Serial Troponin Measurements Research Articles

Diagnostic Performance of High-Sensitive Troponin T in Patients With Renal Insufficiency

In the present study, we wanted to (1) evaluate whether high-sensitive troponin T levels correlate with the grade of renal insufficiency and (2) test the accuracy of high-sensitive troponin T determination in patients with renal insufficiency for diagnosis of acute myocardial infarction (AMI). In this cross-sectional analysis, all patients who received serial measurements of high-sensitive troponin T from August 1, 2010, to October 31, 2012, at the Department of Emergency Medicine were included. We analyzed data on baseline characteristics, reason for referral, medication, cardiovascular risk factors, and outcome in terms of presence of AMI along with laboratory data (high-sensitive troponin T, creatinine). A total of 1,514 patients (67% male, aged 65 ± 16years) were included, of which 382 patients (25%) had moderate to severe renal insufficiency and significantly higher levels of high-sensitive troponin T on admission (0.028 vs 0.009, p <0.0001). In patients without AMI, high-sensitive troponin T correlated inversely with the estimated glomerular filtration rate (R=-0.12, p <0.0001). Overall, sensitivity of an elevated high-sensitive troponin for diagnosis of AMI was 0.64 (0.56 to 0.71) and the specificity was 0.48 (0.45 to 0.51). The area under the curve of the receiver operating characteristic for all patients was 0.613 (standard error [SE] 0.023), whereas it was 0.741 (SE 0.029) for patients with a Modification of Diet in Renal Disease estimated glomerular filtration rate >60ml/min presenting with acute chest pain or dyspnea and 0.535 (SE 0.056) for patients with moderate to severe renal insufficiency presenting with acute chest pain or dyspnea. In conclusion, the diagnostic accuracy for presence of AMI of a baseline measurement of high-sensitive troponin in patients with renal insufficiency was poor and resembles tossing a coin.

Cardiac involvement of lung cancer mimicking myocardial infarction

A 58-year-old man (a heavy smoker), without prior medical history, was admitted to the Department of Cardiology in the emergent diagnosis of acute coronary syndrome with ST segment elevation in the third hour of retrosternal pain. The initial ECG revealed sinus rhythm 85/min, left anterior fascicular block, QS pattern in V1–V3 with ST-segment elevation in the leads V2 through V6 (up to 2 mm in V2–V3), with symmetric negative T waves in the leads I, aVL, V2–V5 (Fig. 1). Laboratory tests, except for a small leukocytosis (11 × 109/L, N to 10 × 109/L), and elevations of troponin T (30 ng /L, N to 14 ng/L), were within normal limits. Urgent coronary angiography was performed, which showed critical changes in the distal circumflex branch narrow artery (< 2 mm), with no significant haemodynamic atherosclerosis in other arteries. Due to the location of the stenosis and artery calibre, coronary angioplasty was not performed. Despite typical pharmacological treatment, pain relief was not achieved. The subsequent ECG recorded persistent ST-segment elevation with negative T waves in precordial leads, without a change in troponin values (the II. troponin: 27 ng/L and the III: 28 ng/L). Based on radiological images of the chest, a tumour in the left lung with obliteration of the left heart border was suspected. Transthoracic echocardiography demonstrated the presence of a tumour sized 10 × 7 × 11 cm with involvement of the pericardium (without evidence of fluid), and probably the anterior wall of the left ventricle. To differentiate the cardiac mass, we performed cardiac magnetic resonance imaging and confirmed an anterior mediastinal tumour, causing extensive atelectatic changes in the left lung and infiltrating the anterior wall of the left ventricle (Figs. 2, 3). The patient was referred to the oncology centre where metastatic small cell carcinoma of the left lung was diagnosed. Three months after the start of chemotherapy, the patient died. The most common neoplasms associated with cardiac metastasis are lung cancer, oesophageal cancer, lymphoma, breast cancer, leukaemia, stomach cancer, and melanoma. Their symptomatology is largely dependent on the size of the tumour and its location. Myocardial infiltration by tumour cells may lead to the occurrence of arrhythmias and cardiac conduction, and less non-specific ST segment changes. In this case, the clinical and ECG changes initially showed a myocardial infarction with ST segment elevation anterior wall. However, subsequent ECGs, serial measurements of cardiac troponin and results of imaging studies did not confirm the initial diagnosis. In the era of invasive treatment of myocardial infarction, it is necessary to consider other causes of ST-T changes in the ECG and increased troponin values. Extended cardiac diagnosis and a multidisciplinary approach are often necessary to determine the correct diagnosis.

