Abstract. Introduction. Kitigon Vichairuangthum, MD 1, Anawat Sermsawan, MD 1, and Mala Treewatchareekorn, MSc 2

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Troponin I Assessment Provides Incremental Prognostic Information in Patients with Acute Coronary Syndromes and Borderline Troponin T Values upon Admission Kitigon Vichairuangthum, MD 1, Anawat

1 Troponin I Assessment Provides Incremental Prognostic Information in Patients with Acute Coronary Syndromes and Borderline Troponin T Values upon Admission Kitigon Vichairuangthum, MD 1, Anawat Sermsawan, MD 1, and Mala Treewatchareekorn, MSc 2 1 Division of Cardiology, Faculty of Medicine, Bangkok Metropolitan Administration Medical College and Vajira Hospital, Bangkok, Thailand 2 Division of Clinical Chemistry, Department of Clinical Pathology, Bangkok Metropolitan Administration Medical College and Vajira Hospital, Bangkok, Thailand Abstract Objectives: The purpose of this study was to evaluate the incremental prognostic information for short term risk of adverse cardiovascular events from serum cardiac troponin I (ctni) in patients with acute coronary syndrome (ACS) and borderline troponin T (ctnt) levels upon admission. Methods: This was a prospective analytical study design. 75 ACS patients with borderline troponin T upon admission at BMA Medical College and Vajira Hospital were enrolled from April 2009 August Serum cardiac troponin I and other blood chemistries were measured at the time of the study. Main outcome measures were cardiac death, congestive heart failure, interventional procedures such as percutaneous coronary intervention (PCI) and coronary bypass graft (CABG), major bleeding and stroke at 3 months. Results: Sixty four patients (85%) had elevated ctni concentrations more than the ng/ml cut-off, but only seven patients (9%) had ctni concentrations more than the acute myocardial infarction (AMI) cut-off (0.3ng/ml).When using the ng/ml cut-off, there were no significant differences for in-hospital and 1 month adverse events, however cardiovascular events at the 3 month follow up (p = 0.04) were significantly higher. The AMI cut- off value did not shown this benefit. Conclusion: The incremental prognostic information of ctni was not observed for the in-hospital and 1 month period. Notwithstanding, the ng/ml cutoff seems to have a benefit in predicting the cardiovascular events at 3 months in patients with acute coronary syndromes and borderline troponin T values upon admission, whereas the AMI cut off (0.3ng/ml) was not useful for this purpose Keywords: Troponin I, Borderline Troponin T, Acute coronary syndrome, Cardiovascular Events Thai Heart J 2012; 25 : E-Journal : Introduction In the normal population cardiac troponin is regarded as the most sensitive and specific marker in the detection of myocardial injury and is used routinely for the diagnosis of acute coronary syndrome (1-3). Elevated troponin levels also have been reported for several other purposes, such as being an important predictor of adverse outcomes (1,2,4,5). Corresponding author: Kitigon Vichairuangthum, MD Division of Cardiology, Department of Medicine, BMA Medical College and Vajira Hospital, Bangkok, Thailand E mail address: neozz15@hotmal.co.th Troponin T is a contractile protein not normally found in blood. When detected, it is considered positive evidence for myocardial cell damage. Serum troponin T values < 0.03 ng/ml are considered negative for myocardial damage while values of 0.03 to 0.09 ng/ml are considered borderline and values 0.1 ng/ml are considered positive for myocardial infarction (MI). The meaning of negative and positive for MI is clear but the term borderline is unclear. At present, this borderline value is creating considerable confusion. If there is a high level of suspicion that a patient has an acute coronary syndrome, for example, new onset of myocardial ischemia or evolving MI, a physician has no choice but to admit that patient for

