The effect of streptokinase therapy in STEMI and conventional therapy in NSTEMI patients on TIMI risk index, B-type natriuretic peptide and high-sensitive C-reactive protein/Akut STEMI'de streptokinaz tedavisi ve NSTEMI'de konvansiyonel tedavivinin TIMI risk indeksi, B-tip natriuretik peptit ve yuksek-duyarlikli C-reaktif protein uzerindeki etkisi.
Objective: In this study, it was aimed to investigate the effect of streptokinase therapy in ST elevation myocardial infarction (STEMI) and conventional therapy in non-ST elevation myocardial infarction (NSTEMI) patients on the thrombolysis in myocardial infarction (TIMI) risk index (TRI), B-type natriuretic peptide (BNP), and high-sensitive C-reactive protein (hs-CRP)levels.
Methods: Eighty-six STEMI (male/female ratio: 65/21, mean age 57.52 [+ or -] 9.87 years) and eighty NSTEMI patients (male/female ratio: 50/30, mean age 57.6 [+ or -] 1.7 years) were included in this prospective observational study. Hs-CRP and BNP were measured and TIMI risk index was calculated in all patients. Coronary angiography was performed in all patients for principally determining TIMI flow rate. Chi-square test, paired t-test or Wilcoxon signed rank test, ANOVA and Spearman correlation analysis were used for statistical analysis where appropriate.
Results: STEMI patients had higher systolic blood pressure, heart rate, BNP and hs-CRP values than NSTEMI patients at admission (p=0.04, p=0.01, p=0.001 and p=0.01, respectively). Thrombolytic therapy in STEMI patients resulted in statistically significant higher levels of BNP, hs-CRP and TRI values compared to baseline levels (p=0.001, p=0.001 and p=0.042, respectively). For NSTEMI patients conventional therapy yielded statistically significant decrease in systolic blood pressure levels and increase in TRI (p=0.001 and p=0.041, respectively). We found significantly lower BNP, hs-CRP in patients with higher TIMI flow rate (p=0.001 and p=0.001 respectively).
Conclusion: Thrombolytic therapy with streptokinase failed to decrease BNP, hs-CRP and TRI values in STEMI patients. Conventional therapy in NSTEMI patients also resulted in higher TRI values than baseline values. We reached TIMI 3 flow in only 10.5% of the study patients, which may be responsible for our findings. (Anadolu Kardiyol Derg 2011; 11: 530-5)
Key words: Acute myocardial infarction, thrombolytic therapy, TIMI risk index, B-type natriuretic peptide, high-sensitive C-reactive protein
Amac: Bu calismada akut ST yukselmeli miyokart enfarktusunde (STEMI) streptokinaz tedavisi ve ST yfikselmesiz miyokart enfarktusunde (NSTEMI) standart tedavinin, miyokart enfarktusunde tromboliz risk indeksi (TRI) ve yuksek-duyarlilikli C-reaktif protein (hs-CRP), B-tip natriuretik peptit (BNP) fizerindeki etkilerinin arastirilmasi amaclanmistir.
Yontemler: Bu prospektif, gozlemsel calismaya 86 STEMI (erkek/kadin orani: 65/21, ortalama yas 57.52 [+ or -] 9.87 yil) ve 80 NSTEMI (erkek/kadin orani: 50/30, ortalama yas 57.6 [+ or -] 1.7 yil) hasta alindi. Tum hastalarin hs-CRP, BNP, TRI olculdu ve koroner anjiyografileri cekilerek TIM akimlari tespit edildi. Istatistiksel analiz icin Ki-kare, eslestirilmis t, Wilcoxon isaret siralama, ANOVA ve Spearman korelasyon testleri kullanildi.
