Biochemical Markers Of Myocardial Injury Research Articles

A New Concept in Relation to Blood Biochemical Parameters with Myocardial Infarction in Bangladeshi Population

Background : Blood testing for biochemical markers of Myocardial injury plays an increasingly important role for the evaluation, diagnosis and triage of patients with chest pain. The guidelines for the diagnosis of Myocardial Infarction ((MI) have recently changed and prominently incorporate the results of cardiac marker testing in the clinical definition of MI. We investigated these updated biomarkers and further compare the differing biology and release kinetics of clinically relevant biomarkers. Methods: Biochemical changes that occurred in the blood of acute myocardial infarction (AMI) patients were investigated. Two hundred and fifty two patients, 180 males and 72 females were included in this study. The mean age was 49.3 ± 9.25 years. Biochemical parameters include serum triglyceride, total protein, albumin , total bilirubin and total cholesterol to albumin ratio were analyzed. Results : Biochemical parameters showed that the increased level of triglyceride and total bilirubin were associated with myocardial infarction. Triglyceride and total bilirubin levels in myocardial infarction patients were 2.3 ±1.4 mmol/ L and 12.3±3.2 ?mol/ L respectively, whereas those of healthy controls were 1.7±1.2 mmol/L for triglycerides and 9.7±3.7 ?mol/L for bilirubin. On the other hand, serum total protein and albumin concentrations were lower in MI patients compared to those of controls. Total protein level was 65.5 ±3.1 g/L in MI patients and 76.2±5.3 g/L in healthy controls. Albumin levels in both patients and controls were 40.2 ±3.2 g/L and 45.4 ± 4.5 g/L correspondingly. Conclusion : Interestingly, serum total cholesterol level was not significantly different in MI patients compared to controls. In addition, cholesterol/albumin ratio in myocardial infarction patients (0.14 ± 0.04) found to be significantly higher than in healthy controls (0.11± 0.03). Cardiovascular Journal Volume 6, No. 1, 2013, Page 43-46 DOI: http://dx.doi.org/10.3329/cardio.v6i1.16114

LDH as a predictor of in-hospital and late mortality in acute pulmonary embolism

Purpose: Acute pulmonary embolism (PE) is a common cardiovascular emergency, which can be acute life-threatening and can have a dismal long-term prognosis. Prognostic assessment of these patients is based mainly on hemodynamic status, echocardiography findings and biochemical markers of myocardial injury. However, LDH measurement may have a role in the risk stratification of the patients. The aim of this study was to assess the value of LDH as a mortality predictor in acute PE. Methods: Retrospective, observational study including 165 patients with acute PE (age 72.8±16.4; 76 males), diagnosed by pulmonary CT angiography in the emergency department, between January 2010 and December 2010. The studied endpoints were in-hospital mortality and follow-up all-cause mortality. A receiver operating characteristics (ROC) curve was used to define the best cut-off between two groups [group 1 (LDH > 310 U/L, n=53) and group 2 (LDH ≤ 310 U/L, n=112)], regarding all-cause mortality. Mean follow-up time was 415±358 days. Results: No differences were found between the 2 groups regarding demographic data, symptoms and cardiovascular risk factors. Area under the ROC curve (AUC) was 0.626. The best cut off value was 310 U/L (sensitivity 54.5%, specificity 71.3%). In univariate regression analysis, a LDH higher than 310 U/L was found to be strongly associated with worse outcome [Hazard-ratio: 2.841 (95% CI, 1.226 – 6.584), p=0.015]. Patients from group 1 had a significantly higher in-hospital (18.2% vs. 7.4%, p<0.05) and long-term mortality (22.6% vs. 8.9%, Log-rank p<0.02). ![Figure][1] Kaplan-Meier survival analysis Conclusions: LDH is a predictor of both in-hospital and all-cause mortality at follow-up after acute PE. Its addition to current risk stratifying systems may be of interest. [1]: pending:yes