2 Kitigon Vichairuangthum, MD observation. Patients admitted to the hospital who by traditional criteria are ruled out for acute myocardial infarction but have detectable levels of troponin have a higher in-hospital and short term chance of suffering from adverse cardiac events (6). A recent study showed the different prognostic performance utility among troponin isoforms, where the Architect ctni assay (Abbott Diagnostics, Chicago, Ill., USA) was superior to the Roche troponin T assay when using the admission samples (7). The differences in performance between the two assays were attributed to the additional antibody targeting epitope of the ctni molecule. But another report did not agree with this belief (8). The purpose of this study was to evaluate the incremental prognostic information for short term risk of adverse cardiovascular events of serum cardiac troponin I levels in patients with acute coronary syndrome (ACS) and borderline troponin T levels upon admission. Methods Study design: A prospective analytical study design. Patient population Inclusion criteria The study was approved by the Bangkok Metropolitan Administration Medical College and Vajira Hospital (BMA) Institutional Review Board for Human Subjects Research. Written informed consent was received from all of the participants. A total of 75 patients with acute coronary syndromes (defined by 1.chest discomfort or symptoms of myocardial ischemia 10 minutes and/or one of the following: a) New transient ST elevation at the J-point in two contiguous leads with the cut-off points 0.2 mv in men or 0.15 mv in women in leads V2-V3 and/or 0.1 mv in other leads b) New horizontal or down-sloping ST depression 0.05 mv in two contiguous leads: and/or T inversion 0.1 mv in two contiguous leads with prominent R-wave or R/S ratio > 1 ) and borderline troponin T values (0.03 to 0.09 ng/ml) upon admission into BMA Medical College and Vajira Hospital between April 2009 and August 2009 were included. Exclusion criteria were patients with: 1) history of acute coronary syndrome (unstable angina, myocardial 117 infarction or revascularization) within the preceding 3 months; 2) a history of recent major cardiovascular surgery within the preceding 3 months; 3) renal insufficiency (creatinine 2 mg/dl); and 4) patients who did not agree to participate. The patients were evaluated by a complete medical history and physical examination. Blood samples were drawn; blood urea nitrogen (BUN), creatinine, total cholesterol, triglyceride, high density lipoprotein cholesterol (HDL), low density lipoprotein cholesterol (LDL), creatine kinase MB (CK-MB), troponint and troponin I were measured immediately at the time of admission. Biochemical markers All the serum samples were centrifuged for 5 min at 3,500 revolutions per minute to remove any particular matter. Each tube was labeled with the patient number and accession number. The technicians who performed the assays did not know the clinical data. Specimens were re-analyzed at random or to verify an abnormal result in order to eliminate technical errors. The Architect i 1000 SR (Abbott Laboratories, USA) was used to analyze the serum Tn I level. The level is less than ng/ml in a normal population. The acute myocardial infarction (AMI) cut- off is at 0.3 ng/ml. Cardiac troponin T was measured with an Elecsys 2010 (3 rd generation cardiac troponin T assay, Roche Diagnostics, Switzerland). In a normal healthy population, the serum TnT is less than 0.03 ng/ml while the AMI cut-off is 0.1 ng/ml. The other blood chemistries were measured with an Olympus AU 640 Analyzer using routine methods according to the protocols of the manufacturer. Follow-up The study groups were classified according to the serum troponin I level on initial enrollment. All patients were followed up for 3 months from the time of their initial enrollment into the study. The end points studied were 1) cardiac death; 2) congestive heart failure: (NYHA FC 3); 3) intervention such as PCI or CABG; 4) major bleeding: hemoglobin drop > 5 g/dl with or without an identified site and 5) acute ischemic or hemorrhagic stroke. Hospital records, outpatient clinical records and interviews with the patient or primary physician were used for confirmation of the events.