Bulgular: Calismamizda STEMI hastalarda yatis sirasindaki sistolik kan basinci, nabiz, BNP ve hs-CRP duzeyi NSTEMI hastalara oranla daha yuksekti (p=0.04, p= 0.01, p=0.001 ve p=0.01 sirasiyla). Trombolitik tedavi sonrasi STEMI hastalarda yatistaki BNP, hs-CRP ve TRI degerleri lie karislastirildiginda daha yuksek bulduk (p=0.001, p=0.001 ve p=0.042 sirasiyla). Standart tedavi alan NSTEMI hastalarda ise sistolik kan basinci ve TRI istatistiksel olarak anlami yukselme tespit ettik (p=0.001 ve p=0.047 sirasiyla). Ayrica calismamizda anjiyografik TIMI akim degeri derecesi arttikca BNP ve hs-CRP degerleri azalmaktadir (p=0.001 ve p=0.001 sirasiyla).
Sonuc: Calismamizda STEMI olgularinda trombolitik tedavi icin verilen streptokinaz; BNP, hs-CRP duzeyini ve TRI'i dusurmede yetersiz kaldi. Standart tedavi verilen NSTEMI da ise TRI degeri baslangica oranla daha yuksek bulundu. Bizim bulgularimiza gore hastalann yalnizca %10.5'inde TIMI 3 saglanmis olmasi, bu sonuctan sorumlu olabilir. (Anadolu Kardiyol Derg 2011; 11: 530-5)
Anahtar kelimeler: Akut miyokart enfarktusu, trombolitik tedavi, TIMI risk indeksi, B-tip natriuretik peptit, yuksek-duyarlikli C-reaktif protein
Acute myocardial infarction (MI)is still one of the leading causes of death despite new therapeutic options. Therefore, risk assessment has a paramount importance in decision-making process. Currently, many risk scores are being used for this purpose such as TIMI risk score, which requires multiple variables to be entered (1, 2). However, TIMI risk index (TRI) as a new risk assessment tool in both STEMI and NSTEMI patients has been used for this purpose because of its simplicity, it has been tested in 150.000 STEMI (3) and 5430 NSTEMI patients (4) and was revealed as a strong predictor of 30-day mortality in both patient's groups.
Brain natriuretic peptide (BNP) and high-sensitive C-reactive protein (hs-CRP) are also markers of increased cardiovascular mortality in acute coronary syndrome patients (5-9). However, prognostic significance of these biomarkers has been evaluated especially in both NSTEMI patients and STEMI patients treated with primary coronary intervention approach.
The aim of the present study was to determine levels of all these three markers in NSTEMI and STEMI patients treated thrombolytic therapy. We also tried to evaluate the effects of conventional and reperfusion therapy on TIMI risk index, BNP, hs-CRP levels in both NSTEMI and STEMI patients.
Study population This single-center, prospective, observational study enrolled one hundred and sixty-six patients (115 males, 51 females, mean age 57.7 [+ or -] 10.8 years, median 57 years) who were admitted to the emergency department of Adana Numune Education and Research Hospital between May 2007 and April 2008 with the diagnosis acute myocardial infarction. Eighty-six of these patients (52%) were STEMI cases (65 males, 21 females; mean age 57.52 [+ or -] 9.87 years, median 58 years) and 80 of them (48%) were NSTEMI cases (50 males, 30 females, mean age 57.6 [+ or -] 1.7 years, median 57 years).
Patients were excluded from the study based on following criteria: patients undergoing rescue percutaneous coronary intervention (PCI) due to failed thrombolysis determined as the absence of [greater than or equal to] 50% ST segment elevation resolution at 90th minutes; patients admitted to emergency service after 12 hours of onset of symptoms; patients with pericarditis, aortic dissection, chronic inflammation, renal failure (serum creatinine >1.5 mg/ dl), active infection (determined as hs-CRP level >10 mg/dl), and presence of any malignancy.
The study was executed upon the consent received from the patients as per the protocol followed by the approval of the Ethics Committee of our hospital.
