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Clinical manifestations and diagnosis of diastolic heart

failure

AuthorMichael R Zile, MD

Section EditorWilson S Colucci, MD

Deputy EditorSusan B Yeon, MD, JD, FACC

Last literature review for version 16.1:January 31, 2008 | This topic last updated:February

14, 2008

INTRODUCTION Diastolic heart failure (HF) refers to a clinical syndrome in which patients have

symptoms and signs of HF, normal or near normal left ventricular systolic function, and evidence of

diastolic dysfunction (eg, abnormal left ventricular filling and elevated filling pressures) ( show table 1)

[1-3] . Among patients with HF, as many as 40 to 60 percent have a normal or near normal left

ventricular ejection fraction (LVEF) [1,4-9] . This condition has been labeled diastolic heart failure (DHF)or "heart failure with normal ejection fraction" (HFNEF) [ 10] . In such patients, diastolic dysfunction is

the presumed cause of the HF, which can be confirmed by objective measures [1,11,12] . However, heart

failure with normal ejection fraction can occur due to conditions other than diastolic dysfunction ( show

table 2) [13] .

The etiology, clinical manifestations, and diagnosis of patients with diastolic heart failure will be reviewed

here. Issues related to treatment, prognosis, and pathophysiology are discussed separately. (See

"Treatment and prognosis of diastolic heart failure"and see "Pathophysiology of diastolic heart failure"

and see "Cellular mechanisms of diastolic dysfunction").

PREVALENCE AND DEMOGRAPHICS The prevalence of diastolic heart failure as the cause of HF

increases with age [1,6,14] . This was illustrated in a review in which the estimated prevalence of

diastolic heart failure among patients with HF was 15, 33, and 50 percent at ages less than 50, 50 to 70,

and more than 70 years, respectively [1] . In addition, another 15 percent of elderly patients with HF

have only mildly abnormal systolic function (LVEF 45 to 54 percent), which should not produce symptoms

on its own and is therefore probably associated with an important component of diastolic dysfunction

[14] . The development of diastolic dysfunction in the elderly may be independent of left ventricular

mass, heart rate, contractility, or systemic blood pressure [15] .

A greater proportion of women than men have diastolic heart failure [16-19] . In a chart study of over

19,000 Medicare beneficiaries hospitalized with the principal discharge diagnosis of HF, 35 percent had a

normal ejection fraction [16] . Among patients with normal ejection fraction, 79 percent were women,

while among those with decreased ejection fraction, 49 percent were women.

Asymptomatic diastolic dysfunction is much more common than symptomatic disease. This was

illustrated in a community-based survey from the Mayo Clinic, which evaluated 2042 subjects 45 years

of age [5] . The prevalence of symptomatic HF was 2.2 percent overall, 44 percent of whom had diastolic

heart failure. Among subjects without symptoms of HF, 28.1 percent had some degree of diastolic

dysfunction, which was moderate or severe in 7.3 percent using Doppler echocardiographic criteria. ( See

"Echocardiographic evaluation of left ventricular diastolic function" ).

Using data from more than 100,000 hospitalizations due to acute decompensated heart failure, the 50

percent of patients with a normal ejection fraction (ie, those with diastolic heart failure) had the following


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clinical characteristics compared to those with systolic dysfunction [9] :

More likely to be older, female, and hypertensive

Less likely to have had a prior myocardial infarction or to be receiving an angiotensin

converting enzyme inhibitor or angiotensin II receptor blocker.

Lower in-hospital mortality (3 versus 4 percent) but similar ICU and hospital length of stay.

