Ponad 7000 publikacji medycznych!
Statystyki za 2021 rok:
odsłony: 8 805 378
Artykuły w Czytelni Medycznej o SARS-CoV-2/Covid-19

Poniżej zamieściliśmy fragment artykułu. Informacja nt. dostępu do pełnej treści artykułu
© Borgis - Postępy Nauk Medycznych 10/2013, s. 667-672
Maria Maliszewska1, *Urszula Fiszer1, Witold Palasik1, Michał Morton1, Wiesław Tadeusiak2
Podwyższony poziom troponiny I – czynnik złego rokowania w udarach niedokrwiennych mózgu
Elevated troponin I level – a predictor of poor prognosis after ischemic stroke**
1Department of Neurology and Epileptology, Medical Centre of Postgraduate Education, Warszawa
Head of Department: prof. Urszula Fiszer, MD, PhD
2Department of Anaesthesiology and Intensive Therapy, Medical Centre of Postgraduate Education, Warszawa
Head of Department: A.i. Małgorzata Malec-Milewska, MD, PhD
Wstęp. W ostrej fazie udaru niedokrwiennego mózgu (UNM) obserwuje się liczne zaburzenia kardiologiczne, przede wszystkim w zapisie krzywej EKG. Dodatkowym czynnikiem ryzyka wystąpienia zaburzeń kardiologicznych jest udar w obrębie prawej wyspy. Monitorowanie zapisu EKG oraz kontrola poziomu troponiny I (cTnI) mogą być pomocne w rozpoznawaniu tych zaburzeń.
Cel pracy. Celem tej pracy było ustalenie, czy podwyższone stężenie cTnI wpływa na przeżycie i prognozę u pacjentów z UNM, ustalenie czynników predysponujących do jego wzrostu oraz określenie korelacji pomiędzy lokalizacją udaru a wzrostem stężenia cTnI.
Materiał i metody. Przy przyjęciu u pacjentów z UNM oznaczano stężenie cTnI, wykonywano badanie tomografii komputerowej głowy i badanie EKG z 12 odprowadzeniami. Po miesiącu i sześciu miesiącach od UNM badano ponownie chorego i/lub rejestrowano zgon.
Wyniki. Pacjenci z podwyższonym stężeniem cTnI mieli 2,22-krotnie (95% CI 1,14-4,34; p < 0,019) i 2,33-krotnie (95% CI 1,37-3,96; p < 0,002) odpowiednio wyższe ryzyko zgonu w ciągu 30 i 180 dni. Niezależnymi czynnikami ryzyka wpływającymi na wzrost stężenia cTnI były: zaburzenia repolaryzacji (OR = 3,49; 95% CI 1,08-11,28; p < 0,037), dodatkowe pobudzenia komorowe (VEB) (OR = 10,12; 95% CI 1,57-65,03; p < 0,015), wzrost stężenia glukozy (OR = 7,38; 95% CI 2,07-26,37; p < 0,002), ognisko udaru w zakresie prawej tętnicy środkowej mózgu (MCA) (OR = 6,60; 95% CI 1,90-22,93; p < 0,003) i wzrost stężenia białka ostrej fazy (CRP) (OR = 5,90; 95% CI 1,89-18,45; p < 0,002).
Wnioski. U pacjentów z UNM występuje istotny wzrost ryzyka pojawienia się zaburzeń kardiologicznych. W identyfikacji tych pacjentów pomóc może pomiar stężenia cTn.
Introduction. Multiple ECG abnormalities can be observed during the acute phase of ischemic stroke (IS). Right-hemisphere stroke with insular involvement is also a risk factor for cardiac complications. ECG monitoring and levels of cardiac-specific troponin (cTn) may help to identify these disorders.
Aim. The aim of this study was to evaluate the influence of elevated concentrations of cTnI on survival and prognosis in patients with IS to identify factors predisposing to cTnI elevation and to determine whether stroke location and elevated cTnI concentration were correlated.
Material and methods. The cTnI concentration, CT imaging study and a standard 12-lead ECG were performed on admission in patients with IS. At one and six months after IS, the neurological status was re-evaluated or the death of the patient was registered.
Results. Patients with elevated cTnI concentrations had 2.22-fold (95% CI 1.14-4.34; p < 0.019) and 2.33-fold (95% CI on 1.37-3.96; p < 0.002) higher 30- and 180-day mortality risk, respectively. Other independent prognostic factors influencing elevated cTnI concentration were: repolarization abnormalities (OR = 3.49; 95% CI 1.08-11.28; p < 0.037). Ventricular ectopic beats (VEB) (OR = 10.12; 95% CI 1.57-65.03; p < 0.015), increased glucose level (OR = 7.38; 95% CI 2.07-26.37; p < 0.002), lesion in the right MCA perfusion territory (OR = 6.60; 95% CI 1.90-22.93; p < 0.003) and increased CRP concentration (OR = 5.90; 95% CI 1.89-18.45; p < 0.002).
Conclusion. There is a significantly increased risk of cardiac complications among patients with IS. Measurement of cTnI concentrations may improve clinical identification of at-risk patients.

