Detection Of Myocardial Injury Research Articles

Prediction of mid-term outcome after cryo-balloon ablation of atrial fibrillation using post-procedure high-sensitivity troponin level.

ObjectiveHigh-sensitivity troponin I (hsTnI) assays lead to, among other things, improvement in the detection of myocardial injury and improved risk stratification of patients with atrial fibrillation (AF). The aim of this study was to investigate the association between post-procedure cardiac biomarkers and clinical outcome in patients undergoing cryo-balloon ablation (CA) for AF.MethodsA total of 57 patients (mean age 55.1 ± 12.2 years, 50.9% female) with symptomatic paroxysmal AF underwent the CA procedure. Two hundred and twenty-eight pulmonary veins (PVs) were attempted for pulmonary vein isolation (PVI) with a second-generation cryo-balloon. hsTnI, CK-MB mass and myoglobin samples were prospectively obtained before and 24 hours after ablation.ResultAt a mean follow up of 214.6 ± 24.3 days, the probability of being arrhythmia free after a single procedure was 86%. Post-ablation hsTnI (p = 0.001), left atrial (LA) diameter (p = 0.002), duration of AF (p = 0.002), mean minimal temperature of the left superior pulmonary vein (p = 0.005), and age (p = 0.021) were associated with increased AF recurrence rate. On multivariate analysis, lower hsTnI level was the only independent predictor for AF recurrence (p = 0.012). Post-ablation hsTnI levels lower than 4.40 ng/ml predicted AF recurrence during follow up, with a sensitivity of 86% and a specificity of 96%.ConclusionIt is well recognised that the PV antrum contributes to initiation and/or perpetuation of AF. A lower postablation hsTnI level may predict an increased AF recurrence rate, suggesting inadequate ablation of the PV antrum. This may be used as a non-invasive marker to predict the outcome of AF.

High-sensitivity troponin: where are we now and where do we go from here?

High-sensitivity troponin (hsTn) assays are used clinically in most parts of the world and are expected to be approved by the US FDA for clinical use in the USA soon. Clinical use of hsTn leads to improvements in the detection of myocardial injury, shorter time to ruling out acute myocardial infarction, improved risk-stratification of patients with heart failure and atrial fibrillation among others. HsTn may also guide strategies for primary and secondary prevention of cardiovascular disease. However, unmet challenges remain, including distinguishing between acute and chronic hsTn elevations, distinguishing between type 1 and type 2 acute myocardial infarction and determining whether to use gender-neutral or gender-specific reference values.

Detection of Myocardial Injury by CMR After Transcatheter Aortic Valve Replacement

BackgroundMyocardial injury after transcatheter aortic valve replacement (TAVR) is common, but its cause and relationship to the extent of myocardial tissue loss remain unclear. ObjectivesThis study sought to examine the incidence and degree of ischemic myocardial damage using cardiac magnetic resonance imaging and myocardial biomarkers in patients undergoing TAVR. MethodsPatients with severe aortic stenosis (n = 61) underwent cardiac magnetic resonance imaging before and after TAVR for the assessment of new myocardial injury. High-sensitivity cardiac troponin T and creatine kinase-myocardial band were measured before and at 24, 48, and 72 h after TAVR. ResultsAfter TAVR, new myocardial late enhancement (LE) with an ischemic pattern occurred in 11 patients (18%), with a mean mass of 3.7 g (interquartile range: 1.2 to 6 g) or 1.8% (interquartile range: 1.3% to 4.1%) of the left ventricular mass. Patients with new LE had a decreased left ventricular function (ejection fraction: pre, 55.5 ± 14.1% vs. post, 45.3 ± 14.9%; p = 0.001). In patients without new LE, no differences were observed (ejection fraction: pre, 53.9 ± 17.3% vs. post, 54.6 ± 16.3%; p = NS) after TAVR. ConclusionsNew ischemic-type myocardial LE after TAVR can be observed in a notable proportion of patients and is assumed to be of embolic origin. Patients with new LE feature a significant decrease in left ventricular function at discharge.

