Diagnostic value of serial measurement of cardiac markers in patients with chest pain: limited value of adding myoglobin to troponin I for exclusion of myocardial infarction

Background

Despite improved laboratory assays for cardiac markers and a revised standard for definition of myocardial infarction (AMI), early detection of coronary ischemia in unselected patients with chest pain remains a difficult challenge.

Methods

Rapid measurements of troponin I (TnI), creatine kinase MB (CK-MB), and myoglobin were performed in 197 consecutive patients with chest pain and a nondiagnostic electrocardiogram for AMI. The early diagnostic performances of these markers and different multimarker strategies were evaluated and compared. Diagnosis of AMI was based on European Society of Cardiology/American College of Cardiology criteria.

Results

At a given specificity of 95%, TnI yielded the highest sensitivity of all markers at all time points. A TnI cutoff corresponding to the 10% coefficient of variation (0.1 μg/L) demonstrated a cumulative sensitivity of 93% with a corresponding specificity of 81% at 2 hours. The sensitivity was considerably higher compared to CK-MB and myoglobin, even considering patients with a short delay until admission. Using the 99th percentile of TnI results as a cutoff (0.07 μg/L) produced a cumulative sensitivity of 98% at 2 hours, but its usefulness was limited due to low specificities. Multimarker strategies including TnI and/or myoglobin did not provide a superior overall diagnostic performance compared to TnI using the 0.1 μg/L cutoff.

Conclusion

A TnI cutoff corresponding to the 10% coefficient of variation was most appropriate for early diagnosis of AMI. A lower TnI cutoff may be useful for very early exclusion of AMI. CK-MB and in particular myoglobin did not offer additional diagnostic value.     

Prognostic implications of C-reactive protein and troponin following percutaneous coronary intervention

BACKGROUND:

C-reactive protein (CRP), a marker of inflammation, plays a role in the pathophysiology of atherosclerotic events. The relationship between CRP levels and myocardial necrosis assessed by troponin T (TnT) in patients undergoing percutaneous coronary intervention (PCI) has not been established. In addition, the long-term significance of TnT rise following PCI is not clear.

OBJECTIVES:

To examine the relationship between CRP and the rise in TnT levels, and evaluate the long-term prognostic implications of TnT rise following PCI.

METHODS:

A total of 1208 patients underwent successful nonemergent PCI. Baseline demographic characteristics, CRP and TnT levels were prospectively collected before and 12 h to 18 h following PCI. Long-term follow-up data over two years were available.

RESULTS:

Among the patients studied (mean age 62 years), 64% presented with acute coronary syndrome. A PCI procedure was associated with a significant increase in TnT levels (higher than 0.1 μg/L) in 238 patients (20%). Multivariate logistic regression identified presentation with acute coronary syndrome or myocardial infarction, no statin use at the time of the procedure, increased CRP and increasing length of stent as independent predictors of TnT rise following PCI. Periprocedural TnT rise was not associated with adverse events in follow-up examinations (OR 1.09, 95% CI 0.73 to 1.65).

CONCLUSIONS:

Myocardial necrosis commonly occurred in otherwise successful PCI and was particularly prevalent in the proinflammatory milieu of a recent myocardial infarction. This response was blunted with statin therapy. However, there was no long-term adverse sequelae of these troponin rises following otherwise uncomplicated PCI.     

Evaluation of troponin T criteria for periprocedural myocardial infarction in patients with acute coronary syndromes

In patients with acute coronary syndromes undergoing percutaneous coronary intervention (PCI), the diagnosis of periprocedural myocardial infarction is often problematic when the pre-PCI levels of cardiac troponin T (TnT) are elevated. Thus, we examined different TnT criteria for periprocedural myocardial infarction when the pre-PCI TnT levels were elevated and also the associations between the post-PCI cardiac marker levels and outcomes. We established the relation between the post-PCI creatine kinase-MB (CKMB) and TnT levels in 582 patients (315 with acute coronary syndromes and 272 with stable coronary heart disease). A post-PCI increase in the CKMB levels to 14.7 μg/L (3 × the upper reference limit [URL] in men) corresponded to a TnT of 0.23 μg/L. In the 85 patients with acute coronary syndromes and normal CKMB, but elevated post peak TnT levels before PCI (performed at a median of 5 days, interquartile range 3 to 7), the post-PCI cardiac marker increases were as follows: 21 (24.7%) with a ≥ 20% increase in TnT, 10 (11.8%) with an CKMB level >3 × URL, and 12 (14%) with an absolute TnT increase of >0.09 μg/L (p <0.005 for both). In the patients with stable coronary heart disease and post-PCI cardiac markers > 3× URL compared to those without markers elevations, the rate of freedom from death or nonfatal myocardial infarction was 88% for those with TnT elevations versus 99% (p <0.001, log-rank) and 84% for those with CKMB elevations versus 98% (p <0.001, log-rank). Of the patients with acute coronary syndromes, the post-PCI marker levels did not influence the outcomes. In conclusion, in patients with acute coronary syndromes and elevated TnT levels undergoing PCI several days later, ≥20% increases in TnT were more common than absolute increments in the TnT or CKMB levels of >3× URL. Also, periprocedural cardiac marker elevations in patients with acute coronary syndromes did not have prognostic significance.     