The efficacy of parecoxib on systemic inflammatory response associated with cardiopulmonary bypass during cardiac surgery

Cardiopulmonary bypass (CPB) during cardiac surgery is well known to be associated with the development of a systemic inflammatory response. The efficacy of parecoxib in attenuating this systemic inflammatory response is still unknown. Patients undergoing elective mitral valve replacement with CPB were assessed, enrolled and randomly allocated to receive parecoxib (80 mg) or placebo. Blood samples were collected in EDTA vials for measuring serum cytokine concentrations, troponin T, creatinekinase myocardial-brain isoenzyme CK-MB concentrations and white cell counts. Compared with the control group, IL-6 and IL-8-values in the parecoxib group increased to a lesser extent, peaking at 2 h after the end of CPB (IL-6 31.8 pg ml⁻¹ ± 4.7 vs. 77.0 pg ml⁻¹ ± 14.1, 95% CI -47.6, -42.8, P < 0.001; IL-8 53.6 pg ml⁻¹ ± 12.6 vs. 105.7 pg ml⁻¹ ± 10.8, 95% CI -54.8, -49.4, P < 0.001). Peak concentrations of anti-inflammatory cytokine IL-10 occurred immediately after termination of CPB and were higher in the parecoxib group (115.7 pg ml⁻¹ ± 10.5 vs. 88.4 pg ml⁻¹ ± 12.3, 95% CI 24.7, 29.9, P < 0.001). Furthermore, the increase in neutrophil counts caused by CPB during cardiac surgery was inhibited by parecoxib. The increases in serum troponin T and CK-MB concentrations were also significantly attenuated by parecoxib in the early post-operative days. Peak serum concentrations of CK-MB in both groups occurred at 24 h post-CPB (17.4 μg l⁻¹ ± 5.2 vs. 26.9 μg l⁻¹ ± 6.9, 95% CI -10.9, -8.1, P < 0.001). Peak troponin T concentrations occurred at 6 h post-bypass (2 μg l⁻¹ ± 0.62 vs. 3.5 μg l⁻¹ ± 0.78, 95% CI -1.7, -1.3, P < 0.001). Intra-operative parecoxib attenuated the systemic inflammatory response associated with CPB during cardiac surgery and lowered the biochemical markers of myocardial injury.

Changes in Diagnosing Non-ST-Segment Elevation Myocardial Infarction after the Introduction of a New High-Sensitivity Cardiac Troponin T Assay: A Single-Centre Experience

Cardiac troponins are the most sensitive and specific biochemical markers of myocardial injury and with the new high-sensitivity troponin methods very minor injuries of the heart muscle can be detected. The introduction of high-sensitivity assays has facilitated reference range adjustments and a revised cut-off point for myocardial infarction (MI) due to an improved performance in the lower concentration range. The objective of this study was to investigate whether implementing a high-sensitivity cardiac troponin T (hs-cTnT) assay with subsequent lowering of the cut-off point changed the hospital evaluation and diagnosis of acute non-ST-segment elevation myocardial infarction (NSTEMI) in a general hospital population. NSTEMI patients admitted to our hospital during two periods each lasting one year were retrospectively compared. During period 1 (August 2007 - July 2008) patients were diagnosed with a conventional troponin T assay, and during period 2 (August 2009 - July 2010) patients were diagnosed using an hs-cTnT assay. A significant increase in the number of NSTEMI admissions was observed using the hs-cTnT assay (225 vs. 341, risk ratio 1.57, 95% confidence interval 1.33 to 1.85). The proportion of patients examined with acute coronary angiography was similar (25.8% vs. 23.8%). Due to the higher number of NSTEMI admissions the total number of angiographies was higher in period 2 (58 vs. 81, p < 0.05), and significantly more patients were examined without signs of coronary artery disease (CAD) (0% vs. 8.6%, p < 0.05). A smaller proportion diagnosed with the high-sensitivity assay had significant dynamic cTnT changes between the highest and lowest cTnT measurement during each admission (96.2% vs. 88.7%, p < 0.01). More patients were diagnosed with NSTEMI and underwent coronary angiography after introducing the hs-cTnT assay. At the same time there was an increase in the frequency of coronary angiograms without signs of CAD, and fewer had significant dynamic cTnT concentration changes.