Detection of myocardial injury due to defi brillation threshold checking after insertion of implantable cardioverter/defi brillators

Aims Possible myocardial damage caused by defi brillation threshold (DFT) control and its extent after insertion of implantable cardioverter/defi brillators (ICD) is still a matter for debate. This study aimed to identify the eff ect of DFT checking during ICD implantation, compared with permanent pacemaker (PPM) implantation, on the magnitude of myocardial damage as assessed by cardiac troponin-T (cTNT) and CK-MB.Methods and results A total of 133 candidates for ICD implantation were enrolled in the ICD group (mean age 60.66 ± 12.25 years; males 111 [83.5%]) as well as 130 candidates in the PPM group (mean age 69.56 ± 12.86 years; males 64 [49.2%]). DFT was controlled in all of the ICD patients. Serum levels of cTNT and CK-MB were measured at baseline plus 8 and 24 hours following the procedure. The results were adjusted for age, gender, and other confounding factors. The amount of cTNT rise after 8 and 24 hours in the ICD group was signifi cantly higher than in the PPM group (p < 0.001 for both). These diff erences remained signifi cant after adjustment for confounding factors. The level of CK-MB rise after 8 and 24 hours was also signifi cantly higher in the ICD group, although it lost its signifi cance after adjustment for age, gender and other confounding variables. There was no signifi cant relationship between the amount of energy delivered and enzyme elevation.Conclusion Elevation of cTNT and CK-MB after the ICD implantation was signifi cantly higher than that after the PPM implantation and may be attributed to the DFT testing shock and resulting myocardial injury.

Quantification of Circulating Donor Specific Cell Free DNA Is an Exquisitely Sensitive Non-Invasive Indicator of Injury to the Donor Heart

Purpose The detection and quantification of circulating donor specific cell free DNA (DS cf-DNA) has been proposed as a non-invasive biomarker for the detection of rejection following cardiac transplantation. The purpose of this study was to investigate the sensitivity of a novel approach based on targeted quantification of DS cf-DNA in detecting injury to the donor organ. Methods and Materials A prospective blinded study was conducted in 45 samples from 17 pediatric patients post heart transplantation. In 11 patients, blood samples were drawn at each of three time points: 1) 14 to 36 hours, 2) 84-126 hours, and 3) 160-206 hours post cross clamp removal (33 samples). In 6 patients samples were drawn both immediately before and within 35 min following standard bioptome surveillance cardiac biopsy (12 samples). Total cf-DNA was determined by quantitative real time PCR; percent donor specific DNA was measured using targeted next generation sequencing (DANSRtm, Ariosa Diagnostics). Results All 11 patient samples were elevated on post op time 1 compared to times 2 and 3 (p figure ). All 6 patient samples were at baseline levels at time of surveillance biopsy. All surveillance biopsies were negative for rejection. All 6 post bioptome biopsy samples were significantly elevated compared to their pre biopsy levels (p figure ). Conclusions Circulating levels of DS cf-DNA are elevated post clamp removal and decrease to baseline within 5 days. The sensitivity of the approach allows unambiguous detection of myocardial injury at the level of that produced by standard surveillance biopsy. Quantification of circulating DS cf-DNA may be a sensitive non-invasive biomarker for rejection.

Diagnostic performance of T2-weighted CMR for evaluation of acute myocardial injury