Implications of elevated cardiac troponin T in ambulatory patients with heart failure: a prospective analysis

Background

Elevated concentrations of cardiac troponin T (TnT) have been reported in patients hospitalized for decompensated heart failure (HF). We assessed whether elevated TnT levels are associated with the severity, etiology, and prognosis of HF in stable, ambulatory patients.

Methods

From 1998-1999, we prospectively collected data from 136 ambulatory patients with HF, New York Heart Association functional class II to IV, ejection fraction ≤35%, and no recent unstable angina, myocardial infarction, surgery, or coronary revascularization. Blood was obtained and analyzed by immunoassay for TnT, and patients were followed for 14.0 ± 4.3 months for death or HF hospitalization (primary end point) and other adverse cardiovascular outcomes.

Results

Thirty-three patients (24%) had an elevated TnT level (≥0.02 ng/mL). Mean TnT concentration did not differ by etiology of HF (0.002 ± 0.03 ng/mL vs 0.02 ± 0.04 ng/mL for ischemic and nonischemic etiologies, P = .25). Compared with patients with normal (undetectable) levels of TnT, patients with elevated TnT were significantly older, had worse functional class, and had poorer renal function. Elevated TnT concentrations were associated with increased relative risks (RR) of death or HF hospitalization (RR 2.7, 95% CI 1.7-4.3, P = .001) and death alone (RR 4.2, 95% CI 1.8-9.5, P = .001) during follow-up. Elevated TnT and New York Heart Association class were significant, independent predictors of death or HF hospitalization. Increased age and serum creatinine concentrations were significant independent predictors of death alone.

Conclusions

Nearly one fourth of ambulatory patients with chronic HF have ongoing myocardial necrosis as shown by abnormal TnT values, which are associated with increased mortality and morbidity.     

Effect of Dexamethasone on Myocardial Injury After Total Knee Arthroplasty: A Substudy of the Randomized Clinical DEX-2-TKA Trial

BackgroundMyocardial injury after noncardiac surgery (MINS) carries a high postoperative mortality. In this preplanned, subgroup analysis of the randomized DEX-2-TKA Trial, we investigated the effect of dexamethasone versus placebo on the concentration of cardiac troponin I and T (TnI and TnT) on the first postoperative morning after total knee arthroplasty. In addition, frequency of MINS, myocardial infarction, and major adverse cardiovascular events where evaluated.MethodsWe included 290 patients who received either 24 mg of dexamethasone intravenously (given perioperatively) or placebo. Blood samples were analyzed as either TnI or T depending on trial site.ResultsA total of 236 samples were eligible for analysis of TnI and 38 samples for TnT on the first postoperative morning. The median (IQR) TnI concentration was 4.6 ng/L (0-7.2 ng/L) in the dexamethasone group and 4.5ng/l (0-7.0 ng/L) in the placebo group (P = .96) on the first postoperative morning. The median TnT was 9 ng/L (6-11 ng/L) in the dexamethasone group and 8 ng/L (5-10 ng/L) in the placebo group (P = .68). The frequencies of MINS, myocardial infarction, and major adverse cardiovascular events were similar in the compared groups, but these analyses were underpowered.ConclusionWe found no effect of dexamethasone on postoperative concentration of troponin I or T on the first postoperative morning after total knee arthroplasty.     

Usefulness of diastolic deceleration time assessed by transthoracic Doppler measurement in the detection of sustained microvascular obstruction in STEMI patients treated by primary PTCA

Aims

To assess the value of coronary flow measurement by transthoracic Doppler technique in the detection of “no-reflow” phenomenon.