3 118 Troponin I Assessment Provides Incremental Prognostic Information in Patients with Acute Coronary Syndromes and Borderline Troponin T Values upon Admission Statistical analysis Continuous variables are expressed as the mean value ± SD and were analyzed by an unpaired student t test. Categorical variables are expressed as percentages and were analyzed by a Chi-square and Fisher s Exact Test. A twotailed p value 0.05 was considered significant. All of the statistical analyses were performed using SPSS, version 12.0 (SPSS Inc., Chicago, Illinois). Results Sixty four patients (85%) had elevated ctni concentrations more than the ng/ml cut off, but only seven patients (9%) had ctni concentrations more than the AMI cut-off (0.3 ng/ml). The drug data for the patients are shown in Figure 1, and about half of all the patients received an aspirin, beta blocker or statin. The first time the ng/ml cut-off level was used, the baseline characteristics of patients with normal troponin I levels were similar to those with elevated levels ( ng/ml) (Table 1). Similarly, there were no significant differences in baseline biochemical profiles between the two groups (Table 2). There was no significant difference in major adverse cardiovascular events between the two groups in the in-hospital and at 1 month but these adverse events occurred at a significantly higher incidence in the elevated group at the 3 month follow-up (44 of 64 patients [69%] vs. 4 of 11 patients [36%]; p = 0.04)(Table 3). When done a second time the AMI cut-off level (0.3 ng/ml) was used and the baseline characteristics and baseline serum biochemical profiles showed no significant differences between the two groups (Table 4 and 5). There was no significant difference in cardiovascular events between the two groups at in-hospital, 1 month and 3 months (p=1.00)(table 6). When combined with the provisional cut-off point from the manufacturer (the ng/ml and 0.3 ng/ml cutoff) and used as the cut-off level, there was no significant difference of adverse events during the follow up period (Table7). The overall add on accuracies of troponin I for discrimination between patients with or without MACE were evaluated by ROC analysis (Figure 2). The areas under ROC curves for Tn I for discrimination in-hospital, 1 month and 3 months MACE were 0.55 (95%CI ), 0.59 (95%CI ) and 0.60 (95%CI ) respectively. Because of their low AUC, there was no benefit for this purpose. Discussion Some patients are known to have coronary artery disease (CAD) and have symptoms of myocardial ischemia manifested by classic angina pectoris and transient electrocardiographic (ECG) changes. However, a large majority of them have neither classic symptom of myocardial ischemia nor ECG changes compatible with ischemia. Thus, the chest pain in these patients should be classified as chest pain of uncertain etiology. It is becoming standard practice to obtain a serum troponin T in these patients. Measurement of cardiac troponins has gained a leading position in the field of biochemical diagnosis of myocardial necrosis, as compared with the conventional creatine kinase-mb (CK-MB) measurement. Data reported during the past decade have indicated a superior efficacy, higher sensitivity and specificity for troponin I (ctn-i), and cardiac troponin T (ctn-t) in the diagnosis and prognostication of myocardial damage (9-12). The meaning of negative and positive for MI is understood. But the term borderline is unclear when added to the usual emergent diagnostic testing - ECG, total CK and CK-MB, and, in some instances, high sensitivity C-reactive protein and two-dimensional cardiac ultrasound. If all diagnostic tests are negative but troponin T is borderline should the patient be admitted, or discharged for further outpatient workup? From the past, there was no fundamental difference between troponin T (ctnt) and troponin I (ctni) testing (13, 14). Recent study shows the different prognostic performance utility among troponin isoforms. The ARCHITECT Stat troponin I is a chemiluminescent microparticle immunoassay. It is a two-step sandwich configured with monoclonal antibodies for both the microparticles and the acridinium-derivative conjugate. It included a monoclonal antibody directed toward epitope This method provides an increase in sensitivity to diagnose AMI patients (7). In this study, we postulated that troponin I may have an additive benefit in the borderline troponin T group. In the present study, troponin I showed no additive benefit for prediction of adverse events due to

4 Kitigon Vichairuangthum, MD 119 Table 1. Baseline clinical characteristics: Comparison between patients with normal ctni levels and those with elevated levels, when using the ng/ml cutoff (n=75) ctni cutoff ng/ml Baseline clinical Normal ctni Elevated ctni p-value characteristics (< ng/ml) ( ng/ml) (n = 11) (n = 64) Male** 6 (55%) 34 (53%) 0.93 Age (yrs.)* 73 ± ± BMI (m/kg 2 )* 24.8 ± ± Hypertension 11 (100%) 52 (81%) 0.19 Diabetes 6 (54%) 35 (55%) 1.00 Dyslipidemia 6 (54%) 41 (64%) 0.73 Smoker 6 (54%) 28 (44%) 0.53 Family history 0 (0%) 2 (3%) 1.00 Previous MI** 3 (27%) 36 (56%) 0.07 LVEF (%)* 59 ± ± Data are presented as number (%) of patients. The data were analyzed by a Fisher s exact test * These data were analyzed by an unpaired student t test and data are presented as mean ± SD **These data are presented as number (%) of patients. The data were analyzed by a Chi-square test Table 2. Baseline serum biochemical profiles: Comparison between patients with normal ctni levels and those with elevated levels, using the ng/ml cutoff (n = 75). ctni cutoff ng/ml Blood Chemistries Normal ctni Elevated ctni p-value (< ng/ml) ( ng/ml) (n = 11) (n = 64) Cholesterol (mg/dl) 169 ± ± Triglyceride (mg/dl) 142 ± ± HDL (mg/dl) 32 ± ± LDL (mg/dl) 100 ± ± BUN (mg/dl) 18 ± ± Creatinine (mg/dl) 1.35 ± ± CK-MB (U/L) 18 ± ± Data are presented as the mean value ± SD. The data were analyzed by an unpaired student t test

