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Nejm Systolic Vs Diastolic HF
Nejm Systolic Vs Diastolic HF
7 2007
Review Articles
ABSTRACT
Background: Diastolic heart failure (DHF) and systolic heart failure (SHF) are 2 clinical subsets of the
syndrome of chronic heart failure that are most commonly encountered in clinical practice.
Methods and Results: The clinically overt DHF and SHF appear to be 2 separate syndromes with
distinctive morphologic and functional changes although signs, symptoms, and prognosis are very similar.
In DHF, the left ventricle is not dilated and the ejection fraction is preserved. In contrast in SHF, it is
dilated and the ejection fraction is reduced. The neurohormonal abnormalities in DHF and SHF appear
to be similar. The stimuli and the signals that ultimately produce these 2 different phenotypes of chronic
heart failure remain, presently, largely unknown.
Conclusions: Although there has been considerable progress in the management of SHF, the management
of DHF remains mostly empirical because of lack of knowledge of the molecular and biochemical mechanisms which produce myocardial structural and functional changes in this syndrome. Further research
and investigations are urgently required. (J Cardiac Fail 2007;13:569e576)
Key Words: Systolic heart failure, diastolic heart failure, remodeling, function.
569
Diagnosis
Based on the proposed definitions, it appears that for
establishing the diagnosis of DHF or SHF, it is only necessary to measure left ventricular ejection fraction after
confirming the presence of heart failure. If ejection fraction
is preserved it is DHF, and if reduced it is SHF. It is highly
desirable to establish the normal range of ejection fraction
for any technique employed, preferably under similar loading conditions. It should be appreciated that signs and
symptoms, radiologic and electrocardiographic findings
and neurohormonal profile cannot distinguish between
DHF and SHF.6,11
Is Cardiac Catheterization Necessary?
Asymptomatic left ventricular systolic dysfunction constitutes Stage B systolic heart failure.16 The prevalence of
Stage B systolic heart failure in the community is between
3% and 6%.17 The risk of development of symptomatic
heart failure is reported to be between 5.1% and
10.5%.17e21
The echo-Doppler studies have reported that patients
with asymptomatic left ventricular diastolic dysfunction
have a higher incidence of all-case mortality adjusted for
age, sex, and ejection fraction.12 Mild diastolic dysfunction
was associated with 8.3-fold, and moderate-to-severe
dysfunction with 10.2-fold increased risk of mortality.12
Natural History in Symptomatic Patients
571
Fig. 1. One-year mortality morbidity in patients with severe systolic (open bar) and diastolic (closed bar) heart failure. Although the mortality morbidity rate in patients with preserved systolic function is lower than that of patients with reduced systolic function, the mortality
rate in both groups with severe heart failure was high. (Published with permission of Dauterman KW, Go AS, Rowell R, Gebretsadik T,
Gettner S, Massie BM. Congestive heart failure with preserved systolic function in a statewide sample of community hospitals. J Card
Failure 2001;7:221e8.25)
Risk Factors
Diastolic Heart
Failure
Systolic Heart
Failure
Normal or decreased
Increased
Increased
Increased
Increased
Increased
Normal
Normal
Normal or decreased
Normal
May be present
Increased
Normal or decreased
Decreased
Increased
Increased
Increased
Increased
Decreased
May be present
Usually remains
unchanged
Spherical
Fig. 2. Ventricular remodeling in systolic and diastolic heart failure. (Left) Autopsy examples; (right) cross-sectional 2-dimensional echocardiographic views of systolic and diastolic heart failures compared with normals are illustrated. In systolic heart failure, the left ventricular cavity is markedly dilated and wall thickness is not increased. In diastolic heart failure, the cavity size is normal or decreased and wall
thickness is markedly increased. (Reprinted with permission.33)
Systolic Heart
Failure
192
137
31
232
1.22
6
6
6
6
6
10*
9*
2*
9*
0.14
287
28
Diastolic Heart
Failure
6
6
6
6
6
Systolic Heart
Failure
Diastolic Heart
Failure
e
e
e
e
87
37
60
160
2.12
10
9
2y
9y
0.14z
306; P 5 .007
56; P 5 .02
Myocyte
Hypertrophy
Apoptosis
Necrosis
Myocardial fibrosis
Calcium regulation
MMPs/TIMPs
Collagen cross-links
Titin isoforms N2BA/
N2B
, increased; e, decreased or impaired; MMPs, matrix metalloproteinases; TIMPs, tissue inhibitors of metalloproteinases.
573
Fig. 3. Changes in myocytes (left) and in extracellular matrix (right) in systolic heart failure resulting from dilated cardiomyopathy, and
diastolic heart failure resulting from pressure over load compared with normals in animal models. In systolic heart failure, the myocyte
length is increased without any change in the cross-sectional area; in diastolic heart failure, the cross-sectional area of the myocyte is increased without a significant change in its length. In systolic heart failure, collagen degradation and disruption occur; in diastolic heart
failure, there is increased width and continuity of fibrillar collagen. (Reprinted with permission.34)
Fig. 4. Schematic diagram of pressure-volume relations in normals, systolic and diastolic heart failure. In systolic heart failure, a downward
and rightward shift of the end-systolic pressure-volume line indicates decreased contractile function, which is the principal cause of reduced
ejection fraction and forward stroke volume. In primary diastolic heart failure, diastolic pressure-volume relation (dashed line) shifts upward and to the left, indicating a disproportionate and a greater increase in diastolic pressure for any increase in diastolic volumes. If there
is also a decrease in end-diastolic volume, then a decrease in stroke volume also occurs. (Reprinted with permission.44)
Fig. 5. The changes in the diastolic pressure-volume relation in patients with overt diastolic heart failure, illustrating its shifts upward and to
the left. (Reprinted with permission.45)
68
67
14
3.4
6
6
6
6
9
3
3
0.6
End of Follow-up
76
60
26
6.3
6
6
6
6
8
4
2*
0.9*
ejection fraction remain unchanged, but end-diastolic pressure and stiffness index increase, suggesting that in DHF
ventricular dilatation does not occur and worsening
diastolic function is the mechanism for development and
progression of heart failure (Table 4).46,47 Thus left ventricle size remains unchanged and it does not dilate without an
ischemic insult.
Differences in Therapeutic Options
17.
18.
19.
20.
Acknowledgment
21.
The authors are grateful to Marci Yellin for her invaluable assistance in preparing the manuscript.
22.
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