Summary We compared the performances of two different fat suppression T2-weighted fast spin echo sequences and demonstrated that T2-weighted CMR has high specificity but overall low sensitivity for detection of myocardial injury. More robust CMR techniques are needed for the detection of acute myocardial injury. Background Edema-sensitive T2-weighted cardiac magnetic resonance (CMR) based on fast spin-echo (FSE) imaging is a useful modality to detect acute myocardial injury. Conventional T2-weighted CMR uses three inversion-recovery (IR) pulses, the first two to null the blood signal, and the last one (STIR) to null fat signal, but suffers from reduced myocardial signal and signal dropout. We compared the performances of two different fat suppression T2-weighted FSE sequences: a) STIR (FSE-STIR) and b) spectral adiabatic inversion recovery fat suppression (FSE-SPAIR) for detection of myocardial injury in patients with cardiomyopathy. Methods 65 consecutive patients referred for CMR evaluation of myocardial structure and function underwent FSE-STIR and FSE-SPAIR in addition to cine and late gadolinium enhancement CMR as part of the routine clinical protocol. T2-weighted FSE images were independently evaluated by two readers, blinded to the clinical history and type of sequence, for image quality and artifacts (Likert scale 1-5), and presence of increased myocardial T2 signal suggestive of edema. Disagreements in interpretation of myocardial edema were resolved by consensus. In addition, presence of increased T2 signal suggestive of myocardial edema based on the clinical CMR interpretation, incorporating all CMR sequences available in the study, was also recorded for comparison. Troponin levels acquired during the time of the referral were recorded, and patients with recent (<30 days) troponin elevation greater than 2 times upper limit of normal were diagnosed with acute myocardial injury. The diagnostic performance of each T2-weighted FSE technique for detection of myocardial injury was evaluated. Results There were 22/65 patients (34%) with evidence of acute myocardial injury. Image quality and artifact scores were significantly better with the FSE-SPAIR technique compared to FSE-STIR (2.15 vs 2.68, p<0.01; 2.62 vs 3.05, p<0.01, respectively). The sensitivity, specificity, positive predictive value and negative predictive value are as follows: 27%, 93%, 67%, 71% for FSE-SPAIR, 36%, 91%, 67%, 74% for FSE-STIR and 68%, 98%, 94%, 84% for clinical interpretations. There was a statistically significant difference in sensitivity between the clinical interpretation and each of the T2-weighted techniques, but not between the independent T2-weighted techniques. Conclusions

OT1-02-12: Early Detection of Cardiotoxicity by Advanced Cardiac Imaging and a Novel Biomarker in Breast Cancer Patients Undergoing Chemotherapy.

Abstract Background The survival rate of breast cancer patients has increased due to improvements in cancer treatment. However, many survivors develop irreversible or reversible cardiotoxicity associated with anthracycline or trastuzumab therapy, respectively. To detect cardiac damage, the currently accepted method is to measure left ventricular ejection fraction (LVEF) by echocardiography, which lacks the sensitivity to predict early cardiac dysfunction. Early identification of cardiotoxicity is essential to cancer survivors, as development of cardiomyopathy carries a worse outcome independent of cancer prognosis. Currently, there are no accepted guidelines for the early detection of myocardial injury. The use of cardiac biomarkers and more sensitive echocardiographic techniques have expanded options for monitoring, but have yet to reach a consensus. Hence, our study will evaluate the potential predictive value of novel cardiac biomarkers and advanced echocardiographic and cardiac magnetic resonance imaging (CMR) techniques to detect subclinical myocardial damage. Our findings may be applicable for monitoring new antineoplastic agents during food and drug administration (FDA) clinical trials. Trial Design Prospective cohort study with internal control of 20 patients newly diagnosed with breast cancer. The trial will assess endpoints at baseline, 2 weeks after initiation of therapy, and 2 weeks and 6 months after chemotherapy completion. 1. Primary Endpoint a. Decline in left ventricular ejection fraction assessed by CMR and 3D-echo not detected by conventional methods b. Presence of either myocardial fibrosis or edema detected by CMR c. Changes in myocardial deformation detected by echo or CMR strain d. Increase in cardiac biomarkers (Serum caspase-3 p17 peptide, Troponin I, B-type natriuretic peptide) and possible correlation with imaging parameters 2. Secondary Endpoint a. Development New York Heart Association class 1 to 4 symptoms b. Decrease in LVEF of ≥5% to ≤50% with or without symptoms Eligibility Criteria Inclusion Criteria: 1. Newly diagnosed stage I, II, or III breast cancer 2. Age between 18 and 75 years old. 3. Treatment with trastuzumab or anthracycline-based chemotherapy Exclusion Criteria: 1. History of cardiovascular disease 2. Pacemaker 3. History of mediastinal radiotherapy 4. Creatinine clearance &amp;lt;30 ml/min 5. Serum bilirubin &amp;gt;2.0 mg/dl, ALT and AST &amp;gt; 100 U/1) 6. Hypertension, uncontrolled &amp;gt;140/90 7. LVEF &amp;lt;55% per 2-D echocardiogram 8. Claustrophobia Specific Aims 1. Detect early myocardial injury. 2. Evaluate early predictors of left ventricular dysfunction. 3. Evaluate timing of monitoring during or post treatment Statistical Method This is a pilot study and 20 patients are required to reach statistical significance with 85% power. All values will be analyzed as mean±SD or n (%). Categorical indicators will be analyzed using nonparametric statistics such as Cochran's Q. Changes in imaging and biomarker parameters will be assessed using analysis of variance, while correlation between the two will be assessed using mixed models appropriate for binary outcome. Significance will be accepted at p ≤0.05 for all tests. Present accrual and target accrual Nine subjects are enrolled with a goal of 20. Contact for people interested in trial: 1. Dr. Erick Avelar, eavelar@uchc.edu 2. Dr. Susan Tannenbaum, stannenbaum@uchc.edu Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr OT1-02-12.