GW24-e2277 Cardiac Diastolic Dysfunction may Hold Promise as Markers of Cardiotoxicity during Daunorubicin Treatment in Acute Nonlymphocytic Leukemia Patients

ObjectivesDaunorubicin causes cardiac injury in acute nonlymphocytic leukemia. Early identifying caridotoxicity induced by daunorubicin might help individualise cardiac protect treatment. Dexrazoxane can reduce cardiac damage. In this study, we assess...

Serial measurements of cardiac troponin I in patients with myasthenia gravis-related cardiomyopathy

Myasthenia gravis (MG) primarily affects skeletal muscle through the production of autoantibodies against the nicotinic acetylcholine receptor in the motor endplates; in addition, heart muscle is an autoimmune target [1,2]. Although MG is believed to be relatively rare, 16% of patients with MG exhibit several types of cardiac involvement, ranging from asymptomatic electrocardiogram (ECG) changes to myocarditis, heart failure, and sudden death [2]. A persistent increase in cardiac troponins reportedly indicates ongoing myocardial damage during heart failure and a poor prognosis [3–6].

Serial measurement of hFABP and high-sensitivity troponin I post-PCI in STEMI: how fast and accurate can myocardial infarct size and no-reflow be predicted?

The objective of this study was to compare heart-specific fatty acid binding protein (hFABP) and high-sensitivity troponin I (hsTnI) via serial measurements to identify early time points to accurately quantify infarct size and no-reflow in a preclinical swine model of ST-elevated myocardial infarction (STEMI). Myocardial necrosis, usually confirmed by hsTnI or TnT, takes several hours of ischemia before plasma levels rise in the absence of reperfusion. We evaluated the fast marker hFABP compared with hsTnI to estimate infarct size and no-reflow upon reperfused (2 h occlusion) and nonreperfused (8 h occlusion) STEMI in swine. In STEMI (n = 4) and STEMI + reperfusion (n = 8) induced in swine, serial blood samples were taken for hFABP and hsTnI and compared with triphenyl tetrazolium chloride and thioflavin-S staining for infarct size and no-reflow at the time of euthanasia. hFABP increased faster than hsTnI upon occlusion (82 ± 29 vs. 180 ± 73 min, P < 0.05) and increased immediately upon reperfusion while hsTnI release was delayed 16 ± 3 min (P < 0.05). Peak hFABP and hsTnI reperfusion values were reached at 30 ± 5 and 139 ± 21 min, respectively (P < 0.05). Infarct size (containing 84 ± 0.6% no-reflow) correlated well with area under the curve for hFABP (r(2) = 0.92) but less for hsTnI (r(2) = 0.53). At 50 and 60 min reperfusion, hFABP correlated best with infarct size (r(2) = 0.94 and 0.93) and no-reflow (r(2) = 0.96 and 0.94) and showed high sensitivity for myocardial necrosis (2.3 ± 0.6 and 0.4 ± 0.6 g). hFABP rises faster and correlates better with infarct size and no-reflow than hsTnI in STEMI + reperfusion when measured early after reperfusion. The highest sensitivity detecting myocardial necrosis, 0.4 ± 0.6 g at 60 min postreperfusion, provides an accurate and early measurement of infarct size and no-reflow.