Methods

Fourteen patients with first anterior wall infarction treated by successful (TIMI3) primary percutaneous angioplasty and left descending coronary artery stenting were investigated. Myocardial perfusion following PCI was assessed by (i) ST-segment resolution, (ii) MRI-detected microvascular obstruction (early hypoenhancement), (iii) coronary flow pattern measurement by transthoracic Doppler technique.

Results

Sustained impairment of myocardial perfusion following PCI was observed in a large proportion of the cohort (36% by MRI, 43% by ST regression analysis). Patients with a diastolic deceleration time inferior to 482 ms had higher troponin and CK peak value, higher wall motion index score, lower ST resolution and lower LVEF assessed by MRI. The concordance of the three methods was 80%.

Conclusion

The measurement of diastolic deceleration time by transthoracic Doppler technique is a reliable technique to identify microvascular obstruction following PCI in acute anterior STEMI. A DDT inferior to 482 ms is associated with sustained “no-reflow” phenomenon.     

Optical Coherence Tomography-Guided Primary Percutaneous Coronary Intervention in ST-Segment Elevation Myocardial Infarction Patients: A Pilot Study

Background

The objective of our study was to assess whether optical coherence tomography (OCT) guidance could guide intervention to avoid balloon angioplasty and stenting during primary percutaneous coronary intervention.

Methods

One hundred patients with ST-segment elevation myocardial infarction and thrombus-containing lesion were enrolled in this study. Thrombus aspiration was performed in all cases followed by an OCT study. After thrombectomy, no stent was implanted in residual significant stenosis (> 50%) if examination using OCT suggested that the occlusion was mostly thrombotic, provided that the patient was symptom-free and the Thrombolysis in Myocardial Infarction (TIMI) flow was ≥ 2. All patients managed only using thrombectomy underwent 1-week and 9-month angiography and OCT. Patients with significant lesion or those in whom thrombectomy failed to re-establish flow underwent standard treatment.

Results

Based on the OCT information, 20 patients (20%) were treated only with aspiration even in the presence of angiographically detected “high-grade stenosis.” Angiogram and OCT performed at 1 week and 9 months showed a “normal vessel” without significant stenosis in all 20 cases. There were no cases of major adverse cardiovascular event (including death, myocardial infarction, and target lesion revascularization) during the in-hospital period or at the 12-month follow-up.

Conclusions

The results of our pilot study suggest that ST segment elevation myocardial infarction patients with TIMI 2/3 flow in the angiogram and without significant coronary narrowing using OCT examination (even in the presence of angiographically detected “high-grade stenosis”), in whom thrombus aspiration is performed in addition to optimal medical therapy might benefit only from thrombus aspiration without plain old balloon angioplasty/stenting during primary percutaneous coronary intervention. Validation of these preliminary data in larger randomized studies is warranted.     

Use of neutrophil count in early diagnosis and risk stratification of AMI

Background

Neutrophils are rapidly released into the circulation upon acute stress such as trauma or acute myocardial infarction (AMI). We hypothesized that neutrophil count might provide incremental value in the early diagnosis and risk stratification of AMI.

Methods

We conducted a prospective observational multicenter study to examine the diagnostic accuracy of the combination of neutrophil count and cardiac troponin T from 1125 consecutive patients who presented to the Emergency Department with symptoms suggestive of acute myocardial infarction. The final diagnosis was adjudicated by 2 independent cardiologists.

Results

Neutrophil count was higher in patients with acute myocardial infarction compared with other diagnoses (median 6.7 vs. 5.0 × 10⁹/L, respectively, P <.001). The accuracy of the neutrophil count for diagnosing acute myocardial infarction, quantified by the area under the receiver operating characteristic curve (AUC) was 0.69, which was significantly lower than that of cardiac troponin T (AUC 0.89, P <.001). The combination of the neutrophil count and cardiac troponin T did not improve the early diagnosis of acute myocardial infarction versus cardiac troponin T alone (P = .79). The prognostic accuracy of neutrophil count for death and AMI was significantly lower than that of cardiac troponin T. However, patients in the highest tertile of neutrophil count had a significantly increased risk of death and AMI at 90 and 360 days compared with patients in the lowest tertile (hazard ratios 2.47 [95% confidence interval, 1.63–3.72] and 2.28 [95% confidence interval, 1.55–3.36], respectively).