Myocardial protection with prophylactic oral metoprolol during coronary artery bypass grafting surgery: evaluation by troponin I

IntroductionBiochemical markers of myocardial injury are frequently altered after cardiac surgery. So far there is no evidence whether oral beta-blockers may reduce myocardial injury after coronary artery bypass grafting. ObjectiveTo determine if oral administration of prophylactic metoprolol reduces the release of cardiac troponin I in isolated coronary artery bypass grafting, not complicated by new Q waves. MethodsA prospective randomized study, including 68 patients, divided in 2 groups: Group A (n=33, control) and B (n=35, beta-blockers). In group B, metoprolol tartrate was administered 200 mg/day. The myocardial injury was assessed by troponin I with 1 hour and 12 hours after coronary artery bypass grafting. ResultsNo significant difference between groups regarding pre-surgical, surgical, complication in intensive care (15% versus 14%, P=0.92) and the total number of hospital events (21% versus 14%, P=0.45) was observed. The median value of troponin I with 12 hours in the study population was 3.3 ng/ml and was lower in group B than in group A (2.5 ng/ml versus 3.7 ng/ml, P<0,05). In the multivariate analysis, the variables that have shown to be independent predictors of troponin I release after 12 hours were: no beta-blockers administration and number of vessels treated. ConclusionThe results of this study in uncomplicated coronary artery bypass grafting, comparing the postoperative release of troponin I at 12 hours between the control group and who used oral prophylactic metoprolol for at least 72 hours, allow to conclude that there was less myocardial injury in the betablocker group, giving some degree of myocardial protection.

Correlation of cardiac magnetic resonance imaging and biochemical markers of myocardial injury in a multi-centre study: PROTECTION AMI CMR substudy

The purpose of this study was to determine predictors of 90-day left ventricular function following acute ST-segment elevation myocardial infarction (STEMI) using variables from clinical presentation, biomarker testing, and cardiovascular magnetic resonance imaging (CMR).

Correlation of CMR and Biochemical Markers of Myocardial Injury in a Multi-centre Study: PROTECTION AMI CMR Substudy

Correlation of CMR and Biochemical Markers of Myocardial Injury in a Multi-centre Study: PROTECTION AMI CMR Substudy

Reflections on the Evolution of Cardiac Biomarkers

I was asked for this special issue to reflect on the area of laboratory tests for identifying cardiac injury. I will include my own experiences in this area, as well as some of others and a bit of personal perspective. I have published elements of this history previously (1–3) and freely admit to drawing on my prior publications. Considerations for a blood protein biomarker to identify the death of any cell involve 3 major factors: sensitivity, which will be affected by the abundance and location of the protein in the cell; the timing of sampling, which is influenced by the mode of entry into blood and the half-life of elimination; and specificity for the cell of interest. A compounding factor in myocardial infarction (MI)2 (acute coronary syndrome) is that the acute event is caused by blockage of blood flow in a coronary artery or arteries that leads to hypoxia and cell death. This blockage delays protein markers from reaching the blood because they cannot readily diffuse into the blood; instead, they reach the blood via the lymphatics, which is somewhat akin to traveling on city streets rather than on an interstate. Today, we have several discovery tools for identifying candidate cell injury biomarkers via gene expression (4) or proteomics (5) in a reasonably straightforward manner. It is noteworthy that cardiac biomarkers evolved without such tools, and appropriate biomarkers were found intuitively and empirically (Table 1), probably because the heart's major function is contraction, which requires energy. The biomarkers used were all involved in energy production or control of contraction. View this table: Table 1. History of use of biochemical markers of myocardial injury. The first practical test used was serum glutamic-oxaloacetic transaminase (SGOT), now called “aspartate aminotransferase” (AST) (6). Practical use of this test in clinical laboratories required the development of robust, temperature-controlled spectrophotometers, such as the Gilford 300N developed by …

