal muscle cell lines, smooth muscle cells, and a variety of stem cells, either adult or embryonic. With many of these cells, encouraging results in experimental ischemic and nonischemic heart disease have been obtained including successful cell survival after transplantation, integration into the host myocardium, and improvement of the function of diseased hearts. Most of these studies found cardiac contractility improved and some found enhanced angiogenesis. However, the mechanisms of these effects remain obscure, and the impact of dosage (cell number) on functional response is completely unclear. In addition, not enough comparative studies were performed to allow preference of one cell type over the other. The current data suggest that whatever cell species is used, the best survival and integration may be accomplished if immature and undifferentiated cells are used. Any kind of stem cell has obvious advantages in terms of endless reproducibility and plasticity, but the complete differentiation and maturation into cardiac myocytes still needs to be proven. At present several clinical studies are exploring the therapeutic benefits of cellular cardiomyoplasty in patients with ischemic heart disease, but it has to be noted that there are many issues that need to be addressed before this strategy will add to the therapeutic options for patients with heart disease.
{"title":"Cellular cardiomyoplasty--a novel approach to treat heart disease.","authors":"J. Müller-Ehmsen, L. Kedes, R. Schwinger, R. Kloner","doi":"10.1111/J.1527-5299.2002.00292.X","DOIUrl":"https://doi.org/10.1111/J.1527-5299.2002.00292.X","url":null,"abstract":"Cell transplantation is a novel experimental strategy to treat heart disease, such as myocardial infarction and heart failure. Its beneficial effects may include active contribution of transplanted cells to contractile function, passive improvement of the mechanics of the heart, induction of neoangiogenesis or other indirect influences on the biology of the heart. Several cell types have been used for cardiac cell transplantation including cardiac cells from fetal or newborn animals and cardiac muscle cell lines, skeletal myoblasts and skeletal muscle cell lines, smooth muscle cells, and a variety of stem cells, either adult or embryonic. With many of these cells, encouraging results in experimental ischemic and nonischemic heart disease have been obtained including successful cell survival after transplantation, integration into the host myocardium, and improvement of the function of diseased hearts. Most of these studies found cardiac contractility improved and some found enhanced angiogenesis. However, the mechanisms of these effects remain obscure, and the impact of dosage (cell number) on functional response is completely unclear. In addition, not enough comparative studies were performed to allow preference of one cell type over the other. The current data suggest that whatever cell species is used, the best survival and integration may be accomplished if immature and undifferentiated cells are used. Any kind of stem cell has obvious advantages in terms of endless reproducibility and plasticity, but the complete differentiation and maturation into cardiac myocytes still needs to be proven. At present several clinical studies are exploring the therapeutic benefits of cellular cardiomyoplasty in patients with ischemic heart disease, but it has to be noted that there are many issues that need to be addressed before this strategy will add to the therapeutic options for patients with heart disease.","PeriodicalId":10536,"journal":{"name":"Congestive heart failure","volume":"13 1","pages":"220-7"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76824804","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 : 2002-07-01DOI: 10.1111/J.1527-5299.2002.01715.X
M. Silver
In a recent excellent editorial message, Dr. Dean Ornish emphasized to all of us the need to use diet and lifestyle measures as well as statin therapies for patients with hyperlipidemias—in other words, he urged us to not fail to use all of the tools in our tool belt.1 And so it is with heart failure; we have long paid attention (or lip-service it sometimes seems) to the many other options for treating patients with symptomatic heart failure including the roles of dietary salt restriction, exercise, smoking cessation, stress reduction, and so on. In this issue of Congestive Heart Failure, and in issues to come, papers on surgical therapies for heart failure are part of the content, along with drug therapies such as diuretics and angiotensin II receptor blockers. At first glance one might say that surgical therapies such as coronary artery bypass surgery and heart transplantation have long been important parts of our heart failure armamentarium. However, beginning to think about surgical approaches as a “standard” or “routine” is in fact going to be a bit of a culture shift for some. As our understanding of the pathophysiology of heart failure grows and we recognize that once developed, heart failure in many ways begets itself, so, too, will our understanding and acceptance of surgical therapies for heart failure. This step is critical, I believe, since my observation has been that aside from the few “early adopters” of new surgical approaches, most professionals taking care of patients with advanced heart failure often share the lay perspective that a patient is so sick—they might not “make it through” the surgical procedure—when, in fact, without a surgical correction, the patient will most certainly die. And so, as we have learned about many of our drug therapies with heart failure (treating earlier is better), we need to get over the cultural shock of what a surgical therapy really is—a big fix for a big problem that has gone on too long. It is incumbent on our surgical colleges and device manufacturers as well to begin to reduce the surgical intensity needed to effect a surgical treatment. So as you read the reviews in this issue of CHF be reminded that they are here because this is where they need to be—in the hands and minds of the heart failure therapists of the world. And if this is a little uncomfortable for you right now, I suggest you try, as Suzuki implored us, to keep a “beginner’s mind.”
