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Heart failure with preserved ejection fraction (HFpEF) is a form of heart failure in which the ejection fraction – the percentage of the volume of blood ejected from the left ventricle with each heartbeat divided by the volume of blood when the left ventricle is maximally filled – is normal, defined as greater than 50%; [1] this may be measured by echocardiography or cardiac catheterization.
In clinical cardiology the term "diastolic function" is most commonly referred as how the heart fills. [1] Parallel to "diastolic function", the term "systolic function" is usually referenced in terms of the left ventricular ejection fraction (LVEF), which is the ratio of stroke volume and end-diastolic volume. [2]
The EF of the left heart, known as the left ventricular ejection fraction (LVEF), is calculated by dividing the volume of blood pumped from the left ventricle per beat (stroke volume) by the volume of blood present in the left ventricle at the end of diastolic filling (end-diastolic volume).
The reversal of the E/A ratio ('A' velocity becomes greater than 'E' velocity) is often accepted as a clinical marker of diastolic dysfunction, in which the left ventricular wall becomes so stiff as to impair proper filling, which can lead to diastolic heart failure. This can occur, for instance, with longstanding untreated hypertension.
Diastolic dysfunction is associated with a reduced compliance, or increased stiffness, of the ventricle wall. This reduced compliance results in an inadequate filling of the ventricle and a decrease in the end-diastolic volume. The decreased end-diastolic volume then leads to a reduction in stroke volume because of the Frank-Starling mechanism. [1]
Illustration of a Normal Heart vs. Heart with Dilated Cardiomyopathy. The progression of heart failure is associated with left ventricular remodeling, which manifests as gradual increases in left ventricular end-diastolic and end-systolic volumes, wall thinning, and a change in chamber geometry to a more spherical, less elongated shape.
In diastolic dysfunction, the end-diastolic ventricular pressure will be high. This increase in volume or pressure backs up to the left atrium and then to the pulmonary veins. Increased volume or pressure in the pulmonary veins impairs the normal drainage of the alveoli and favors the flow of fluid from the capillaries to the lung parenchyma ...
Defects in cellular processes such as autophagy and mitophagy are thought to contribute to the development of diabetic cardiomyopathy. [2] Diabetic cardiomyopathy is characterized functionally by ventricular dilation, enlargement of heart cells, prominent interstitial fibrosis and decreased or preserved systolic function [5] in the presence of a diastolic dysfunction.
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