Combined analyses of creatine kinase MB, cardiac troponin I and myoglobin in pericardial and cerebrospinal fluids to investigate myocardial and skeletal muscle injury in medicolegal autopsy cases

Creatine kinase-MB (CK-MB), cardiac troponin I (cTnI) and myoglobin (Mb) are biochemical markers of myocardial injury; however, Mb is more abundant in skeletal muscles. The present study involved analysis of these markers in pericardial and cerebrospinal fluids (PCF and CSF) from serial medicolegal autopsy cases ( n = 295, within 48 h) to examine their efficacy in determining the cause of death. Although these markers showed a slight postmortem time-dependent elevation, except for CK-MB in CSF, the distribution depended on the cause of death. Mb levels in PCF and CSF were higher in fatal hyperthermia (heat stroke) and methamphetamine abuse, and CK-MB in both fluids was also higher in the latter. In psychotropic drug intoxication, CK-MB, cTnI and Mb were higher in PCF, but only cTnI was elevated in CSF. In electrocution and cerebrovascular disease, each marker was higher in PCF and also relatively high in CSF. PCF cTnI level was higher in acute pulmonary embolism without significant elevation of any other markers, whereas CSF CK-MB was higher in acute blunt brain injury death and methamphetamine abuse. In most cases of delayed brain injury death, hypothermia (cold exposure) and pneumonia, these markers were low or intermediate in both PCF and CSF; however, sudden cardiac death, asphyxiation and fire fatality cases showed few characteristic findings. These observations suggest that combined analyses of these markers in postmortem PCF and CSF, in addition to blood samples, are helpful for evaluating the severity of myocardial and/or skeletal muscle damage in death processes, in particular for investigating deaths due to hyperthermia, hypothermia, electrocution and intoxication.

The research progress on the diagnosis of myocardial injury of heart-type fatty acid-binding protein

Background The correct application of cardiac markers have played a revolutionary role for clinical accurate diagnosis,identification and treatment of cardiovascular disease. Now more and more cardiac biochemical markers have been applied in clinic researches,and the latest research progress in the field of H-FABP is reviewed in this paper.Objective To understand the physical and chemical properties and clinical detection methods of H-FABP,to recognize the unique advantages in diagnosis of the early AMI.Content To survey the basic and clinical research of H-FABP by reviewing domestic and international literatures, and to introduce the current clinical detection methods.Trend With the development of H-FABP determination methods and clinical research,H-FABP is becoming an important biochemical marker of myocardial injury. Key words: Myocardial injury; Heart-type fatty acid-binding protein; Biochemical marker

Relationship of troponin T to cardiac MRI criteria for acute myocarditis

Background Cardiac MR criteria for acute myocarditis (“Lake Louise Criteria”) include scarring as defined by high-signalintensity areas in late gadolinium enhancement (LGE), and inflammatory markers as defined by an increased early contrast uptake (early gadolinium enhancement, EGE) and edema (increased signal intensity in T2 signal weighted images). Troponin is a widely used clinical marker for cardiomyocyte death; however, the relationship between biochemical markers of myocardial injury and these imaging features has not been clearly established.

Elevated Biochemical Markers of Myocardial Injury are not Associated with Postoperative Cognitive Dysfunction after Coronary Artery Surgery

