FREQUENCY OF QTc PROLONGATION IN PATIENTS WITH HEMORRHAGIC STROKE

Authors

  • Sarwar Malik
  • Rukhsana Abdul Sattar
  • Shahnaz Shah
  • Hisala Rehman
  • Tahira Tahira
  • Muhammad Ali Ismail

Abstract

Jinnah Postgraduate Medical Centre, Karachi, PakistanBackground: Acute cerebral events play an important role in generating autonomic imbalance especially cardiac rhythm disturbances. This forms the basis of significant lethal abnormalities of heart rate and rhythm like QTc prolongation, ventricular fibrillation, asystole, and ultimately death. This study was conducted to determine the frequency of QTc prolongation in patients presenting with acute haemorrhagic stroke at a tertiary care hospital. Methods: This descriptive case series was conducted at Medical Unit-I, ward-5, Jinnah Postgraduate Medical Centre (JPMC), Karachi, from 13 October, 2009 to 12 April, 2010. Patients of either gender and age >18 years who presented within 48 hours of onset of acute hemorrhagic stroke for the first time, confirmed by computerized tomography (CT) scan of brain were included. A 12 lead electrocardiogram (ECG) was performed. Lead III and VI were used for this due to their importance in this aspect. QTc was then calculated by using Bazetts formula. Data was analysed using SPSS-12. Results: Among 95 patients of acute haemorrhagic stroke, 48 (50.5%) had prolonged QTc in lead III, 47 (49.5%) had prolonged QTc in lead VI. The average QTc interval in lead III was 440.4±45.2 (Range=364–571). Proportion of prolonged QTc in lead III was higher in males than females. Frequency of QTc III prolongation was higher in comparatively younger age groups than older age groups. Conclusion: The frequency of prolonged QTc interval among patients of acute hemorrhagic stroke is alarmingly higher in our setup. Prolonged QTc is a useful predictor of impending clinical deterioration and provide an opportunity for early intervention to reduce severe loss like mortality.Keywords: Haemorrhagic stroke, QTc prolongation

References

Warlow C, Gijn J, Dennis M. Stroke: practical management. New Eng J Med 2008;359:1188–9.

World Health Organization. Preventing chronic diseases: a vital investment. Geneva: World Health Organization, 2005.

Alam I, Haider I, Wahab F, Khan W, Taqweem MA, Nowsherwan. Risk factors stratification in 100 patients of acute stroke. J Postgrad Med Inst 2004;18:583–91.

Saleheen D, Bukhari S, Haider SR, Nazir A, Khanum S, Shafqat S, et al. Association of Phosphodiesterase 4D gene with ischemic stroke in a Pakistani population. Stroke 2005;36:2275–7.

Shafqat S. Clinical practice guidelines for the management of ischemic stroke in Pakistan. J Pak Med Assoc 2003;53:600–2.

Hacke W, Donnan G, Fieschi C, Kaste N, von Kummer R, Broderick JP, et al. Association of outcome with early stroke treatment: pooled analysis of ATLANTIS, ECASS, and NINDS rt-PA stroke trials. Lancet 2004;363:768–74.

Lai SM, Studenski S, Duncan PW, Perera S. Persisting consequences of stroke measured by the stroke impact scale. Stroke 2002;33:1840–4.

Aminoff MJ. Nervous system disorders. Current medical diagnosis and treatment. 49th ed. USA: Mc Graw Hill; 2010.

Colivicchi F, Bassi A, Santini M, Caltagirone C. Prognostic implication of right sided insular damage, cardiac autonomic derangement, and arrhythmias after acute ischemic stroke. Stroke 2005;36:1710–5.

Fure B, Wyller TB, Thommessen B. Electrocardiographic and troponin T changes an acute ischemic stroke. J Intern Med 2006;259:592–7.

Akbar MA, Awan MM, Taseer I, Qureshi A, Chaudhary GM. Electrocardiographic predictors of mortality in acute stroke. Pak J Med Res 2007;46(1):15–9.

Calder K. QTc dispersion in intracerebral hemorrhage. Am J Emerg Med 2005;23:98.