Cardiac biomarkers: The troponins and CK- MB

With the prevalence of ischemic heart disease, early diagnosis and management of myocardial infarction is important, and necessitates the need for cardiac biomarkers. Since several markers have evolved over time, it becomes important to understand which markers are best in different clinical situations. After a review of the literature, we have summarized the most frequent markers used. Though the search for an ideal cardiac biomarker remains, troponins seem to have evolved as the most advantageous. Features of troponins include high specificity, sensitivity, a wide diagnostic window allowing prompt, early diagnosis, as well as enhancing detection of myocardial injury in patients presenting late. Enabling risk stratification, estimation of infarct size, detecting reperfusion, usefulness in predicting prognostic outcomes, and offering therapeutic guidance also are among the advantageous features of troponins. Troponins also aid in detecting perioperative myocardial injuries and cardiac injury in renal failure patients. CK myocardial band (CK-MB), however, seems to be more advantageous in detecting reinfarction, though it has limitations in terms of early diagnosis. Troponins are being increasingly used, compared to other cardiac biomarkers, in the detection of acute coronary events and myocardial damage, though CK-MB is still preferred in selective situations.

MicroRNAs as Novel Myocardial Biomarkers

The search for new biomarkers of cardiovascular disease remains a large and growing enterprise. Biomarkers are used to identify the risk, presence, and/or severity of disease; to guide diagnostic and therapeutic interventions; and to provide clues to disease mechanisms and pathophysiological distinctions within clinically similar populations. Among cardiovascular biomarkers, those used for identifying the presence or severity of myocardial injury have the most extensive history. Beginning with the first report 55 years ago that circulating transaminases are increased in acute myocardial infarction (1), the search for new and better biomarkers of myocardial injury has continuously evolved. As recently reviewed (2), cardiac troponin has emerged after decades of clinical and laboratory investigation as a highly diagnostically sensitive and specific biomarker of myocardial injury, with a currently indispensable role in the accurate and timely diagnosis of patients with suspected acute coronary syndromes (ACSs).1 Central to this preeminence is the tissue specificity of cardiac troponin isoforms, increases in assay sensitivity, and an extensive body of evidence validating the diagnostic, prognostic, and therapy-guiding utility of cardiac troponins in diverse clinical settings. Because the benefits of ACS treatments are favorably influenced by the speed with which they are applied, the ideal myocardial injury biomarker must also permit rapid measurement; cardiac troponin assays have also proved satisfactory in this regard. Despite the established strengths of cardiac troponins for prompt and reliable detection of myocardial injury, the ability to reliably detect ischemia in the absence of myocyte necrosis and the ability to distinguish alternative causes and mechanisms of myocyte damage (inflammation, oxidative stress, apoptosis) represent unmet needs and opportunities for new biomarkers, which have been highlighted in recent reviews (2)(3). Resistance to inaccuracy caused by confounding factors such as renal failure is another favorable attribute that is not ideally achieved with cardiac troponin assays. …

The Use of Biochip Cardiac Array Technology for Early Diagnosis of Acute Coronary Syndromes

