Infarction Research Articles

Effects of individualized antiplatelet therapy based on CYP2C19 genotype and platelet function on the prognosis of patients after PCI.

To evaluate the effect of individualized antiplatelet therapy based on CYP2C19 genotype and platelet function on the prognosis of patients after percutaneous coronary intervention (PCI) compared with conventional antiplatelet therapy. Patients diagnosed with acute coronary syndromes (ACS) in Shandong Provincial Qianfoshan Hospital from December 2014 to December 2017 were included in this prospective study and randomly divided into conventional (CA) and individualized antiplatelet therapy group (IA) at 1:1 ratio. Patients in the CA group received clopidogrel 75 mg once a day (QD). Group IA was divided into extensive, intermediate, and poor metabolizers according to the results of the CYP2C19 gene test. Three genotypes were given clopidogrel 75 mg QD, 75 mg twice daily (BID) and ticagrelor 90 mg BID respectively. After taking these medicines for a period of time, platelet function was monitored by thromboelastography (TEG) and MAADP values were recorded. MAADP indicates the adenosine diphosphate (ADP) induced platelet function that not inhibited by medicine. High platelet reactivity (HPR) was defined as MAADP > 47mm, indicating a high risk of thrombus, and MAADP ≤ 31 mm indicates a high risk of hemorrhage. For extensive metabolizers (EMs) and intermediate metabolizers (IMs) patients with HPR, the antiplatelet therapy would be changed by the clinician according to the patient's conditions. Major adverse cardiovascular events (MACE) and hemorrhage events were monitored during 1-year follow-up. The patients with MAADP > 47 mm were 89 (28.6%) in the IA group. There were 50 EMs patients with MAADP > 47 mm (33.3%). Of which, there were 2 cases which changed the dosage of clopidogrel to 75 mg BID, 14 cases who changed clopidogrel to ticagrelor. There were 36 IMs patients with MAADP > 47 mm (30.8%). Of which, there were 19 cases who changed clopidogrel to ticagrelor. There was no significant difference in the value of MAADP between EMs and IMs patients. Within 1 year after PCI, the occurrence of MACE in the IA group was significantly lower than that in the CA group (p=0.010). (1) Patients with a CYP2C19 loss-of-function (LOF) gene who take double doses of clopidogrel overcome the decreased efficacy of clopidogrel which partly due to CYP2C19 LOF gene, without increasing the risk of hemorrhage. (2) Individualized antiplatelet therapy based on CYP2C19 genotype and platelet function can significantly reduce the occurrence of MACE (mainly acute non-fatal myocardial infarction) after PCI without increasing the risk of moderate or severe hemorrhage.

Vom Oesophaguskarzinom zum Hirninfarkt

Vom Oesophaguskarzinom zum Hirninfarkt

Acute ST-segment Elevation Myocardial Infarction in Argentina. Data from the continuous ARGEN-IAM-ST registry

Introduccion: A traves del Registro Nacional de Infarto Agudo de Miocardio (IAM) con Elevacion del ST (ARGEN IAM-ST) realizadoen 2015 se conocieron datos de la realidad del IAM en Argentina; en esta ocasion, se presenta un reporte actual.Material y metodos: Estudio prospectivo multicentrico, con alcance nacional. Luego de la primera fase de la encuesta ARGEN-IAMST,se invito a los centros a continuar con el registro de IAM. Se incluyeron pacientes con IAM con elevacion del segmento ST en elelectrocardiograma de hasta 36 horas de evolucion.Resultados: La poblacion analizada abarco 2464 pacientes asistidos en 78 centros. La media de edad fue 60 ± 12 anos y el 80% fuede genero masculino. Los factores de riesgo prevenibles se distribuyeron del siguiente modo: tabaquismo 45%, hipertension arterial58%, diabetes 24% y dislipidemia 41%. El 11% tuvo antecedente de enfermedad coronaria. El 88% recibio reperfusion; el 21% de estospacientes recibieron tromboliticos y al 89% se le realizo angioplastia. La demora desde el inicio de los sintomas hasta la admision fuede 130 minutos (RIC 25-75: 60-305); los medicos reportaron demoras hasta el tratamiento en el 49% de los casos, con impacto en lostiempos totales de isquemia (TTI). La mortalidad intrahospitalaria fue del 8,7%. En el analisis multivariado, ser tratado en un centrocon hemodinamia no se asocio de forma independiente con la supervivencia.Conclusiones: Los datos actuales del registro continuo de IAM en la Argentina son similares a los que mostro la encuesta de 2015.Las demoras hasta el tratamiento son importantes, especialmente por el tiempo de demora en la consulta de los pacientes, lo queimpacta en gran medida en los TTI.