Conclusion

The neutrophil count does not improve the early diagnosis of AMI in patients presenting with chest pain but identifies patients at increased risk of death.     

Frequency and significance of troponin T elevation in acute ischemic stroke

Elevated levels of troponin have been reported in patients with acute ischemic stroke. In this prospective study, the prevalence and characteristics of troponin elevation were examined in 244 patients with acute ischemic stroke but without overt ischemic heart disease. Troponin T (TnT) and creatine kinase-MB (CK-MB) concentrations were measured and 12-lead electrocardiograms obtained daily during the first 5 days of admission. Myocardial perfusion scintigraphy was performed in patients with TnT levels of 0.10 micro g/L and in comparable controls without elevation of TnT. Patients were followed for a mean of 19 +/- 7 months, with all-cause mortality as the clinical end point. Elevated levels of TnT (>0.03 micro g/L) and creatine kinase-MB (> or =10 micro g/L) were observed in 10% and 9% of patients, respectively. Patients with elevated TnT had higher frequencies of heart and/or renal failure. Perfusion abnormalities on myocardial perfusion scintigraphy at rest were not more frequent or pronounced in patients with TnT levels of > or =0.10 micro g/L than in the control group. Only 7 patients (3%) had elevations of TnT or creatine kinase-MB and electrocardiographic changes suggesting acute myocardial infarctions. According to univariate and multivariate analyses, elevation of TnT was significantly associated with mortality. In conclusion, elevated levels of TnT are rare in patients presenting with ischemic stroke but without overt ischemic heart disease. Heart and renal failure rather than myocardial infarction are the most likely causes. When present, elevation of TnT seems to be useful in identifying patients who are at increased risk of dying within the following 2 years.     

Takotsubo cardiomyopathy has a unique cardiac biomarker profile: NT-proBNP/myoglobin and NT-proBNP/troponin T ratios for the differential diagnosis of acute coronary syndromes and stress induced cardiomyopathy

Background

Takotsubo cardiomyopathy (TC) usually is not recognized until heart catheterization reveals typical wall motion abnormalities in the absence of significant coronary artery disease. It was our aim to identify TC by its unique cardiac biomarker profile at an early stage and, preferably, with non-invasive procedures only.

Methods

Ratios of N-terminal prohormone of brain natriuretic peptide (NT-proBNP) and myoglobin, NT-proBNP and troponin T (TnT), NT-proBNP and creatinekinase-MB (CK-MB) were compared in patients with TC (n = 39), patients with ST-elevation myocardial infarction (STEMI, n = 48) and patients with non-ST-elevation myocardial infarction (NSTEMI, n = 34). Biomarkers were recorded serially at admission and at the three consecutive days. Optimal cut-off values to distinguish TC from STEMI and NSTEMI were calculated with receiver operator characteristic (ROC) curves.

Results

At admission a NT-proBNP (ng/l)/myoglobin (μg/l) ratio of 3.8, distinguished TC from STEMI (sensitivity: 89%, specificity: 90%), while a NT-proBNP (ng/l)/myoglobin (μg/l) ratio of 14 separated well between TC and NSTEMI (sensitivity: 65%, specificity: 90%). Best differentiation of TC and ACS was possible with the ratio of peak levels of NT-proBNP (ng/l)/TnT (μg/l). A cut-off value of NT-proBNP (ng/l)/TnT (μg/l) ratio of 2889, distinguished TC from STEMI (sensitivity: 91%, specificity: 95%), while a NT-proBNP (ng/l)/TnT (μg/l) ratio of 5000 separated well between TC and NSTEMI (sensitivity: 83%, specificity: 95%).

Conclusions

TC goes along with a singular cardiac biomarker profile, which might be useful to identify patients with TC among patients presenting with acute coronary syndromes (ACS).     

Ischemia modified albumin (IMA) in acute coronary syndrome (ACS) and left bundle branch block (LBBB). Does it make the difference?

Background

Management of patients with a suspected ACS and LBBB is a challenge to the clinician.

Different Causes of Death in Patients with Myocardial Infarction Type 1, Type 2, and Myocardial Injury

Background

Data outlining the mortality and the causes of death in patients with type 1 myocardial infarction, type 2 myocardial infarction, and those with myocardial injury are limited.