ETIOLOGY The major causes of diastolic heart failure include [1] :

Chronic hypertension with left ventricular hypertrophy (LVH) [20] ; a hypertensive

hypertrophic cardiomyopathy with LVEF above 75 percent has been described in the elderly [ 6]

Hypertrophic cardiomyopathy (HCM) (see "Clinical manifestations of hypertrophic

cardiomyopathy")

Aortic stenosis with a normal LVEF [21]

Ischemic heart disease

Restrictive cardiomyopathy, which can be idiopathic or caused by infiltrative diseases of the

heart (see "Idiopathic restrictive cardiomyopathy"and see "Cardiac sarcoidosis"and see

"Clinical manifestations of hereditary hemochromatosis" and see "Amyloid cardiomyopathy")

PATHOPHYSIOLOGY Diastolic function is determined by two factors, the process of myocardial

relaxation (which is an active process that requires metabolic energy) and the elasticity or distensibility

of the left ventricle, which is a passive phenomenon [2] .

Relaxation of the contracted myocardium occurs at the onset of diastole. The rapid pressure

decay and the concomitant "untwisting" of the left ventricle (LV) produces a suction effect that

augments the left atrial-to-left ventricular pressure gradient, thereby promoting diastolic

filling.

During the later phases of diastole, the normal LV is composed of completely relaxed myocytes

and is very compliant and easily distensible, offering minimal resistance to LV filling over a

normal volume range. As a result, LV filling can normally be accomplished by very low filling

pressures in the left atrium and pulmonary veins, preserving a low pulmonary capillary

pressure (


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generally less severe, manifestations (reduced exercise capacity, neurohumoral activation, and

diminished quality of life).

The exercise intolerance seen with diastolic heart failure is largely due to the impairment in left

ventricular filling, which leads to elevations in left atrial and pulmonary venous pressures and pulmonary

congestion [26,27] . In addition, inadequate cardiac output during exercise leads to fatigue of skeletal

muscles, especially the leg muscles and the accessory muscles of respiration [ 28,29] .

Patients with diastolic heart failure have particular difficulty in tolerating certain kinds of hemodynamic

stress:

They tolerate atrial fibrillation (AF) poorly, since the loss of atrial contraction can dramatically

reduce left atrial emptying, LV filling, and LV stroke volume. ( See "Hemodynamic

consequences of atrial fibrillation and cardioversion to sinus rhythm" ).

They do not tolerate tachycardia well, since the increase in heart rate shortens the duration of

diastole and truncates the important late phase of diastolic filling.

Elevations in systemic blood pressure, especially the abrupt, severe, or refractory elevations

often seen with renovascular hypertension, increase left ventricular wall stress, which can

worsen myocardial relaxation in patients with diastolic heart failure. ( See "Treatment of

hypertension in heart failure", section on Diastolic dysfunction and see "Who should be

screened for renovascular or secondary hypertension?").

The acute induction or worsening of diastolic dysfunction by ischemia raises left atrial and

therefore pulmonary venous pressure. This explains why many patients with coronary heart

disease (CHD) have respiratory symptoms with their anginal pain, including wheezing, an

inability to take a deep breath, shortness of breath, and overt pulmonary edema. These

respiratory symptoms can occur in the absence of anginal pain and are often referred to as

"anginal equivalents."

Episodes of hemodynamic decompensation may result in pulmonary congestion or edema severe enough

to be life-threatening. This phenomenon, called flash pulmonary edema, is discussed in detail separately.(See "Pathophysiology and evaluation of acute decompensated heart failure").

DIAGNOSIS The diagnosis of diastolic heart failure is often made, or presumed, in patients who have

symptoms of HF and a normal LVEF by echocardiography [30] . There is controversy about whether such

patients require further testing to establish the diagnosis of diastolic heart failure [ 4] . Some experts

argue that specific testing confirms but is not needed to establish the diagnosis [ 11,25] . In one report of

63 patients with a history of HF and, on echocardiography, LVH and a normal LVEF, every patient had

one or more of the indices of abnormal diastolic function [11] . However, others insist that it is necessary

to have objective evidence of abnormal left ventricular relaxation and distensibility [ 22,23] .

The 2007 consensus statement of the Heart Failure and Echocardiography Associations of the European

Society of Cardiology requires the following three conditions for diagnosis of DHF or HFNEF ( show table 1)

[3] :

Signs or symptoms of HF;

Normal or mildly abnormal LV systolic function (both LVEF >50 percent and an LV

end-diastolic volume


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The tissue Doppler requirement of E/E'> 8 which would exclude patients with normal resting

filling pressures but elevated diastolic pressure with exercise.