Reduction of Myocardial Necrosis After Glycosaminoglycan Administration: Effects of a Single Intravenous Administration of Heparin or N-Acetylheparin 2 Hours Before Regional Ischemia and Reperfusion.

BACKGROUND: We determined if a single administration of heparin or nonanticoagulant N-acetylheparin could reduce myocardial injury resulting from a 90-minute occlusion of the left circumflex coronary artery (LCX) and 6 hours of reperfusion in the anesthetized canine. METHODS AND RESULTS: Heparin (2 mg/kg), N-acetylheparin (2 mg/kg), or vehicle, 0.9% sodium chloride (control), was administered intravenously to separate groups of animals 2 hours before LCX occlusion. To ensure parity of LCX ischemia, only animals with ischemic zone regional blood flow < 0.16 mL/min/g tissue were included in the final analysis. Hemodynamics did not differ among the three study groups. Infarct size as a percentage of the left ventricular area at risk was obtained for each group. Myocardial infarct size was 43.0 +/- 3.9% in the vehicle, 28.8 +/- 5.8% in the heparin (P <.05 vs vehicle) and 24.7 +/- 4.6% (P <.05 vs vehicle) in the N-acetylheparin-treated animals. CONCLUSIONS: Pretreatment with heparin or its nonanticoagulant derivative, N-acetylheparin, provides significant protection to the regionally ischemic and reperfused canine myocardium independent of either plasma glycosaminoglycan concentration or alterations in the coagulation system.

Intervenções de emergência ao paciente com suspeita de infarto agudo do miocárdio

O Infarto Agudo do Miocárdio (IAM) representa um importante problema de saúde pública no Brasil e no mundo, apresentando altas taxas de incidência e mortalidade. Objetivou-se realizar um levantamento bibliográfico acerca das intervenções de emergência ao paciente com suspeita de infarto agudo no miocárdio. Trata-se de uma revisão integrativa da literatura, a busca ocorreu nas bases de dados: LILACS, SCIELO e BDENF, via BVS. Os artigos foram coletados no período de maio e junho de 2020. Foram utilizados os descritores: Emergência, Assistência ao paciente e Infarto agudo do miocárdio. Após a aplicação dos critérios de inclusão, restaram 10 estudos. Os indivíduos que apresentam infarto agudo no miocárdio necessitam de intervenção o mais rápido possível, sendo que os cuidados iniciais realizados, dizem respeito a procedimentos emergenciais, visando impedir que o quadro evolua para um estado mais grave, ou mesmo para o óbito. Concluiu-se que as intervenções de emergência prestadas ao paciente com suspeita de infarto são imprescindíveis para o prognóstico do paciente, e que a avaliação correta, o rápido diagnóstico e o início do tratamento adequado previnem as lesões decorrentes desse quadro clínico.

Inflammation, apoptosis and autophagy as critical players in vascular dementia.

Vascular dementia is the second-most cause of dementia, characterized by cerebral infarcts, white matter lesions, myelin loss and often amyloid angiopathy. Hence, vascular damage is a critical cause of neuronal loss and synaptic disintegration. Abnormal neuroinflammation, autophagy and apoptosis are the prerequisite factors for endothelial and neuronal cell damage. This leads to the onset and progression of cerebrovascular disorders and cognitive dysfunction. The innate immune cells, pattern recognition receptors, Toll-like receptor-4 and related inflammatory mechanisms disrupt cerebrovascular integrity via glial activation and increased pro-inflammatory interleukins and TNFα. Inflammasome polymorphisms and multi-faceted neuro-immune interactions further integrate systemic and central inflammatory pathways, which induce vascular tissue injury and neurodegeneration. Specifically, chronic cerebral hypoperfusion disrupts the self-cannibalization mechanism of autophagy via altered expression of autophagy-specific proteins, Beclin-1, LC3 and P62. The deregulated autophagy pathway causes neuronal loss, hippocampal shrinkage, and ultimate loss in synaptic plasticity. The vascular dementia models typically exhibit downregulated anti-apoptotic Bcl-2 and upregulated pro-apoptotic Bax, cleaved caspase-3, and cleaved-PARP levels in the brain, for which modulated p38 MAPK and JNK phosphorylation pathways play a vital role. Endoplasmic stress-induced apoptosis, calcium overload and glutamate excitotoxicity in combination with ASK1-MAPK signaling mechanism also contribute to the cerebrovascular pathology. Vascular injury reduces neurological scores and increases the infarct volume, DNA damage and neuronal apoptosis in ischemia/reperfusion injury. Additionally, synergistic and additive interactions between inflammasome, autophagy and apoptotic signaling pathways augment symptoms of vascular neurodegeneration. Overall, the current review enlightens the key risk factors and underlying mechanism triggering vascular dementia. The review additionally informs the challenges associated while treating vascular dysfunction, and highlights the need for targeted drugs for reducing cerebrovascular damage.

