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                        Arterial hypertension
is the most common risk factor for heart failure in the general population.1 The progression of hypertensive left
ventricular (LV) involvement toward heart failure includes serial structural
abnormalities (mainly myocardial fibrosis) and geometric changes of the left
ventricle—LV concentric remodelling and LV hypertrophy (LVH) with high LV
mass/volume ratio—whose prognostic role is recognized.2–4 In the presence of these abnormalities,
parallel abnormalities of LV diastolic properties occur. These abnormalities
are globally defined as LV diastolic dysfunction (DD). They include alterations
of both relaxation and filling,5,6 precede
alterations of LV chamber systolic function and can per se induce
symptoms/signs of heart failure even when ejection fraction (EF) is normal
(heart failure with normal ejection fraction (HFNEF)). Noteworthy, compared to
those with reduced systolic function, patients with HFNEF are more often
female, older, and less predisposed to have coronary artery disease and more
likely to have hypertension.7 The growing
interest for DD and HFNEF rises from the knowledge that ~60% of patients with
heart failure have a normal or near normal EF.

The prevalence of HFNEF
has increased over the last 15-year period—it possibly reflects also on the
greater number of patients undergoing Doppler-echocardiographic
examination—while the rate of death from this disorder remained unchanged.8 Accordingly, diagnosis, prognosis, and
therapeutic management of DD and HFNEF in hypertensive patients is a growing
public health problem.

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The traditional definition of diastole (?????o?? =
“expansion”), includes the part of the cardiac cycle starting at the aortic
valve closure—when LV pressure falls below aortic pressure—and finishing at the
mitral valve closure. A normal diastolic function is clinically defined as the
capacity of the left ventricle to receive a filling volume and its ability to
guarantee an adequate stroke volume, operating at a low pressure regimen.

 In descriptive terms,
diastole can be divided in four phases:

1.  
Isovolumetric relaxation: This is the period occurring between the end of systolic
ejection (aortic valve closure) and the opening of the mitral valve, when LV
pressure continues its rapid fall, while LV volume remains constant.

2.  
 LV rapid filling: This begins when LV pressure falls below left atrial (LA)
pressure and the mitral valve opens. During this period the blood has an
acceleration which achieves a maximal extent, directly related to the magnitude
of atrio-ventricular pressure, and stops when this gradient ends. This period
represents a complex interaction between LV suction (active relaxation) and
visco-elastic properties of the myocardium (compliance).

3.  
Diastasis: This occurs when LA and LV pressures are almost equal and LV
filling is essentially maintained by the flow coming from pulmonary veins—with
left atrium representing a passive conduit—with an amount depending on LV pressure,
function of LV “compliance”.

4.  
Atrial systole: This corresponds to LA contraction and ends at the mitral
valve closure. This period depends on LV compliance and, to a lower extent, on
pericardial resistance, atrial force, and atrio-ventricular synchronicity
(electrocardiogram-derived PR interval).

 

Globally, LV filling is
determined by interaction between LV filling pressure (LVFP) and filling
properties, which in turn are regulated by extrinsic factors (mainly
pericardial restraint and ventricular interaction) and by intrinsic factors
such as chamber stiffness (cardiomyocytes and extracellular matrix), myocardial
tone, chamber geometry, and wall thickness. Increased LVFP is the main
physio-pathologic consequence of DD. It is determined by filling and passive
properties of LV walls, and may be additionally controlled by incomplete LV
relaxation and alterations of myocardial diastolic tone. Main morphological and
functional correlates of DD include LV concentric geometry, LA enlargement and
function, and pulmonary arterial hypertension.

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