Background: The systemic inflammatory response to cardiopulmonary bypass (CPB) and organ hypoperfusion during CPB contribute to cerebral and myocardial dysfunction in patients undergoing cardiac surgery. We hypothesized that biochemical markers of myocardial injury [creatine kinase - myocardial band (CK-MB), troponin-I] may be independently associated with postoperative cognitive dysfunction (POCD; an indicator of cerebral dysfunction) in patients undergoing coronary artery bypass graft (CABG) surgery using CPB. Methods: Eighty-eight age- and education-balanced patients=55 years of age undergoing elective CABG with CPB and 28 nonsurgical controls with coronary artery disease were enrolled. Recent verbal and nonverbal memory and executive functions were assessed before surgery, 1 week, and 3 months after surgery using a standard psychometric test battery. Plasma CK-MB and troponin-I concentrations were determined before and at the end of surgery. Plasma troponin-I concentrations were also measured 24 hours after surgery. Results: Performance on two cognitive tests decreased at least two standard deviations (SD) from baseline and performance on five additional tests decreased 1 SD 1 week after surgery. After 3 months, performance on six tests was at least a 1 SD below baseline. CK-MB and troponin-I concentrations were significantly (p<0.00001) elevated after surgery. There was no correlation between overall cognitive function (measured by average z-score) and postoperative CK-MB or troponin-I concentrations 1 week or 3 months after surgery. Conclusion: The results suggest that elevated postoperative CK-MB or troponin-I concentration alone is not associated with the subsequent development of short- and medium-term impairment of cognitive functions after CABG.

Pre-operative High-sensitive Troponin Concentration in Higher-risk Patients Undergoing Elective Non-cardiac Surgery

Background: Cardiac troponins are the most sensitive biochemical marker of myocardial injury, with newer high-sensitive troponin (hs-TnT) assays allowing the detection of lesser degrees of myocardial damage. Hs-TnT is elevated in approximately 10% of patients with stable coronary artery disease, and is significantly associated with adverse long-term cardiovascular outcomes. The aim of our study was to investigate baseline troponin (both 4th generation and hs-TnT) concentrations in high-risk patients undergoing elective non-cardiac surgery. Methods: Consecutive patients undergoing elective non-cardiac surgery, currently prescribed anti-platelet therapy because they were deemed high risk, were included. Patient demographics and comorbidities were collected. Baseline hs-TnT (Roche Diagnostics, ninety-ninth percentile 13 ng/L, limit of detection 2 ng/L), and fourth generation TnT (Roche Diagnostics, 99th percentile 10 ng/L, limit of detection 10 ng/L) were collected in all patients. Results: One hundred and ten consecutive patients were recruited (mean age: 72 ± 9.7 years, 64% male). Hs-TnT concentration was elevated above the ninety-ninth percentile in 29 (26%) patients, with only seven (6%) elevated using the older fourth generation assay. Multivariate predictors of elevated hs-TnT included; age (r = 0.42, p < 0.01); estimated glomerular filtration rate (r = −0.67, p < 0.01); and haemoglobin (r = −0.42, p < 0.01). A similar trend was observed for ischaemic heart disease history, however this was not statistically significant (p = 0.08). Conclusion: In stable high risk patients undergoing elective non-cardiac surgery, approximately one-quarter will have an elevated pre-operative hs-TnT. Factors associated with this include age, renal dysfunction, and anaemia. Given an elevated hs-TnT in stable populations is associated with worse cardiovascular outcomes, the impact on peri-operative morbidity and mortality merits further evaluation.

Troponin elevation in coronary vs. non-coronary disease

Acute myocardial infarction is defined as myocardial cell death due to prolonged myocardial ischaemia. Cardiac troponins (cTn) are the most sensitive and specific biochemical markers of myocardial injury and with the new high-sensitivity troponin methods very minor damages on the heart muscle can be detected. However, elevated cTn levels indicate cardiac injury, but do not define the cause of the injury. Thus, cTn elevations are common in many disease states and do not necessarily indicate the presence of a thrombotic acute coronary syndrome (ACS). In the clinical work it may be difficult to interpret dynamic changes of troponin in conditions such as stroke, pulmonary embolism, sepsis, acute perimyocarditis, Tako-tsubo, acute heart failure, and tachycardia. There are no guidelines to treat patients with elevated cTn levels and no coronary disease. The current strategy of treatment of patients with elevated troponin and non-acute coronary syndrome involves treating the underlying causes. The aim of this paper is to review data from studies of non-ACS patients with acutely elevated troponin who in clinical practice may be difficult to discriminate from ACS patients.