Age, gender, blood pressure, heart rate, presence of diabetes or hypertension, smoking status, alcohol use and chest pain duration was determined in all patients at admission. Blood samples for biochemistry analysis including lipid panel and electrocardiographic (ECG) recordings were undertaken. Patients had STEMI diagnosis in the presence of two of three following criteria (10):
--Chest pain and/or discomfort for at least 30 minutes;
--ST-segment elevation of >0.1 mm in at least two adjacent leads in the extremity leads and ST-segment elevation of >0.2 mm in the precordial leads in a standard 12-lead ECG;
--A more than two-fold increase in CK-MB value compared to normal.
NSTEMI patients had at least 10 minutes of typical chest pain and on one of the following: elevated biomarkers of myonecrosis and ST-depression [greater than or equal to] 0.1 mV (8).
All patients were given non-enteric 300 mg acetylsalicylic acid chewable tablets. Those patients with aspirin intolerance or allergy were given clopidogrel 300 mg by oral route. In STEMI patients 1.5 million IU streptokinase was administered by I.V. infusion over 1 hour if there was no contraindication for thrombolytic therapy. Beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, Low-molecular-weight heparin (LMWH), IV nitrates and statins were also used at the discretion of responsible physician. In NSTEMI patients, we used conventional therapy including beta-blockers, ACE inhibitors, IV nitrates and statins, clopidogrel, LMWH (enoxaparine 1 mg/kg).
Patients had undergone coronary angiography after the thrombolytic therapy by using standard Judkins technique before discharge (median time for coronary angiography was 5 days). The coronary angiographic procedure was performed by Shimadzu device (AUD 150 G-Digitex, Kyoto, Japan). Coronary angiograms were interpreted by two independent, experienced interventional cardiologists who were uninformed about the clinical and laboratory data of patients. Angiographic TIMI flow rates of the culprit vessel were determined after thrombolytic therapy by previously established grading system (11): TIMI 0: no flow or perfusion atthe distal of stenosis; TIMI 1: penetration at the distal of stenosis but no perfusion; TIMI 2: partial perfusion; TIMI 3: complete perfusion).
TIMI risk index calculation
The thrombolysis in myocardial infarction risk index was calculated by using the following formula in all patients at admission and atthe day of discharge: Heart rate*(age/10)2/SBP, where SBP is systolic blood pressure (12).
Peripheral blood samples for plasma BNP and hs CRP determination were obtained at admission by direct venipuncture of an antecubital vein after the patient had been in the supine position for 30 minutes. Blood samples were immediately centrifuged. High sensitive-CRP levels were measured by using immune nephelometric method (IMMAGE Immunochemistry Systems; Beckman Coulter, California, USA). BNP measurements were done using Triage Meter Plus equipment (Willich, Germany).
The SPSS 16.0 software package (SPSS Inc., Chicago, III, USA) was used for statistical analysis of the data. Categorical analyses were expressed as numbers (n) and percentages (%), whereas continuous analyses were reported as mean and standard deviation and as median and minimum-maximum where appropriate. Chi-square test was used to compare categorical variables between the treatment groups. For comparison of continuous variables in time (before and after the treatment) within groups, the paired t-test or Wilcoxon signed rank test was used depending on whether the statistical hypotheses were fulfilled or not; and the Student's t-test or Mann-Whitney U test was used for comparisons between groups. The analysis of variance (ANOVA) or KruskaI-Wallis Test were used for comparisons between TIMI values. The correlation between certain variables of the treatment groups was performed using the Spearman correlation analysis. The statistical level of significance for all tests was considered to be 0.05.
Six patients (3.2%) undergoing rescue PCI for persistent chest pain following thrombolytic therapy and 8 patients who died (4.2%) were excluded from the study. In STEMI patients 41 (47.7%) had anterior and 45 (52.3%) had non-anterior MI localization. Chest pain duration at admission in STEMI was less than 1 hour in 28 patients (32.6%), 1-6 hours in 36 subjects (41.8%) and 6-12 hours in 22 patients (25.6%).
Patient characteristics including medication used at admission and affected coronary artery presented in Table 1 which revealed higher SBP and heart rate in STEMI patients (p=0.04 and 0.01, respectively). Moreover, BNP and hs-CRP were also significantly higher in STEMI patients compared to NSTEMI patients (p=0.001 and p=0.01)(Table 1). With thrombolytic therapy in STEMI patients we found statistically significant decrease in systolic-diastolic blood pressure levels and heart rate (p=0.001, p=0.001 and p=0.004, respectively)(Table 2).
