By G. Hasenfuss, E. Marbán (auth.), Prof. Dr. med. Gerd Hasenfuss, Eduardo Marbán M.D., Ph.D. (eds.)
G. HASENFUSS, E. MARBAN center failure embodies the relevant irony of recent drugs. As we've turn into more and more adept at treating the key proximate motives of dying in Western society, we've successfully switched over acute sickness into persistent illness. The final two decades have witnessed a revolution within the remedy of acute coronary syndromes, myocardial infarction specifically. sufferers who succeed in the health facility now have each expectation of leaving alive, yet no longer unavoidably good. Our skill to blunt the sting of ischemic insults has en gendered new difficulties: a brand new cohort of sufferers whose hearts functionality good sufficient to permit temporary survival, yet on the price of reduced ex ercise tolerance, dyspnea and elevated long term mortality. The irony is compounded via our more and more subtle pharmacopeia for the deal with ment of middle failure, which, via slowing the development of ventricular dys functionality, has created a protracted ailment. the actual fact of its chronicity makes middle failure no much less lethal. In symptomatic sufferers, mortality exceeds 5-10% in keeping with yr regardless of the easiest modern treatment. now not all center failure is ischemic, after all, however the ultimate universal phenotype is eerily concordant whatever the proximate reason. No ask yourself, then, that center failure is the best reason behind hospitalization in the United States and in Western Europe and that the superiority of the ailment keeps to upward push. medications have certainly revolutionized middle failure remedy, ACE inhibitors and beta-adrenergic blockers having the main striking files to date.
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Limbird LE, Vaughan DE (1999) Augmenting p-receptors in the heart: short-term gains offset by long-term pains? Proc Nat! Acad Sci USA 96:7125-7127 31. Lohse MJ (1995) G-protein coupled receptor kinases and the heart. Trends Cardiovasc Med 5:63-68 2 Cardiac overexpression of p-adrenergic receptors 32. Lohse MJ, Benovic JL, Codina J, Caron MG, Lefkowitz RJ (1990) p-Arrestin: a protein that regulates p-adrenergic function. Science 248: 1547 -1550 33. Lohse MJ, Andexinger S, Pitcher J, Trukawinski S, Codina J, Faure J-p, Caron MG, Lefkowitz RJ (1992) Receptor-specific desensitization with purified proteins: kinase dependence and receptor-specificity of p-arrestin and arrestin in the Pr adrenergic receptor and rhodopsin systems.
B Representative sections from 20-week old wild-type (left) and transgenic (right) hearts are shown. 33 34 M. J. Lohse, s. Engelhardt Differences between cardiac receptor overexpression Pl- and P2-adrenergic Comparing the phenotypes of 131- and f32-overexpressing mice, striking differences become apparent. While 200-fold overexpression of the f3radrenergic receptor did not induce detrimental myocardial changes [35, 51], overexpression of the f31-adrenergic receptor at relatively low levels (IS-fold at young age) led to progressive hypertrophy, fibrosis and heart failure [18].
Beyond these in vitro studies, experiments in intact systems demonstrate that phospholamban is a key regulator of basal contractility and fJ-adrenergic stimulatory effects [22]. However, until recently, little was known about the functional significance of phospholamban in vivo. The development of genetic techniques to modify a specific gene product, and the ability to characterize the functional consequences of such manipulations, greatly improved our understanding of the mechanisms and cellular players regulating contractility under physiological and pathophysiological conditions [16].