"Echo - bloodflow Doppler" criteria include E/A ratio and DT (deceleration time) parameters

consistent with impaired relaxation (E/A 280 ms) but do not include parameters

for restrictive filling (eg E/A >1,5 and DT


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In addition, other causes of HFNEF can be identified including:

Constrictive pericarditis (show echocardiogram 6)

Severe mitral regurgitation show echocardiogram 7show echocardiogram 8

Severe aortic regurgitation (show echocardiogram 9show echocardiogram 10

The distinction among causes of HFNEF, whether by echocardiography or by other means, is important,

because some are responsive to specific therapies directed at the underlying disease. (See "Treatmentand prognosis of diastolic heart failure").

Doppler echocardiography Doppler echocardiography is an effective method to establish the

presence of abnormalities in diastolic function [1,5,11,35,36] . In patients with impaired relaxation,

assessment of mitral valve inflow velocity may demonstrate diminished early diastolic filling velocity,

manifested by an abnormally low E wave, and increased late diastolic filling, manifested by an increased

A wave; as a result, the E/A ratio is less than one (show figure 3) [1] . In contrast, patients with reduced

LV compliance have a restrictive pattern, which is associated with an increased E/A ratio. Tissue Doppler

imaging and measurement of pulmonary vein blood flow velocity also may be helpful. ( See

"Echocardiographic evaluation of left ventricular diastolic function" ).

Systolic function Patients with diastolic HF have, by definition an LVEF >50 percent. However, inseveral series, sophisticated imaging techniques (eg, tissue Doppler imaging) have identified subtle

abnormalities of regional systolic function in approximately 20 to 50 percent of patients with diastolic

dysfunction [37-40] . These abnormalities are usually noted in longitudinal contraction and motion of the

basal left ventricle in the region of the mitral annulus. The clinical significance of these abnormalities has

not been established.

This issue was directly assessed in a study in which the systolic properties of the left ventricle was

evaluated by echocardiography and cardiac catheterization in 75 patients with diastolic heart failure and

75 normal controls [41] . There was no difference between the two groups in a variety of measures of LV

systolic performance, such as stroke work, the relationship between stroke work and end-diastolic

volume, and the peak dP/dt. Thus, the pathophysiology of diastolic HF does not appear to be associatedwith significant abnormalities in systolic function [ 42] . (See "Pathophysiology of diastolic heart failure" ,

section on Systolic function in DHF).

Occult CHD Occult CHD is a potentially reversible cause of diastolic heart failure [ 43] . Although there

are limited data on how often this occurs in patients with diastolic heart failure [ 32] , it is a relatively

common finding in patients with systolic heart failure. In a study of cardiac transplant recipients,

ischemic cardiomyopathy was found in 9 of 38 patients with a pretransplant diagnosis of idiopathic

dilated cardiomyopathy (IDC) and in three of four with presumptive alcoholic cardiomyopathy [ 44] .

Findings suggesting the possible presence of ischemic cardiomyopathy include dyspnea at rest or on

exertion (symptoms that may reflect anginal equivalents), the presence of multiple risk factors for

atherosclerosis, and ischemic changes on exercise testing. Regional wall abnormalities are common in but

are not specific for ischemia, since they also occur in 50 to 60 percent of patients with IDC [ 45,46] .

However, IDC is typically associated with an enlarged heart and systolic dysfunction.

When attempting to diagnose coronary ischemia, the presence of LVH on the surface ECG may preclude

an accurate evaluation with exercise ECG testing. In such patients, evidence of ischemia can be detected

by myocardial perfusion imaging or stress echocardiography. (See "Exercise myocardial perfusion

imaging in the diagnosis and prognosis of coronary heart disease"and see "Stress echocardiography in

the diagnosis and prognosis of coronary heart disease").