In contrast, we detected higher BNP, hs-CRP and TRI values in STEMI patients with reperfusion therapy which reached statistical significance (p=0.001, p=0.001 and p=0.042, respectively) (Table 2). For NSTEMI patients conventional therapy yielded statistically significant decrease in systolic-diastolic blood pressure levels and increase in TRI (p=0.001, p=0.004 and p=0.047, respectively) (Table 2).
TRI, BNP and hs-CRP levels according to TIMI flow rate, and MI localization
Coronary angiographic evaluation performed after the thrombolytic therapy yielded the following TIMI grading: TIMI 0 in 12 patients (14.0%); TIMI 1 in 20 patients (23.3%); TIMI 2 in 45 patients (52.3%); TIMI 3 in 9 patients (10.5%). We found significantly lower BNP, hs-CRP levels in patients with higher TIMI flow rate (p=0.001, and p=0.001 respectively) (Table 3).
We also determined that pre-treatment BNP (p=0.001) and post-treatment BNP, hs-CRP values were significantly higher in STEMI patients having non-anterior MI localization (p=0.001 and p=0.001 respectively)(Table 4).
Relationship between TIMI risk score and BNP and hs-CRP levels
According to correlation analysis we detected a weak but statistically significant correlation coefficient between TRI and BNP levels in patients with STEMI only after reperfusion therapy (p=0.030) (Table 5).
In our study, we found that STEMI patients had higher BNP and hs-CRP values both before and after reperfusion therapy. Likewise, higher TRI values were determined in STEMI and NSTEMI patients even in the presence of appropriate treatment. BNP and hs-CRP were increased in STEMI patients having non-anterior localization but had a tendency to decrease with increasing TIMI flow rate. Moreover, we also found a correlation between TRI and BNP levels in STEMI patients only after reperfusion therapy.
TIMI risk index is relatively strong and independent predictor of mortality in STEMI and NSTEMI patients (3, 4, 13). TIMI risk index scores can be divided into low risk (<12.5), intermediate risk (12.5-30) and high risk groups (>30)(14) and every 5 percentage points increase in TIMI risk index results in a 43% increase in 30-day mortality (14). Predictive power of TIMI risk index is decreased in patients older 65 years (12, 15), which was not the case in our study because median was 57 years in our patients.
TIMI risk index calculation is directly related to heart rate/ SBP ratio, which was higher in STEMI patients (0.61) compared to NSTEMI patients (0.59) at admission in our study. Although SBP and heart rate decreased after reperfusion therapy in STEMI and conventional therapy in NSTEMI patients, heart rate/ SBP ratio was still higher in STEMI patients than NSTEMI patients (0.66 vs 0.63), which explains higher TRI values in this patients group. Therefore we can assume that reperfusion or conventional therapy in our acute coronary syndrome patients did not decrease TIMI risk score and hence patient's mortality risk. Underlying reasons for this finding in spite of early presentation of patients (74.4% of them within 6 hours) is not clear but we thought streptokinase was the cause in STEMI patients for low TIMI flow rates (only in 10.5% of the patients having TIMI 3 flow rate) and lower SBP levels. This lack of satisfactory TIMI flow rate in our study groups may also be responsible for higher TRI values in NSTEMI patients at discharge than at admission.
Brain natriuretic peptide is released in acute MI due to increased wall stress (5). It begins to rise during first 24 hours of MI but is generally more useful for prognostic purpose when measured in 2 to 5 days of admission (5, 16-18). BNP levels were higher in our STEMI patients than NSTEMI patients, which reflect greater ischemia burden and more severe left ventricular impairment in our opinion. Even higher BNP levels in STEMI patients after reperfusion therapy can be explained by our failure to provide satisfactory TIMI flow rate, and hence, to salvage myocardium at risk with streptokinase. Mega et al. (19) previously showed that patients with BNP >80 pg/ml were at significantly higher risk of death and were also more likely to have impaired coronary flow. Indeed, we found gradual increase in BNP levels with decreasing TIMI flow rates.
