The heart failure epidemic: exactly how big is it?

Cleland, John G.F.; Khand, Aleem; Clark, Andrew L.

doi:10.1053/euhj.2000.2493

Cited by 282 publications

(189 citation statements)

References 25 publications

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“…Heart failure is a leading cause of morbidity and mortality in industrial countries, affecting over 10 million Americans and Western Europeans, with a 5-year mortality approaching 50% despite current medical therapy (1). 1 These mortality figures reflect the lack of biologically efficacious therapies directed against the underlying disease processes that lead to maladaptive left ventricular remodeling and, ultimately, failure itself.…”

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“…1 These mortality figures reflect the lack of biologically efficacious therapies directed against the underlying disease processes that lead to maladaptive left ventricular remodeling and, ultimately, failure itself. In response to a plethora of intra-and extracardiac stimuli, cardiomyocytes exhibit cellular enlargement or hypertrophy as a compensatory adaptation to increased ventricular wall stress (3).…”

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Requirement of Nuclear Factor of Activated T-cells in Calcineurin-mediated Cardiomyocyte Hypertrophy

Rooij¹,

Doevendans²,

Theije³

et al. 2002

Journal of Biological Chemistry

115

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The calcium-activated phosphatase calcineurin has been implicated as a critical intracellular signal transducer of cardiomyocyte hypertrophy. Although previous data suggested the nuclear factor of activated T-cells (NFAT) as its sole transcriptional effector, the absolute requirement of NFAT as a mediator of calcineurin signaling has not been examined in the heart. We therefore investigated the expression and activation profile of NFAT genes in the heart. Four members (NFATc1-c4) are expressed in cardiomyocytes, elicit nuclear translocation upon calcineurin activation, and are able to drive transactivation of cardiac promoter luciferase constructs. To define the necessary function of NFAT factors as hypertrophic transducers, a dominant negative NFAT construct was created, encompassing part of the N-terminal region of NFATc4 containing a conserved calcineurin-binding motif. Cotransfection of this construct dose-dependently abrogated promoter activation, irrespective of the NFAT isoform used, whereas a control construct with the calcineurin-binding motif mutated displayed no such effects. Adenoviral gene transfer of dominant negative NFAT rendered cardiomyocytes resistant toward all aspects of calcineurin or agonist-induced cardiomyocyte hypertrophy, whereas adenoviral gene transfer of the control construct had no discernable effect on these parameters. These results indicate that multiple NFAT isoforms are expressed in cardiomyocytes where they function as necessary transducers of calcineurin in facilitating cardiomyocyte hypertrophy.Heart failure is a leading cause of morbidity and mortality in industrial countries, affecting over 10 million Americans and Western Europeans, with a 5-year mortality approaching 50% despite current medical therapy (1).1 These mortality figures reflect the lack of biologically efficacious therapies directed against the underlying disease processes that lead to maladaptive left ventricular remodeling and, ultimately, failure itself. In response to a plethora of intra-and extracardiac stimuli, cardiomyocytes exhibit cellular enlargement or hypertrophy as a compensatory adaptation to increased ventricular wall stress (3). However, sustained cardiac hypertrophy is the single most important risk factor for the development of heart failure (4, 5). Because intracellular signaling pathways are thought to both initiate and perpetuate the cardiac hypertrophic response and its transition to dilated failure, recent investigation has attempted the identification of key regulatory factors with the goal of defining novel therapeutic targets (3).One recently characterized intracellular signaling pathway that links extracellular stimuli to a hypertrophic transcriptional response employs the phosphatase calcineurin and its downstream transcriptional effector nuclear factor of activated T-cells (NFAT).2 Four of the five NFAT proteins (NFATc1, NFAT2, or NFATc; NFATc2, NFAT1, or NFATp; NFATc3, NFAT4, or NFATx; and NFATc4 or NFAT3) reside in the cytoplasm in unstimulated cells but quickly translocate to ...