Beating-Heart Valve Surgery: A Systematic Review

Beating-heart continuous coronary perfusion (BHCCP) has been promoted as an alternative to the technique of cardioplegic arrest in valve surgery. Its potential advantage is the elimination of cardioplegia and the corollary risk of ischemic reperfusion injury. The use of CCP has been recommended especially when performing more complex operations, such as mitral valve repair, and particularly as surgeons become more familiar with beating-heart coronary surgery. We conducted a systematic review to assess the strength of the evidence supporting the efficacy of BHCCP compared to cardioplegia in valve surgery. Thirty nine reports were identified. Of these, only two were randomized control trials. Overall the studies were generally of poor quality and had a low evidence level. In those studies, mortality and major morbidity from BHCCP were within acceptable levels, nevertheless, there was no advantage over cardioplegic arrest. On the other hand there is weak evidence that it may reduce functional and biochemical markers of myocardial injury. In conclusion, BHCCP is an operative strategy in valve surgery with some potential benefits. There is, however a need for a high quality, prospective, randomized control trial to establish the exact role for BHCCP in complex valve surgery.

Exercise above the ischemic threshold and serum markers of myocardial injury

Current guidelines for exercise training in coronary patients state that in the presence of exercise-induced ischemia, the heart rate during exercise should be at least 10 beats/min below the heart rate associated with an ST segment depression of 1 mm or greater. For patients with a relatively low ischemic threshold, this recommendation does not allow for a sufficient training stimulus. To document the effects of a single session of exercise above the ischemic threshold on biochemical markers of myocardial injury in stable coronary patients with exercise-induced ischemia. Because creatine kinase (CK) and its MB isoenzyme (CK-MB) can both increase after exercise because of skeletal muscle injury, troponin T was also measured. Twenty-one patients with documented coronary artery disease underwent two 20 min exercise sessions. The intensity of the first exercise training session was fixed at a heart rate below the ischemic threshold (ie, approximately 10 beats/min lower than the heart rate associated with the appearance of an ST segment depression of 1 mm or greater). The intensity of the second exercise session was fixed at a heart rate above the ischemic threshold. Blood test measurements at baseline, 6 h after and 24 h after the exercise sessions did not show any increase in total CK, CK-MB or troponin. The value of all measurements remained well below the lower limits associated with myocardial damage. A 20 min period of exercise above the ischemic threshold did not result in myocardial necrosis.

Trimetazidine May Protect the Myocardium during Cardiac Surgery

Trimetazidine is an anti-ischemic agent with cardioprotective effects. The purpose of this double-blind, controlled, prospective randomized study was to investigate the possible effects of the preoperative use of trimetazidine on the biochemical markers of myocardial injury during open heart surgery and to determine if it has any myocardial protective effects. Thirty patients undergoing coronary artery bypass grafting surgery, received either trimetazidine (study group, n = 15) or not (control group, n = 15). Pretreatment began 2 weeks before the operation with trimetazidine (60 mg/day orally), and the control group received no medication. We measured the levels of serum creatine kinase (CK), CK isoenzyme MB (CK-MB), myoglobin, and troponin T in venous blood samples obtained before and after the operation to evaluate the effect of this drug against myocardial damage. We also took serial blood samples from the radial artery and the coronary sinus before the institution of cardiopulmonary bypass (CPB) and at 2 and 15 minutes after the removal of the cross-clamp to measure lactate levels and calculate the lactate extraction of the myocardium. Postoperative levels of myoglobin, troponin T, CK, and CK-MB were significantly lower in the trimetazidine group than in the control group (P < .05). There was also a significant difference in the values for the lactate extraction calculation between the groups at minute 2 after the removal of the cross-clamp (P < .05). We conclude that pretreatment with trimetazidine has some beneficial effects in protecting the myocardium and decreasing myocardial injury during the cardioplegic arrest period in open heart surgery without affecting postoperative hemodynamics.