5 120 Troponin I Assessment Provides Incremental Prognostic Information in Patients with Acute Coronary Syndromes and Borderline Troponin T Values upon Admission Table 3. Cardiovascular events: Comparison between patients with normal cardiac troponin I levels and those with elevated levels, using the ng/ml cutoff (n = 75). ctni cutoff ng/ml Normal ctni Elevated ctni p-value (< ng/ml) ( ng/ml) (n = 11) (n = 64) In hospital MACE No MACE 8 (73%) 32 (50%) MACE 3 (27%) 32 (50%) 0.16 MACE at 1 month No MACE 7 (64%) 27 (42%) MACE 4 (36%) 37 (58%) 0.20 MACE at 3 months No MACE 7 (64%) 20 (31%) MACE 4 (36%) 44 (69%) 0.04 Data are presented as the number (%) of patients and were analyzed by a Fisher s Exact Test Table 4. Baseline clinical characteristics: Comparison between normal ctni levels and those with elevated levels, when using the AMI cutoff (n = 75). ctni cutoff 0.3 ng/ml Baseline clinical Normal ctni Elevated ctni p-value characteristics (< 0.3 ng/ml) ( 0.3 ng/ml) (n = 68) (n = 7) Male 37 (54%) 3 (42%) 0.69 Age (yrs.)* 73 ± ± BMI (m/kg 2 )* 24.3 ± ± Hypertension 59 (86%) 4 (57%) 0.07 Diabetes 36 (52%) 5 (71%) 0.44 Dyslipidemia 44 (65%) 3 (43%) 0.41 Smoker 31 (45%) 3 (43%) 1.00 Family History 2 (3%) 0 (0%) 1.00 Previous MI 35 (51%) 4 (57%) 1.00 LV EF (%)* 53 ± ± Data are presented as number (%) of patients. The data were analyzed by a Fisher s Exact test * These data were analyzed by an unpaired student t test and data are presented as mean ± SD

6 Kitigon Vichairuangthum, MD 121 Table 5. Baseline serum biochemical profiles: Comparison between patients with normal ctni levels and those with elevated levels, using the AMI cutoff (n = 75). ctni cutoff 0.3 ng/ml Blood Chemistries Normal ctni Elevated ctni p-value (< 0.3 ng/ml) ( 0.3 ng/ml) (n = 68) (n = 7) Cholesterol (mg/dl) 176 ± ± Triglyceride(mg/dl) 142 ± ± HDL (mg/dl) 34 ± ± LDL (mg/dl) 107 ± ± BUN (mg/dl) 22 ± ± Creatinine (mg/dl) 1.38 ± ± CK-MB (U/L) ± ± Data are presented as the mean value ± SD. The data were analyzed by an unpaired student t test Table 6. Cardiovascular events: Comparison between patients with normal cardiac troponin I levels and those with elevated levels, using the AMI cutoff (n = 75). ctni cutoff 0.3 ng/ml Blood Chemistries Normal ctni Elevated ctni p-value (< 0.3 ng/ml) ( 0.3 ng/ml) (n = 68) (n = 7) In hospital MACE No MACE 36 (53%) 4 (57%) MACE 32 (47%) 3 (43%) 1.00 MACE at 1 month No MACE 31 (46%) 3 (43%) MACE 37 (54%) 4 (57%) 1.00 MACE at 3 months No MACE 25 (37%) 2 (29%) MACE 43 (63%) 5 (71%) 1.00 Data are presented as the number (%) of patients and were analyzed by a Fisher s Exact Test

122 Troponin I Assessment Provides Incremental Prognostic Information in Patients with Acute Coronary Syndromes and Borderline Troponin T Values upon Admission Table 7.

7 122 Troponin I Assessment Provides Incremental Prognostic Information in Patients with Acute Coronary Syndromes and Borderline Troponin T Values upon Admission Table 7. Analysis when combined with the provisional cut-off point from the manufacturer (the ng/ml & 0.3 ng/ ml cutoff) as the cut-off level No MACE MACE p-value In hospital MACE TnI < ng/ml 8 (73%) 3 (27%) ng/ml Tn I <0.3 ng/ml 28 (50%) 29 (50%) Tn I 0.3 ng/ml 4 (57%) 3 (43%) MACE at 1 month TnI < ng/ml 7 (64%) 4 (36%) ng/ml Tn I <0.3 ng/ml 24 (42%) 33 (58%) Tn I 0.3 ng/ml 3 (43%) 4 (57%) MACE at 3 month TnI < ng/ml 7 (64%) 4 (36%) ng/ml Tn I <0.3 ng/ml 18 (31%) 39 (69%) Tn I 0.3 ng/ml 2 (29%) 5 (71%) Data are presented as the number (%) of patients and were analyzed by a Fisher s Exact Test Figure 1. The number (%) of patient s medication

