Gülhan SARIÇAM, Oğuzhan KURŞUN, Şerefnur ÖZTÜRK

İntraserebral hematomlu hastalarda kardiyak etkilenme ve prognoza etkisi

Amaç: Serebrovasküler hastalıkların kardiyak fonksiyonlar üzerine negatif etkileri olduğu bilinmektedir. Ek olarak, inme kliniğinde uzun dönem izlemde en sık ve en önemli ölüm nedeni kardiyak disfonksiyondur. Bu çalışmanın amacı hemorajik inmeli hastalarda kardiyak enzim ve inflamasyon belirteçlerinin değişimini incelemek ve bu belirteçlerin inme prognozuna etklerini araştırmaktır. Materyal ve Metot: Bu çalışmaya intraserebral hematom (ISH) tanısı ile yatırılan ve hastalığın başlangıcının ilk 24 saati içinde olan 53 hasta ile 48 kontrol dahil edildi. Her iki grubun da 1., 5. ve 10. gün kreatinin kinaz (CK), kreatinin kinaz myokardiyal band (CKMB), troponin-I (Trop-I), C reaktif protein (CRP) ve lökosit değerleri incelendi.Bulgular: Çalışmaya dâhil edilen 53 hasta ile 48 kontrol grubu arasında yaş açısından anlamlı farklılık tespit edilmedi (P=0.062). 1.gün CK, CRP ve lökosit değerleri ile 5. ve 10 gün CRP ve lökosit değerleri, ISH grubunda kontrol grubuna göre anlamlı olarak daha yüksek idi. Bununla beraber, ISH grubunda CK-MB ve troponin değerlerinin giderek azaldığı, CRP değerlerinin ise giderek arttığı tespit edildi. 53 kişilik hasta grubunun 13 tanesi takipte exitus oldu. Yaşayan hastalar ile karşılaştırıldığında, exitus olan hastalarda 1. gün CK, CRP ve lökosit, 5. gün CK, CK-MB ve CRP ile 10. gün CK, CK-MB ve troponin değerleri anlamlı olarak daha yüksek idi. Sonuç: Çalışmamızda, intraserebral hematom tanılı hastalarda CK-MB ve troponin değerlerinde 1.günden itibaren bir azalma olduğunu, CRP değerlerinde ise 1. günden itibaren bir artma olduğunu tespit ettik. Ek olarak, exitus olan hastalarda kardiyak enzim ve inflamatuvar belirteçlerin daha yüksek olduğunu tespit ettik. Dolayısıyla hemorajik inmeli hastalarda myokardiyal hasarın ve inflamasyonun erken dönemde tanınmasının, morbidite ve mortaliteyi büyük ölçüde azaltabileceğini düşünüyoruz.

Anahtar Kelimeler:

Kreatin kinaz, kreatin kinaz miyokardiyal band, C-reaktif protein

Cardiac impairment and its effect on prognosis in patients with intracerebral hematoma

Background: Cerebrovascular diseases are known to have negative effects on cardiac functions. In addition, cardiac dysfunction is the most common and most important cause of death in the stroke clinic during long-term follow-up. The aim of this study was to investigate the changes in cardiac enzyme and inflammation markers in patients with hemorrhagic stroke and to investigate the effects of these markers on stroke prognosis.Methods: This study included 53 patients and 48 controls who were hospitalized for intracerebral hematoma (ICH) and were within the first 24 hours of the onset of the disease. Creatinine kinase (CK), creatinine kinase myocardial band (CKMB), troponin-I (Trop-I), C-reactive protein (CRP) and leukocyte values of both groups were evaluated on the 1st, 5th and 10th days.Results: There were no significant differences in age between 53 patients and 48 control groups (68.50 ± 10.22 versus 71.70 ± 6.02, P = 0.062). CK, CRP and leukocyte values on day 1 and CRP and leukocyte values on day 5 and 10 were significantly higher in the ICH group than in the control group. However, CK-MB and Troponin levels decreased and CRP values increased gradually in ICH group. Thirteen patients of 53 patients died during follow-up. Compared with the surviving patients, CK, CRP and leukocytes on day 1, CK, CK-MB and CRP on day 5 and CK, CK-MB and Troponin on day 10 were significantly higher in patients with exitus. Conclusions: In our study, we found a decrease in CK-MB and troponin values from day 1 and an increase in CRP values from day 1 in patients with intracerebral hematoma. In addition, we found that cardiac enzymes and inflammatory markers were higher in patients with exitus. Therefore, we believe that early recognition of myocardial damage and inflammation in hemorrhagic stroke patients may significantly reduce morbidity and mortality.

