Editing Heart failure (section)

==Pathophysiology==
{{Main|Pathophysiology of heart failure}}
[[File:Right side heart failure.jpg|thumb|upright=1.6|Model of a normal heart (left); and a weakened heart, with over-stretched muscle and dilation of [[left ventricle]] (right); both during [[diastole]]]] Heart failure is caused by any condition that reduces the efficiency of the heart muscle, through damage or [[Volume overload|overloading]]. Over time, these increases in workload, which are mediated by long-term activation of neurohormonal systems such as the [[renin–angiotensin system]] and the sympathoadrenal system, lead to [[fibrosis]], dilation, and structural changes in the shape of the left ventricle from elliptical to spherical.<ref name="Lancet2017"/>

The heart of a person with heart failure may have a reduced force of contraction due to overloading of the [[Ventricle (heart)|ventricle]]. In a normal heart, increased filling of the ventricle results in increased contraction force by the [[Frank–Starling law of the heart]], and thus a rise in [[cardiac output]]. In heart failure, this mechanism fails, as the ventricle is loaded with blood to the point where heart muscle contraction becomes less efficient. This is due to the reduced ability to cross-link [[actin]] and [[myosin]] [[myofilament]]s in over-stretched heart muscle.<ref>{{cite book | vauthors = Boron WF, Boulpaep EL |title=Medical Physiology: A Cellular and Molecular Approach |publisher=Saunders |edition=Updated |year=2005  |isbn=978-0-7216-3256-8 |page=533 }}</ref>