CRP has an active role in MI because it reflects inflammatory reaction, which has prominent role in plaque rupturethrombosis and infarct expansion (20, 21). Serum hs-CRP increases within the first few days of acute MI in response to myocardial necrosis (22). It has been reported that addition of hs-CRP level to TIMI risk score allowed risk stratification and provided additional prognostic information in patients with acute coronary syndromes (23). Moreover, plasma hs-CRP level at admission was suggested as a predictor for short-term and long-term reperfusion failure in AMI (24, 25). We showed higher hs-CRP levels in STEMI patients than in NSTEMI patients. In addition, we also determined even higher hs-CRP levels in STEMI patients after reperfusion therapy but not in NSTEMI patients. Possible explanations for this finding can be more powerful inflammatory response due to larger myocardial necrotic area and ensuing infarct expansion.
We showed a weak but statistically significant correlation between TRI and BNP in STEMI patients only after reperfusion therapy. If we look at this result from different perspective, we cannot use a clinical variable (TIMI risk index) and a biomarker BNP levels interchangeably. Indeed, Kuklinska et al. (8) previously postulated that only BNP and hs-CRP but not TRI could provide independent and incremental prognostic information.
In addition to small number of subjects recruited, our study has other major limitations to be mentioned. We did not provide mortality data because our primary aim was to determine BNP, hs-CRP and TRI values. Mortality data and its relation to BNP, hs-CRP and TRI should be investigated in other trials. We also did not measure infarct area with which we can reach to further conclusions.
Ineffective reperfusion achieved with streptokinase can be used to explain persistently increased biomarker's levels and TIMI risk index in our STEMI patients. For, NSTEMI patients, conventional treatment strategy did not affect BNP or hs-CRP levels but caused a possible adverse result: an increase in TRI. Therefore, we need further trials for both confirming our study results and finding answers for other important questions: Are our findings also valid for other thrombolytics in STEMI patients and early invasive strategy in NSTEMI patients?
Conflict of interest: None declared.
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Ibrahim Hall/Kurt, Mustafa Kemal Batur , Ilker Unal  Department of Cardiology, Adana Numune Education and Research Hospital, Adana
 Department of Cardiology, Faculty of Medicine Acibadem University, Adana
 Department of Biostatistics, Faculty of Medicine, Cukurova University, Adana. Turkey
Address for Correspondence/Yazisma Adresi: Dr. Ibrahim Halil Kurt, Department of Cardiology, Adana Nimune Education and Research Hospital, 01330 Adana-Turkey Phone: +90 322 458 32 52 Fax: +90 322 459 51 63 E-mail: email@example.com
