Background Image
Table of Contents Table of Contents
Previous Page  58 / 60 Next Page
Information
Show Menu
Previous Page 58 / 60 Next Page
Page Background

CARDIOVASCULAR JOURNAL OF AFRICA • Volume 32, No 2, March/April 2021

112

AFRICA

Although research is still needed to delineate the time of day

when melatonin therapy should be given, pre-clinical findings,

strengthened by the findings that melatonin levels are lower in

patients suffering from PAH, strongly suggest that melatonin,

given via a diet rich in melatonin, is worth testing as a safe,

simple and inexpensive therapy that could benefit PAH patients,

especially in resource-limited settings where patients cannot

receive expensive, targeted PAH therapies.

Professor S Lecour receives funding from Winetech for part of her research.

References

1.

Suzuki S, Dennerstein L, Greenwood KM,

et al

. Melatonin and hormo-

nal changes in disturbed sleep during late pregnancy.

J Pineal Res

1993;

15

: 191–198.

2.

Nduhirabandi F, Maarman GJ. Melatonin in heart failure: a promising

therapeutic strategy?

Molecules

2018;

23

(7): 1819

3.

Zhang J, Lu X, Liu M,

et al

. Melatonin inhibits inflammasome-associat-

ed activation of endothelium and macrophages attenuating pulmonary

arterial hypertension.

Cardiovasc Res

2020;

116

(13): 2156–2169.

4.

Cai Z, Klein T, Geenen LW,

et al

. Lower plasma melatonin levels predict

worse long-term survival in pulmonary arterial hypertension.

J Clin

Med

2020;

9

(5): 1248.

5.

Astorga CR, Gonzalez-Candia A, Candia AA,

et al.

Melatonin decreas-

es pulmonary vascular remodeling and oxygen sensitivity in pulmonary

hypertensive newborn lambs.

Front Physiol

2018;

9

: 185.

6.

Hung MW, Yeung HM, Lau CF,

et al.

Melatonin attenuates pulmonary

hypertension in chronically hypoxic rats.

Int J Mol Sci

2017;

18

(6): 1125.

7.

Maarman G, Blackhurst D, Thienemann F,

et al

. Melatonin as a preven-

tive and curative therapy against pulmonary hypertension.

J Pineal Res

2015;

59

: 343–353.

8.

Dominguez-Rodriguez A, Abreu-Gonzalez P, de la Torre-Hernandez

JM,

et al

. Effect of intravenous and intracoronary melatonin as an

adjunct to primary percutaneous coronary intervention for acute

ST-elevation myocardial infarction: Results of the Melatonin Adjunct in

the acute myocaRdial Infarction treated with Angioplasty trial.

J Pineal

Res

2017;

62

(1). Epub 2016 Nov 5.

9.

Dwaich KH, Al-Amran FGY, AL-Sheibani BIM,

et al

. Melatonin

effects on myocardial ischemia–reperfusion injury: Impact on the

outcome in patients undergoing coronary artery bypass grafting surgery.

Int J Cardiol

2016;

221

: 977–986.

10. Baltatu OC, Senar S, Campos LA,

et al

. Cardioprotective melatonin:

translating from proof-of-concept studies to therapeutic use.

Int J Mol

Sci

2019;

20

(18): 4342.

11. Andersen LP, Gogenur I, Rosenberg J,

et al

. The safety of melatonin in

humans.

Clin Drug Investig

2016;

36

: 169–175.

12. Jiki Z, Lecour S, Nduhirabandi F. Cardiovascular benefits of dietary

melatonin: a myth or a reality?

Frontiers Physiol

2018;

9

: 528–528.

Even low-dose steroid treatments substantially increase cardiovascular disease risk

While high doses of steroids are known to increase the risk

of cardiovascular disease (CVD), the impact of lower doses

is unknown. A Leeds University study in

PLOS Medicine

suggests that even low doses of glucocorticoid may increase

the risk of CVD.

Why was this study done?

Glucocorticoids (steroids) are widely used to reduce

disease activity and inflammation in patients with a range

of immune-mediated inflammatory diseases, such as

rheumatoid arthritis, polymyalgia rheumatica, giant cell

arteritis and inflammatory bowel disease.

Adequate assessment of cost-effectiveness of new steroid-

sparing treatments for immune and inflammatory diseases

requires modelling of estimates of risk and cost of the

main treatment complications of steroids.

It is widely recognised that high-dose steroids may increase

the risk of CVD (heart disease, stroke, or other vascular

diseases), but it is debated whether this increase also

applies to lower steroid doses.

Earlier studies of CVD risk associated with glucocorticoid

therapy failed to account for changes in dose over time

and for use of non-oral steroids and other potentially

confounding therapies.

What did the researchers do and find?

In 87 794 adults with immune-mediated inflammatory

diseases and no prior CVD (five-year median follow up),

we studied the risk of six common CVDs associated with

the steroid dose prescribed, quantified either as current or

as cumulative dose.

We found strong dose-dependent risks of all CVDs,

including myocardial infarction, heart failure, atrial fibril-

lation and cerebrovascular disease, in patients diagnosed

with the six inflammatory diseases studied.

After one year, the overall absolute risk of CVD doubled

for individuals using less than 5 mg prednisolone per day

and was six times higher for users of 25 mg or greater.

Many individuals had known modifiable cardiovascular

risk factors, including current smoking (24%), obesity

(25%) or hypertension (25%).

What do these findings mean?

We have provided evidence that individuals receiving

steroids have an increased risk of developing a broad

spectrum of fatal and non-fatal CVDs and that this risk

increases with the dose of steroids and with the duration

of steroid treatment.

It was previously believed that less than 5 mg of predniso-

lone was safe long term, but even at this ‘low dose’ patients

with immune-mediated inflammatory diseases have a

doubling of their underlying risk of CVD.

New treatment approaches that avoid the need for long-

term steroid treatment and have better cardiovascular

safety profile are required for immune-mediated inflam-

matory diseases.

All patients requiring long-term steroid treatment should

be prescribed the lowest effective steroid dose and have

a personalised CVD risk-prevention plan that takes into

account current and prior steroid use.

Source:

Medical Brief 2020