Serial measurements of high-sensitivity cardiac troponin T after exercise stress test in stable coronary artery disease

Objective: The aim was to assess serial measurements of high-sensitivity cardiac troponin T (hs-cTNT) post-exercise in patients with stable coronary artery disease (CAD).Methods: Twelve patients with positive coronary angiograms (CAD positives) and 12 controls performed an exercise stress test.Results: CAD positive had higher baseline and peak concentrations of hs-cTNT than controls. Significant increases in hs-cTNT were seen in both groups after exercise. In two-third of patients the peak in hs-cTNT was above the 99th percentile.Conclusion: hs-cTNT is higher in patients with stable coronary disease than in controls and exceeds the diagnostic cut-off value for myocardial infarction in a majority of patients with CAD after exercise.

Incremental value of objective cardiac testing in addition to physician impression and serial contemporary troponin measurements in women.

Guidelines recommend that patients presenting to the emergency department (ED) with chest pain who are at low risk for acute coronary syndrome (ACS) receive an objective cardiac evaluation with a stress test or coronary imaging. It is uncertain whether all women derive benefit from this process. The study aim was to determine the incremental value of objective cardiac testing after serial cardiac markers and physician risk assessment. Women enrolled in the 18-site Myeloperoxidase in the Diagnosis of Acute Coronary Syndrome (MIDAS) study had serial troponin I measured at time 0 and 90 minutes and physician risk assessment for the presence of ACS. Risk estimates obtained at the time of ED evaluation were dichotomized as high or non-high risk. The primary outcome was the composite of acute myocardial infarction (AMI) or revascularization at 30 days. Logistic regression with receiver operator characteristic (ROC) curves and net reclassification index were used to determine the diagnostic accuracy for the composite outcome of 30-day MI or revascularization for two models: 1) troponin I results and physician risk assessment alone and 2) troponin I results, physician risk assessment, and objective cardiac testing. A total of 460 women with a median age 58 years (interquartile range [IQR] = 48.5 to 68 years) were included, and 32 (6.9%) experienced AMI or revascularization by 30 days. Comparison of the area under the ROC curves (AUC) showed that the addition of objective cardiac testing to the combination of troponin I results and physician risk assessment did not significantly improve prediction of 30-day AMI or revascularization (AUC = 0.85 vs. 0.89; p = .053). Using a threshold of 1%, net reclassification index showed that the addition of objective cardiac testing to troponin I results and physician risk assessment worsened the prediction for 30-day AMI and revascularization. All of the reclassified patients were false positives, with nine (2.1%) patients incorrectly reclassified from <1% risk to ≥ 1% risk of 30-day AMI or revascularization. In the era of contemporary troponin assays, objective cardiac testing after an ED clinician risk assessment of non-high risk and negative troponin I results at 0 and 90 minutes does not improve the prediction of 30-day AMI or revascularization in women presenting with chest pain or other symptoms of cardiac ischemia.

Abstract WP131: Correlation of Cardiac Derangement in Patients with Right-Sided Ischemic Stroke and the Severity of Insular Damage