The targeted regulation of miR-26a on PTEN-PI3K/AKT signaling pathway in myocardial fibrosis after myocardial infarction.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "The targeted regulation of miR-26a on PTEN-PI3K/AKT signaling pathway in myocardial fibrosis after myocardial infarction, by S. Zhang, R. Cui, published in Eur Rev Med Pharmacol Sci 2018; 22 (2): 523-531-DOI: 10.26355/eurrev_201801_14205-PMID: 29424913" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/14205.

Clinical significance of miR-492 in peripheral blood of acute myocardial infarction.

To detect the potential of microRNA-492 (miR-492) as a diagnostic biomarker of acute myocardial infarction (AMI) in the acute phase. A total of 100 AMI patients and 100 controls (non-AMI patients with chest pain) were retrospectively analyzed. Blood samples were collected at 0, 6, 12, and 24 h after admission, followed by detection of the serum miR-492 level. Serum levels of cTnI and creatine kinase-MB (CK-MB) in AMI patients were examined by enzyme-linked immunosorbent assay (ELISA). The potential relationship between miR-492 level with cTnI and CK-MB levels was analyzed by Pearson correlation test. Moreover, diagnostic value of miR-492 was assessed by depicting receiver operating characteristic (ROC) curves. Serum level of miR-492 achieved the peak at 6 h after admission, which was time-dependently reduced at 12 h and 24 h. Serum levels of cTnI and CK-MB were higher in AMI patients than those of controls. However, miR-492 level achieved the peak before cTnI and CK-MB increased to the highest levels. MiR-492 level was positively correlated to cTnI and CK-MB levels. ROC curves verified the diagnostic value of miR-492 in AMI (AUC=0.8621, 95% CI=0.8129-0.9112, sensitivity=80%, specificity=75%). Serum level of miR-492 remarkably increases in the acute phase of AMI, which may be used as an effective biomarker for diagnosing AMI.

Oxycodone protects cardiomyocytes from ischemia-reperfusion-induced apoptosis via PI3K/Akt pathway.

Ischemia/reperfusion (I/R) cause secondary myocardial damage following a blood reflow after myocardial infarction. This study aimed to explore oxycodone as a myocardial protector after an I/R injury in rats. Oxycodone reduced myocardial infarction volume, an I/R-induced apoptosis of the cardiomyocytes, the serum levels of CK-MB and LDH. The ejection fraction and fraction shortening in the I/R rats also increased. From the molecular mechanism, it was evident that oxycodone not only decreased the expression levels of Bax, active-caspase 3 protein but also increased the expression levels of Bcl2, p-PI3K, and p-Akt protein in heart tissue of the I/R rats. In vitro, oxycodone induced anti-H9c2 cell apoptosis after hypoxia/reoxygenation (H/R). However, its ability to act as a myocardial protector deteriorated in the presence of a PI3K/Akt pathway inhibitor.