Myocardial cell injury is common in children with septic shock

To determine the prevalence of myocardial cell injury in children with septic shock by estimating the levels of biochemical markers of myocardial injury, troponin I (TnI) and creatine kinase MB (CK-MB). Children aged 3 months to 16 years were admitted to paediatric intensive care unit (PICU) with septic shock. Children with sepsis without shock and children with hypovolaemic shock were enrolled as controls. Serum TnI and CK-MB levels were measured at admission and serially at 24 h, 48 h and 96 h in children with septic shock, while baseline measurement of the same markers was taken from the controls. In total, 88% (15/18) of children with septic shock had elevated TnI levels compared with 25% (5/20) with sepsis and 6.7% (1/15) with hypovolaemic shock (p < 0.001). Serial TnI levels at admission, 24 h, 48 h and 96 h were higher in the nonsurvivors. There was a positive correlation between the baseline TnI levels and the predicted mortality using the paediatric index of mortality (PIM2) scores at admission (r = 0.51, p = 0.03). A majority of children with septic shock have evidence of myocardial cell injury. The estimation of serum TnI levels may help in better prognostication of children with septic shock.

Elevated serum cardiac troponin in non-acute coronary syndrome.

Cardiac troponins (CTn) are the most sensitive and specific biochemical markers of myocardial injury and risk stratification. The assay for troponin T (cTnI) is standardized, and results obtained from different institutions are comparable. This is not the case with troponin I (cTnT), and clinicians should be aware that each institution must analyze and standardize its own results. Elevated cTn levels indicate cardiac injury, but do not define the mechanical injury. The differentiation of cTn elevation caused by coronary events from those not related to an acute coronary syndrome (ACS) is tiresome, at times vexing, and often costly. Elevation of cTn in non-ACS is a marker of increased cardiac and all-cause morbidity and mortality. The cause of these elevations may involve serious medical conditions that require meticulous diagnostic evaluation and aggressive therapy. At present, there are no guidelines to treat patients with elevated troponin levels and no coronary disease. The current strategy of treatment of patients with elevated troponin and non-ACS involves treating the underlying causes.

Ressonância magnética vs cintilografia com pirofosfato marcado com tecnécio-99m para a detecção de necrose miocárdica perioperatória

Perioperative myocardial infarction (POMI) is a complication of coronary artery bypass grafting (CABG) with a potential prognostic impact. Technetium-99m pyrophosphate myocardial scintigraphy (MS) is used in the diagnosis of POMI; however it shows a limited sensitivity for subendocardial lesions. Cardiovascular magnetic resonance imaging (CMRI), in turn, has a high accuracy in the detection of myocardial necrosis. To compare CMRI and MS for the detection of POMI after CABG. A total of 24 patients with chronic coronary artery disease were studied using the delayed contrast enhanced CMRI and MS before and after CABG by analyzing the development of areas of perioperative myocardial necrosis (POMI). Biochemical markers of myocardial injury (CKMB and troponin I) were also determined before and after surgery. Nineteen patients completed the study. Of these, 6 (32%) presented POMI on CMRI and 4 (21%) on MS (p = NS). Of the 323 left ventricular segments assessed, 17 (5.3%) showed perioperative necrosis on CMRI and 7 (2.2%) on MS (p = 0.013). Moderate agreement was observed between the methods (kappa = 0.46). There was disagreement regarding the diagnosis of POMI in 4 (21%) cases, most of them with small areas of perioperative necrosis on CMRI which were not visualized on MS. In all cases with POMI on CMRI, significant CKMB and troponin I elevations were observed. Moderate diagnostic agreement was observed between the methods for the detection of POMI, but CMRI enabled visualization of small areas of perioperative myocardial necrosis which were not identified on MS and were associated with elevation of biochemical markers of myocardial injury.