8 Kitigon Vichairuangthum, MD 123 Figure 2. Receiver operating characteristic curve (ROC curve) for the troponin I in the prediction of MACE A. In-hospital MACE; AUC Tn I = 0.55 (95%CI; ) C. 3 months MACE; AUC Tn I = 0.60 (95%CI ; ) B. 1 month MACE; AUC Tn I = 0.59 (95%CI; ) the low AUC in the ROC curve analysis. Thus, the 0.03 ng/ml cut-off seems to have a correlation with the major adverse cardiovascular outcomes at a 3 month follow up. More significant benefit may show up in long term outcome after 3 months. Further studies are needed to clarify this hypothesis. However, there was no correlation when using the AMI cutoff. Because of the high incidence of adverse events found in the borderline population the term borderline appears not to be a benign condition. So we suggest an aggressive approach in this borderline group. The limitation of our study was first, the sample size although it was adequately powered, it was too small and it was just a single center study. Second, the short term follow-up time might be considered a limitation. So a larger population and longer follow up period more than 3 months may show more significant results. Conclusion The ctni did not show any incremental prognostic information for in-hospital and at 1 month follow up, however, the ng/ml cut-off appears to have benefit in predicting cardiovascular events at 3 months in patients

9 124 Troponin I Assessment Provides Incremental Prognostic Information in Patients with Acute Coronary Syndromes and Borderline Troponin T Values upon Admission with acute coronary syndromes and borderline troponin T values upon admission. The AMI cut off (0.3ng/ml) was not useful for this purpose. Acknowledgements We wish to thank the Bangkok Metropolitan Administration Medical College and the Vajira Hospital Research Fund as well as the Clinical Research Center for their support of this study. We are also grateful to all the patients, cardiovascular unit nursing staff and the BMA laboratory technicians for their cooperation in this study and their dedication to the care of these patients. Conflict of interest There is no conflict of interest for our study. References 1. Sribhen K. Cardiac Troponins: Novel myocardial markers with high diagnostic performance and prognostic value. Siriraj Hosp Gaz 2001;53: Sunil VE, Magnus O, Christopher BG, et al. Prognostic Value of Isolated Troponin Elevation Across the Spectrum of Chest Pain Syndromes. Am J Cardiol 2003;91: Sarko J, Pollack CV. Clinical laboratory in Emergency Medicine. J Emerg Med 2002; 23: Roberto L, Serge M, Inder SA. Prognostic value of very low plasma concentration of troponin t in patients with stable chronic heart failure. Circulation 2007;116: Healey JS, Davies RF, Smith SJ, Davies RA, Ooi DS. Prognostic use of cardiac troponin T and troponin I in patients with heart failure. Can J Cardiol. 2003;19: Heidenreich PA, Go A, Melsop KA, et al. Prediction of risk for patients with unstable angina. Evidence Report/Technology Assessment no. 31 (prepared by the UCSF-Standford Evidence based Practice Center under Contract No ). AHRQ Publication No.01-E001. Rockville, MD. Agency for Healthcare Research and Quality, December James S, Flodin M, Johnston N, Lindahl B, Venge P. The antibody configurations of cardiac troponin I assays may determine their clinical performance. Clin Chem, 2006;52: Charoenpanichkit C, Sritara P, Yamwong S, et al. Comparison between cardiac troponin I or troponin T in acute myocardial infarction diagnosis. Thai Heart J 2008;1: Fred S, Mary A, Lesly AP, et al. Prognostic value of the Ortho vitros cardiac troponin I assay in patients with symptoms of Myocardial ischemia risk stratification using European Society of Cardiology/American College of Cardiology Recommended cutoff value. Am J Clin Pathol 2003;120: Stein R, Gupta B, Agarwal S etal. Prognostic implications of normal (<0.10 ng/ml) and borderline ( ng/ml) troponin elevation levels in critically ill patients without acute coronary syndrome. Am J Cardiol 2008;102: Babuin L, Vasile VC, Rio Perez JA, et al. Elevated cardiac troponin is an independent risk factor for short- and long-term mortality in medical intensive care unit patients. Crit Care Med. 2008;36: Melloni C, Alexander KP, Milford BS, et al. Prognostic value of troponins in patients with non-st segment elevation acute coronary syndromes and chronic kidney disease. Clin Cardiol. 2008;31: Heeschen C, DA, Langenbrink L, Goldmann BU, et al. Analytical and diagnostic performance of troponin assays in patients suspicious for acute coronary syndromes. Clin Biochem 2000;33: Tucker JF, C.R., Anderson AJ, et al., Early diagnostic efficiency of cardiac troponin I and troponin T for acute myocardial infarction. Acad Emerg Med1997;4:13-21.