Multiple electrocardiographic (ECG) abnormalities can be observed during the acute phase of ischemic stroke (IS), the most common of which are arrhythmias and repolarization abnormalities with QT interval prolongation and/or ST segment depression. These abnormalities may be transient or may indicate an existing cardiac disorder (1-4). Right-hemisphere stroke with insular involvement is an additional risk factor for cardiac complications of cerebral origin and also for sudden death during this period (5-7). Stimulation of the right insula increases blood pressure and heart rate, whereas stimulation of the left insula causes a decrease in blood pressure and bradycardia (8). Such abnormalities are often observed in patients despite the absence of any previous cardiac history and justify the necessity for ECG monitoring during the acute phase of stroke. The concentration of cardiac-specific troponin (cTn) may be helpful in identifying these disorders. It is a highly sensitive and specific marker of cardiomyocyte damage. Troponin I concentration begins to rise within the first 3 to 8 hours after the onset of chest pain, peaks at 18 to 24 hours and remains elevated for 4 to 7 days after infarction (9).
Studies that have examined the prognostic value of elevated cTn level and its association with a higher risk of death and further vascular events are of interest to cardiologists and other specialists (10-13). These studies emphasize the importance of the cTn concentration measurement to assess mortality risk in patients with internal and/or systemic diseases. The identification of mechanisms contributing to elevated cTnI concentrations in IS patients would enable the identification of patients at especially high risk for cardiac complications. As a result, appropriate treatment would be initiated earlier, resulting in a better prognosis.
The goals of this study were: to assess the influence of elevated cTnI concentration in patients with IS on the course of stroke and survival prognosis; to characterize the potential relationship between cTnI concentration and other factors influencing the course of stroke, and to identify any correlations between lesion location in the central nervous system (CNS) and elevations in cTnI concentrations following IS.
This was a hospital-based, prospective, observational, case-control study conducted at the Department of Neurology and Epileptology, Medical Centre of Postgraduate Education, Warsaw, Poland. The study was approved by the Medical Centre of Postgraduate Education Ethics Committee. Two hundred and sixty-one of acute stroke patients were consecutive admitted to the Department between March 2003 and June 2005. Inclusion criteria included: time from stroke onset less than 72 hours, age less than 85 years, stable coronary artery disease (CAD), without history of myocardial infarction (MI) in the four weeks prior to study entry. The study group consisted of 128 women (49%) and 133 men (51%) with IS who were transferred from the Emergency Room directly to the Department. The study group was divided into subgroups according to their cTnI concentration and patient death or survival. The first subgroup consisted of subjects with IS who demonstrated or did not demonstrate elevated cTnI concentrations on admission. Whereas the second subgroup consisted of patients who died or survived throughout the observation period. For each patient, the study period lasted six months starting from the onset of stroke symptoms. At one and six months after IS, the neurological status was re-evaluated or the death of the patient was registered. Patients who failed to show up for follow-up appointments were telephoned at home, and data concerning their health and course of disease were obtained. When it was otherwise impossible to obtain these data, we asked the Warsaw Registrar’s Office for help in identifying patients who died during the study period. Additional tests were carried out in accordance with the European Stroke Initiative guidelines (14). A computed tomographic (CT) imaging study was performed to confirm IS by excluding other reasons for the observed neurological deficits. A standard 12-lead ECG was also recorded routinely on admission. The cTnI concentration was measured once in a blood sample collected on admission, using the AxSYM Troponin-I and AxSYM Troponin-I ADV (starting in October 2004) tests (Abbott Laboratories). Because it was impossible to linearly convert “earlier” cTnI concentrations to “more modern” ones, two ranges were defined with the following nominal values: 0 = cTnI concentrations within the reference range for the healthy population (99th percentile) (earlier test version 0 – 0.3 ng/ml, modern version 0 – 0.04 ng/ml), 1 = cTnI concentrations above reference values (earlier test version > 0.3 ng/ml, modern version > 0.04 ng/ml).