Makrovasküler Komplikasyon Gelişen Diyabetik Hastalarda Risk Faktörlerinin Değerlendirilmesi

Amaç: Biz çalışmamızda 2015-2018 yılları arasında hastanemize diyabetes mellitusun makrovasküler komplikasyonlarından olan akut miyokard infarktüsü veya serebrovasküler olay tanısı konulan hastaların risk faktörleri açısından araştırılmasını planladık. Gereç ve Yöntemler: Retrospektif olarak yapılan çalışmaya 48 diyabetes mellitus tanılı makrovasküler komplikasyon gelişen hasta alınmış iken kontrol grubu olarak da polikliniğimizden takipli makrovasküler komplikasyon gelişmemiş olan 97 diyabetik hasta çalışmaya dahil edilmiştir. Komplikasyon gelişen hastaların ve kontrol grubu hastaların son 6 ayındaki polikliniğimize olan başvurusunda laboratuar sonuçları incelenerek yaş, BMİ, açlık kan şekeri, Hba1C, MPV, RDW, PLT ve kreatinin parametrelerine göre risk faktörleri belirlenmeye çalışıldı. İstatistiksel analizler SPSS versiyon 17.0 programı ile gerçekleştirilmiştir. Değişkenlerin normal dağılıma uygunluğu histogram grafikleri ve Kolmogorov-Smirnov testi ile normal dağılım gösteren (parametrik) değişkenlerin gruplar arasında değerlendirilirken; bağımsız gruplarda T Testi, normal dağılım göstermeyenler (non parametrik) gruplar arasında değerlendirilirken Mann Whitney U Testi kullanılmıştır. Bulgular: Yaptığımız çalışma sonucunda diyabetik hastalarda makrovasküler komplikasyon gelişimi ile yaştaki artışın, HbA1c düzeyindeki progresyonun, MPV değerinin &amp;gt;11,9 ve kreatinin düzeylerinin 1.2 mg/dl dğerinin üzerinde olması durumuyla istatistiksel olarak anlamlı bir ilişki saptadık fakat cinsiyet, BMI, açlık kan şekeri, RDW ve platelet değerleri her iki grupta benzer olarak bulundu. Sonuç: Elde edilen veriler doğrultusunda diyabetik hastaların takiplerinde ileri yaş, MPV,kreatinin, Hba1c değerlerinin yakın takibinin yapılması ve bu parametrelerdeki bozulmaların makrovasküler komplikasyon gelişimi açısından bize yol gösterebileceğini düşünmekteyiz.

Splenic Infarction: Clinical Features and Associated Conditions

Splenic infarction occurs when the splenic artery or branch is occluded (i.e., thrombus). Patients with splenic infarctions classically present with

Regional Pericarditis Mimicking as ST-segment Elevation Myocardial Infarction

Acute pericarditis is common and often mimics acute coronary syndrome (ACS) in clinical as well as electrographic presentation. It is essential to differentiate between these two conditions, as treatment is different. A rare form of acute pericarditis, regional pericarditis, can be elusive, especially when it presents on EKG as an acute ST-segment elevation MI of a particular wall. We present a case of localized (regional) pericarditis in a 66-year-old female with a history of rheumatoid arthritis who presented to the emergency department with localized left-sided chest pain. Her arrival EKG showed acute anterolateral wall ST-segment elevation. The patient received diagnostic cardiac catheterization, treatment with colchicine and steroid, which produced resolution of symptoms and EKG changes.

Clinical significance of FSTL 1, Bax, Bcl-2 in acute cerebral infarction and its relationship with hemorrhagic transformation.

Acute cerebral infarction (ACI) is the most common type of acute cerebrovascular disease so far, and its incidence rate has been increasing in recent years. At present, the methods of diagnosing ACI in clinic are extremely complicated, and an effective index that can effectively diagnose ACI is urgently needed in clinic. This study is designed to investigate the clinical significance of Follistatin-like protein 1 (FSTL1), Bax and Bcl-2 in ACI. A total of 84 cases of ACI patients admitted to our hospital from September 2017 to September 2019 and 90 cases of healthy subjects undergoing physical examination at the same time were selected as the research objects for prospective analysis. The concentrations of FSTL1, Bax and Bcl-2 in the peripheral blood of objects in the two groups were detected to analyze the diagnostic value of FSTL1, Bax and Bcl-2 for ACI, and the correlation of FSTL 1, Bax and Bcl-2 with the infarct size, treatment method and hemorrhagic transformation. Another 20 SD rats were purchased, among which 10 rats were randomly selected for ACI modeling. FSTL1 concentration, Bax and Bcl-2 protein expression in brain tissues of ACI rats and normal rats were detected. FSTL1 and Bax in peripheral blood of ACI patients were higher than those of healthy subjects (p<0.050), and Bcl-2 was lower than those of healthy subjects (p<0.050). It was detected that FSTL1, Bax and Bcl-2 had good diagnostic value for patients with ACI (p<0.001). FSTL1 and Bax decreased while Bcl-2 increased in patients treated with thrombolytic therapy (p<0.050). And FSTL1, Bax and Bcl-2 were closely related to infarct size and hemorrhagic transformation (p<0.050). Logistic regression analysis showed that NIHSS score, atrial fibrillation, infarct volume, FSTL1 and Bax were independent risk factors affecting hemorrhagic transformation in ACI patients (p<0.050), and Bcl-2 was an independent protective factor affecting hemorrhagic transformation in ACI patients (p<0.050). The concentration of FSTL1 and the expression of Bax protein in rat brain tissue were also higher than that in normal rats, while Bcl-2 was lower than that in normal rats (p < 0.001). FSTL1, Bax and Bcl-2 are involved in the occurrence and development of ACI and are closely related to the hemorrhagic transformation of patients. The mechanism by which FSTL1 promotes the occurrence of ACI might be related to promoting the occurrence of inflammatory responses in the brain tissue of patients or accelerating the apoptosis of neurons.