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Plasma BNP The plasma concentrations of brain natriuretic peptide (BNP) and N-terminal pro-BNP are

increased in patients with asymptomatic and symptomatic left ventricular systolic dysfunction and can be

used for both diagnosis and prognosis. (See "Brain natriuretic peptide measurement in left ventricular

dysfunction and other cardiac diseases").

Plasma BNP and N-terminal pro-BNP also elevated in patients with diastolic heart failure, but cannot be

used to distinguish diastolic from systolic dysfunction [47-50] . In one report, for example, plasma BNP

was measured in 400 patients referred for echocardiography to evaluate left ventricular function [ 47] .

Among those with normal left ventricular function, the mean plasma BNP was 30 pg/mL. A plasma BNP75 pg/mL had a sensitivity of 85 percent and a specificity of 97 percent in detecting any ventricular

dysfunction, but could not discriminate systolic from diastolic dysfunction. Among patients with normal

systolic function on echocardiogram, a plasma BNP 57 pg/mL detected the 28 patients with isolated

abnormal diastolic function with 100 percent positive predictive value.

Another report evaluated 294 patients referred for echocardiography who had normal left ventricular

function, which included some patients from the previous report [49] . Patients were classified by

echocardiography as having normal, impaired relaxation, pseudonormal, or restrictive filling patterns

based upon the E/A ratio and deceleration time (show figure 3). Mean plasma BNP was significantly

higher in the patients with diastolic dysfunction than in normals (286 versus 33 pg/mL). Those with

impaired relaxation, pseudonormal, and restrictive filling patterns had plasma BNP concentrations of 202,294, and 402 pg/mL, respectively. A plasma BNP 62 pg/mL had a sensitivity of 85 percent and a

specificity of 83 percent for the diagnosis of diastolic dysfunction.

Endomyocardial biopsy Endomyocardial biopsy may be helpful in selected settings, such as

identifying a specific infiltrative disease or monitoring for anthracycline cardiotoxicity. The indications for

this procedure are discussed elsewhere. (See "Indications for endomyocardial biopsy").

INFORMATION FOR PATIENTS Educational materials on this topic are available for patients. ( See

"Patient information: Heart failure causes, symptoms, and diagnosis" and see "Patient information: Heart

failure treatments"). We encourage you to print or e-mail these topic reviews, or to refer patients to our

public web site, www.uptodate.com/patients, which includes these and other topics.

Use of UpToDateis subject to the Subscription and License Agreement.

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Paulus, WJ, Tschope, C, Sanderson, JE, et al. How to diagnose diastolic heart failure: aconsensus statement on the diagnosis of heart failure with normal left ventricular ejectionfraction by the Heart Failure and Echocardiography Associations of the European Society ofCardiology. Eur Heart J 2007; 28:2539.

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Topol, EJ, Traill, TA, Fortuin, NJ. Hypertensive hypertrophic cardiomyopathy of theelderly. NEngl J Med 1985; 312:277.

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Yancy, CW, Lopatin, M, Stevenson, LW, et al. Clinical presentation, management, andin-hospital outcomes of patients admitted with acute decompensated heart failure withpreserved systolic function: a report from the Acute Decompensated Heart Failure NationalRegistry (ADHERE) Database. J Am Coll Cardiol 2006; 47:76.

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Hogg, K, Swedberg, K, McMurray, J. Heart failure with preserved left ventricular systolicfunction; epidemiology, clinical characteristics, and prognosis. J Am Coll Cardiol 2004; 43:317.

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Zile, MR, Gaasch, WH, Carroll, JD, et al. Heart failure with a normal ejection fraction: ismeasurement of diastolic function necessary to make the diagnosis of diastolic heart failure?.Circulation 2001; 104:779.

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Zile, MR, Baicu, CF, Gaasch, WH. Diastolic heart failure--abnormalities in active relaxation andpassive stiffness of the left ventricle. N Engl J Med 2004; 350:1953.

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Oh, JK, Hatle, L, Tajik, AJ, Little, WC. Diastolic heart failure can be diagnosed bycomprehensive two-dimensional and Doppler echocardiography. J Am Coll Cardiol 2006;47:500.