Colkesen AY, Sen O, Giray S, Acil T, Ozin B, Muderrisoglu H. Correlation between QTc interval and clinical severity of subarachnoid hemorrhage depends on QTc formula used. Pacing Clin Electrophysiol 2007;30(12):1482–6.

Akbar MA, Haider SA, Awan MM, Chaudhary GM. Electrocardiographic changes in acute stroke. Professional Med J 2008;15(1):91–5.

Huang CH, Chen WJ, Chang WT, Yip PK, Lee YT. QTc dispersion as a prognostic factor in intracerebral haemorrhage. Am J Emerg Med 2004;22(3):141–4.

Cook NL, Kleinig TJ, Heuvel CVD, Vink R. Reference genes for normalising gene expression data in collagenase-induced rat intracerebral haemorrhage. BMC Mol Biol 2010;11:7.

Sakr YL, Lim N, Amaral ACKB, Ghosn I, Carvalho FB, Renard M, et al. Relation of ECG changes to neurological outcome in patients with aneurysmal subarachnoid hemorrhage. Int J Cardiol 2004;96:369–73.

Bergh WMVD, Algra A, Rinkel GJ. Electrocardiographic abnormalities and serum magnesium in patients with subarachnoid hemorrhage. Stroke 2004;35:644–8.

Maramattom BY, Manno EM, Fulghsm JR, Jaffe AS, Wijdicks EF. Clinical importance of cardiac troponin release and cardiac abnormalities in patients with supratentorial cerebral hemorrhages. Mayo Clin Proc 2006;81(2):192–6.

Schuiling WJ, Algra, A, de Weerd AW, Leemans P, Rinkel CJ. ECG abnormalities in predicting secondary cerebral ischemia after subarachnoid haemorrhage. Acta Neurochir (Wien) 2006;148:853–8.

Kawasaki T, Azuma A, Sawada T, Sugihara H, Kuribayashi T, Satoh M, et al. Electrocardiographic score as a predictor of mortality after subarachnoid haemorrhage. Circ J 2002;66:567–70.

Fukui S, Katoh H, Tsuzuki N, Ishihara S, Otani N, Ooigawa H. et al. Multivariate analysis of risk factors for QT prolongation following subarachnoid hemorrhage. Crit Care 2003;7:R7–R12.

Randell T, Tanskanen P, Scheinin M, Kytta J, Ohman J, Lindgren L. QT dispersion after subarachnoid hemorrhage. J Neurosurg Anesthesiol 1999;11:163–6.

Lanzino G, Kongable GL, Kassell NF. Electrocardiographic abnormalities after nontraumatic subarachnoid hemorrhage. J Neurosurg Anesthesiol 1994;6:156–62

Published

2013-07-01

Issue

Vol. 25 No. 3-4 (2013): JOURNAL OF AYUB MEDICAL COLLEGE, ABBOTTABAD

Section

ORIGINAL ARTICLE

License

Journal of Ayub Medical College, Abbottabad is an OPEN ACCESS JOURNAL which means that all content is FREELY available without charge to all users whether registered with the journal or not. The work published by J Ayub Med Coll Abbottabad is licensed and distributed under the creative commons License  CC BY ND Attribution-NoDerivs. Material printed in this journal is OPEN to access, and are FREE for use in academic and research work with proper citation. J Ayub Med Coll Abbottabad accepts only original material for publication with the understanding that except for abstracts, no part of the data has been published or will be submitted for publication elsewhere before appearing in J Ayub Med Coll Abbottabad. The Editorial Board of J Ayub Med Coll Abbottabad makes every effort to ensure the accuracy and authenticity of material printed in J Ayub Med Coll Abbottabad. However, conclusions and statements expressed are views of the authors and do not reflect the opinion/policy of J Ayub Med Coll Abbottabad or the Editorial Board.

USERS are allowed to read, download, copy, distribute, print, search, or link to the full texts of the articles, or use them for any other lawful purpose, without asking prior permission from the publisher or the author. This is in accordance with the BOAI definition of open access.

AUTHORS retain the rights of free downloading/unlimited e-print of full text and sharing/disseminating the article without any restriction, by any means including twitter, scholarly collaboration networks such as ResearchGate, Academia.eu, and social media sites such as Twitter, LinkedIn, Google Scholar and any other professional or academic networking site.