The Use of Biochip Cardiac Array Technology for Early Diagnosis of Acute Coronary SyndromesSerum troponin is the best biomarker for the diagnosis of acute coronary syndrome, but it takes considerable time before a definitive diagnosis is available. The purpose of this study was to evaluate whether a multimarker approach, using the biochip cardiac array, would facilitate the early diagnosis. Serum biomarkers were determined on admission (≤6 hrs) and after 6 hours in 42 patients suspected for ACS. Cardiac troponin I was measured by a sensitive assay (STATcTnI) and cardiac markers (H-FABP, myoglobin, cTnI, CK-MB mass, carbonic anhydrase III) were assayed with the use of Biochip Array Technology.STATcTnI concentrations, within the first 6 hours, were elevated &gt;99thpercentile for the reference population in 83.3% of subjects, but none reached the cut-off for AMI. On admission H-FABP was the only marker with 90.5% sensitivity in all ACS cases and 100% sensitivity in STEMI/NSTEMI patients. The sensitivity of myoglobin at presentation was 71.4% in ACS, however, combined sensitivity of myoglobin and H-FABP reached 95.2%. Lowering the cut-off for cTnI allowed early diagnosis (≤6 hrs) in only 26.2% of ACS patients and 95.2% after the next 6 hours. In unstable angina the cardiac panel was not sufficiently accurate for early risk stratification. In conclusion, testing for both markers, H-FABP and sensitive cardiac troponin, available with the cardiac array may facilitate the early detection of myocardial injury in clinical practice.

Detection of myocardial injury in patients with unstable angina using a novel nanoparticle cardiac troponin I assay: Observations from the PROTECT-TIMI 30 Trial

At least 30% of patients with non-ST-elevation acute coronary syndrome present without evidence of myonecrosis using current generation troponin assays. A new generation of research assays for troponin that offer a >10-fold increase in analytical sensitivity has emerged. To perform a pilot study to evaluate the clinical sensitivity of a new ultra-sensitive nanoparticle assay for cardiac troponin I (nano-cTnI), we identified 50 patients with unstable angina (serial negative cTnI) and 50 patients with non-ST-elevation myocardial infarction with an initially negative current generation cTnI result. We measured cTnI using an assay (Nanosphere, Northbrook, IL) that can detect pg/mL concentrations of cTnI (detection-limit 0.0002 microg/L). Measured at 0, 2, and 8 hours with the nano-cTnI assay 44%, 62%, and 82% of patients with unstable angina defined by the current-generation assay had an elevated nano-cTnI result (> or =0.003 microg/L, 99 th percentile decision-limit, coefficient of variation <10%). In patients with definite myocardial injury (current-generation cTnI > or =0.1 microg/L) but an initially negative cTnI, 72% and 98% had a nano-cTnI > or =0.003 microg/L at 0 and 2 hours. No patient had a positive current-generation cTnI without an elevated nano-cTnI level. In this pilot study using a nanoparticle assay for cTnI, myocardial injury was detectable in a substantial proportion of patients presently classified as having unstable angina, suggesting that ischemia with rest pain without injury is rare. The emergence of a new generation of troponin assays has the potential to lead to new clinical applications based on enhanced analytical performance at very low concentrations of troponin.

Use of the biochip microarray system in detection of myocardial injury caused by radiofrequency catheter ablation

In a prospective study, we measured plasma markers of myocardial damage induced by radiofrequency catheter ablation (RFA) with the protein biochip microarray system. A total of 32 consecutive patients undergoing RFA for atrioventricular nodal re-entry tachycardia (AVNRT), right atrial flutter (AFL) and atrial fibrillation (AF) were included in the study. Cardiac troponin I (cTnI), creatine kinase isoenzyme MB (CK-MB), heart-type fatty acid binding protein (hFABP) and glycogen phosphorylase BB (GPBB) were measured using biochip array technology at baseline and 24 h after the procedure. Values for all markers increased 24 h after RFA (cTnI: 0.92+/-0.49 microg/L vs. 0.33+/-0.06 microg/L, p<0.001; CK-MB: 3.79+/-2.04 microg/L vs. 1.85+/-0.55 microg/L, p<0.001; hFABP: 2.82+/-0.95 microg/L vs. 2.00+/-0.95 microg/L, p<0.001; GPBB: 9.07+/-5.83 microg/L vs. 4.70+/-2.50 microg/L, p<0.001). The correlations between plasma marker levels and RFA time were cTnI: r=0.63, p<0.01; CK-MB: r=0.75, p<0.01; hFABP: r=0.55, p<0.05, GPBB: r=0.51, p<0.05; the correlation between RFA time and number of RF applications was significant (r=0.81, p<0.001). Patients with RFA due to AF or flutter had elevated cTnI, CK-MB and hFABP levels compared to patients with AVNRT (cTnI: 1.14+/- 0.49 microg/L vs. 0.59+/-0.25 microg/L, p<0.05; CK-MB: 4.46+/- 2.07 microg/L vs. 2.81+/-1.54 mug/L, p<0.05; hFABP: 3.21+/- 0.98 microg/L vs. 2.25+/-0.54 microg/L, p<0.01). Myocardial injury induced by RFA can be detected by cTnI, CK-MB, hFABP and GPBB. Plasma cTnI, CK-MB and hFABP levels significantly increased in patients with AFL and AF compared to patients with AVNRT. The increase of cTnI, CK-MB and GPBB levels correlates with the total duration of RFA.