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Gottdiener, JS, McClelland, RL, Marshall, R, et al. Outcome of congestive heart failure inelderly persons: influence of left ventricular systolic function. The Cardiovascular Health Study.

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Kitzman, DW, Sheikh, KH, Beere, PA, et al. Age-related alterations of Doppler left ventricularfilling indexes in normal subjects are independent of left ventricular mass, heart rate,contractility and loading conditions. J Am Coll Cardiol 1991; 18:1243.

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Masoudi, FA, Havranek, EP, Smith, G, et al. Gender, age, and heart failure with preserved leftventricular systolic function. J Am Coll Cardiol 2003; 41:217.

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Devereux, RB, Roman, MJ, Liu, JE. Congestive heart failure despite normal left ventricularsystolic function in a population-based sample: the Strong Heart Study. Am J Cardiol 2000;86:1090.

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Smith, GL, Masoudi, FA, Vaccarino, V, et al. Outcomes in heart failure patients with preserved

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Vasan, RS, Levy D. The role of hypertension in the pathogenesis of heart failure. A clinicalmechanistic overview. Arch Intern Med 1996; 156:1789.

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Fifer, MA, Bourdillon, PD, Lorell, BH. Altered left ventricular diastolic properties during pacinginduced anginain patients with aortic stenosis. Circulation 1986; 74:675.

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Vasan, RS, Levy, D. Defining diastolic heart failure: a call for standardized diagnostic criteria.Circulation 2000; 101:2118.

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Burkhoff, D, Maurer, MS, Packer, M. Heart failure with a normal ejection fraction: is it really a

disorder of diastolic function?. Circulation 2003; 107:656.

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Kitzman, DW, Little, WC, Brubaker, PH, et al. Pathophysiological characterization of isolateddiastolic heart failure in comparison to systolic heart failure. JAMA 2002; 288:2144.

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Kitzman, DW, Higginbotham, MB, Cobb, FR, et al. Exercise intolerance in patients with heartfailure and preserved left ventricular systolic function: Failure of the Frank-Starlingmechanism. J Am Coll Cardiol 1991; 17:1065.

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Packer, M. Abnormalities of diastolic function as a potential cause of exercise intolerance inchronic heart failure. Circulation 1990; 81:III78.

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Massie, B, Conway, M, Yonge, R, et al. Skeletal muscle metabolism in patients with congestiveheart failure: relation to clinical severity and blood flow. Circulation 1987; 76:1009.

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Mancini, DM, Henson, D, LaManca, J, et al. Respiratory muscle function and dyspnea in29.


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patients with chronic congestive heart failure. Circulation 1992; 86:909.

Hunt, SA, Abraham, WT, Chin, MH, et al. ACC/AHA 2005 Guideline Update for the Diagnosisand Management of Chronic Heart Failure in the Adult: a report of the American College ofCardiology/American Heart Association Task Force on Practice Guidelines (Writing Committeeto Update the 2001 Guidelines for the Evaluation and Management of Heart Failure):developed in collaboration with the American College of Chest Physicians and the InternationalSociety for Heart and Lung Transplantation: endorsed by the Heart Rhythm Society. Circulation2005; 112:e154.

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Hatle, L. How to diagnose diastolic heart failure a consensus statement. Eur Heart J 2007;

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Caruana, L, Petrie, MC, Davie, AP, McMurray, JJ. Do patients with suspected heart failure andpreserved left ventricular systolic function suffer from "diastolic heart failure" or frommisdiagnosis? A prospective descriptive study. BMJ 2000; 321:215.

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Kass, DA. Assessment of diastolic dysfunction. Invasive modalities. Cardiol Clin 2000; 18:571.33.

Angeja, BG, Grossman, W. Evaluation and management of diastolic heart failure. Circulation2003; 107:659.

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Cohen, GI, Pietrolungo, JF, Thomas, JD, et al. A practical guide to assessment of ventriculardiastolic function using Doppler echocardiography. J Am Coll Cardiol 1996; 27:1753.

