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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 31, No 2, March/April 2020

64

AFRICA

ment from the European Society of Cardiology Working Group on

Peripheral Circulation.

Eur J Cardiovasc Prev Rehabil

2011;

18

(6):

775–789.

36. Mancia G, Fagard R, Narkiewicz K, Redon J, Zanchetti A, Bohm M,

et al

. 2013 ESH/ESC guidelines for the management of arterial hyper-

tension: the Task Force for the Management of Arterial Hypertension

of the European Society of Hypertension (ESH) and of the European

Society of Cardiology (ESC).

Eur Heart J

2013;

34

(28): 2159–2219.

37. Van Bortel LM, De Backer T, Segers P. Standardization of arterial stiff-

ness measurements make them ready for use in clinical practice.

Am J

Hypertens

2016;

29

(11): 1234–1236.

38. Triant VA, Meigs JB, Grinspoon SK. Association of C-reactive protein

and HIV infection with acute myocardial infarction.

J Acquir Immune

Defic Syndr

2009;

51

(3): 268–273.

39. Baker J, Quick H, Hullsiek KH, Tracy R, Duprez D, Henry K,

et al.

Interleukin-6 and d-dimer levels are associated with vascular dysfunc-

tion in patients with untreated HIV infection.

HIV Med

2010;

11

(9):

608–609.

40. Kelesidis T, Kendall MA, Yang OO, Hodis HN, Currier JS. Biomarkers

of microbial translocation and macrophage activation: association with

progression of subclinical atherosclerosis in HIV-1 infection.

J Infect Dis

2012;

206

(10): 1558–1567.

41. Knudsen A, Katzenstein TL, Benfield T, Jorgensen NR, Kronborg

G, Gerstoft J,

et al

. Plasma plasminogen activator inhibitor-1 predicts

myocardial infarction in HIV-1-infected individuals.

AIDS

2014;

28

(8):

1171–1179.

42. Fourie CM, Schutte AE, Smith W, Kruger A, van Rooyen JM.

Endothelial activation and cardiometabolic profiles of treated and

never-treated HIV infected Africans.

Atherosclerosis

2015;

240

(1):

154–160.

43. Blankenberg S, Barbaux S, Tiret L. Adhesion molecules and atheroscle-

rosis.

Atherosclerosis

2003;

170

(2): 191–203.

44. Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis.

Circulation

2002;

105

(9): 1135–1143.

45. Hulten E, Mitchell J, Scally J, Gibbs B, Villines TC. HIV positivity,

protease inhibitor exposure and subclinical atherosclerosis: a systematic

review and meta-analysis of observational studies.

Heart

2009;

95

(22):

1826–1835.

46. D’Ascenzo F, Cerrato E, Calcagno A, Grossomarra W, Ballocca F,

Omede P,

et al

. High prevalence at computed coronary tomography

of non-calcified plaques in asymptomatic HIV patients treated with

HAART: a meta-analysis.

Atherosclerosis

2015;

240

(1): 197–204.

47. Stein JH, Currier JS, Hsue PY. Arterial disease in patients with human

immunodeficiency virus infection: what has imaging taught us?

J Am

Coll Cardiol Cardiovasc Imaging

2014;

7

(5): 515–525.

48. McComsey GA, O’Riordan M, Hazen SL, El-Bejjani D, Bhatt S,

Brennan ML,

et al

. Increased carotid intima–media thickness and cardi-

ac biomarkers in HIV infected children.

AIDS

2007;

21

(8): 921–927.

49. Baker JV, Henry WK, Patel P, Bush TJ, Conley LJ, Mack WJ,

et al

.

Progression of carotid intima–media thickness in a contemporary

human immunodeficiency virus cohort.

Clin Infect Dis

2011;

53

(8):

826–835.

50. Kablak-Ziembicka A, Tracz W, Przewlocki T, Pieniazek P, Sokolowski

A, Konieczynska M. Association of increased carotid intima–media

thickness with the extent of coronary artery disease.

Heart

2004;

90

(11):

1286–1290.

One-off DNA test could predict heart attack risk in childhood

People at high risk of a heart attack in adulthood could be

spotted much earlier in life with a reasonably inexpensive,

one-off DNA test, according to research funded, among

others, by the British and Australian heart foundations.

An international team led by researchers from the

University of Leicester, University of Cambridge and the

Baker Heart and Diabetes Institute in Australia used UK

Biobank data to develop and test a powerful scoring system,

called a genomic risk score (GRS), which can identify

people who are at risk of developing coronary heart disease

prematurely because of their genetic make-up.

Genetic factors have long been known to be major

contributors of someone’s risk of developing coronary heart

disease – the leading cause of heart attacks. Currently, to

identify those at risk, doctors use scores based on lifestyle

and clinical conditions associated with coronary heart

disease, such as cholesterol level, blood pressure, diabetes

and smoking. But these scores are imprecise, age-dependent

and miss a large proportion of people who appear ‘healthy’,

but will still develop the disease.

The ‘big-data’ GRS technique takes into account 1.7

million genetic variants in a person’s DNA to calculate their

underlying genetic risk for coronary heart disease. The team

analysed genomic data of nearly half a million people, aged

between 40 and 69 years, from the UK Biobank research

project. This included over 22 000 people who had coronary

heart disease.

The GRS was better at predicting someone’s risk of

developing heart disease than each of the classic risk factors

for coronary heart disease alone. The ability of the GRS to

predict coronary heart disease was also largely independent

of these known risk factors. This showed that the genes that

increase the risk of coronary heart disease don’t simply work

by elevating blood pressure or cholesterol, for example.

People with a genomic risk score in the top 20% of the

population were over four times more likely to develop

coronary heart disease than someone with a genomic risk

score in the bottom 20%. In fact, men who appeared healthy

by current NHS health check standards but had a high

GRS were just as likely to develop coronary heart disease

as someone with a low GRS and two conventional risk

factors such as high cholesterol or high blood pressure. These

findings help to explain why people with healthy lifestyles

and no conventional risk factors can still be struck by a

devastating heart attack.

continued on page 74…