A parametric Students t-test for independent groups and its nonparametric counterpart, the U-test, were used to determine the significance of the differences between variables in the groups analyzed. A chi-square test with Yates’ correction and Fisher’s exact test for counts less than five were employed to demonstrate a relationship between studied variables. A chi-square Mantel-Haenszel test was applied to analyze the mutual influence of given variables in separate subgroups for several independent two-way tables (2 x 2). A Kaplan-Meier method and log-rank test were employed to analyze the survival time. Multivariate logistic regression analysis using Enter and Forward stepwise Wald modeling was applied to determine the influence of selected independent factors on the prevalence of elevated cTnI concentration. A nonparametric Cox proportional hazard model using the Forward stepwise Wald method was employed to determine the influence of analyzed factors on increased prediction of mortality during the first 30 and 180 days after onset of IS symptoms. The results were assumed to be reliable at a significance level α < 0.05. Statistical analyses were performed using the SPSS version 11.5 (SPSS Inc.).
Sixty-seven patients (25.7%) died during the six-month observation period. Early mortality (< 30 days) occurred in 42 cases (16.1%). Elevated cTnI concentration on admission was observed in 16.5% (43/261) of the patients included in the study and in 28.4% (19/67) of the patients who died during the observation period (p < 0.002) (U-test). An elevated cTnI on admission was observed regardless of the length of the survival period i.e. either < 30 days (p < 0.021) or > 30 days after IS (p < 0.002) (U-test). The most common locations for the ischemic lesion were the right (42%, 73/174) and left (33.3%, 58/174) middle cerebral artery (MCA) territories. There was a significant difference between groups with respect to frequency of lesion location in the right MCA territory. This lesion location was observed in 35.1% (46) of patients who survived throughout and 62.8% (26) of patients who died during the study period (p < 0.001) (U-test). The features of cerebral edema in the CT scan taken on admission to hospital in 19.4% (50) patients with IS but in 28.8% (19) of those who died and in 16.1% (31) patients who survived were present (p < 0.025) (U-test). No abnormalities on 12-lead ECG were observed in 27.2% (72) of patients with IS. On ECG, the frequency of abnormalities was significantly different between groups (heart rate [HR] > 100/min and features of previous MI). The prevalence of features of acute MI, HR < 50/min and repolarization abnormalities trended towards significance (U-test) (tab. 1).
Table 1. Prevalence of certain ECG abnormalities in patients with ischemic stroke who survived or died during the observation period.
ECG abnormality% (n) of patients who lived through the study period% (n) of patients who died during the study periodp-value
HR < 50/min12.9% (25)4.5% (3)< 0.056
HR > 100/min3.1% (6)11.9% (8)< 0.006
AF 21.1% (41)26.9% (18)ns
Features of acute infarction1.5% (3)6.0% (4)< 0.054
Features of previous infarction31.4% (61)14.9% (10)< 0.009
Repolarization abnormalities27.8% (54)40.3% (27)< 0.058
SVEB 4.6% (9)4.5% (3)ns
VEB 9.3% (18)7.5% (5)ns
LBBB 7.7% (15)10.4% (7)ns
RBBB 7.2% (14)ns
A-V I° block 4.1% (8)7.5% (5)ns
HR – Heart Rate; AF – Atrial Fibrillation; SVEB – Supraventricular Ectopic Beats; VEB – Ventricular Ectopic Beats; LBBB – Left Bundle- -Branch Block; RBBB – Right Bundle-Branch Block; A-V I° block – Atrioventricular Block first degree

