Cardiovascular Journal of Africa: Vol 27 No 2 (March/April 2016)

CARDIOVASCULAR JOURNAL OF AFRICA • Volume 27, No 2, March/April 2016

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AFRICA

the pregnancy becomes advanced, disruption in this oxidative

balance can lead to inappropriate activation of the inflammatory

cascade, which produces harmful effects, including premature

labour and complications such as pre-eclampsia.

The inflammatory response in pregnancy

At the start of pregnancy an inflammatory cascade is activated,

which allows the formation and invasion of the foreign

trophoblastic material into the maternal tissues.

Medawar

al.

proposed a model by which suppression of the mother’s

immune system allows invasion of the foreign material.

This

model suggests that maternal lymphocyte suppression allows

this invasion.

The immune system uses two basic components: the

non-specific inbuilt innate immune response and the specific

‘learned’ adaptive immune system.

The innate immune system is

primitive. Its primary function is to differentiate self from non-self

and it only copes with the most fundamental immune challenges,

such as pathogens.

The innate immune system presents antigens

in association with major histocompatibility complex (MHC)

class I and II molecules to the lymphocytes. The more specific

adaptive immune system has a delayed response. The cells learn

and develop an acquired defence against external threats.

Human pregnancy presents a unique challenge to the immune

system.

The uterus is surrounded by a mucosal barrier, the

decidua.

It is, however, not impenetrable to the maternal

immune system.

The trophoblast cells do not express MHC

class I or II molecules, thereby escaping the maternal innate

immune response. Imbalances in the innate immune response

in the placenta and decidua have been implicated in the

development of pre-eclampsia.

Adaptive immune responses are suppressed by placental

products such as prostaglandins and interleukins 4, 6 and 10

(IL-4, IL-6 and IL-10). IL-6 is an important cytokine in the

immune inflammatory response in adaptive immunity during

pregnancy.

Excessive IL-6 response has been implicated in

pathological conditions of pregnancy, such as miscarriage and

pre-eclampsia.

Women and cardiovascular disease

Cardiovascular disease, once thought to be a ‘male problem’,

is now recognised as equally affecting women.

The American

Heart Association published the first women-specific clinical

recommendations in 1999, which led to an increase in awareness

and prevention of CVD in women.

The rate of deaths resulting

from CVD are however still increasing, due to diseases of

lifestyle leading to an increase in hypertension and diabetes.

Around 81% of CVD deaths in women occur in lower-income

countries.

In women with pre-existing heart disease, changes in the

circulatory system during pregnancy can cause decompensation

or death of the foetus or mother.

Atkins and colleagues

investigated the differences in risk factors in American women

of Caucasian and African racial groups.

Caucasian women

have been found to have higher rates of hyperhomocysteinaemia

and higher body mass index (BMI). African women were found

to have an increase in blood pressure, BMI and iron-deficiency

anaemia. Physiological changes during pregnancy in women

with no known pre-existing CVD may lead to the development

of PPCM and pre-eclampsia.

Pre-eclampsia occurring in late or early pregnancy is

characterised by hypertension, oedema and the presence of

protein in the urine.

Hypertensive disorders are the most

frequent complication in pregnancy and cause of maternal death

in Africa.

There have also been limited insights into the exact

pathophysiological mechanisms of the disease.

A suggested

pathophysiological mechanism is an increase in oxidative stress

during pregnancy.

PPCM presents in the final month of pregnancy and during

the first five months postpartum.

Distinguished from other

forms of cardiomyopathy by its rapid development in the

peripartum period, the exact mechanism of PPCM is not well

understood.

In countries with large populations of African

descent, such as South Africa and Haiti, the prevalence is

higher, with one in 1 000 and one in 299 births, respectively.

More epidemiological studies are needed to fully determine the

prevalence rates in Europe and Asia.

Studies have suggested that an increase in oxidative stress

during pregnancy leads to the cleavage of the breastfeeding

hormone, prolactin, into a 16-Kda pro-apoptotic, which

may contribute to the development of PPCM.

Increases in

pro-inflammatory cytokines such as C-reactive protein (CRP)

have also been suggested to contribute to the condition.

Depression as a risk factor for cardiovascular

disease

Since the time of the ancient Greeks, affective dispositions

have been thought to be associated with physical disease.

The

World Health Organisation (WHO) estimates that, by the year

2030, mental disorders will rise to first place in hospitalisation

morbidity, overtaking road traffic accidents and heart disease.

Depression is known to be a risk factor for the development of

CVD, as well as a predictor of poor prognosis following a cardiac

event.

Established risk factors, such as hypercholesterolaemia,

hypertension and smoking, leave unexplained inconsistencies

in ischaemic heart disease data.

It has been suggested that

psychosocial factors may account for these differences.

The

mental and physiological changes of a depressive individual

may also negatively affect the course of CVD.

The decrease

in the depressive patient’s motivation and inability to function

in day-to-day tasks, as well as fear of side effects, may result in

non-compliance with medical recommendations.

Depression

also increases the incidence of other risk indicators, such as

smoking and hypertension.

Previous animal and human models have suggested links in

the pathways between depression and physiological responses,

such as nervous system activation, an increase in inflammation,

changes in sleep patterns and cardiac rhythm disturbances.

8,30

Rosengren and colleagues investigated the association of

psychosocial factors with the risk of myocardial infarction.

This

study found that patients with myocardial infarction reported

high psychosocial stress factors, such as depression and financial

and work stress, compared to healthy individuals.

The increased

risk for CVD is potentially due to the physiological response to

these psychosocial stressors.

Depressionhas been shown to increase inflammatory cytokines,

which are known to contribute to CVD.

Inflammatory markers