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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.
Modalities applied to measurement of ejection fraction is an emerging field of medical mathematics and subsequent computational applications. The first common measurement method is echocardiography, [7] [8] although cardiac magnetic resonance imaging (MRI), [8] [9] cardiac computed tomography, [8] [9] ventriculography and nuclear medicine (gated SPECT and radionuclide angiography) [8] [10 ...
Heart failure with mildly reduced ejection fraction (HFmrEF), previously called "heart failure with mid-range ejection fraction", [63] is defined by an ejection fraction of 41–49%. [ 63 ] Heart failure with preserved ejection fraction (HFpEF): Synonyms no longer recommended include "diastolic heart failure" and "heart failure with normal ...
CRT: People with NYHA class III or IV, left ventricular ejection fraction (LVEF) of 35% or less and a QRS interval of 120 ms or more may benefit from cardiac resynchronization therapy (CRT; pacing both the left and right ventricles), through implantation of a bi-ventricular pacemaker. This treatment modality may alleviate symptoms, improving ...
This is defined as a left ventricular ejection fraction (LVEF) of 40% or less. About half of heart failure patients have a reduced ejection fraction. [2] Other types of heart failure are heart failure with mildly reduced ejection fraction (LVEF between 40% and 50%) and heart failure with preserved ejection fraction (LVEF 50% or higher). [1] [3]
[35] Each leaflet is composed of three layers of tissue: the atrialis, fibrosa, and spongiosa. Patients with classic mitral valve prolapse have excess connective tissue that thickens the spongiosa and separates collagen bundles in the fibrosa. This is due to an excess of dermatan sulfate, a glycosaminoglycan.
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Due to non-compaction cardiomyopathy being a relatively new disease, its impact on human life expectancy is not very well understood. In a 2005 study [3] that documented the long-term follow-up of 34 patients with NCC, 35% had died at the age of 42 +/- 40 months, with a further 12% having to undergo a heart transplant due to heart failure ...
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