58 / 72
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 27, No 2, March/April 2016
112
AFRICA
The first trimester is characterised by increased cardiac
output brought about by increased heart rate and stroke volume.
These changes are partly induced by the onset of an expanded
intravascular volume, set against peripheral arteriolar dilatation.
Human chorionic gonadotrophin, which has some thyroid
stimulating factor homology and activity, may also contribute to
the rise in cardiac output. This is followed by progressive volume
expansion secondary to physiological hyperaldosteronism with
renal sodium and water retention.
15
In the second trimester the volume expansion continues and
peripheral vasodilatation dominates the pregnancy adaptation,
leading to a fall in blood pressure.
16
Early in the third trimester,
the volume expansion peaks and vascular resistance rises.
Labour is accompanied by a further increase in cardiac output,
which may be catecholamine mediated as a result of painful
contractions. Delivery has complex haemodynamic effects,
including blood loss and autotransfusion of blood from the
contracted uterus immediately after delivery. In the puerperium,
the extracellular fluid retention of pregnancy dissipates, with
resolving peripheral oedema, and the hyperdynamic effects of
pregnancy persist for days to weeks. Further cardiovascular
disturbance may arise from common morbidity such as
postpartum anaemia.
Pregnancy induces a procoagulant haematological profile
with accelerated rates of thrombus formation and fibrinolysis.
17
This is necessary to secure haemostasis within the choriodecidual
space of the placenta and is also one of the mechanisms
by which blood loss at the point of delivery is curtailed.
This adaptation will increase the risk of thrombotic events in
susceptible individuals.
In summary, the cardiac consequences of pregnancy are those
of increased preload, reduced afterload, and increased heart
rate, stroke volume and cardiac output in a hypercoagulable
circulation subject to progressive change throughout pregnancy
but also confronted by acutely increased demands during labour
and immediately after delivery.
Valvular heart disease
Acute rheumatic fever is a possible complication of pregnancy
but is rarely seen. Most patients present with established post-
rheumatic valvular disease. Valvular heart disease is present
in 80% of patients with heart disease during pregnancy in
developing countries, with rheumatic fever as the most common
aetiology.
18
It may present for the first time during pregnancy.
Stenotic lesions that limit the ability to increase cardiac
output may not be well tolerated during pregnancy and delivery.
Regurgitant lesions are generally better tolerated, especially
if the underlying cardiac function is normal.
19
Occasionally,
deterioration of regurgitation or left ventricular function is seen,
requiring medical treatment.
Stenotic lesions
The mitral valve is the most commonly affected valve following
the development of acute rheumatic fever. A study of routine
echocardiographic screening among a population of children
under the age of 17 years in Mozambique and Cambodia
identified mitral valve disease in 87–98% of cases.
20
An earlier
South African study showed that overall, mitral stenosis was
the single most prevalent abnormality, affecting 38% of those
presenting with valvular disease, although mitral incompetence
was more common in the first two decades of life.
21
The latter
study identified mitral incompetence in 30% of patients, with
mixed lesions making up the balance.
In the recently published REMEDY registry, children in
the first decade of life presented predominantly with pure
mitral regurgitation, with mixed mitral and mixed aortic valve
disease emerging as a dominant mitral valve lesion from the
second decade of life. Most of the cases of mitral stenosis and
mitral regurgitation among other forms of valvular disease had
moderate-to-severe disease.
11
Mitral stenosis (MS)
Rheumatic mitral stenosis is poorly tolerated in pregnancy,
and it is the leading cardiac cause of maternal mortality in the
developing world.
22
It may be an incidental finding on physical
examination, with many women unaware of the condition until
the haemodynamic changes of pregnancy precipitate symptoms,
usually in the mid-second trimester. They develop exertional
dyspnoea and postural symptoms, including orthopnoea and
paroxysmal nocturnal dyspnoea. Occasionally the condition
may have been misdiagnosed as bronchial asthma. The classical
signs of mid-diastolic rumbling murmur at the apex may be
difficult to detect in patients with pulmonary oedema and a
rapid tachycardia. Radiological signs of an enlarged left atrium
and ECG evidence of a bifid P wave are all useful investigations.
Pregnancy may, however, result in a mitralised cardiac shadow in
the absence of any valvular pathology.
Pregnancy-related tachycardia and the increased blood
volume are less likely to be tolerated without an increase in
pulmonary capillary pressures, with increasing degrees of mitral
stenosis. The increasing systemic vascular resistance of the third
trimester tends to increase left-sided filling pressures further and
there is a risk of pulmonary oedema during pregnancy. This risk
escalates further during labour and immediately postpartum
because of an increasingly hyperdynamic circulation and the
acute increase in blood volume during the third stage of labour.
Significant mitral stenosis results in left atrial dilatation and
an increased risk of atrial fibrillation. As pregnancy is already
a hypercoagulable state, these patients are at an increased
risk of developing intracardiac thrombus, and they should be
anticoagulated with therapeutic low-molecular-weight heparin
(LMWH).
In a South American study of 88 women with rheumatic
mitral stenosis (54 of whom had moderate-to-severe mitral
stenosis), eight maternal deaths occurred as a result of heart
failure.
23
In sub-Saharan Africa, a study of 50 pregnancies in
women with heart disease, most of whom had rheumatic mitral
stenosis, the maternal mortality rate was high at 32%.
23
The general principles of medical management are to control
the heart rate, limit the volume expansion and prevent the
development of co-morbidity due to anaemia, hyperthyroidism
and sepsis. In addition to controlling heart rate, beta-blockade
will preserve sinus rhythm and prolong diastolic filling of the left
ventricle. Atrial fibrillation and atrial flutter should be treated
promptly with rate control, and early cardioversion should be
considered.
24
All drugs should be given with caution. Afterload
reduction can cause reflex tachycardia with declining diastolic