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confidence: 99%

mentioning

confidence: 99%

Requirement of Nuclear Factor of Activated T-cells in Calcineurin-mediated Cardiomyocyte Hypertrophy

Rooij¹,

Doevendans²,

Theije³

et al. 2002

Journal of Biological Chemistry

115

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“…Takođe se očekuje povećavanje broja pacijenata sa SI u zemljama u razvoju i nerazvijenim zemljama, sa velikom incidencom hipertenzije, dijabetesa i gojaznosti. Prema nekim projekcijama procenat starijih ljudi sa SI u 2040. godini prevazići će 20% [5,6].…”

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Bolesnik sa srčanom insuficijencijom – izazov za lekara porodične medicine

Bunc¹

2017

Biomedicinska istraž.

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Katedra za porodičnu medicinu, Medicinski fakultet, Univerzitet u Mariboru, Slovenija Zdravstveni dom dr Adolfa Drolca, Maribor, Slovenija Kratak sadržajSrčana insuficijencija (SI) predstavlja veliki problem javnog zdravlja. Učestalost se, za razliku od drugih kardiovaskularnih bolesti, povećava. Tome doprinosi starenje stanovništva i efikasnost lečenja etioloških činilaca kardiovaskularnih bolesti, naročito ishemijske bolesti srca. Pacijenti sa SI najčešće traže pomoć kod svog izabranog doktora, pa su tako oni česti posetioci ambulanti porodične medicine. Njihovo stanje je ozbiljno, sa lošom prognozom i kvalitetom života, sa potrebom za čestim hospitalizacijama, a prosečno preživljavanje nakon postavljanja dijagnoze je pet godina. Vođenje bolesnika sa SI predstavlja izazov za svakog lekara porodične medicine. Pažljivo uzimanje anamneze je od velike važnosti, jer simptomi upozoravaju lekara na mogućnost postojanja SI. Ipak, oni su relativno česti u opštoj populaciji i ponekad ih je teško objasniti, posebno kod starih osoba, gojaznih i kod žena. Njihova prediktivna vrednost je niska, zato ih treba tumačiti oprezno i sprovoditi detaljnu dijagnostiku pomoću metoda koje su dostupne i na raspolaganju lekaru porodične medicine u svakodnevnoj praksi. Pacijentima sa SI potreban je pregled kardiologa koji će dopunskim pretragama potvrditi dijagnozu SI. U lečenju SI, lekar porodične medicine ima važnu ulogu ne samo u pružanju savremene terapije nego i u savetovanju i podsticanju pacijenta da provodi nefarmakološke mere, kao i da odgovori na pitanja pacijenta koja se ne odnose samo na bolest, nego i na kvalitet života. Na kraju života, u terminalnoj fazi SI, lekar porodične medicine je često jedini koji ostaje na raspolaganju pacijentima i porodicama u palijativnom zbrinjavanju.Ključne reči: lekar porodične medicine, srčana insuficiencija UvodSrčana insuficijencija (SI) je progresivni klinički sindrom, čijem nastanku doprinose različiti etiološki faktori, najčešće hipertenzija i ishemijska bolest srca. To je često stanje, njegova učestalost raste, prate ga komorbiditeti, a pacijenti imaju loš kvalitet živo-ta. Česte su hospitalizacije, dok je mortalitet visok i može se upoređivati sa mortalitetom kod malignih bolesti. SI kao krajnji rezultat različitih kardiovaskularnih bolesti predstavlja veliki problem javnog zdravlja sa kojima se suočavaju

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“…Actualmente es incuestionable el papel que juegan la hipertensión arterial (HTA) y la cardiopatía isquémica (CI) en la etiopatogenia de la insuficiencia cardiaca (IC) (2), ambas patologías crónicas que requieren tratamiento diario, en el cual fármacos como los inhibidores del enzima convertidor de angiotensina (IECA) (3), antagonistas del receptor de angiotensina II (ARA-II) (4) y beta-bloqueantes (5) han demostrado su utilidad y la mayor supervivencia en las tres patologías (HTA, CI e IC), lo que añadido a un envejecimiento poblacional está aumentando progresivamente la prevalencia de IC, que alcanza el 10% en mayores de 70 años (6), hasta el punto de ser la primera causa de ingreso hospitalario en España (5% de los ingresos), lo que refleja que la IC, a pesar de presentar mayor supervivencia, limita notablemente la calidad de vida de los pacientes (7).…”

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