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Vol. 216. Issue 2.
Pages 99-105 (March 2016)
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Vol. 216. Issue 2.
Pages 99-105 (March 2016)
Symposium. Heart Failure
Target organ damage in acute heart failure
Lesión de órganos diana en la insuficiencia cardiaca aguda
Visits
8
J. Casado Cerradaa,
Corresponding author
casadocerrada@telefonica.net

Corresponding author.
, J.P. Zabaleta Caminob, M. Fontecha Ortegaa
a Servicio de Medicina Interna, Hospital Universitario de Getafe, Madrid, Spain
b Servicio de Urgencias, Hospital Universitario de Getafe, Madrid, Spain
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Tables (3)
Table 1. Diagnosis and classification criteria for acute renal damage.
Table 2. Association between biomarker levels in the first 48h of hospitalization for acute heart failure and mortality at 180 days.
Table 3. Clinical trials with potentially useful drugs for the organ protection mechanism in patients hospitalized for acute heart failure.
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Abstract

Acute heart failure is a prognostic factor due to its high mortality during the acute phase and the increased frequency of medium- to long-term adverse events. The pathophysiological mechanisms triggered during these exacerbations can persist after reaching clinical stability, remaining even after the acute episode has ended. A certain degree of neurohormonal activation, oxidative stress, apoptosis, and inflammation (among other conditions) can therefore persist, resulting in organ damage, not just of the myocardium but also likely for the entire cardiovascular apparatus. This new insight into the persistence of harmful mechanisms that last beyond the exacerbations could be the start of a change in perspective for developing new therapeutic strategies that seek an overall control of hemodynamic and congestive changes that occur during acute decompensated heart failure and changes that remain after achieving clinical stability.

Keyword:
Target organs
Resumen

La insuficiencia cardiaca aguda es un condicionante pronóstico, tanto por su alta morbimortalidad durante el episodio agudo, como por el incremento de acontecimientos adversos a medio y largo plazo. Los mecanismos fisiopatológicos desencadenados durante la agudización podrían no cesar al alcanzarse la estabilidad clínica, manteniéndose una vez pasado el episodio agudo. De este modo, persistiría cierto grado de activación neurohormonal, estrés oxidativo, apoptosis e inflamación, entre otros, que conllevaría daño orgánico, no exclusivamente miocárdico, sino probablemente generalizado sobre el aparato cardiovascular. Esta nueva percepción de la persistencia de los mecanismos lesivos más allá de las agudizaciones puede ser el inicio de un cambio de perspectiva para el desarrollo de nuevas estrategias terapéuticas que persiguen un control global, tanto de los cambios hemodinámicos y congestivos que acontecen durante la descompensación cardiaca aguda, como de los remanentes tras alcanzarse la estabilidad clínica.

Palabras clave:
Órganos diana

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