{"title":"Surgical therapies for heart failure--making the tool belt for heart failure bigger.","authors":"M. Silver","doi":"10.1111/J.1527-5299.2002.01715.X","DOIUrl":"https://doi.org/10.1111/J.1527-5299.2002.01715.X","url":null,"abstract":"In a recent excellent editorial message, Dr. Dean Ornish emphasized to all of us the need to use diet and lifestyle measures as well as statin therapies for patients with hyperlipidemias—in other words, he urged us to not fail to use all of the tools in our tool belt.1 And so it is with heart failure; we have long paid attention (or lip-service it sometimes seems) to the many other options for treating patients with symptomatic heart failure including the roles of dietary salt restriction, exercise, smoking cessation, stress reduction, and so on. In this issue of Congestive Heart Failure, and in issues to come, papers on surgical therapies for heart failure are part of the content, along with drug therapies such as diuretics and angiotensin II receptor blockers. At first glance one might say that surgical therapies such as coronary artery bypass surgery and heart transplantation have long been important parts of our heart failure armamentarium. However, beginning to think about surgical approaches as a “standard” or “routine” is in fact going to be a bit of a culture shift for some. As our understanding of the pathophysiology of heart failure grows and we recognize that once developed, heart failure in many ways begets itself, so, too, will our understanding and acceptance of surgical therapies for heart failure. This step is critical, I believe, since my observation has been that aside from the few “early adopters” of new surgical approaches, most professionals taking care of patients with advanced heart failure often share the lay perspective that a patient is so sick—they might not “make it through” the surgical procedure—when, in fact, without a surgical correction, the patient will most certainly die. And so, as we have learned about many of our drug therapies with heart failure (treating earlier is better), we need to get over the cultural shock of what a surgical therapy really is—a big fix for a big problem that has gone on too long. It is incumbent on our surgical colleges and device manufacturers as well to begin to reduce the surgical intensity needed to effect a surgical treatment. So as you read the reviews in this issue of CHF be reminded that they are here because this is where they need to be—in the hands and minds of the heart failure therapists of the world. And if this is a little uncomfortable for you right now, I suggest you try, as Suzuki implored us, to keep a “beginner’s mind.”","PeriodicalId":10536,"journal":{"name":"Congestive heart failure","volume":"12 1","pages":"200"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86601962","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 : 2002-07-01DOI: 10.1111/J.1527-5299.2002.01731.X
O. Soran, B. Fleishman, T. DeMarco, W. Grossman, V. M. Schneider, K. Manzo, P. de Lame, A. Feldman
To assess the feasibility of using enhanced external counterpulsation to treat patients with heart failure, 26 patients with stable heart failure (New York Heart Association classes II-III), with a left ventricular ejection fraction at or below 35%, and without fluid overload, were treated with enhanced external counterpulsation (1 hour daily, 5 days a week, to a total of 35 hours). Patients were followed for 6 months after completing the course of enhanced external counterpulsation. The primary parameter was safety as reflected by adverse events or by changes in laboratory parameters. Secondary end points included changes in exercise capacity and quality of life. There were no clinically significant problems associated with the administration of enhanced external counterpulsation. Significant improvements were seen in exercise capacity (peak oxygen uptake and exercise duration), and in quality of life assessments, at 1 week and 6 months after the course of enhanced external counterpulsation. This study suggests that enhanced external counterpulsation is safe and well tolerated in patients with stable heart failure, and that a randomized, controlled study of enhanced external counterpulsation in these patients is warranted.
