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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 28, No 1, January/February 2017
64
AFRICA
Discussion
A thorough and complete echocardiographic examination has
been shown to be a useful diagnostic test in the evaluation of
patients with HF.
15
Although it is widely used to evaluate cardiac
structure and function in patients with HF, few data are available
regarding its ability to predict outcomes.
16
In the case of acute HF, the precise association of LVEF with
cardiovascular outcomes in patients with acute decompensated
HF is controversial.
17
Because the LVEF measure is load
dependent and varies with haemodynamic status, it may
underestimate or overestimate true myocardial function in
various pathophysiological conditions and precipitants of acute
decompensation. A prospective study reported that LVEF was
weakly correlated with haemodynamic measures and clinical
outcomes in patients with acute HF.
18
Various therapeutic interventions can reduce the risk
of re-admissions and death in patients admitted with HF.
Therefore, identification of patients at the highest risk of
re-admission or death could help provide targeted cost-
effective interventions. Although several studies have assessed
potential echocardiographic predictors, the results have been
inconsistent.
19,20
A large number of variables can be measured
or calculated by echocardiographic and Doppler imaging. It
is not clear which echocardiographic measurements provide
independent prognostic information.
In our study, echocardiographic parameters showed only
limited associations between echocardiographic measures and
outcomes. Heart rate (which can be obtained by simple physical
examination) and left atrial size were associated with death or
re-admission within 60 days, and left ventricular posterior wall
thickness and presence of aortic stenosis were associated with
the risk of death up to 180 days. In agreement with the results of
the PROTECT study modelling,
10
LVEF was not associated with
60-day death or re-admission or with 180-day mortality.
This finding contrasts with data from the ESCAPE study,
where echocardiographic measures of LV size and function did
change from baseline to follow up and were associated with
some outcomes.
21
However, the ESCAPE study enrolled patients
with end-stage cardiomyopathy who had very significant LV
dysfunction at baseline. These patients were different from the
majority of acute HF patients, particularly those enrolled in the
THESUS registry.
The results of the current study confirming the preliminary
findings of Gandhi
et al
.
9
and the retrospective analysis of the
PROTECT study
10
raise the question of why in the general
population of patients admitted for acute HF, echocardiographic
measures of left ventricular function and size were not
associated with outcomes. This puzzling finding suggests that
the pathophysiology of acute HF may differ from that of
chronic HF by being less dependent on systolic function and,
as suggested by Gandhi
et al
.,
9
more driven by factors that
cause cardiac and vascular stiffening, manifesting as diastolic
dysfunction.
Left ventricular hypertrophy (LVH) is a recognised
complication of systemic hypertension and the best-studied
marker of hypertensive heart disease.
22
LVH strongly predicts
cardiovascular morbidity and mortality in hypertensive patients,
and is an independent risk factor for overall cardiovascular
mortality and morbidity.
23
It is known to cause a reduction in
myocardial coronary reserve, which predisposes to myocardial
ischaemia and left ventricular dysfunction, thereby causing
increased incidence of coronary heart disease among
hypertensives.
24
This finding should encourage increased efforts
for screening and treatment of young hypertensive patients, in
Africa and throughout the world, to prevent the progression of
hypertension to LVH.
The increased risk of patients with severe valvular heart
disease, particularly aortic stenosis, is well documented.
25
The
Table 3. Univariate associations between echo predictors and 180-day death by diagnosis groups
Echocardiographic parameter
Hypertensive CMP (
n
=
338)
Valvular (
n
=
217)
Other (
n
=
399)
Interaction
p
-value
Hazard ratio
(95% CI)
p
-value
Hazard ratio
(95% CI)
p
-value
Hazard ratio
(95% CI)
p
-value
LVEDD (mm)
0.98 (0.96–1.01)
0.25
1.01 (0.98–1.04)
0.47 1.02 (1.00–1.04)
0.12 0.17
LVESD (mm)
0.99 (0.96–1.01)
0.28
1.01 (0.99–1.04)
0.32 1.01 (0.99–1.03)
0.19 0.20
IVSTd (mm)
0.95 (0.85–1.06)
0.34
0.99 (0.89–1.09)
0.80 0.91 (0.84–1.00)
0.041 0.50
PWTd (mm)
≤ 9 mm
0.58 (0.42–0.80)
0.0011
0.79 (0.57–1.10)
0.32
0.82 (0.67–1.00)
0.072 0.30
>
9 mm
1.73 (1.16–2.59)
1.38 (0.91– 2.11)
1.19 (0.88–1.62)
LV mass
1.00 (0.99–1.00)
0.097 1.00 (1.00–1.00)
0.85 1.00 (1.00–1.00)
0.62 0.36
LVEF (%), per 5% increment
1.00 (0.90–1.11)
0.99
0.95 (0.85–1.06)
0.36 0.93 (0.86–1.02)
0.11 0.59
Left atrial size (A-P) (mm)
0.99 (0.94–1.03)
0.52
1.01 (0.97–1.04)
0.79 0.99 (0.96–1.02)
0.63 0.79
Left atrial size (planimetry) mm
2
1.00 (1.00–1.00)
0.70
1.00 (1.00–1.00)
0.78 1.00 (1.00–1.00)
0.34 0.72
E/A ratio, per doubling
1.03 (0.74–1.43)
0.89
2.07 (1.01–4.26)
0.049 1.13 (0.86–1.49)
0.38 0.21
E-wave deceleration time (ms)
1.00 (0.99–1.00)
0.23
1.00 (1.00–1.00)
0.42 1.00 (0.99–1.00)
0.15 0.68
MV A-wave duration
1.00 (0.99–1.01)
0.63
1.01 (1.00–1.01)
0.12 1.00 (0.99–1.01)
0.47 0.26
MV E/A ratio grades
Grade 1: impaired relaxation
(reference group)
0.50
(reference group)
0.14
(reference group)
0.20 0.27
Grade 2: pseudonormal
1.63 (0.67–3.98)
0.82 (0.07–8.99)
2.71 (0.91–8.04)
Grade 3: restrictive filling
1.14 (0.50–2.61)
3.01 (0.40–22.68)
2.16 (0.76–6.15)
LVEDD, left ventricular end-diastolic diameter; LVESD, left ventricular end-systolic diameter; IVSTd, interventricular septal thickness in diastole;
PWTd, posterior wall thickness in diastole; LV, left ventricular; LVEF, left ventricular ejection fraction; A-P, antero-posterior; MV, mitral valve.
Heart rates are for an increment of one unit in the predictor unless otherwise noted. Valvular group defined as rheumatic heart disease or having
severe mitral stenosis/regurgitation, aortic stenosis/regurgitation.