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Labovitz, AJ, Pearson, AC. Evaluation of left ventricular diastolic function: Clinical relevanceand recent Doppler echocardiographic insights. Am Heart J 1987; 114:836.

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Yu, CM, Lin, H, Yang, H, et al. Progression of systolic abnormalities in patients with "isolated"diastolic heart failure and diastolic dysfunction. Circulation 2002; 105:1195.

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Yip, G, Wang, M, Zhang, Y, et al. Left ventricular long axis function in diastolic heart failure isreduced in both diastole and systole: time for a redefinition?. Heart 2002; 87:121.

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Petrie, MC, Caruana, L, Berry, C, McMurray, JJ. "Diastolic heart failure" or heart failure causedby subtle left ventricular systolic dysfunction?. Heart 2002; 87:29.

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Nikitin, NP, Witte, KK, Clark, AL, Cleland, JG. Color tissue Doppler-derived long-axis leftventricular function in heart failure with preserved global systolic function. Am J Cardiol 2002;90:1174.

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Baicu, CF, Zile, MR, Aurigemma, GP, Gaasch, WH. Left ventricular systolic performance,function, and contractility in patients with diastolic heart failure. Circulation 2005; 111:2306.

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Aurigemma, GP, Zile, MR, Gaasch, WH. Contractile behavior of the left ventricle in diastolicheart failure: with emphasis on regional systolic function. Circulation 2006; 113:296.42.

Choudhury, L, Gheorghiade, M, Bonow, RO. Coronary artery disease in patients with heartfailure and preserved systolic function. Am J Cardiol 2002; 89:719.

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Bortman, G, Sellanes, M, Odell, DS, et al. Discrepancy between pre- and post-transplantdiagnosis of end-stage dilated cardiomyopathy. Am J Cardiol 1994; 74:921.

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Yamaguchi, S, Tsuiki, K, Hayasaka, M, Yasui, S. Segmental wall motion abnormalities indilatedcardiomyopathy: Hemodynamic characteristics and comparison with thallium-201myocardial scintigraphy. Am Heart J 1987; 113:1123.

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Glamann, DB, Lange, RA, Corbett, JR, Hillis, LD. Utility of various radionuclide techniques fordistinguishing ischemic from nonischemic dilated cardiomyopathy. Arch Intern Med 1992;152:769.

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Maisel, AS, Koon, J, Krishnaswamy, P, et al. Utility of B-natriuretic peptide as a rapid,point-of-care test for screening patients undergoing echocardiography to determine leftventricular dysfunction. Am Heart J 2001; 141:367.

47.

Krishnaswamy, P, Lubien, E, Clopton, P, Koon, J. Utility of B-natriuretic peptide levels inidentifying patients with left ventricular systolic or diastolic dysfunction. Am J Med 2001;111:274.

48.

Lubien, E, DeMaria, A, Krishnaswamy, P, et al. Utility of B-natriuretic peptide in detectingdiastolic dysfunction: comparison with Doppler velocity recordings. Circulation 2002; 105:595.

49.

Tschope, C, Kasner, M, Westermann, D, et al. The role of NT-proBNP in the diagnostics ofisolated diastolic dysfunction: correlation with echocardiographic and invasive measurements.Eur Heart J 2005; 26:2277.

50.


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GRAPHICS

Diagnostic flowchart on "How to diagnose HFNEF" in a patientsuspected of HFNEF

LVEDVI: left ventricular end-diastolic volume index; mPCW: mean pulmonary capillary wedge

pressure; LVEDP: left ventricular end-diastolic pressure; t: time constant of left ventricular

relaxation; b: constant of left ventricular chamber stiffness; TD: tissue Doppler; E: early mitralvalve flow velocity; E': early TD lengthening velocity; NT-proBNP: N-terminal-pro brain natriuretic

peptide; BNP: brain natriuretic peptide; E/A: ratio of early (E) to late (A) mitral valve flow velocity;

DT: deceleration time; LVMI: left ventricular mass index; LAVI: left atrial volume index; Ard:

duration of reverse pulmonary vein atrial systole flow; Ad: duration of mitral valve atrial wave flow.

