Table Of ContentAFRICA
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20. Williams B, Lacy PS, Yan P, Hwee CN, Liang C, Ting CM. Development 26. European Society of Cardiology. 2007 Guidelines for the Management
and validation of a novel method to derive central aortic systolic pres- of Arterial Hypertension: The Task Force for the Management of
sure from the radial pressure waveform using an N-point moving aver- Arterial Hypertension of the European Society of Hypertension (ESH)
age method. J Am Coll Cardiol 2011; 57(8): 951–961. and of the European Society of Cardiology (ESC). J Hypertens 2007;
21. Nair D, Tan SY, Gan HW, Lim SF, Tan J, Zhu M, et al. The use of ambu- 25(6): 1105–1187.
latory tonometric radial arterial wave capture to measure ambulatory 27. Schlieper G, Aretz A, Verberckmoes SC, Kruger T, Behets GJ, Ghadimi
blood pressure: the validation of a novel wrist-bound device in adults. J R, et al. Ultrastructural analysis of vascular calcifications in uremia. J
Hum Hypertens 2008; 22(3): 220–222. Am Soc Nephrol 2010; 21(4): 689–696.
22. Mansia G, De Backer G, Dominiczak A, Cifkova R, Fagard R, 28. Roman MJ, Okin PM, Kizer JR, Lee ET, Howard BV, Devereux RB.
Germano G, et al. 2007 ESH-ESC Guidelines for the management Relations of central and brachial blood pressure to left ventricular
of arterial hypertension: the task force for the management of arterial hypertrophy and geometry: the Strong Heart Study. J Hypertens 2010;
hypertension of the European Society of Hypertension (ESH) and of 28(2): 384–388.
the European Society of Cardiology (ESC). Blood Press 2007; 16(3): 29. Minutolo R, Agarwal R, Borrelli S, Chiodini P, Bellizzi V, Nappi F,
135–232. et al. Prognostic role of ambulatory blood pressure measurement in
23. Agatston AS, Janowitz WR, Hildner FJ, Zusmer NR, Viamonte M, Jr, patients with nondialysis chronic kidney disease. Arch Intern Med
Detrano R. Quantification of coronary artery calcium using ultrafast 2011; 171(12): 1090–1098.
computed tomography. J Am Coll Cardiol 1990; 15(4): 827–832. 30. Covic A, Goldsmith DJ. Ambulatory blood pressure monitoring in
24. Kauppila LI, Polak JF, Cupples LA, Hannan MT, Kiel DP, Wilson nephrology: focus on BP variability. J Nephrol; 12(4): 220–229.
PW. New indices to classify location, severity and progression of 31. Agarwal R, Andersen MJ, Bishu K, Saha C. Home blood pressure
calcific lesions in the abdominal aorta: a 25-year follow-up study. monitoring improves the diagnosis of hypertension in hemodialysis
Atherosclerosis 1997; 132(2): 245–250. patients. Kidney Int 2006; 69(5): 900–906.
25. Devereux RB, Alonso DR, Lutas EM, Gottlieb GJ, Campo E, Sachs 32. Agarwal R, Peixoto AJ, Santos SF, Zoccali C. Out-of-office blood pres-
I, et al. Echocardiographic assessment of left ventricular hypertrophy: sure monitoring in chronic kidney disease. Blood Press Monit 2009;
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letter to the Editor
Non-compaction is not a simple genetic disorder
dear sir The authors reported that systolic function improved after
We read with interest the article by Osmonov et al. about ablation. Did the patient also receive angiotensin converting
an asymptomatic 16-year-old boy with left ventricular enzyme inhibitors, angiotensin 2 blockers, beta-blockers or
hypertrabeculation/non-compaction (LVHT) who was incidentally diuretics, or do the authors attribute improvement of systolic
investigated cardiologically for repetitive monomorphic couplets/ dysfunction within two months after the procedure exclusively
triplets of premature ventricular ectopic beats with left bundle to the ablation?
branch block morphology and inferior QRS axis.1 We have the The authors mentioned that the boy was scheduled for plastic
following comments and concerns. surgery. Which operation was the patient intended to undergo?
We do not agree with the definition of LVHT as a genetic Did the patient present with dysmorphism, any skin problems,
disorder. Although frequently associated with genetic disease, or bone abnormalities, which are occasionally found in patients
a clear-cut genotype/phenotype correlation has never been with LVHT?3 LVHT has not only been misdiagnosed as distal
established for any of the mutated genes so far described heterotrophic cardiomyopathy, dilated cardiomyopathy, or left
in association with LVHT. An argument against a causal ventricular apical thrombus, but has also been mixed up with
relationship is that in the majority of hereditary neuromuscular aberrant bands, papillary muscles, apical type of hypertrophic
disorders (NMDs) associated with LVHT, LVHT is absent.2 Since cardiomyopathy, myocardial abscess and toxoplasmosis.4
the exact cause and pathomechanism of LVHT remains elusive, it
is not justified to classify LVHT as a genetic disease. continued on page 20…
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20 CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 1, January/February 2014
1681–1687. cal activation. J Am Soc Echocardiogr 2005; 18(9): 940–944.