Objective: Although it is known that neurogenic cardiac damage can occur after an ischemic stroke, the mapping of the neuroanatomic correlation of ischemic stroke-related myocardial injury remains to be defined. Our previous animal study found a higher incidence of myocardial damage from left-sided insular infarction comparing to the right side. However, the results from various clinical studies have been inconclusive. This clinical study aims to identify a quantitative correlation between adverse cardiac outcomes and insular infarction, left-sided versus right-sided, as well as potential prognostic factors that may be used to aid in assessing patient outcomes and making treatment decisions. Methods and Results: A serial measurements of cardiac troponin T (cTnT) and creatine phosphokinase-MB (CK-MB), 12-lead EKG, and two- dimensional echocardiography were performed in 42 patients with MRI-confirmed ischemic stroke involving the insular cortex. The severity of insular damage was measured with diffusion-weighted imaging studies (DWI). Patients with renal failure, recent cardiac ischemic events, or congestive heart failure were excluded. Twenty-two patients (52.4%) had left-sided middle cerebral artery (MCA) infarcts with insular involvement, whereas 20 (47.6%) had a right-sided MCA infarcts involving the insular cortex. When compared to patients with left MCA infarcts involving the insular cortex, patients with right MCA infarcts with insular involvement had significantly higher levels of cTnT elevation. By using the linear regression analysis we also identified a statistically significant correlation between cTnT elevation and severity of right insular damage, instead of the NIH stroke score (NIHSS) as commonly assumed. Moreover, two patients were found to have transient left ventricular wall hypokinesis which mimics Takotsubo cardiomyopathy. Conclusions: This study showed that patients with right MCA ischemic stroke involving the insular cortex, comparing to those with left-sided insular stroke, tend to have more severe cardiac insult leading to higher levels of cTnT. The study also identified severity of insular damage as a potential prognostic factor in assessing cardiac derangement as a complication of insular infarction.

A Nonthoracotomy Myocardial Infarction Model in an Ovine Using Autologous Platelets

Objective. There is a paucity of a biological large animal model of myocardial infarction (MI). We hypothesized that, using autologous-aggregated platelets, we could create an ovine model that was reproducible and more closely mimicked the pathophysiology of MI. Methods. Mepacrine stained autologous platelets from male sheep (n = 7) were used to create a myocardial infarction via catheter injection into the mid-left anterior descending (LAD) coronary artery. Serial daily serum troponin measurements were taken and tissue harvested on post-embolization day three. Immunofluorescence microscopy was used to detect the mepacrine-stained platelet-induced thrombus, and histology performed to identify three distinct myocardial (infarct, peri-ischemic “border zone,” and remote) zones. Results. Serial serum troponin levels (μg/mL) measured 0.0 ± 0.0 at baseline and peaked at 297.4 ± 58.0 on post-embolization day 1, followed by 153.0 ± 38.8 on day 2 and 76.7 ± 19.8 on day 3. Staining confirmed distinct myocardial regions of inflammation and fibrosis as well as mepacrine-stained platelets as the cause of intravascular thrombosis. Conclusion. We report a reproducible, unique model of a biological myocardial infarction in a large animal model. This technique can be used to study acute, regional myocardial changes following a thrombotic injury.

Diagnosing myocardial infarction by serial measurement of high sensitivity troponin — What type of relative change value (delta) and how much should it be?

Diagnosing myocardial infarction by serial measurement of high sensitivity troponin — What type of relative change value (delta) and how much should it be?

What Is the Role of Serial High-Sensitivity Troponin Measurements in Chronic Heart Failure?

In the past decade, there has been a veritable explosion of studies examining cardiac biomarkers in heart failure (HF).2 Among the many reasons for this fact is that measurements of such biomarkers as natriuretic peptides (the current gold standard biomarker for HF diagnosis, prognosis, and management decision-making) are easy and safe to obtain, and they can potentially reveal important information about the patient at the biological level. Another class of cardiac biomarkers, the cardiac troponins, also provides important information about the prognosis of patients with HF. Studies have shown that cardiac troponins are typically measurable and sometimes frankly increased in HF patients, with values being closely linked with the severity of illness. Patients with more severe HF usually show higher cardiac troponin concentrations, intriguingly often independently of a diagnosis of coronary artery disease. Interestingly, cardiac troponins have been shown to be independently prognostic in both acute HF (1) and chronic HF (2), even after adjusting for natriuretic peptide concentrations. With a new generation of high-sensitivity cardiac troponin assays now or soon to be available, it is possible to detect minute amounts of circulating cardiac troponins with high precision. A substantial percentage of the patients with HF have measurable cardiac troponin values in high-sensitivity assays, often above the 99th percentile for a normal healthy population. For example, in a prior study, Latini and colleagues used a high-sensitivity cardiac troponin T (hs-cTnT) assay to measure cTnT among patients in the Valsartan Heart Failure Trial (Val-HeFT) (3) and reported the biomarker to be measurable in 92% of the study participants and—importantly for prognosis—before and after an adjustment for natriuretic peptides. This finding is of importance for both monitoring and managing HF, because high-sensitivity cardiac troponin measurements could theoretically be leveraged for monitoring chronic HF stability. If therapies specifically tailored for ameliorating the …

How Safe Is the Outpatient Management of Patients with Acute Chest Pain and Mildly Increased Cardiac Troponin Concentrations?