Keywords:

Creatine kinase, creatine kinase myocardial band,

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1. Albertson M, Sharma J. Stroke: current concepts. S D Med. 2014;11(67):455-465.
2.Liu Q, Ding Y, Yan P, Zhang JH, Lei H. Electrocardiographic abnormalities in patients with intracerebral hemorrhage. Acta Neurochir Suppl. 2011;111:353-6.
3. Arab D, Yahia AM, Qureshi AI. Cardiovascular manifestations of acute intracranial lesions: pathophysiology, manifestations, and treatment. J Intensive Care Med. 2003;3(18):119-29.
4. Hays A, Diringer MN. Elevated troponin levels are associated with higher mortality following intracerebral hemorrhage. Neurology. 2006; 9(66):1330-4
5. Apak I, Iltumur K, Tamam Y, Kaya N. Serum cardiac troponin T levels as an indicator of myocardial injury in ischemic and hemorrhagic stroke patients. Tohoku J Exp Med. 2005;2(205): 93-101.
6. Michael J. Aminof. Manifestations of Acute Neurologial Lesions. Neurology And General Medicine 4th Edition; 2007.
7.Liang XM, Chen J, Zhang T, Liu J, Jiang XJ, Xu ZQ. Cerebral hemorrhage increases plasma concentrations of noradrenalin and creatine kinase MB fraction with induction of cardiomyocyte damage in rats. Cell Biochem Biophys. 2014;3(70):1807-11.
8.Maramattom BV, Manno EM, Fulgham JR, Jaffe AS, Wijdicks EF. Clinical importance of cardiac troponin release and cardiac abnormalities in patients with supratentorial cerebral hemorrhages. Mayo Clin Proc. 2006;2(81):192-6
9. Tobias SL, Bookatz BJ, Diamond TH. Myocardial damage and electrocardiographic cahanges in acute cerebrovascular hemorrhage; A report of three cases and review. Heart Lung 1987;16(5):521-526
10.Wıllıam P. Cheshıre, Jr, Clıfford BS. The insular cortex and cardiac response to stroke: Neurology . 2006;3(66):1296-1297
11. Wybraniec M, Mizia-Stec K, Krzych L. Stress cardiomyopathy: yet another type of neurocardiogenic injury: 'stress cardiomyopathy'.Cardiovasc Pathol. 2014;3(23):113-20.
12. Dziedzic T. Clinical Significance of Acute Phase Reaction in Stroke Patients. Front Biosci. 2008;1(13):2922-7
13.Ay H, Arsava EM, Sarıbaş O. Creatine Kinase-MB Elevation After Stroke is not Cardiac in Origin: Stroke 2002;1(33):286-289
14. Collinson PO, Stubbs PJ, Kessler AC. Multicentre Evaluation Of Routine Immunoassay Of Troponin T Study. Multicentre evaluation of the diagnostic value of cardiac troponin T, CK-MB mass, and myoglobin for assessing patients with suspected acute coronary syndromes in routine clinical practice. Heart. 2003;3(89):280-6.
15.Norris JW, Hachinski VC, Myers MG, Callow J. Serum cardiac enzymes in stroke. Stroke. 1979; 5(10):548-53
16.Lang K, Borner A, Figulla HR. Comparision of biochemical markers fort he detection of minimal myocardial injury: superior sensitivity of cardiac troponin t elisa. J İntern Med 2000;247:119-123
17. Garrett MC, Komotar RJ, Starke RM, Doshi D, Otten ML, Connolly ES. Elevated troponin levels are predictive of mortality in surgical intracerebral hemorrhage patients. Neurocrit Care. 2010;2(12):199-203.
18. Xu M, Lin J, Wang D, Liu M, Hao Z, Lei C. Cardiac troponin and cerebral herniation in acute intracerebral hemorrhage. Brain Behav.2017;7(6):e00697.
19. Morotti A, Phuah CL, Anderson CD, Jessel MJ, Schwab K, Ayres AM, et al. Leukocyte Count and Intracerebral Hemorrhage Expansion. Stroke. 2016;47(6):1473-8.
20.Hjalmarsson C, Bergfeldt L, Bokemark L, Manhem K, Andersson B. Electrocardiographic abnormalities and elevated cTNT at admission for intracerebral hemorrhage: predictors for survival? Ann Noninvasive Electrocardiol. 2013;5(18):441-9.
21. Katsanos AH, Korantzopoulos P, Tsivgoulis G, Kyritsis AP, Kosmidou M, Giannopoulos S.Electrocardiographic abnormalities and cardiac arrhythmias in structural brain lesions. nt J Cardiol. 2013;2(167):328-34.