Diastolic heart failure had been for the most part a diagnosis of exclusion.Symptoms and physical signs of heart failure (Hf) and an elevated natriuretic hormone level in the face of a normal ejection fraction (EF) as determined by echocardiography or gated myocardial perfusion imaging are the elements of the diagnosis.More recently echo studies of flow through the mitral valve opening have allowed a diagnosis of inclusion based on various indicators of diastolic flow and ventricular filling but evidence of diastolic dysfunction is not sufficient to make the diagnosis of diastolic heart failure with preserved systolic function abbreviated as HFpEF.
In the classic physiology text book's 70 kilogram man the stroke volume is 70 ml and the volume of blood poised in the left ventricle at the end of diastole is 120 ml, and the volume at the end of systole is 50 ml giving a EF ( 70/120) of 0.58 ( 58%)) where EF = EDV-ESV/EDV, Clinicians like to use the term pre load. Pre load is the end diastolic volume.
But the percentage ejected per beat is not even close to whole story of cardiac pump function because first the ventricle has to fill and it has become apparent than at least as many patients have filling problems as have lower ejection fractions. The HF from filling problems is known as diastolic failure or in the jargon HFpEF ( heart failure with preserved ejection fraction) as opposed to HFrEF (heart failure with reduced ejection fraction)
Of course all patients with HFrEF also have diastolic dysfunction., i.e.failure of normal filling of the ventricles.
Echocardiography has become the major tool to diagnose diastolic dysfunction. Doppler techniques measure blood flow early and late in diastole.In the healthy compliant heart most the flow occurs early and that phase is is designated the A phase and the second phase is the E phase and the E.A ratio has become a useful indicator of diastolic dysfunction. As the ventricle become more stiff , for whatever reasons,the ratio of E to A decreases and diastolic filling relies more on the atrial kick phase.
A model or stylized working hypothesis concerning the heart stiffness has been proposed in which two major elements. are considered: 1) reduced compliance which is defined a change in volume/change in pressure in the left ventricle The relevant pressure is the difference between the left atrial and left ventricular pressure and 2) ventricular muscle relaxation.
Compliance is assessed to some degree and imperfectly by the E and A and E/A ratio and the E/E prime ratio while the relaxation is measured by the isovolumic relaxation time of the left ventricle (IVRT) This is the period after the closing of the aortic value and before the opening of the mitral valve.An increased value denotes poor relaxation.The E/A ratio can be deceptive because as diastolic function decreases,the left atrial pressure may rise to help push the blood into the ventricle which tends to increase the E/A ratio that may have become depressed in an earlier phase of filling problems resulting in a "pseudo-normal" pattern.
To help sort out normal and pseudo normal ratios, tissue Doppler Imaging (TDI) can be helpful. TDI measures the movement of the mitral annulus as it move upwards as the ventricle fills and is designated as E prime.
It has been recognized that the e/a ratio decreases with aging and some cardiologists recommend using an age adjusted set of value to determine if a value is abnormal just as values for lung function test indices are age adjusted. So is it normal or is it the case that everyone get a bit of diastolic failure as they get older or for that matter a little bit of lung impairment.It has been suggested than the aging lung is a bit like early COPD.
Several groups of researchers have taken the optimistic view that regular endurance type exercise over the years can help prevent at least some of the age related stiffness of the heart. There are data that suggest that is the case as at least some groups of older long time endurance athletes have better e/a ratios than their otherwise apparently healthy more sedentary cohorts. However the IVRT does not differ between the two groups, so the impaired relaxation of the myocardium that accompanies aging does not seem to be mitigated by regular endurance exercise.
The putative underlying cellular mechanisms for increased stiffness and the sluggish myocardial relaxation are topics for another day.Basically the narrative is that myocardial cells die with aging (apoptosis) and the surviving cells hypertrophy plus subendocardial fibrosis develops and maybe long time regular aerobic exercise might mitigate that process a bit.
addendum:5/30/16 Hitting the wrong key lead to publishing a uncorrected version. I think I fixed most of the typos ,etc now .
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