Mitochondrion: Key factors in acute heart failure

Abstract

Mitochondria are largely abundant in the myocardium, not only because they provide the large part of energy in an organ that consumes a lot of adenosine triphosphate (ATP) for its mechanical activity and its cellular processes, but also because mitochondria play a potent role in cardiac homeostasis. Acute heart failure (AHF), defined as a reversible incapacity of the myocardium to provide a sufficient output for cellular metabolism of all the organs, is very common. Mechanisms leading to AHF have been largely investigated. Because the mitochondrial functional state is able to modulate force development and then pump function [1], impairment in cardiac contractile functions, as seen in AHF, may be the consequence of alterations in mitochondria function and metabolism. The role of mitochondria in AHF has been largely studied after ischemia-reperfusion injury and in septic shock. Besides these two situations, evidence of the role of mitochondria in AHF comes also from carbon monoxide (CO) poisoning where swollen mitochondria with rupture of mitochondrial cristae were described [2]. © 2008 Springer-Verlag London.