Powyżej zamieściliśmy fragment artykułu, do którego możesz uzyskać pełny dostęp.
Mam kod dostępu
  • Aby uzyskać płatny dostęp do pełnej treści powyższego artykułu albo wszystkich artykułów (w zależności od wybranej opcji), należy wprowadzić kod.
  • Wprowadzając kod, akceptują Państwo treść Regulaminu oraz potwierdzają zapoznanie się z nim.
  • Aby kupić kod proszę skorzystać z jednej z poniższych opcji.

Opcja #1


  • dostęp do tego artykułu
  • dostęp na 7 dni

uzyskany kod musi być wprowadzony na stronie artykułu, do którego został wykupiony

Opcja #2


  • dostęp do tego i pozostałych ponad 7000 artykułów
  • dostęp na 30 dni
  • najpopularniejsza opcja

Opcja #3


  • dostęp do tego i pozostałych ponad 7000 artykułów
  • dostęp na 90 dni
  • oszczędzasz 28 zł
1. Berrior S, Amarenco P: Anomalies electrocardiographiques a la phase aigue de l’infarctus cerebral. Sang Thromb Vaiss 2001; 13: 224-230.
2. Kopelnik A, Zaroff JG: Neurocardiogenic injury in neurovascular disorders. Crit Care Clin 2006; 22: 733-752.
3. Oppenheimer SM: Neurogenic cardiac effects of cerebrovascular disease. Curr Opin Neurol 1994; 7: 20-24.
4. Tatschl C, Stollberger C, Matz K et al.: Insular involvement is associated with QT prolongation: ECG abnormalities in patients with acute stroke. Cerebrovasc Dis 2006; 21: 47-53.
5. Abboud H, Berroir S, Labreuche J et al.: Insular involvement in brain infarction increases risk for cardiac arrhythmia and death. Ann Neurol 2006; 59: 691-699.
6. Cheung RT, Hachinski V: The insula and cerebrogenic sudden death. Arch Neurol 2000; 57: 1685-1688.
7. Tokgozoglu SL, Batur MK, Topuoglu MA et al.: Effects of stroke localization on cardiac autonomic balance and sudden death. Stroke 1999; 30: 1307-1311.
8. Sander D, Klingelhofer J: Stroke-associated pathological sympathetic activation related to size infarction and extent of insular damage. Cerebrovasc Dis 1995; 5: 381-385.
9. Bodor GS: Cardiac troponin-I: A highly specific marker for myocardial infarction. J Clin Immunoassay 1994; 17: 40-44.
10. Heidenreich PA, Alloggiamento T, Melsop K et al.: The prognostic value of troponin in patients with non-ST elevation acute coronary syndromes: a meta-analysis. J Am Coll Cardiol 2001; 38: 478-485.
11. Hudson MP, O’Connor CM, Gattis W et al.: Implications of elevated cardiac troponin T in ambulatory patients with heart failure: a prospective analysis. Am Heart J 2004; 147: 546-552.
12. Ammann P, Maggiorini M, Bertel O et al.: Troponin as a risk factor for mortality in critically ill patients without acute coronary syndromes. J Am Coll Cardiol 2003; 41: 2004-2009.
13. Mehta NJ, Khan IA, Gupta V et al.: Cardiac troponin I predicts myocardial dysfunction and adverse outcome in septic shock. Int J Cardiol 2004; 95: 13-17.
14. European Stroke Initiative Executive Committee, EUSI Writing Committee, Olsen TS, Langhorne P, Diener HC et al.: European Stroke Initiative Executive Committee Recommendations for Stroke Management-update 2003. Cerebrovasc Dis 2003; 16: 311-337.
15. Barber M, Morton JJ Macfarlane PW et al.: Elevated troponin levels are associated with sympathoadrenal activation in acute ischaemic stroke. Cerebrovasc Dis 2007; 23: 260-266.
16. Ghali J, Allison D, Kleinig T et al.: Elevated serum concentrations of troponin T in acute stroke: what do they mean? J Clin Neurosci 2010; 17: 69-73.