{"title":"Enhanced external counterpulsation in patients with heart failure: a multicenter feasibility study.","authors":"O. Soran, B. Fleishman, T. DeMarco, W. Grossman, V. M. Schneider, K. Manzo, P. de Lame, A. Feldman","doi":"10.1111/J.1527-5299.2002.01731.X","DOIUrl":"https://doi.org/10.1111/J.1527-5299.2002.01731.X","url":null,"abstract":"To assess the feasibility of using enhanced external counterpulsation to treat patients with heart failure, 26 patients with stable heart failure (New York Heart Association classes II-III), with a left ventricular ejection fraction at or below 35%, and without fluid overload, were treated with enhanced external counterpulsation (1 hour daily, 5 days a week, to a total of 35 hours). Patients were followed for 6 months after completing the course of enhanced external counterpulsation. The primary parameter was safety as reflected by adverse events or by changes in laboratory parameters. Secondary end points included changes in exercise capacity and quality of life. There were no clinically significant problems associated with the administration of enhanced external counterpulsation. Significant improvements were seen in exercise capacity (peak oxygen uptake and exercise duration), and in quality of life assessments, at 1 week and 6 months after the course of enhanced external counterpulsation. This study suggests that enhanced external counterpulsation is safe and well tolerated in patients with stable heart failure, and that a randomized, controlled study of enhanced external counterpulsation in these patients is warranted.","PeriodicalId":10536,"journal":{"name":"Congestive heart failure","volume":"1 1","pages":"204-8, 227"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80158116","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 : 2002-07-01DOI: 10.1111/J.1527-5299.2002.01213.X
V. Badhwar, S. Bolling
Mitral regurgitation (MR) is a frequent complication of end-stage cardiomyopathy. Historically, these patients were managed either medically or with mitral valve replacement, both associated with poor outcomes. We studied 150 patients with cardiomyopathy and severe MR who were managed with mitral reconstruction. One hundred fifty patients with 4+ MR, left ventricular ejection fractions of 8%-24% (mean, 14%), and New York Heart Association class III or IV symptoms were prospectively studied. All patients underwent mitral valve repair with an undersized, flexible annuloplasty ring. There was one intraoperative death and seven 30-day mortalities. Intraoperative echocardiography revealed no residual MR in the majority of patients and mild to trivial MR in seven patients. There were 27 late deaths; three of these patients had progression of the disease and underwent transplantation. The 1-, 2-, and 5-year actuarial survival rates are 82%, 71%, and 57%, respectively. New York Heart Association class has improved for all patients, from a preoperative mean of 3.2+/-0.2 to 1.8+/-0.4 postoperatively. At 24-month follow-up, all patients showed improvement in ejection fraction, cardiac output, and end-diastolic volumes, along with a reduction in the sphericity index and regurgitant volume. Mitral valve repair with an undersized, flexible annuloplasty ring is a safe and effective approach to correction of MR, even in cardiomyopathy patients. All observed changes contribute to reverse remodeling and the restoration of the normal left ventricular geometric relationship. Mitral reconstruction provides a new first-line management strategy for patients with MR and end-stage heart failure.