The appropriate management of patients discharged from the emergency department (ED) with increased high-sensitivity cardiac troponin T (hs-cTnT) but normal or borderline-high conventional cardiac troponin concentrations is unknown. We investigated 643 consecutive ED patients with acute chest pain who had been discharged for outpatient management after acute myocardial infarction (AMI) had been ruled out by serial measurements of conventional cardiac troponin. hs-cTnT was measured blindly, and we calculated the rates of all-cause mortality (primary endpoint) and subsequent AMI (secondary endpoint) at 30, 90, and 360 days. hs-cTnT concentrations were increased (>14 ng/L) in 114 patients (18%) but <30 ng/L in 95% of these patients. Of those 114 patients, 96 (84%) had an adjudicated noncoronary cause of chest pain. Thirty-day mortality (95% CI) was 0.9% (0.1%-6.1%), 90-day mortality was 2.7% (0.9%-8.1%), and 360-day mortality was 5.2% (2.2%-11.9%) in patients with increased hs-cTnT; respective rates (95% CI) of AMI were 0.0%, 1.9% (0.5%-7.2%), and 7.6% (3.7%-15.3%). Increased hs-cTnT was associated with increased mortality and AMI at 90 days (P = 0.006 and P = 0.081, respectively) and 360 days (P = 0.001 for both). hs-cTnT is a strong prognosticator of intermediate and long-term mortality and AMI in low-risk patients discharged from the ED after AMI has been ruled out. The relatively low rate of 30-day events may suggest that patients without acute coronary syndrome and small increases in cardiac troponin are in need of further investigations and treatments, but not necessarily immediate hospitalization.

LONG-TERM SAFETY OF A CORONARY COMPUTED TOMOGRAPHY ANGIOGRAPHY-GUIDED STRATEGY FOR ASSESSMENT OF CHEST PAIN IN THE EMERGENCY DEPARTMENT

Background: Coronary computed tomography angiography (CCTA) is increasingly being used in Emergency Departments (ED) for the diagnostic work-up of patients with low-to-intermediate risk chest pain, however limited data exists on the safety of such an approach. Methods: We prospectively evaluated 335 consecutive patients who presented to ED between September 2008 and March 2010 with low-to-intermediate risk (TIMI 0–4) ischaemic-type chest pain and were evaluated with 320-detector CCTA (dose-modulated retrospective electrocardiogram-triggering) after normal single or serial troponin measurement and normal electrocardiogram. Patients with previous significant coronary stenoses or previous revascularisation were excluded. Patients without anyplaque ormild stenoses onCCTAweredischarged with no further investigation. Patients with moderate s d f t d

Changes in Cardiac Biomarkers During Doxorubicin Treatment of Pediatric Patients With High-Risk Acute Lymphoblastic Leukemia: Associations With Long-Term Echocardiographic Outcomes

