CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 1, January/February 2014
20
AFRICA
1681–1687.
28. Pytkowski M, Jankowska A, Maciag A,
et al
. Paroxysmal atrial fibrilla-
tion is associated with increased intra-atrial conduction delay.
Europace
2008;
10
(12): 1415–1420.
29. Yavuzkir M, Ozturk A, Dagli N,
et al
. Effect of ongoing inflammation
in rheumatoid arthritis on P-wave dispersion.
J Int Med Res
2007;
35
:
796–802.
30. Dogan SM, Aydin M, Gursurer M,
et al
. The increase in P-wave disper-
sion is associated with the duration of disease in patientswith Behcet’s
disease.
Int J Cardiol
2008;
124
: 407–410.
31. Ozmen N, Cebeci BS, Yiginer O, Muhcu M, Kardesoglu E, Dincturk
M. P-wave dispersion is increased in pregnancy due to shortening of
minimum duration of P: does this have clinical significance.
J Int Med
Res
2006;
34
(5): 468–474.
32. Merckx KL, De Vos CB, Palmans A, Habets J, Cheriex EC, Crijns HJ,
et al
. Atrial activation time determined by transthoracic Doppler tissue
imaging can be used as an estimate of the total duration of atrial electri-
cal activation.
J Am Soc Echocardiogr
2005;
18
(9): 940–944.
33. Daubert JC, Pavin D, Jauvert G, Mabo P. Intra and interatrial conduc-
tion delay: Implications for cardiac pacing.
Pacing Clin Electrophysiol
2004;
27
: 507–525.
34. De Vos CB, Weijs B, Crijns HJ, Cheriex EC, Palmans A, Habets J,
et al
.
Atrial tissue Doppler imaging for prediction of new-onset atrial fibril-
lation.
Heart
2009;
95
: 835–840.
35. Park S M, Kim YH, Choi JI, Pak HN, Kim YH, Shim WJ. Left atrial
electromechanical conduction time can predict six-month maintenance
of sinus rhythm after electrical cardioversion in persistent atrial fibrilla-
tion by Doppler tissueechocardiography.
J Am Soc Echocardiogr
2010;
23
: 309–314.
36. Pala S, Tigen K, Karaahmet T, Dundar C, Kilicgedik A, Güler A,
et al
.
Assessment of atrial electromechanical delay by tissue Doppler echo-
cardiography in patients with nonischemic dilated cardiomyopathy.
J
Electrocardiol
2010;
43
: 344–350.
… continued from page 8
LVHT frequently occurs familiarly.
5
Were any other first-
degree relatives investigated for LVHT? Did any of the first-
degree relatives present with clinical cardiac disease? Was
the family history positive for syncope, severe arrhythmias or
sudden cardiac death?
LVHT is frequently associated with chromosomal aberrations
or NMDs. Did the boy undergo cytogenetic investigations to
confirm a chromosomal defect or was he ever investigated by
a myologist to confirm or rule out NMD? When examining
the patient cardiologically, did he present with myopathic face,
weakness of the limb, axial or respiratory muscles, wasting, or
with fasciculations? What was the level of serum creatine kinase
and serum lactate?
We do not agree with the view that LVHT may develop into
cardiomyopathy (discussion). LVHT is
per se
classified as an
unclassified cardiomyopathy by the European and American
Cardiological Society.
A follow up of two months is very short. It would be
interesting to know about any long-term results. Did ventricular
arrhythmias recur? Did left ventricular dysfunction or dilatation
of the cardiac cavities re-emerge?
Overall, it would be helpful to receive more detailed
information about the affected patient and his relatives to
assess whether LVHT was associated with hereditary disease
or not. Long-term data would help to assess whether the
applied therapeutic measures truly had a long-term effect in this
particular patient without developing arrhythmias other than
ventricular ectopic beats or heart failure since then.
Josef Finsterer, MD, PhD,
Krankenanstalt Rudolfstiftung, Vienna, Austria
Sinda Zarrouk-Mahjoub, PhD
Laboratory of Biochemistry, UR Human Nutrition and
Metabolic Disorders, Faculty of Medicine, Monastir, Tunisia
References
1.
Osmonov D, Ozcan KS, Ekmekçi A, Güngör B, Alper AT, Gürkan K.
Tachycardia-induced cardiomyopathy due to repetitive monomorphic
ventricular ectopy in association with isolated left ventricular non-
compaction.
Cardiovasc J Afr
2013;
24
: 1–3.
2.
Finsterer J, Stöllberger C, Fazio G. Neuromuscular disorders in left
ventricular hypertrabeculation/noncompaction.
Curr Pharm Des
2010;
16
: 2895–2904.
3.
Patil MB, Patil SM. Left-ventricular noncompaction in an infant with
trisomy 21.
Pediatr Cardiol
2013;
34
: 722–724.
4.
Finsterer J, Stöllberger C. Toxoplasmosis or left ventricular hypertra-
beculation/non-compaction.
J Med Life
2012;
5
: 258–259.
5.
Finsterer J, Stöllberger C, Blazek G, Sehnal E. Familal left ventricular
hypertrabeculation (noncompaction) is myopathic.
Int J Cardiol
2013;
164
: 312–317.