Type 1 and 2 Myocardial Infarction and Myocardial Injury: Clinical Transition to High-Sensitivity Cardiac Troponin I

Background

Studies addressing patients with type 2 myocardial infarction and myocardial injury, including the impact of using high-sensitivity (hs) cardiac troponin (cTn) assays on their incidence are needed.

Short-Term Prognosis of Myocardial Injury,Type 1, and Type 2 Myocardial Infarction in the Emergency Unit

BACKGROUND

Type 2 myocardial infarction and nonischemic myocardial injury, corresponding to troponin elevation without atherothrombosis, are emerging concepts suspected of being common in emergency departments (ED). However, their respective frequencies, risk profiles, and short-term prognoses remain to be investigated.

A score predicts failure of reperfusion after fibrinolytic therapy for acute myocardial infarction

Background A rapid, accurate, noninvasive means of predicting the likelihood of failure to achieve Thrombolysis In Myocardial Infarction (TIMI) grade 3 flow within 90 minutes after the start of fibrinolysis with streptokinase could help to identify patients who might benefit from additional therapies that aim to preserve myocytes. Methods We measured ST recovery, which was assessed as the sum of ST deviation on a 12-lead electrocardiogram, and blood levels of the myocardial proteins, troponin T, creatine kinase myocardial band (CK-MB), and myoglobin before and 60 minutes after commencing streptokinase infused for 30 to 60 minutes in 107 patients, who presented within 12 hours of symptom onset and underwent angiography at 90 minutes. Results At 90 minutes, 56% of patients (95% CI 46-66) had TIMI-3 flow. The baseline levels of troponin T, CK-MB, and myoglobin were more commonly below the discrimination values in patients with TIMI-3 flow than in patients without TIMI-3 flow (all P < .005). On multivariate analysis, the factors associated with failure to achieve TIMI-3 flow were ST recovery of <70% (P = .009), a 60-minute/baseline troponin T ratio of ≤5 (P = .0004), a baseline CK-MB level of >4 μg/L (P = .039), or a baseline myoglobin level of >85 μg/L (P = .048). Age and a history of myocardial infarction were added into the multivariate model, and a risk score was developed to predict the likelihood of failure to achieve TIMI-3 flow. A score of ≤2 excluded failure to achieve TIMI-3 flow with 96% accuracy, and a score of ≥7 predicted failure to achieve TIMI-3 flow with 90% accuracy. Conclusion Failure to achieve TIMI-3 flow in the infarct-related artery within 90 minutes after the start of fibrinolysis can be accurately predicted at approximately 60 minutes by a score incorporating clinical variables, ST recovery, and the 60-minute/baseline ratios of troponin T, CK-MB, and/or myoglobin levels. This score may facilitate triage of patients at 60 minutes after fibrinolysis to additional reperfusion therapies. (Am Heart J 2003;145:508-14.)     

Prognostic Value of Megatroponinemia After Myocardial Infarction

Purpose

The purpose of this study is to investigate the prognostic value of megatroponinemia (troponins >100 ng/mL), as a predictor of major adverse cardiac events such as recurrent angina, myocardial infarction, and death in patients presenting with acute myocardial infarction.

Methods

Over a period of 2 years, we identified 27 patients admitted with acute myocardial infarction and troponin I values >100 ng/mL. These patients were followed-up for the short term during their hospitalization as well as for an intermediate term of 18 ± 14 months after their initial presentation with acute myocardial infarction for major adverse cardiac events including recurrent angina, myocardial infarction, and death.

Results

Of the 27 patients, one died 5 days after myocardial infarction and 26 were discharged home in stable condition, with few requiring timely intervention. Six patients were lost to follow-up. Five patients died during follow-up, 4 from recurrent myocardial infarction and 1 died from metastatic renal cell carcinoma. Twelve patients had non-fatal myocardial infarction, with 10 being acute ST elevation; 3 patients had recurrent angina.

Conclusion

Patients presenting with an acute myocardial infarction and troponins >100 ng/mL have continued incremental risk of excessive major adverse cardiac events during short and intermediate follow-up period.     

Single High-Sensitivity Cardiac Troponin I to Rule Out Acute Myocardial Infarction

Background

This study examined the performance of single high-sensitivity cardiac troponin I (hs-cTnI) measurement strategies to rule out acute myocardial infarction.