Reproduced with permission from: Paulus, WJ, Tschope, C, Sanderson, JE, et al. How todiagnose diastolic heart failure: a consensus statement on the diagnosis of heart failurewith normal left ventricular ejection fraction by the Heart Failure and Echocardiography

Associations of the European Society of Cardiology. Eur Heart J 2007; 28:2539. Copyright2007 Oxford University Press.

Examples of heart failure with normal left ventricular ejection fraction

Diastolic heart failure


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Hypertension

Restrictive cardiomyopathy

Infiltrative cardiomyopathy

Hypertrophic cardiomyopathy

Noncompaction cardiomyopathy

Right heart failure

Severe pulmonary hypertension

Right ventricular infarct

Arrhythmogenic right ventricular dysplasia

Atrial septal defect

Valvular heart diseases

Severe valvular stenosis

Severe valvular regurgitation

Pericardial disease

Cardiac tamponade

Constrictive pericarditis

Intracardiac mass

Atrial myxoma

Apical eosinophilic thrombus

Pulmonary vein stenosis

Congenital heart diseases

Oh, JK, Hatle, L, Tajik, AJ, Little, WC. Diastolic heart failure can be diagnosed by comprehensive two-dimensional andDoppler echocardiography. J Am Coll Cardiol 2006; 47:500.

Mechanisms and causes of diastolic dysfunction

Physiologic abnormalityAlteration in parameter of

assessment Common etiology

Delayed or incomplete relaxation Increased tau

Increased IVRT

Reduced E/A ratio

LV hypertrophy

Myocardial ischemia

LV asynchrony

Abnormal loading

Early diastolic fillingabnormalities

Reduced peak filling rate

Increased time to peak filling

Reduced E/A ratio

Delayed relaxation

LV asynchrony

Late diastolic filling abnormalities Increased diastolic P/V

relationship

Normal or increased E/A ratio

LV chamber dilation

Restrictive/constrictive filling

pattern

Increased LV passive chamberstiffness

Increased diastolic P/V

relationship

Increased stiffness constant

Increased collagen and fibrosis

Myocardial infiltration (eg,amyloid)

Increased vascular turgor

Concentric LVH

Post-MI hypertrophy and fibrosis

LV chamber dilation

LV: left ventricular; LVH: LV hypertrophy; Tau: time constant of isovolumic pressure decay; IVRT: isovolumic relaxation time; E/A

ratio: ratio of early and late LV inflow as detected by Doppler echocardiography; peak filling rate: dV/dt max; time to peak filling: time

to dV/dt max; increased diastolic P/V relationship: upward shift and/or increased slope of LV diastolic pressure/volume relationship;

stiffness constant: Kp.


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Left ventricular pressure tracing in diastolic dysfunction

The left ventricular pressure is initially recorded with a scale of 0 to 200mmHg and then at 0 to 40 mmHg. Although the systolic and diastolicpressures are normal, the pressure waveform in diastole is abnormal;there is a continuing decline of pressure over the mid-diastolic period (asopposed to the gradual rise seen in normal subjects) with the pressurenadir occurring midway through the diastolic period and there is aprominent "a" wave generated by left atrial contraction. Reproduced with

permission from Kern, MJ. ACC Current Journal Review, 1997.

PCWP increases during exercise in diastolic dysfunction

During symptom-limited upright exercise, normal subjects have anincrease in left ventricular end diastolic volume (LVEDV), associated with

a modest increase in pulmonary capillary wedge pressure (PCWP) whichremains within a normal range (red arrow). In contrast, patients withnormal systolic function who have left ventricular hypertrophy, diastolicdysfunction, and a stiff, nondistensible left ventricle have a markedincrease in PCWP with exercise, often to levels associated with pulmonaryedema (blue arrow), but no change in LVEDV. This is consistent withexercise-induced ischemia and an exaggerated impairment of diastolicrelaxation of the hypertrophied myocardium. Data from Kitzman, DW,Higginbotham, MB, Cobb, FR, et al, J Am Coll Cardiol 1991; 17:1065.