17. Etgen T, Baum H, Sander K et al.: Cardiac troponins and N-terminal pro-brain natriuretic peptide in acute ischemic stroke do not relate to clinical prognosis. Stroke 2005; 36: 270-275.
18. James P, Ellis CJ, Whitlock RML et al.: Relation between troponin T concentration and mortality in patients presenting with an acute stroke: observational study. BMJ 2000; 320: 1502-1504.
19. Gilmore RM, Bhagra A, Stead LG: Serum troponin as a predictor of mortality after acute ischemic stroke. Acad Emerg Med 2005; 12 (suppl. 1): 169.
20. Di Angelantonio E, Fiorelli M, Toni D et al.: Prognostic significance of admission levels of troponin I in patients with acute ischaemic stroke. J Neurol Neurosurg Psychiatry 2005; 76: 76-81.
21. Christensen H, Johannesen HH, Christensen AF et al.: Serum cardiac troponin I in acute stroke is related to serum cortisol and TNF-alpha. Cerebrovasc Dis 2004; 18: 194-199.
22. Fure B, Bruun Wyller T, Thommessen B: Electrocardiographic and troponin T changes in acute ischaemic stroke. J Intern Med 2006; 259: 592-597.
23. Jensen JK, Kristensen SR, Bak S et al.: Frequency and significance of troponin T elevation in acute ischemic stroke. Am J Cardiol 2007; 99: 102-108.
24. Kerr G, Ray G, Wu O et al.: Elevated troponin after stroke: a systematic review. Cerebrovasc Dis 2009; 28: 220-226.
25. Ay H, Koroshetz WJ, Benner T et al.: Neuroanatomic correlates of stroke-related myocardial injury. Neurology 2006; 66: 1325-1329.
26. Song HS, Back JH, Jin D et al.: Cardiac troponin T elevation after stroke: relationships between elevated serum troponin T, stroke location, and prognosis. J Clin Neurol 2008; 4: 75-83.
27. Baumgart D, Heusch G: Neuronal control of coronary blood flow. Basic Res Cardiol 1995; 90: 142-159.
28. Christensen H, Boysen G, Christensen AF: Insular lesions, ECG abnormalities, and outcome in acute stroke. J Neurol Neurosurg Psychiatry 2005; 76: 269-271.
29. Christensen H, Christensen AF, Boysen G: Abnormalities on ECG and telemetry predict stroke outcome at 3 months. J Neurol Sci 2005; 234: 99-103.
30. Apak I, Iltumur K, Tamam Y et al.: Serum cardiac troponin T levels as an indicator of myocardial injury in ischemic and hemorrhagic stroke patients. Tohoku J Exp Med 2005; 205: 93-101.
31. Iltumur K, Yavavli A, Apak I et al.: Elevated plasma N-terminal pro-brain natriuretic peptide levels in acute ischemic stroke. Am Heart J 2006; 151: 1115-1122.
32. Trooyen M, Indredavik B, Rossvoll O et al.: Myocardial injury in acute stroke assessed by troponin I. Tidsskr Nor Laegeforen 2001; 121: 421-415.
33. Kennon S, Barakat K, Hitman GA et al.: Angiotensin-converting enzyme inhibition is associated with reduced troponin release in non-ST-elevation acute coronary syndromes. J Am Coll Cardiol 2001; 38: 724-728.
34. Schechter M, Merz NB, Paul-Labrador MJ et al.: Blood glucose and platelet-dependent thrombosis in patients with coronary artery disease. J Am Coll Cardiol 2000; 35: 300-307.
35. Allport LE, Butcher KS, Baird TA et al.: Insular cortical ischemia is independently associated with acute stress hyperglycemia. Stroke 2004; 35: 1886-1891.
otrzymano: 2013-07-17
zaakceptowano do druku: 2013-09-04

Adres do korespondencji:
*Urszula Fiszer
Department of Neurology and Epileptology
Medical Centre of Postgraduate Education
ul. Czerniakowska 231, 00-416 Warszawa
tel.: +48 (22) 629-43-49; fax: +48 (22) 584-13-06
e-mail: kl.neurologii@szpital-orlowskiego.pl

Postępy Nauk Medycznych 10/2013
Strona internetowa czasopisma Postępy Nauk Medycznych