Doxorubicin causes cardiac injury and cardiomyopathy in children with acute lymphoblastic leukemia (ALL). Measuring biomarkers during therapy might help individualize treatment by immediately identifying cardiac injury and cardiomyopathy. Children with high-risk ALL were randomly assigned to receive doxorubicin alone (n = 100; 75 analyzed) or doxorubicin with dexrazoxane (n = 105; 81 analyzed). Echocardiograms and serial serum measurements of cardiac troponin T (cTnT; cardiac injury biomarker), N-terminal pro-brain natriuretic peptide (NT-proBNP; cardiomyopathy biomarker), and high-sensitivity C-reactive protein (hsCRP; inflammatory biomarker) were obtained before, during, and after treatment. cTnT levels were increased in 12% of children in the doxorubicin group and in 13% of the doxorubicin-dexrazoxane group before treatment but in 47% and 13%, respectively, after treatment (P = .005). NT-proBNP levels were increased in 89% of children in the doxorubicin group and in 92% of children in the doxorubicin-dexrazoxane group before treatment but in only 48% and 20%, respectively, after treatment (P = .07). The percentage of children with increased hsCRP levels did not differ between groups at any time. In the first 90 days of treatment, detectable increases in cTnT were associated with abnormally reduced left ventricular (LV) mass and LV end-diastolic posterior wall thickness 4 years later (P < .01); increases in NT-proBNP were related to an abnormal LV thickness-to-dimension ratio, suggesting LV remodeling, 4 years later (P = .01). Increases in hsCRP were not associated with any echocardiographic variables. cTnT and NT-proBNP may hold promise as biomarkers of cardiotoxicity in children with high-risk ALL. Definitive validation studies are required to fully establish their range of clinical utility.

Serial Measurement of Cardiac Troponin T Using a Highly Sensitive Assay in Patients With Chronic Heart Failure

Background— Cardiac troponins are emerging as important prognostic markers in chronic cardiovascular conditions like stable coronary artery disease or chronic heart failure (HF). Less is known about the relation between serial measurements of high-sensitivity cardiac troponin T (hs-cTnT) and future events in HF. We determined the association between changes over time in hs-cTnT and outcome in patients with chronic HF. Methods and Results— We analyzed 5284 patients with chronic HF from 2 independent randomized clinical trials, the Valsartan Heart Failure Trial (Val-HeFT) (n=4053) and the Gruppo Italiano per lo Studio della Sopravvivenza nell'Insufficienza Cardiaca–Heart Failure (GISSI-HF) trial (n=1231). hs-cTnT was measured at randomization and after 3 months (GISSI-HF) or 4 months of follow-up (Val-HeFT). The association between changes over time of hs-cTnT and various outcomes was tested in multivariable models. In both studies, increases in hs-cTnT levels over time were associated with age, diabetes mellitus, worsening of renal function (reduction in estimated glomerular filtration rate), and baseline and increases in N-terminal pro-brain natriuretic peptide concentrations. Increases in hs-cTnT concentrations were associated with all-cause mortality (incidence rates, 8.19 [7.51–8.88] and 6.79 [5.98–7.61] per 100 person-years in Val-HeFT and GISSI-HF, respectively, with hazard ratios [95% confidence intervals] of 1.59 [1.39–1.82] and 1.88 [1.50–2.35]) after adjustment for conventional risk factors and baseline levels of hs-cTnT and N-terminal pro-brain natriuretic peptide. Changes in hs-cTnT concentration modestly improved prognostic discrimination beyond baseline values for fatal outcomes only. Conclusions— Despite very low circulating concentrations, changes in hs-cTnT concentrations over time are robust predictors of future cardiovascular events in patients with chronic HF but add limited prognostic discrimination. Clinical Trial Registration— http://www.clinicaltrials.gov . Unique identifier: NCT00336336.

Circulation: Clinical Summaries

<i>Circulation:</i> Clinical Summaries

A Novel Coronary Computed Tomography Angiography-guided Algorithm for Chest Pain Evaluation in the Emergency Department is Effective and Safe at Long-term Follow-up

