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Molecular Approaches to Heart Failure Therapy

Specificaties
Paperback, 357 blz. | Engels
Steinkopff | 0e druk, 2012
ISBN13: 9783642633324
Rubricering
Steinkopff 0e druk, 2012 9783642633324
Verwachte levertijd ongeveer 9 werkdagen

Samenvatting

G. HASENFUSS, E. MARBAN Heart failure embodies the central irony of modern medicine. As we have become increasingly adept at treating the major proximate causes of death in Western society, we have effectively converted acute illness into chronic malady. The last twenty years have witnessed a revolution in the treatment of acute coronary syndromes, myocardial infarction in particular. Patients who reach the hospital now have every expectation of leaving alive, but not necessarily well. Our ability to blunt the edge of ischemic insults has en­ gendered new problems: a new cohort of patients whose hearts function well enough to enable short-term survival, but at the cost of decreased ex­ ercise tolerance, dyspnea and increased long-term mortality. The irony is compounded by our increasingly sophisticated pharmacopeia for the treat­ ment of heart failure, which, by slowing the progression of ventricular dys­ function, has created a chronic illness. The fact of its chronicity makes heart failure no less deadly. In symptomatic patients, mortality exceeds 5-10% per year even with the best contemporary therapy. Not all heart failure is ischemic, of course, but the final common phenotype is eerily concordant regardless of the proximate cause. No wonder, then, that heart failure is the leading cause of hospitalization in America and in Western Europe and that the prevalence of the disease continues to rise. Drugs have indeed revolutionized heart failure therapy, ACE inhibitors and beta-adrenergic blockers having the most outstanding records to date.

Specificaties

ISBN13:9783642633324
Taal:Engels
Bindwijze:paperback
Aantal pagina's:357
Uitgever:Steinkopff
Druk:0

Inhoudsopgave

Alterations in excitation-contraction coupling and potential gene thrapy targets in failing human hearts.- Cardiac overexpression of ß-adrenergic receptors.- Genetic approaches to elucidate the regulatory role of phospholamban in the heart-. Manipulation of SERCA2a in the heart by gene transfer-. Changing the cardiac calcium transient: SERCA2 overexpression versus phospholamban inhibition.- Adenovirus-mediated gene transfer of SERCA isoforms.- Overexpression of FKBP12.6 to influenxe SR function.- Adenovirus-mediated myocardial gene therapy.- Adenovirus-mediated transfection of multicellular cardiac preparations.- Myocardial-specific gene delivery.- Transfection studies using a new cardiac 3D gel system.- Cellular mechanisms of cardiac arrhythmias - do they play a role in heart failure?.- Potassium channel overexpression.- Mechanisms and relevance of apoptosis.- Strategies to prevent apoptosis.- Neurohumoral modulation of metalloproeinases in cardiac failure: impact on remodeling.- Oxidative stress in heart failure.- Modulation of cardiac function by essential myosin light chains in health and disease.- Mycardial infarction, infarct repair, and strategies for muscle regeneration.- Cardiomyocytes can induce rhythmic contraction of skeletal muscle cells. Potenial use for infarct repair.- Strategies to identify cardimyocyte xell cycle regulatory genes.

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        Molecular Approaches to Heart Failure Therapy