22 / 62
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 31, No 4, July/August 2020
184
AFRICA
Keirns C. Non- compacted cardiomyopathy: clinical-echocardiographic
study.
Cardiovasc Ultrasound
2006;
4
: 35.
13. Ichida F, Hamamichi Y, Miyawaki T, Ono Y, Kamiya T, Akagi T,
et al
.
Clinical features of isolated noncompaction of the ventricular myocar-
dium: long-term clinical course, hemodynamic properties, and genetic
background.
J Am Coll Cardiol
1999;
34
: 233–240
.
14. Lofiego C, Biagini E, Pasquale F, Ferlito M,
et al
. Wide spectrum of
presentation and variable outcomes of isolated left ventricular noncom-
paction.
Heart
2007;
93
: 65–71
.
15. Murphy RT, Thaman R, Blanes JG, Ward D,
et al
. Natural history and
familial characteristics of isolated left ventricular non-compaction.
Eur
Heart J
2005;
26
: 187–192.
16. Hoedemaekers YM, Caliskan K, Michels M,
et al
. The importance of
genetic counseling, DNA diagnostics, and cardiologic family screening
in left ventricular noncompaction cardiomyopathy.
Circ Cardiovasc
Genet
2010;
3
: 232–239.
17. Van Waning JI, Caliskan K, Hoedemaekers YM,
et al
. Genetics, clinical
features, and long-term outcome of noncompaction cardiomyopathy.
J
Am Coll of Cardiol
2018;
71
(7): 711–722.
18. Hermida-Prieto M, Monserrat Beiras A,
et al
. Familial dilated cardio-
myopathy and isolated left ventricular noncompaction associated with
lamin A/C gene mutation.
Am J Cardiol
2004;
94
: 50–54.
19. Camuglia AC, Younger JF, McGaughran J, Lo A, Atherton JJ. Cardiac
myosin-binding protein C gene mutation expressed as hypertrophic
cardiomyopathy and left ventricular noncompaction within two fami-
lies: insights from cardiac magnetic resonance in clinical screening:
Camuglia MYBPC3 gene mutation and MRI.
Int J Cardiol
2013;
168
:
2950–2952.
20. Bagnall RD, Molloy LK, Kalman JM, Semsarian C. Exome sequencing
identifies a mutation in the ACTN2 gene in a family with idiopathic
ventricular fibrillation, left ventricular noncompaction, and sudden
death.
BMC Med Genet
2014;
15
: 99.
21. Serio A, Narula N, Kodama T, Favalli V, Arbustini E. Familial dilated
cardiomyopathy. Clinical and genetic characteristics.
Hertz
2012;
37
(8):
822–829.
22. Caliskan K, Michels M, Geleijnnse M,
et al
. Frequency of asymptomat-
ic disease among family members with noncompaction cardiomyopathy.
Am J Cardiol
2012;
110
: 1512–1517.
23. Nugent AW, Daubeney PE, Chondros P, Carlin JB, Cheung M,
Wilkinson LC,
et al
. The epidemiology of childhood cardiomyopathy in
Australia.
N Engl J Med
2003;
348
: 1639–1646.
24. Diwadkar S, Nallamshetty L, Rojas C,
et al.
Echocardiography fails
to detect left ventricular noncompaction in a cohort of patients with
noncompaction on cardiac magnetic resonance imaging.
Clin Cardiol
2017;
40
: 364–369.
25. Kohli SK, Pantazis AA, Shah JS,
et al
. Diagnosis of left-ventricular
non-compaction in patients with left-ventricular systolic dysfunction:
time for a reappraisal of diagnostic criteria?
Eur Heart J
2008;
29
: 89–95.
26. Saleeb SF, Margossian R, Spencer CT, Alexander ME, Smoot LB,
et al
.
Reproducibility of echocardiographic diagnosis of left ventricular non-
compaction.
J Am Soc Echocardiogr
2012;
25
: 194–202.
27. Steffel J, Kobza R, Oechslin E,
et al
. Electrocardiographic characteristics
at initial diagnosis in patients with isolated left ventricular noncompac-
tion.
Am J Cardiol
2009;
104
(7): 984–989.
28. Lohrmann GM, Peters F, Srivathsan K,
et al.
Electrocardiographic
abnormalities in disease-free black South Africans and correlation with
echocardiographic indexes and early repolarization.
Am J Cardiol
2016;
118
(5): 765–770.
Landmark study highlights importance of cholesterol monitoring of young adults
Adults as young as 25 years, not only older people, need to
know their ‘bad cholesterol’ [non-high-density lipoprotein
cholesterol (non-HDL-C)] levels so they can change their
lifestyle or take drugs to protect themselves against heart
attacks and strokes in later life. The landmark study,
involving data from nearly 400 000 people in 19 countries,
establishes for the first time that levels of non-HDL-C or
‘bad cholesterol’ in the blood, are closely linked to the risk of
heart disease across the entire life course.
The research could lead to many younger people taking
statins to lower their cholesterol levels. At the moment GPs
prescribe the cholesterol-lowering drugs mostly to people in
middle age. The authors said it was important to know your
‘bad cholesterol’ level from young adulthood; it gave you the
chance to lower the level through exercise, a healthier diet, or
by taking statins.
‘We need to start it early,’ said Stefan Blankenberg, a
professor in Hamburg, Germany, who was part of the
multinational cardiovascular risk consortium that carried
out the modelling study. He said would he like to see new
guidance for doctors. ‘We should at least put into the
guidelines that non-HDL-C determination should be an
obligation. At a very young age – 25 to 30 years. You need
to know it.’
He added: ‘In German schools we have large anti-smoking
programmes. We persuade populations not to smoke. We
have no programme to let people know about cholesterol.
The first thing I would do is establish a cholesterol knowledge
programme.’ For young adults the first remedy for high
non-HDL-C would be exercise and losing extra weight,
followed by eating a healthier diet, said Blankenberg.
Colin Baigent, director of the MRC Population Health
Research Unit, at the University of Oxford, is quoted in
the report as saying: ‘This is an important paper because it
shows what could be achieved if, starting early in their 40s,
healthy people were to start taking a statin so that their bad
cholesterol is halved for the rest of their lives.
‘Of course, despite the fact that statins are safe and well
tolerated, many healthy people would be reluctant to take a
statin from early middle age. But the striking findings of this
study show that a policy of recommending such treatment
might be a long-term investment that leads to a substantial
improvement in the health of older people in the years to
come.’
Source:
Medical Brief 2020