Serum and Plasma Cardiac Troponin I 99th Percentile Reference Values for 3 2nd-Generation Assays

Clinical and laboratory medicine associations have endorsed the implementation of the 99th percentile reference value for cardiac troponin I (cTnI) and T (cTnT) for the detection of myocardial injury (1)(2). In the presence of ischemia, cTn above the 99th percentile has become the cornerstone for the definition of acute myocardial infarction (MI) in non–ST-elevation MI (1)(2), leading manufacturers of in vitro diagnostic tests to improve low-end analytic sensitivity and precision. We determined the 99th percentile values for 3 2nd-generation cTnI assays in serum and/or plasma. After receiving appropriate institutional review board approval, we obtained frozen (−20 °C up to 30 days) serum samples from 2992 apparently healthy volunteers. Because this group of samples was collected for another study, data on donor age and sex were unavailable, a study limitation. We also obtained 2000 plasma (heparin) samples from a separate group of healthy individuals, 75% male, age 18–66 years. These fresh specimens were refrigerated for 24–48 h before analysis. cTnI concentrations were measured by use of the following US Food and Drug …

The viral genetic background determines the outcome of coxsackievirus B3 infection in outbred NMRI mice

The reasons for the different outcome of coxsackievirus B3 (CVB3)-induced heart disease in humans are not well understood. Since there are no experimental data on the course of disease after infection with genetically different CVB3 in a natural variable population until now, we studied the outcome of virus infection in outbred NMRI mice after inoculation of genetically different CVB3 variants. Adult male mice were inoculated with seven closely related CVB3 variants. The histopathological changes of heart and pancreas tissue, antibody induction, virus titers, and persistence of viral positive- as well as negative-strand RNA in spleen and heart tissue were compared at day 7 or day 28 after infection to detect prerequisites and predictive factors for chronic myocarditis. Six CVB3 variants infected NMRI mice. CVB3 infection (i) did not induce detectable myocardial injury, (ii) caused signs of healing up acute myocarditis or (iii) ongoing chronic myocarditis. Neither IgG antibody responses nor the extent of destruction of exocrine pancreatic tissue or viral RNA load in spleen did correlate with myocardial histopathology. In contrast, a high persistent viral RNA load in heart tissue specimens was characteristic for mice developing chronic myocarditis. The results of the present study corroborate high viral load in the acute stage of myocarditis and high amounts of persisting CVB3 RNA in heart tissue as predictive marker of chronic myocarditis. The outcome of CVB3-induced heart disease in outbred NMRI mice depends strongly on the viral genetic background. In particular an important role of viral capsid proteins is suggested.

Bovine Cardiac Troponin T is Not Accurately Quantified with a Common Human Clinical Immunoassay

The detection of myocardial injury in cattle caused by the ingestion of cardiotoxic compounds or cardiac diseases would be facilitated by the availability of a rapid and specific quantitative serum assay for cardiac troponins. Therefore, the accuracy of the only cardiac troponin T (cTnT) immunoassay to receive approval by the US Food and Drug Administration for the measurement of cTnT in human serum was evaluated to quantify the protein in bovine serum. Recovery experiments were performed by the addition of purified bovine cTnT to normal bovine serum. Cardiac troponin T was quantified using an immunoassay commonly used for the measurement of cTnT in human serum. The immunoassay demonstrated a well correlated (r = 0.99) and linear dose-dependent response to bovine cTnT but with poor accuracy (slope = 0.024; 95% CI = 0.018 to 0.030). The mean recovery of bovine cTnT was 2.4% across a concentration range of 10 ng/ml to 1,000 ng/ml. These studies demonstrate that a commonly used immunoassay for the measurement of cTnT in human serum demonstrates poor accuracy for the quantification of bovine cTnT.