Table 1. Demographic characteristics, clinical, laboratory and angiographic findings STEMI NSTEMI p * Variables (n=86) (n=80) Age, years 57.52[+ or -]9.87 57.6[+ or -]11.7 0.987 Gender, m/f, n 65/21 50/30 0.092 Diabetes, n (%) 1406.3) 1407.5) 0.43 Hypertension, 24 (27.9) 34 (42.5) 0.053 n (%) Smoking, n (%) 28 (32.6) 35 (43.8) 0.152 Alcohol on, 7(8.1) 10 (12.5) 0.445 n (%) Systolic BP 131.10[+ or -]26.44 124.5[+ or -]14.0 0.044 mmHg Diastolic BP 78.12[+ or -]16.04 75.4[+ or -]9.8 0.193 mmHg Pulse, bpm 80.00[+ or -]16.21 74.0[+ or -]14.4 0.013 Total 189.16[+ or -]4.86 187.4[+ or -]37.7 0.784 cholesterol, mg/dl H D L, m g/dl 38.86[+ or -]0.92 40.5[+ or -]10.7 0.273 TG, mg/dl 170.10[+ or -]13.65 160.1[+ or -]78.2 0.538 LDL, mg/dl 116.55[+ or -]3.88 113.4[+ or -]27.7 0.527 BUN, mg/dl 33.4[+ or -]1.0 35.3[+ or -]13.2 0.631 Creatinine, 1.03[+ or -]0.03 1.04[+ or -]0.27 0.882 mg/dl Medications ACEI, n (%) 37 (43.0) 35 (43.8) 0.999 83 (96.5) 78 (97.5) 0.999 Beta-blockers, 66 (76.7) 61 (76.3) 0.999 n (%) Nitrates, n (%) 26 (30.2) 31 (38.8) 0.258 Statins, n (%) 43 (50.0) 44 (55.0) 0.538 Affected coronary artery LAD, n (%) 60 (69.8) 58 (72.5) 0.734 CX, n (%) 53 (61.6) 45 (56.3) 0.529 RCA, n (%) 55 (64.0) 45 (56.3) 0.343 Data are presented as mean-SD and number (percentages) * Chi-square, unpaired t, and Mann-Whitney U tests ACEI-angiotensin-converting enzyme, ASA-acetyl salicylic acid, BP-blood pressure BUN-blood urine nitrogen, CX-circumflex, DBP-diastolic blood pressure, HDL-high density lipoprotein, LAD-left anterior descending artery, LDL -low-density lipoprotein NSTEMI-non-ST-elevation myocardial infarction, RCA-right coronary artery, STEMI-ST elevation myocardial infarction, TG -triglyceride Table 2. Pre-and post-treatment vital signs and laboratory findings in STEMI and NSTEMI patients STEMI (n=86) Variables Pre-treatment Post-treatment p * SBP mmHg 131.10[+ or -]26.44 114.22[+ or -]19.09 0.001 DBP mmHg 78.12[+ or -]16.04 69.23[+ or -]10.96 0.001 Pulse, bpm 80.00[+ or -]16.21 75.14[+ or -]13.32 0.004 248.2[+ or -]32.7 0.001 BNP pg/ml 104.8[+ or -]24.3 163.5 (18.6-2389) 32.9 (1-1794.1) hs-CRP mg/dl 0.86[+ or -]0.09 1.65[+ or -]0.16 0.001 0.56 (0-3.5) 1.125 (0.1-9.5) TRI 21.19[+ or -]9.14 22.78[+ or -]9.28 0.042 19.7 (2.95-46.21) 21.6 (8.08-67.34) NSTEMI (n=80) Variables Pre-treatment Post-treatment p * SBP mmHg 124.5[+ or -]14.0 118.4[+ or -]18.6 0.001 DBP mmHg 75.4[+ or -]9.8 72.1[+ or -]9.4 0.004 Pulse, bpm 74.0[+ or -]14.4 74.1[+ or -]11.3 0.930 2.21[+ or -]1.95 2.11[+ or -]1.58 0.526 BNP pg/ml 1.65 (0.1-9.8) 1.62 (0.1-6.8) hs-CRP mg/dl 0.52[+ or -]0.50 0.58[+ or -]0.86 0.944 0.45 (0-2.6) 0.35 (0-6.6) TRI 20.64[+ or -]9.18 21.80[+ or -]10.03 0.047 19.8 (4.64-57.76) 21.2 (5.83-68.14) Data are presented as meantSD and median (range) values * Paired samples t-test and Wilcoxon signed rank test BNP-brain natriuretic peptide, DBP-diastolic blood pressure, hs-CRP-high-sensitivity C-reactive protein, NSTEMI-non-ST-elevation myocardial infarction, SBP-systolic blood pressure, STEMI-ST-elevation myocardial infarction, TRI-TIMI risk index