{"title":"Mitral valve surgery: when is it appropriate?","authors":"V. Badhwar, S. Bolling","doi":"10.1111/J.1527-5299.2002.01213.X","DOIUrl":"https://doi.org/10.1111/J.1527-5299.2002.01213.X","url":null,"abstract":"Mitral regurgitation (MR) is a frequent complication of end-stage cardiomyopathy. Historically, these patients were managed either medically or with mitral valve replacement, both associated with poor outcomes. We studied 150 patients with cardiomyopathy and severe MR who were managed with mitral reconstruction. One hundred fifty patients with 4+ MR, left ventricular ejection fractions of 8%-24% (mean, 14%), and New York Heart Association class III or IV symptoms were prospectively studied. All patients underwent mitral valve repair with an undersized, flexible annuloplasty ring. There was one intraoperative death and seven 30-day mortalities. Intraoperative echocardiography revealed no residual MR in the majority of patients and mild to trivial MR in seven patients. There were 27 late deaths; three of these patients had progression of the disease and underwent transplantation. The 1-, 2-, and 5-year actuarial survival rates are 82%, 71%, and 57%, respectively. New York Heart Association class has improved for all patients, from a preoperative mean of 3.2+/-0.2 to 1.8+/-0.4 postoperatively. At 24-month follow-up, all patients showed improvement in ejection fraction, cardiac output, and end-diastolic volumes, along with a reduction in the sphericity index and regurgitant volume. Mitral valve repair with an undersized, flexible annuloplasty ring is a safe and effective approach to correction of MR, even in cardiomyopathy patients. All observed changes contribute to reverse remodeling and the restoration of the normal left ventricular geometric relationship. Mitral reconstruction provides a new first-line management strategy for patients with MR and end-stage heart failure.","PeriodicalId":10536,"journal":{"name":"Congestive heart failure","volume":"31 1","pages":"210-3"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86708391","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 : 2002-07-01DOI: 10.1111/J.1527-5299.2002.01417.X
M. Mehra, P. Uber
A large number of chronic heart failure patients escape from the benefits of neurohormonal blockade only to transit into a discouragingly miserable state of what the physician often refers to as end-stage heart failure. Conceptually, the designation of end-stage as a description of a clinical scenario implies pessimism concerning recourse to a therapeutic avenue. A variety of surgical therapeutic techniques that take advantage of the law of Laplace, designed to effectively restore the cardiac shape from a spherical, mechanically inefficient pump to a more elliptical, structurally sound organ are now being employed. Additionally, the field of mechanical device implantation is surging ahead at a rapid pace. The weight of evidence regarding mechanical unloading using assist devices suggests that hemodynamic restoration is accompanied by regression of cellular hypertrophy, normalization of the neuroendocrine axis, improved expression of contractile proteins, enhanced cellular respiratory control, and decreases in markers of apoptosis and cellular stress. Thus, these lines of data point toward discarding the notion of end-stage heart failure. We are at a new crossroad in our quest to tackle chronic heart failure. It is our contention that the use of antiremodeling strategies, including device approaches, will soon signal the end of end-stage heart failure.
{"title":"Emergence of Laplace therapeutics: declaring an end to end-stage heart failure.","authors":"M. Mehra, P. Uber","doi":"10.1111/J.1527-5299.2002.01417.X","DOIUrl":"https://doi.org/10.1111/J.1527-5299.2002.01417.X","url":null,"abstract":"A large number of chronic heart failure patients escape from the benefits of neurohormonal blockade only to transit into a discouragingly miserable state of what the physician often refers to as end-stage heart failure. Conceptually, the designation of end-stage as a description of a clinical scenario implies pessimism concerning recourse to a therapeutic avenue. A variety of surgical therapeutic techniques that take advantage of the law of Laplace, designed to effectively restore the cardiac shape from a spherical, mechanically inefficient pump to a more elliptical, structurally sound organ are now being employed. Additionally, the field of mechanical device implantation is surging ahead at a rapid pace. The weight of evidence regarding mechanical unloading using assist devices suggests that hemodynamic restoration is accompanied by regression of cellular hypertrophy, normalization of the neuroendocrine axis, improved expression of contractile proteins, enhanced cellular respiratory control, and decreases in markers of apoptosis and cellular stress. Thus, these lines of data point toward discarding the notion of end-stage heart failure. We are at a new crossroad in our quest to tackle chronic heart failure. It is our contention that the use of antiremodeling strategies, including device approaches, will soon signal the end of end-stage heart failure.","PeriodicalId":10536,"journal":{"name":"Congestive heart failure","volume":"47 1","pages":"228-31, 234"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87545795","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 : 2002-07-01DOI: 10.1111/J.1527-5299.2002.01743.X
J. Strobeck
{"title":"Enhanced external counterpulsation in congestive heart failure: possibly the most potent inodilator to date.","authors":"J. Strobeck","doi":"10.1111/J.1527-5299.2002.01743.X","DOIUrl":"https://doi.org/10.1111/J.1527-5299.2002.01743.X","url":null,"abstract":"","PeriodicalId":10536,"journal":{"name":"Congestive heart failure","volume":"17 1","pages":"201-3"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84181236","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 : 2002-07-01DOI: 10.1111/J.1527-5299.2002.01076.X
D. Tepper
{"title":"Anemia Is Associated With Worse Symptoms, Greater Impairment in Functional Capacity, and a Significant Increase in Mortality in Patients With Advanced Heart Failure","authors":"D. Tepper","doi":"10.1111/J.1527-5299.2002.01076.X","DOIUrl":"https://doi.org/10.1111/J.1527-5299.2002.01076.X","url":null,"abstract":"","PeriodicalId":10536,"journal":{"name":"Congestive heart failure","volume":"11 1","pages":"235-236"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81697162","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 : 2002-07-01DOI: 10.1111/J.1527-5299.2002.01078.X
S. Sangha, P. Uber, Myung H. Park, R. Scott, M. Mehra
Often ignored, neurocognitive dysfunction in chronic heart failure represents a daunting morbidity progressing to loss of self-reliance. Although the precise mechanisms arbitrating the development of this disorder remain elusive, microembolization and cerebral hypoperfusion are implicated. Other causes of cognitive decline may include prior cardiac surgery, chronic hypertension, sleep disordered breathing, hyperhomocysteinemia, dementia of aging, and more “traditional causes” such as Alzheimer's disease. The discovery of neurocognitive defects in heart failure must prompt a well-constructed diagnostic evaluation to search for the underlying causes since this process may be at least partially reversible in many cases.