Effects of nicorandil on myocardial infarct size in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention: study design and protocol for the randomized controlled trial.

Previous studies have shown that nicorandil has a protective effect on cardiomyocytes. However, there is no study to investigate whether perioperative intravenous nicorandil can further reduce the myocardial infarct size in patients with ST-segment elevation myocardial infarction (STEMI) compared to the current standard of percutaneous coronary intervention (PCI) regimen. The CHANGE (China-Admini stration of Nicorandil Group) study is a multicenter, prospective, randomized, double-blind and parallel-controlled clinical study of STEMI patients undergoing primary PCI in China, aiming to evaluate the efficacy and safety of intravenous nicorandil in ameliorating the myocar dial infarct size in STEMI patients undergoing primary PCI and provide evidence-based support for myocardial protection strategies of STEMI patients.

Evaluation of profilin 1 as a biomarker in myocardial infarction.

Profilin 1 (Pfn1) is likely to be involved in atherogenesis and myocardial infarction (MI). Clinical data on this subject are very limited. The aim of this study was to search for associations between serum Pfn1 and a number of parameters in MI patients: symptom onset to PCI time (OPT), myocardial necrosis markers, thrombolysis in myocardial infarction (TIMI) flow, antiplatelet drugs, heparin administration and typical atherosclerosis risk factors. We included patients with type 1 MI (according to the Third Universal Definition of Myocardial Infarction) who were able to precisely determine the time of symptom onset. Exclusion criteria involved conditions potentially altering platelet function. We screened 114 patients and included 65. We assessed serum Pfn1 in three time points: on admission (Pfn1_0), 24 hours post PCI (Pfn1_24) and 48 hours post PCI (Pfn1_48) and correlated it with OPT, cardiac necrosis markers (troponin T, CK, CKMB), TIMI flow in the infarct-related artery, pre-hospital P2Y12-antagonist and heparin administration and known atherosclerosis risk factors. Patients with a shorter OPT had higher Pfn1_0 (838.5 vs. 687.1 pg/ml, p=0.007). Patients with impaired coronary flow post PCI had lower Pfn1_24 (748.2 vs. 925.2 pg/ml, p=0.017) and Pfn1_48 (744.5 vs. 879.8, p=0.031. Pfn1_24 and Pfn1_48 were lower in patients who received a P2Y12 antagonist prior to hospital admission. Diabetic patients presented with lower Pfn1_0 concentrations. This is the first study assessing Pfn1 in type 1 MI patients in relation to the chosen parameters. Pfn1 may be a biochemical tool to objectify information on OPT in MI patients. We found an association between Pfn1 and post-PCI TIMI flow, antiplatelet drug administration and diabetes mellitus.