Table 3. Relation between post-treatment angiographic TIMI flow and TRI, BNP, and hs-CRP values Post-treatment Angiographic TIMI flow 0 1 2 TRI 23.49[+ or -] 20.94[+ or -] 24.14[+ or -] 6.75 21.25 5.02 21.21 11.23 22.72 (14.34-39.1) (12.91-29.77) (8.08-67.34) BNP, pg/ml 549.3[+ or -] 221.4[+ or -] 205.1[+ or -] ([pounds 632.9 324.5 184.5 206.8 178.3 159.7 sterling]) (90.2-2389.0) (18.6-759.9) (25.5-878.8) Hs-CRP mg/dl 3.0[+ or -] 1.6[+ or -]1.5 1.4[+ or -] ([pounds 2.4 2.5 1.1(0.1-5.6) 1.0 1.0 sterling]) (0.6-9.5) (0.3-5.1) Chi-square 3 p * (df)* TRI 21.53[+ or -] 0.451 2.63513) 9.85 21.13 (5.83-68.14) BNP, pg/ml 14.3[+ or -] <0.001 109.1131 ([pounds 39.7 1.9 sterling]) (0.1-205.0) Hs-CRP mg/dl 0.7[+ or -] <0.001 56.913) ([pounds 1.0 0.4 sterling]) (0.0-6.6) Data are presented as mean_SD and median (range) values * Kruskal-Wallis test and Bonferroni adjusted Mann-Whitney U test for pairwise comparison: ([pounds sterling])p<0.05 for the comparing the groups as 0 and 2, 0 and 3, 1 and 3, 2 and 3 BNP-brain natriuretic peptide, hs-CRP-high-sensitivity C-reactive protein, TRI-TIMI risk index Table 4. Pretreatment and post-treatment measurements of TRI BNP and hs-CRP according to the STEMI localization STEMI Anterior pre-treatment TRI 20.30[+ or -]8.79 19.98(2.95-46.21) BNP 62.47[+ or -]97.28 20.50 (0.10-430.05) hs-CRP 0.66[+ or -]0.65 0.43 (0.03-3.00) post-treatment TRI 21.43[+ or -]9.79 20.45 (8.08-67.34) BNP 164.28[+ or -]187.04 132.25 (0.20-878.82) hs-CRP 1.23[+ or -]1.23 0.79 (0.00-6.60) STEMI p * Non-anterior pre-treatment TRI 22.52[+ or -]10.00 0.347 19.74(7.71-57.76) BNP 84.60[+ or -]249.41 <0.001 12.55 (0.23-1794.06) hs-CRP 0.79[+ or -]0.80 0.463 0.52 (0.00-3.50) post-treatment TRI 24.05[+ or -]9.87 0.132 22.75(9.99-68.14) BNP 185.11[+ or -]337.54 <0.001 82.30 (0.20-2388.99) hs-CRP 1.48[+ or -]1.65 <0.001 0.94 (0.00-9.46) Data are presented as mean-SD and median (range) values * Mann-Whitney U test BNP--brain natriuretic peptide, hs-CRP-high-sensitivity C--reactive protein, STEMI-ST elevation myocardial infarction, TRI--TIMI risk index Table 5 Correlation of TIMI risk index with BNP and hs-CRP levels Correlation p * Treatment Pairs coefficient * NSTEMI Before TRI--BNP -0.026 0.821 TRI--hs-CRP 0.070 0.538 After TRI--BNP -0.071 0.530 TRI--hs-CRP 0.067 0.552 ST EMI Before TRI--BNP 0.147 0.176 TRI--hs-CRP 0.034 0.757 After TRI--BNP 0.234 0.030 TRI I--hs-CRP -0.082 0.450 * Spearman rank correlation analysis BNP--brain natriuretic peptide, hs-CRP--high-sensitivity C -reactive protein, NSTEMI--non-ST-elevation myocardial infarction, STEMI--ST-elevation myocardial infarction, TRI-TIMI risk index
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|Title Annotation:||Original Investigation/Ozgun Arastirma|
|Author:||Kurt, Ibrahim Halil; Kemal Batur, Mustafa; Unal, Ilker|
|Publication:||The Anatolian Journal of Cardiology (Anadolu Kardiyoloji Dergisi)|
|Article Type:||Clinical report|
|Date:||Sep 1, 2011|
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