{"title":"The Challenge of Neurocognitive Dysfunction in Severe Heart Failure","authors":"S. Sangha, P. Uber, Myung H. Park, R. Scott, M. Mehra","doi":"10.1111/J.1527-5299.2002.01078.X","DOIUrl":"https://doi.org/10.1111/J.1527-5299.2002.01078.X","url":null,"abstract":"Often ignored, neurocognitive dysfunction in chronic heart failure represents a daunting morbidity progressing to loss of self-reliance. Although the precise mechanisms arbitrating the development of this disorder remain elusive, microembolization and cerebral hypoperfusion are implicated. Other causes of cognitive decline may include prior cardiac surgery, chronic hypertension, sleep disordered breathing, hyperhomocysteinemia, dementia of aging, and more “traditional causes” such as Alzheimer's disease. The discovery of neurocognitive defects in heart failure must prompt a well-constructed diagnostic evaluation to search for the underlying causes since this process may be at least partially reversible in many cases.","PeriodicalId":10536,"journal":{"name":"Congestive heart failure","volume":"17 1","pages":"232-234"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80634266","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 : 2002-07-01DOI: 10.1111/J.1527-5299.2002.01114.X
I. Gregoric, O. Frazier, W. J. Couto
Cardiac transplantation is the definitive surgical treatment for patients with severe left ventricular dysfunction and congestive heart failure. Unfortunately, however, the supply of donor hearts remains severely limited, so transplantation is an option for only a minority of these patients. Even after being approved for a heart transplant, patients often have a long wait until a suitable donor heart can be found. This waiting period entails a significant mortality rate. Because the supply of donor hearts is not expected to increase, surgeons have introduced several alternatives to heart transplantation, including partial left ventriculectomy, mitral valve repair, myocardial revascularization, and endoventricular circular patch plasty. For maximal benefit, surgeons must refine the selection criteria for determining which patients are the best candidates for each of these procedures.
{"title":"Surgical treatment of congestive heart failure.","authors":"I. Gregoric, O. Frazier, W. J. Couto","doi":"10.1111/J.1527-5299.2002.01114.X","DOIUrl":"https://doi.org/10.1111/J.1527-5299.2002.01114.X","url":null,"abstract":"Cardiac transplantation is the definitive surgical treatment for patients with severe left ventricular dysfunction and congestive heart failure. Unfortunately, however, the supply of donor hearts remains severely limited, so transplantation is an option for only a minority of these patients. Even after being approved for a heart transplant, patients often have a long wait until a suitable donor heart can be found. This waiting period entails a significant mortality rate. Because the supply of donor hearts is not expected to increase, surgeons have introduced several alternatives to heart transplantation, including partial left ventriculectomy, mitral valve repair, myocardial revascularization, and endoventricular circular patch plasty. For maximal benefit, surgeons must refine the selection criteria for determining which patients are the best candidates for each of these procedures.","PeriodicalId":10536,"journal":{"name":"Congestive heart failure","volume":"138 1","pages":"214-9"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86575595","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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