CARDIOVASCULAR JOURNAL OF AFRICA • Volume 30, No 1, January/February 2019
66
AFRICA
other imaging studies. It noticeable that in some patients,
several mechanisms may be involved in the pathogenesis of
PH in Africa. For example, the interaction between sickle cell
disease-related haemolysis and HIV, chronic lung disease due to
tuberculosis, schistosomiasis, and viral hepatitis could yield very
complex multifactorial and unclear PH.
Limitations of the suggested algorithm
It is important to acknowledge that a major limitation of our
approach lies in the validity of RVSP for diagnosis of PH using
Doppler echo. There is absolutely no doubt that RHC is the
standard to accurately diagnose PH and determine its severity as
well as its impact on right ventricular function. However, RHC
is an invasive procedure, and it is expensive and not available in
most low-resource settings where the majority of patients with
PH are resident, particularly in SSA.
There is abundant literature on the validity of Doppler
echo RVSP estimates in patients with left heart disease using
RHC values as the gold standard. Lanzarini
et al
.
14
reported a
concordance correlation coefficient of 0.88 between RHC and
RVSP, with ± 20 mmHg and 95% limits of agreement. In their
study of Doppler echo evaluation of haemodynamics in patients
with decompensated systolic HF, Nagueh
et al
.
15
reported
that Doppler echo identified patients with invasive systolic
pulmonary artery pressure
>
35 mmHg with 94% sensitivity and
90% specificity.
In an analysis of data from the ESCAPE trial, McClanahan
and Guglin
16
suggested that the accuracy of Doppler echo RVSP
estimates in systolic HF might be inaccurate in the presence
of right ventricular systolic dysfunction. However, at least
two reasons could have explained this lack of accuracy: first,
patients included in the ESCAPE trial
16
were in acute HF and
not haemodynamically stable; and second, echocardiography
in ESCAPE was not protocol driven, and the time differential
between RHC and RVSP evaluation using Doppler echo was
widely variable. In view of the above and provided that patients
are haemodynamically stable and a rigorous Doppler echo
technique is used by experienced observers, it is acceptable and
pragmatic to detect PH using Doppler echo estimates of RVSP,
although we recommend a confirmation with RHC before any
specific therapeutic action is required.
Finally, our recommendations are based on a single study.
Ideally, such a practice algorithm, which is intended to provide
clinicians with recommendations, should be based on systematic
review of the available evidence, and an assessment of the benefits
and harms of care options, with the intention of optimising
patient care and outcomes. However, expert opinion remains a
major part of all such practice guidelines,
17,18
particularly when
high-quality evidence is lacking, as is the case in SSA.
Conclusion
For the busy clinician, it is important to recognise the increasing
burden of PHLHD in low-resource settings and be able to make
an early diagnosis. Adopting a four-step diagnostic algorithm
is recommended and the steps include: (1) a clinical evaluation,
(2) CXR and ECG assessment, (3) Doppler echo, and (4)
exploration of differential aetiologies before classification of
the type of PH. This strategy will help manage the majority of
patients in low-resource settings, especially those with various
types of PHLHD, for which indications of RHC should be
restricted to avoid unnecessary risk.
We acknowledge the Wits/NIH Non-Communicable Diseases Leadership
Program, funded through the Fogarty International Centre of the NIH
Millennium Promise Awards: Non-Communicable Chronic Diseases Research
Training Program (NCoD) (D43), grant number:1D43TW008330-01A1.
The study and publication were partly funded by the Pulmonary Vascular
Research Institute, Bayer Healthcare and the Maurice Hatter Foundation.
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