Cardiac troponin I predicts outcome after ruptured abdominal aortic aneurysm repair

Cardiac troponin I (cTnI) is a highly sensitive and specific marker for myocardial injury that predicts mortality in patients with acute coronary syndromes. This study examined the relationship between perioperative cTnI levels and clinical outcome in patients with ruptured abdominal aortic aneurysm (AAA). Consecutive patients who underwent operative repair of a ruptured AAA over a 22-month interval and survived for more than 24 h were entered into a prospective observational cohort study. Levels of cTnI were measured immediately before, and at 24 and 48 h after surgery, and related to clinical outcome. Of 62 patients who underwent attempted operative repair of ruptured AAA, 50 (81 per cent) survived for more than 24 h and were included in this study. Twenty-three (46 per cent) of the 50 had a detectable cTnI level at one or more time points during the first 48 h. Of these, 11 patients had clinical or electrocardiographic evidence of an acute cardiac event and 12 did not; five patients in each of these two groups died. Of 27 patients with no increase in cTnI in the first 48 h, only three died (P = 0.031 and P = 0.043 respectively, relative to the groups with detectable cTnI). Approximately half of patients who survived repair of ruptured AAA for more than 24 h sustained a detectable myocardial injury within the first 48 h. A perioperative increase in the level of cTnI, with or without clinically apparent cardiac dysfunction, was associated with postoperative death.

Potential of an intracardiac electrogram for the rapid detection of coronary artery occlusion

Early identification of acute MI and prompt intervention can improve clinical outcomes. It would be valuable to identify a method that could allow the earliest possible detection of myocardial injury or ischemia. This article reports one of the first clinical investigations to examine the ability of an intracardiac right ventricular (RV) electrode to identify the early onset of myocardial ischemia/injury in a cohort of patients undergoing balloon occlusion of a coronary artery during percutaneous transluminal coronary angioplasty. The primary data set for analysis included observations from 14 patients with 17 lesions, with a matched comparison of a V6 surface lead and the RV to left upper chest, "intracardiac" lead. The intracardiac lead was sensitive in detecting myocardial injury current/ischemia. There was a 36.4+/-5.6% ST-segment shift, relative to the amplitude of the QRS complex, in the intracardiac lead at 2 min, compared with a 10.1+/-1.9% ST shift from a surface lead (P=.00011). The RV to left upper chest lead detected a >10% shift in ST segment within 2 min in 17 (100%) of 17 cases vs. 8 (47%) of 17 for a V6 surface lead. The intracardiac lead provided detection of ischemia in all three major epicardial coronary distributions. This study demonstrates the ability of an intracardiac (RV apex to left upper chest) lead to rapidly detect myocardial ischemia/injury during acute coronary occlusion in the setting of balloon angioplasty. The results of this study suggest that a simple implantable system resembling a ventricular pacemaker could be programmed to assist in the very early diagnosis of acute myocardial infarction.

Perioperative myocardial injury: individual and population implications

It is generally understood that patients who have cardiovascular disease are at risk of cardiac complications after surgery. In patients undergoing major or vascular surgery, the risk of such complications can be signi®cant. Eagle and colleagues studied patients enrolled on the CASS (Coronary Artery Surgery Study) registry who subsequently underwent non-cardiac surgery. They reported a perioperative myocardial infarction rate of 8.5% in patients with medically managed coronary artery disease who underwent vascular surgery. The authors de®ned high-risk surgery as surgery associated with a risk of perioperative death or myocardial infarction of greater than 4%. Abdominal surgery, thoracic surgery, and head and neck surgery fell into this category. For patients undergoing these types of surgery who had medically treated coronary artery disease, the overall perioperative myocardial infarction rate was 2.7% and the overall death rate 3.3%. This compared with rates of 0.8 and 1% respectively in patients undergoing similar surgery who did not have coronary artery disease. Data such as these are often considered with information on the prevalence of coronary artery disease to obtain some indication of the population burden of disease. For example, in 1990 Mangano stated that 25 million patients undergo major surgery in the USA each year and suggested that perhaps 6±7 million of these people are at risk of perioperative cardiac complications. Such estimates suggest that perioperative cardiac complications are both a major issue in the care of individual surgical patients and a major public health issue. This review will examine in more detail the population impact of perioperative cardiac morbidity and the implications of this for the individual patient.