Diagnostic flow chart on "How to exclude HFNEF" in a patient presentingwith breathlessness and no signs of fluid overload


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S: TD shortening velocity.

Reproduced with permission from: Paulus, WJ, Tschope, C, Sanderson, JE, et al. How todiagnose diastolic heart failure: a consensus statement on the diagnosis of heart failure withnormal left ventricular ejection fraction by the Heart Failure and Echocardiography Associationsof the European Society of Cardiology. Eur Heart J 2007; 28:2539. Copyright 2007 OxfordUniversity Press.

Left ventricular hypertrophy


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M mode echocardiogram recorded within the left ventricle, just below thelevel of the mitral valve annulus. Concentric left ventricular hypertrophyis seen as both the left ventricular septum and posterior left ventricularwall are significantly thickened, measuring almost 3 cm.

M-mode echocardiogram of amyloid cardiomyopathy

The M-mode echocardiogram in a patient with amyloid cardiomyopathy

shows a small left ventricular (LV) cavity, brightly reflective myocardium,and markedly reduced systolic function.IVS: interventricular septum; PWLV: posterior wall of the LV.

Constrictive pericarditis

Two dimensional echocardiogram in constrictive pericarditis. Left panelshows two thickened layers of pericardium separated by a clear layerdevoid of echoes; this process appears to be circumferential (as indicatedby the two sets of arrows) and is seen in constrictive pericarditis. Theappearance of the bright pericardium circumferentially, seen with a darkanechoic layer between the layers, produces the "halo sign." In real time,

the clear area in both the lateral area (horizontal arrows) and apical wall(vertical arrows) maintained the same dimension throughout the cardiaccycle. The thoracic aorta (TAO) sits posterior to the thickenedpericardium. The right panel shows a plethoric or dilated inferior venacava (IVC) and hepatic vein (hv) and the right atrium (RA). The IVC didnot collapse with inspiration; this finding strongly suggests that thepericadial thickening is associated with constrictive physiology.

Continuous wave Doppler in aortic regurgitation


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The severity of aortic regurgitation can be established by the continuouswave Doppler using the pressure half time (PHT), which is computed byplacing a line (arrow) along the slope of velocity decay or decelerationtime (A to B); in this patient the PHT is 99 msec. Values of less than 200msec identify severe aortic regurgitation. In addition, the density of theregurgitant diastolic signal is nearly equal to the systolic signal.

Doppler findings in diastolic heart failure

Schematic representation of LV and left atrial (LA) pressures during diastole, transmitral Doppler

LV inflow velocity, pulmonary vein Doppler velocity, and Doppler tissue velocity in normals and indifferent types of diastolic heart failure. Compared to the normal pattern, Doppler of mitral flowin patients with an abnormality in relaxation due to diastolic dysfunction shows a reduced peakearly diastolic flow velocity (E), a prolonged E wave diastolic deceleration time of early diastolicfilling (DDT), and an increased peak diastolic flow velocity with atrial contraction (A). Withmyocardial restriction, there is an increase in E, but a shortened DDT and a decrease in A. IVRTindicates isovolumic relaxation time; PVs, systolic pulmonary vein velocity; PVd, diastolicpulmonary vein velocity; PVa, pulmonary vein velocity resulting from atrial contraction; Sm,myocardial velocity during systole; Em, myocardial velocity during early filling; and Am,myocardial velocity during filling produced by atrial contraction. Reproduced with permission from:Zile, MR, Brutsaert, DL. New concepts in diastolic dysfunction and diastolic heart failure: Part I:diagnosis, prognosis, and measurements of diastolic function. Circulation 2002; 105:1387. Copyright 2002 Lippincott Williams &Wilkins.


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clinical manifestations and diagnosis of diastolic heart failure.pdf

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