CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 2, March 2012
AFRICA
97
41. Kavanaugh-McHugh AL, Ruff A, Perlman E, Hutton N, Modlin J, Rowe
S. Selenium deficiency and cardiomyopathy in acquired immunodefi-
ciency syndrome. JPEN
J Parenter Enteral Nutr
1991;
15
(3): 347–349.
42. Chetty R, Batitang S, Nair R. Large artery vasculopathy in HIV-positive
patients: another vasculitic enigma.
Hum Pathol
2000;
31
(3): 374–379.
43. Sinzobahamvya N, Kalangu K, Hamel-Kalinowski W. Arterial aneu-
rysms associated with human immunodeficiency virus (HIV) infection.
Acta Chir Belg
1989;
89
(4): 185–188.
44. Chetty R. Vasculitides associated with HIV infection.
J Clin Pathol
2001;
54
(4): 275–278.
Letter to the Editor
Sudden cardiac death due to β
2
-agonist therapy:
is a genetic basis overlooked?
K YALTA, N SIVRI, B GEYİK, Y AKSOY, E YETKIN
β
2
-adrenoceptor agonists have long been widely used for the
management of certain conditions, including chronic obstructive
pulmonary disease (COPD). However, in recent years, sudden
cardiac death (SCD) associated with the use of
β
2
-adrenoceptor
agonists has raised significant concerns about the safety profile
of these agents. These drugs may have the potential to induce
SCD in a proportion of susceptible subjects with structural heart
diseases (SHD) including cardiomyopathies, and should not be
routinely prescribed before ruling out these pathologies.
1
A case of SCD with an undiagnosed cardiomyopathy, possibly
associated with the administration of a
β
2
-adrenoceptor agonist
(for a bronchial asthma attack) has recently been reported,
suggesting the presence of SHD as the most important determi-
nant of SCD due to
β
2
-agonist therapy.
1
However, as described
below, SCD due to
β
2
-agonist therapy may also be closely
associated with individual genetic susceptibility, particularly in
subjects with apparently normal hearts, suggesting the need for
thorough investigation of all candidates of
β
2
-agonist therapy,
with regard to clinical clues to an electrophysiological genetic
basis for
β
2
-agonist-induced SCD, before prescribing these
drugs.
Genetically determined arrhythmogenic entities including
ion channelopathies and catecholaminergic ventricular tachycar-
dia (VT) have been regarded as important aetiologies of SCD,
particularly in young victims
2
with apparently normal hearts. Ion
channelopathies may be overt or obscure in terms of resting ECG
signs (with or without QT-interval prolongation) and generally
present with a spectrum of clinical symptoms (syncopal attacks,
SCD) that may be triggered by a variety of internal or external
factors, including QT-interval-prolonging drugs.
2
Previously, we reported a case of torsades de pointes (TdP)
with a severely prolonged corrected QT (QTc) interval induced
by an initial low-dose sotalol intake in the presence of a normal
basal QTc interval, suggesting an individual genetic susceptibil-
ity to drug-induced pro-arrhythmia.
3
Besides eliciting procliv-
ity for malign arrhythmias in the presence of structural heart
diseases and triggering acute coronary syndromes (ACS) in
susceptible subjects,
β
-receptor stimulation is also well known
to prolong QT interval. Therefore, it may be suggested that TdP
due to a severely prolonged QT interval may be propounded as
one of the fundamental mechanisms of
β
2
-agonist-related SCD
in subjects with a genetic basis for drug-induced pro-arrhythmia.
Consistent with this notion, in a retrospective study comprising
a large population of patients with long-QT syndrome (LQTS),
Cardiology Department, Trakya Üniversity, Edirne, Turkey
K YALTA, MD,
N SIVRI, MD
B GEYİK, MD
Y AKSOY, MD
Cardiology Department, IMC Hospital, Mersin, Turkey
E YETKIN, MD
continued on page 102…