Risk Factor Differences in Calcified and Non-Calcified Cervical Carotid Plaque

Background: Vascular calcification is associated with the inflammatory process. Here, we investigated the relationship of serum lipoprotein-associated phospholipase A2 (Lp-PLA2) and traditional risk factors with carotid plaque calcification in patients with ischemic stroke (IS) or transient ischemic attack (TIA). Methods: Patients with IS or TIA were divided into the calcification (Ca) and non-calcification (nCa) groups according to the results of the CTA of carotid artery with plaque. LP-PLA2 level, demographics, vascular risk factors, and other clinical data were compared to analyze the risk factors for carotid plaque calcification. Results: A total of 260 patients were enrolled, including 134 patients in Group Ca and 126 patients in Group nCa. Multiple logistic regression showed Lp-PLA2 (p = 0.016), age (p = 0.010), and diabetes (p = 0.010) were independent risk factors of carotid artery plaque calcification. The Spearman's rank correlation coefficients showed Lp-PLA2 (r = 0.372, p = 0.000), age (r = 0.325, p = 0.000), and diabetes (r = 0.421, p = 0.000) had a positive correlation with the calcification of the carotid artery. Conclusions: Serum Lp-PLA2, age, and diabetes were associated with carotid plaque calcification in patients with cerebral infarction or TIA. The inflammatory process mediated by Lp-PLA2 and diabetes may be involved in the pathogenesis of carotid calcification.

The prognostic role of high-sensitivity C-reactive protein in patients with acute myocardial infarction.

The prognostic role of high-sensitivity C-reactive protein in patients with acute myocardial infarction.

Nattokinase reduces brain infarction, fibrinogen and activated partial thromboplastin time against cerebral ischemia-reperfusion injury

Natto is a traditional Japanese food prepared from fermented soybeans. nattokinase (NK) is considered one of the most active functional ingredients in natto. The present study evaluated the neuroprotective effects of NK in gerbils subjected to focal cerebral ischemia. The gerbils were separated into four groups: control group, ischemic group and two NK groups (4 and 40 mg/day i.g. for 7 days). All gerbils were fed standard chow with or without NK prior to cerebral ischemia. Focal cerebral ischemia was induced by the occlusion of the right common carotid artery and middle cerebral artery for 60 min, followed by reperfusion. Infarct volumes were determined by 2, 3, 5-triphenyltetrazolium chloride staining. Anti-thrombotic effects of NK, such as fibrinogen, prothrombin time and activated partial thromboplastin time, were also determined. Our data showed that NK significantly reduced infarct volumes by 54-68% (p ＜ 0.01), compared to the ischemic group. Prothrombin time was not significantly different in all groups. However, low dosage NK (4 mg/day) reversed ischemic-induced increase in fibrinogen concentrations and activated partial thromboplastin time. In summary, the data indicated that oral intake of NK for 7 days may alter fibrinolytic activity and provide neuroprotective effects against focal cerebral ischemia in gerbils.

Comparison of Efficacy of Overlapped Versus Long Eluting Stent in Acute Myocardial Infarction Patients with Diffuse Long Lesion

Comparison of Efficacy of Overlapped Versus Long Eluting Stent in Acute Myocardial Infarction Patients with Diffuse Long Lesion

Neutrophil gelatinase-associated lipocalin is a predictor of complications in the early phase of ST-elevation myocardial infarction.

Aim To evaluate a correlation of serum level of neutrophil gelatinase-associated lipocalin (NGAL) to the risk of the occurrence of complications in patients with the early phase of ST-segment elevation myocardical infarction (STEMI) treated with fibrinolytic therapy prior to percutaneous coronary intervention (PCI). Methods A total of 54 patients with the diagnosis of STEMI treated with fibrinolytic therapy (alteplase) prior to PCI were included. Patients were admitted to the Intensive Care Unit (ICU) of Clinic for Heart, Blood Vessel and Rheumatic Diseases in the period January to March 2018. All patients underwent coronary angiography and PCI within the maximum of 48 hours delay after fibrinolysis, according to the hemodynamic and electrical stability and PCI availability. Blood samples were taken immediately after admission prior to fibrinolytic administration. Patients were divided into two groups according to NGAL values (less or more than 134.05 ng/mL). Results Higher values of NGAL have effect on a higher mean systolic and diastolic pressure (p=0.001 and p=0.003, respectively). Patients with higher NGAL values also have higher values of brain natriuretic peptide (p=0.0001) and highly sensitive troponin I (p=0.002). In that group relative risk (RR) for lethal outcome was 6.4 times significantly higher (p=0.002), for the development of heart failure 2.88 times (p=0.0002), for post-myocardial infarction angina pectoris 2.24 times (p=0.0158), and for ventricular rhythm disturbances (ventricular tachycardia, ventricular fibrillation) 1.96 times higher (p=0.0108). Conclusion Increased NGAL value is related to an unfavourable outcome of patients in the early phase of STEMI treated with fibrinolytic therapy prior to PCI.