Usefulness of troponin I as a marker of myocardial injury after pediatric cardiac catheterization

Cardiac troponin I (cTnI) is a sensitive and specific marker of myocardial injury. The degree of myocardial injury associated with pediatric cardiac catheterization is unknown. We sought to investigate cTnI after pediatric cardiac catheterization, and to evaluate the degree of elevation observed with specific types of interventions. Seventy-three pediatric catheterizations were evaluated. Diagnostic procedures and interventions not expected to cause myocardial injury were assigned to group I, whereas interventional procedures expected to be associated with cardiac injury were assigned to group II. Group II procedures were further subdivided based on type of intervention. Serum samples were obtained before and after all procedures and analyzed for cTnI. Postprocedure cTnI levels were compared across groups and correlated with age and weight. Procedures in group II were associated with significantly higher cTnI levels than group I (median 2.65 ng/ml; interquartile range 0.9 to 4.9 ng/ml for group II vs 0.3; 0.3 to 1.6 ng/ml for group I, p <0.001). Within group II, cTnI was inversely correlated with age (p <0.05) and weight (p <0.05). Radiofrequency catheter ablation (RFA) caused higher cTnI levels than other types of interventions (median 3.7 ng/ml; 1.9 to 9.5 ng/ml for RFA vs 1.75; 0.7 to 4.9 ng/ml for non-RFA, p <0.05). Most pediatric interventional catheterization procedures are associated with myocardial injury, as evidenced by elevation of cTnI, with RFA causing higher levels than other interventions. Conversely, most diagnostic procedures are associated with no detectable myocardial injury. When compared with adult studies, pediatric patients seem to be at higher risk for myocardial injury from interventional cardiac catheterization.

Myocardial Injury During Radiofrequency Catheter Ablation: Comparison of Focal and Linear Lesions

The aim of study was to investigate the extent of myocardial injury incurred by creation of continuous RF current induced linear ablation lesions (LL; ablation of atrial fibrillation, right atrial procedure) in comparison to focal RF lesions (FL; AV node reentry tachycardia, WPW tachycardia). In 23 patients with LL (age 51.3 +/- 11.2 years, 18 men, 5 women) and in 16 patients with FL (age 53.9 +/- 5.1 years, 8 men and 8 women), levels of creatine kinase (CK), myoglobin (MG), CKMB mass (CKMB M), CKMB activity (CKMB A), and cardiac troponin T (cTnT) were determined before and 2, 4, 8, 24, and 48 hours after ablation. CKMB A was normal in 87% in LL and 100% in FL (< 6% of CK) with median maximum CK values of 214 (45-1583) U/L in LL and 36 (29-212) U/L in FL. Peak values of all parameters were significantly higher in LL than in FL. The sensitivity of cTnT was 50% in FL and 100% in LL. In FL MG, total CK, and CKMB M were abnormal in only 12.5% of cases while in LL MG and CKMB M were pathological in 100% and total CK was abnormal in 91.3% of patients. The amount of energy and number of RF applications correlated with cTnT, MG, and CKMB M (P = 0.01). In conclusion, (1) long linear RF current lesions for ablation of atrial fibrillation are associated with significantly greater myocardial injury than focal ablations. (2) In focal lesions only cTnT provided a sensitivity of 50% in the detection of myocardial injury while in linear lesions cTnT, CKMBM, and CKMB M seemed suitable for detection of RF current induced myocardial damage with 100% sensitivity. All biochemical parameters do not differentiate patients with coronary ischemia up to 48 hours after an ablation. (3) Further investigations are necessary to determine if RF current linear lesions lead to impaired atrial contractility in cases of extensive tissue damage.