28. Pytkowski M, Jankowska A, Maciag A, et al. Paroxysmal atrial fibrilla- 33. Daubert JC, Pavin D, Jauvert G, Mabo P. Intra and interatrial conduc-
tion is associated with increased intra-atrial conduction delay. Europace tion delay: Implications for cardiac pacing. Pacing Clin Electrophysiol
2008; 10(12): 1415–1420. 2004; 27: 507–525.
29. Yavuzkir M, Ozturk A, Dagli N, et al. Effect of ongoing inflammation 34. De Vos CB, Weijs B, Crijns HJ, Cheriex EC, Palmans A, Habets J, et al.
in rheumatoid arthritis on P-wave dispersion. J Int Med Res 2007; 35: Atrial tissue Doppler imaging for prediction of new-onset atrial fibril-
796–802. lation. Heart 2009; 95: 835–840.
30. Dogan SM, Aydin M, Gursurer M, et al. The increase in P-wave disper- 35. Park S M, Kim YH, Choi JI, Pak HN, Kim YH, Shim WJ. Left atrial
sion is associated with the duration of disease in patientswith Behcet’s electromechanical conduction time can predict six-month maintenance
disease. Int J Cardiol 2008; 124: 407–410. of sinus rhythm after electrical cardioversion in persistent atrial fibrilla-
31. Ozmen N, Cebeci BS, Yiginer O, Muhcu M, Kardesoglu E, Dincturk tion by Doppler tissueechocardiography. J Am Soc Echocardiogr 2010;
M. P-wave dispersion is increased in pregnancy due to shortening of 23: 309–314.
minimum duration of P: does this have clinical significance. J Int Med 36. Pala S, Tigen K, Karaahmet T, Dundar C, Kilicgedik A, Güler A, et al.
Res 2006; 34(5): 468–474. Assessment of atrial electromechanical delay by tissue Doppler echo-
32. Merckx KL, De Vos CB, Palmans A, Habets J, Cheriex EC, Crijns HJ, cardiography in patients with nonischemic dilated cardiomyopathy. J
et al. Atrial activation time determined by transthoracic Doppler tissue Electrocardiol 2010; 43: 344–350.
imaging can be used as an estimate of the total duration of atrial electri-
… continued from page 8 applied therapeutic measures truly had a long-term effect in this
particular patient without developing arrhythmias other than
LVHT frequently occurs familiarly.5 Were any other first- ventricular ectopic beats or heart failure since then.
degree relatives investigated for LVHT? Did any of the first-
degree relatives present with clinical cardiac disease? Was Josef Finsterer, MD, PhD, [email protected]
the family history positive for syncope, severe arrhythmias or Krankenanstalt Rudolfstiftung, Vienna, Austria
sudden cardiac death?
LVHT is frequently associated with chromosomal aberrations Sinda Zarrouk-Mahjoub, PhD
or NMDs. Did the boy undergo cytogenetic investigations to Laboratory of Biochemistry, UR Human Nutrition and
confirm a chromosomal defect or was he ever investigated by Metabolic Disorders, Faculty of Medicine, Monastir, Tunisia
a myologist to confirm or rule out NMD? When examining
the patient cardiologically, did he present with myopathic face,
References
weakness of the limb, axial or respiratory muscles, wasting, or
with fasciculations? What was the level of serum creatine kinase 1. Osmonov D, Ozcan KS, Ekmekçi A, Güngör B, Alper AT, Gürkan K.
and serum lactate? Tachycardia-induced cardiomyopathy due to repetitive monomorphic
We do not agree with the view that LVHT may develop into ventricular ectopy in association with isolated left ventricular non-
cardiomyopathy (discussion). LVHT is per se classified as an compaction. Cardiovasc J Afr 2013; 24: 1–3.
unclassified cardiomyopathy by the European and American 2. Finsterer J, Stöllberger C, Fazio G. Neuromuscular disorders in left
Cardiological Society. ventricular hypertrabeculation/noncompaction. Curr Pharm Des 2010;
A follow up of two months is very short. It would be 16: 2895–2904.
interesting to know about any long-term results. Did ventricular 3. Patil MB, Patil SM. Left-ventricular noncompaction in an infant with
arrhythmias recur? Did left ventricular dysfunction or dilatation trisomy 21. Pediatr Cardiol 2013; 34: 722–724.
of the cardiac cavities re-emerge? 4. Finsterer J, Stöllberger C. Toxoplasmosis or left ventricular hypertra-
Overall, it would be helpful to receive more detailed beculation/non-compaction. J Med Life 2012; 5: 258–259.
information about the affected patient and his relatives to 5. Finsterer J, Stöllberger C, Blazek G, Sehnal E. Familal left ventricular
assess whether LVHT was associated with hereditary disease hypertrabeculation (noncompaction) is myopathic. Int J Cardiol 2013;
or not. Long-term data would help to assess whether the 164: 312–317.