B-type natriuretic peptide in the early diagnosis and risk stratification of acute chest pain

Background

Myocardial ischemia is a strong trigger of B-type natriuretic peptide (BNP) release. As ischemia precedes necrosis in acute myocardial infarction, we hypothesized that BNP might be useful in the early diagnosis and risk stratification of patients with acute chest pain.

Methods

In a prospective, international multicenter study, BNP was measured in 1075 unselected patients with acute chest pain. The final diagnosis was adjudicated by 2 independent cardiologists. Patients were followed long term regarding mortality.

Results

Acute myocardial infarction was the adjudicated final diagnosis in 168 patients (16%). BNP levels at presentation were significantly higher in acute myocardial infarction as compared with patients with other diagnoses (median 224 pg/mL vs. 56 pg/mL, P <.001). The diagnostic accuracy of BNP for the diagnosis of acute myocardial infarction as quantified by the area under the receiver operating characteristic curve (AUC) (0.74; 95% confidence interval [CI], 0.70-0.78) was lower compared with cardiac troponin T at presentation (AUC 0.88; 95% CI, 0.84-0.92; P <.001). Cumulative 24-month mortality rates were 0.5% in the first, 2.1% in the second, 7.0% in the third, and 22.9% in the fourth quartile of BNP (P <.001). BNP predicted all-cause mortality independently of and more accurately than cardiac troponin T: AUC 0.81 (95% CI, 0.76-0.86) versus AUC 0.70 (95% CI, 0.62-0.77; P <.001). Net reclassification improvement for BNP was 0.10 (P = .04), and integrated discrimination improvement 0.068 (P = .01).

Conclusions

BNP accurately predicts mortality in unselected patients with acute chest pain independently of and more accurately than cardiac troponin T, but does not seem to help in the early diagnosis of acute myocardial infarction.     

Remote Ischemic Preconditioning Reduces Myocardial Injury in Patients Undergoing Coronary Stent Implantation

Background

Myocardial necrosis occurs frequently in elective percutaneous coronary intervention (PCI) and is associated with subsequent major adverse cardiovascular events (MACEs). This study assessed the protective effect of remote ischemic preconditioning (RIPC) in patients undergoing successful drug-eluting stent implantation with normal baseline troponin values.

Methods

We analyzed 205 participants with normal baseline troponin values undergoing successful coronary stent implantation. Subjects were randomized to 2 groups: The RIPC group (n = 101), whose members received RIPC (created by three 5-minute inflations of a pneumatic medical tourniquet cuff to 200 mm Hg around the upper arm, interspersed with 5-minute intervals of reperfusion) < 2 hours before the PCI procedure, and the control group (n = 104).

Results

The primary outcomes were high sensitive cardiac troponin I (hscTnI) levels and incidence of myocardial infarction (MI 4a, defined as hscTnI > 0.20 ng/mL) at 16 hours after the PCI procedure. The median hscTnI at 16 hours after PCI was lower in the RIPC group compared with the unpreconditioned, control group (0.11 vs 0.21 ng/mL; P < 0.01). The incidence of MI 4a was lower in the RIPC group compared with the control group (39% vs 54%, P < 0.05). Index of renal function showed no difference between the 2 groups at 16 hours after PCI (P > 0.05).

Conclusion

RIPC reduced post-PCI TnI release and incidence of MI 4a in patients undergoing elective coronary stent implantation.     

The clinical significance of cardiac troponins in medical practice

Troponins are regulatory proteins that form the cornerstone of muscle contraction. The amino acid sequences of cardiac troponins differentiate them from that of skeletal muscles, allowing for the development of monoclonal antibody-based assay of troponin I (TnI) and troponin T (TnT). Along with the patient history, physical examination and electrocardiography, the measurement of highly sensitive and specific cardiac troponin has supplanted the former gold standard biomarker (creatine kinase-MB) to detect myocardial damage and estimate the prognosis of patients with ischemic heart disease. The current guidelines for the diagnosis of non-ST segment elevation myocardial infarction are largely based on an elevated troponin level. The implementation of these new guidelines in clinical practice has led to a substantial increase in the frequency of myocardial infarction diagnosis.Automated assays using cardiac-specific monoclonal antibodies to cardiac TnI and TnT are commercially available. They play a major role in the evaluation of myocardial injury and prediction of cardiovascular outcome in cardiac and non-cardiac causes.In this review we discuss the clinical applications of cardiac troponins and the interpretation of elevated levels in the context of various clinical settings.