Background: Coronary computed tomography angiography (CTA) may be utilised for assessment of patients presenting to the Emergency Department (ED) with chest pain. We designed and tested a novel CTA-guided algorithm for triaging chest pain patients and sought to determine the efficacy and long-term safety of this diagnostic strategy. Methods: We prospectively evaluated 542 consecutive patients who presented to ED between September 2008 and June 2011 with low-to-intermediate risk (TIMI 0–4) ischaemic-sounding chest pain and were evaluated with 320-row CTA after normal single or serial troponin measurements and normal electrocardiogram. Patients with known obstructive coronary stenoses or previous revascularisation were excluded. Patients without plaque or with mild stenoses on CTA were discharged without further investigation. Patients with moderate stenoses were discharged with outpatient stress echocardiography. Patients with severe stenoses were admitted for invasive angiography. Discharged patients and/or their general practitioners were contacted to determine long-term MACE. Results: Mean age was 56.0 ± 11.6 years (58% male). CTA showed no plaque or mild stenoses in 415 patients (77%) who were discharged without further investigation, moderate stenoses in 54 (10%) who were discharged with outpatient stress echocardiography and severe stenoses in 73 (13%) who were admitted. At median 23.3-month follow-up (range 8–41 months), there had been 10 chest pain readmissions (2%, 95%CI 1.2–3.9%), no revsascularisation procedures, no myocardial infarctions and no deaths (95%CI 0–0.8%). Follow-up was 100% complete. Conclusions: Triaging and discharging low-to-intermediate risk chest pain patients from ED after investigation with a novel CTA-guided algorithm is safe with no MACE at long-term follow-up. This approach provides a paradigm for a new model of care for chest pain assessment in ED.

Sustained Ventricular Fibrillation in a Conscious Patient

A 44-YEAR-OLD MAN WITH A NONISCHEMIC DIlated cardiomyopathy treated with an implanted left ventricular assistdevice (LVAD) was admitted to our hospital for diuresis after presenting with acute decompensated heart failure. His admission blood pressure was 95/65 mm Hg. Serial troponin measurements were negative. While hospitalized, the patient developed a wide complex tachycardia on telemetry monitoring resulting in multiple successive discharges from his implantable cardioverterdefibrillator (ICD). On evaluation, the patient was conversant and without complaint of lightheadedness or palpitations. Bilateral radial and femoral pulses were absent. An automated cuff was unable to measure a brachial blood pressure in either arm. An electrocardiogram (ECG) was obtained (Figure 1). Question: How can the patient’s ECG be reconciled with his clinical appearance and physical findings?

A practical assessment of the short-term in vitro stability of troponin I at the 99th percentile

Serial troponin measurement is important for the diagnosis of myocardial infarction. As troponin concentrations approach the cut-off for detectable myocardial necrosis, smaller changes in troponin as a result of decreased in vitro stability may be sufficient to generate changes of apparent clinical significance. This is particularly relevant regarding retrospective 'add-on' testing on samples several hours after venepuncture. We investigated the stability of troponin I (cTnI) at values close to the 99th percentile limit. Serum samples with baseline cTnI concentrations in the range 0.04-0.15 μg/L were analysed routinely using the Siemens TnI-Ultra assay. Follow-up analysis was carried out at 6, 9, 12, 24 and 48 h post-venepuncture after storage at room temperature and in the cold room. There was a significant decrease in cTnI concentration after 6 h post-venepuncture compared with baseline levels (P < 0.001). The maximum percentage change was -17.1% observed after 48 h storage at room temperature. Of samples with baseline cTnI concentration 0.040 μg/L, 80% had a cTnI concentration below 0.040 μg/L on re-analysis after 6 h. Requests for retrospective addition of troponin measurement on samples several hours after venepuncture is commonplace in many laboratories. Analysis of samples drawn >6 h previously may produce values below the cut-off for myocardial necrosis (0.040 μg/L) that would have been detectable if measured earlier as a result of decreased in vitro stability. Significant percentage decreases in cTnI concentration following storage may also have implications in lowering the threshold for an apparently clinically significant change to occur.

Association of serial measurements of cardiac troponin T using a sensitive assay with incident heart failure and cardiovascular mortality in older adults

Association of serial measurements of cardiac troponin T using a sensitive assay with incident heart failure and cardiovascular mortality in older adults