10 Kitigon Vichairuangthum, MD 125 ระด บของ serum cardiac troponin I ในการช วยพยากรณ โรคกล มผ ป วยท ม อาการสงส ย ว าจะเก ดหลอดเล อดห วใจต บเฉ ยบพล น ท ม ระด บ serum cardiac troponin T ก ำก ง ขณะแรกร บในโรงพยาบาล ก ต กร ว ช ยเร องธรรม, อนว ช เสร มสวรรค, มาลา ตร ว ชร กร บทค ดย อ ว ตถ ประสงค : เพ อศ กษาว าการว ดระด บ สารคาร ด แอกโทรโปน น อ ยย ในผ ป วยท ม อาการสงส ยว าจะเก ดหลอดเล อดห วใจ ต บเฉ ยบพล น ท ม ระด บ สารคาร ด แอกโทรโปน น ท ก ำก งขณะแรกร บในโรงพยาบาล สามารถช วยประกอบการต ดส นใจร กษา และม ความส มพ นธ ก บ อ บ ต การณ เก ด ภาวะแทรกซ อนทางหลอดเล อดห วใจ หร อไม ร ปแบบการว จ ย: การว จ ยเช งว เคราะห แบบไปข างหน า กล มต วอย าง: ผ ป วยท ม อาการสงส ยว าจะเก ดหลอดเล อดห วใจต บเฉ ยบพล น ท ม ระด บ สารคาร ด แอกโทรโปน น ท ก ำก ง ขณะแรกร บในว ทยาล ยแพทย ศาสตร กร งเทพมหานครและวช รพยาบาล ระหว างเด อนเมษายน ถ ง เด อนส งหาคม พ.ศ จำนวน 75 ราย ว ธ ดำเน นการว จ ย: ว ดระด บคาร ด แอก โทรโปน น อ ยย และสารเคม อ นในเล อด หล งจากน นทำการเฝ าต ดตาม อ บ ต การณ โรค หลอดเล อดห วใจ ของผ ป วยเป นระยะเวลา 3 เด อนน บจากว นท ได ทำการเจาะเล อด ต วว ดท สำค ญ: การเก ดภาวะแทรกซ อนทางหลอดเล อดห วใจท 3 เด อน ผลการว จ ย: ผ ป วย 64 ราย (85%) ม ระด บคาร ด แอกโทรโปน นอ ยย ส งกว าจ ดต ด นาโนกร ม/มล. ในขณะท พบเพ ยง 7 ราย (9%) ท ม ระด บท ส งกว าจ ดต ดท ใช บอกว าผ ป วยม กล ามเน อห วใจขาดเล อด (0.3 นาโนกร ม/มล.) พบความส มพ นธ ระหว าง ระด บคาร ด แอกโทรโปน นอ ยย ท ส งกว าจ ดต ด 0.3 นาโนกร ม/มล. ก บ การเก ดภาวะแทรกซ อนทางหลอดเล อดห วใจท 3 เด อน ในขณะท ไม พบความส มพ นธ ด งกล าว ก บภาวะแทรกซ อนในขณะร บการร กษาในโรงพยาบาล และ ท 1 เด อน สร ป: พบความส มพ นธ ระหว างระด บสารคาร ด แอกโทรโปน นอ ยย ท ส งกว าจ ดต ด นาโนกร ม/มล. ก บการเก ดเพ มข นของ ภาวะแทรกซ อนทางหลอดเล อดห วใจท 3 เด อน ด งน นจ ดต ดท นาโนกร ม/มล อาจม ประโยชน ในการทำนายภาวะ ด งกล าวได

The Relationship between Serum Concentration of Cardiac Troponin I in Chronic Renal Failure Patients and Cardiovascular Events

The Relationship between Serum Concentration of Cardiac Troponin I in Chronic Renal Failure Patients and Cardiovascular Events Kitigon Vichairuangthum MD*, Wattana Leowattana MD**, Leena Ong-Ajyooth MD***,