11 research outputs found
Acute inferolateral ST-elevation myopericarditis diagnosed by delayed enhancement cardiac computed tomography
SummaryA 20-year-old man with no previous medical history presented to the Emergency Department (ED) complaining of 3h of chest pressure. He denied drug abuse or risk factors for coronary artery disease. He had no symptoms of viral infection. Physical examination was unremarkable. The first electrocardiogram (ECG) showed a 4mm ST-segment elevation in the inferior leads and no PR depression. His troponin and CK-MB levels were abnormal. Urgent coronary angiography showed no lesions. Echocardiography was normal. The patient was investigated with cardiac computed tomography (CT) and late enhancement imaging. Cardiac anatomy and coronary arteries were normal in the first pass images. Later image acquisition showed an inferolateral enhancement. Since cardiac magnetic resonance (CMR) is the gold standard for myocarditis evaluation, the patient was transferred for CMR evaluation which showed edema and late enhancement in the same myocardial territory diagnosed by CT. The patient was discharged with a diagnosis of myocarditis and presented asymptomatic at 1 month follow-up.This is the first report to show the topographic correlation of the ECG ST elevation with the myocarditis diagnosed by CT and CMR. Since CT is more widely available, its use in myocarditis diagnosis might become part of its routine work up
Abnormal elevation of myocardial necrosis biomarkers after coronary artery bypass grafting without established myocardial infarction assessed by cardiac magnetic resonance
Significant elevation of biomarkers of myocardial necrosis after coronary artery bypass grafting without myocardial infarction established assessed by cardiac magnetic resonance
Abnormal elevation of myocardial necrosis biomarkers after coronary artery bypass grafting without established myocardial infarction assessed by cardiac magnetic resonance
Abstract Background The diagnosis of peri-procedural myocardial infarction is complex, especially after the emergence of high-sensitivity markers of myocardial necrosis. Methods In this study, patients with normal baseline cardiac biomarkers and formal indication for elective on-pump coronary bypass surgery were evaluated. Electrocardiograms, cardiac biomarkers, and cardiac magnetic resonance imaging with late gadolinium enhancement were performed before and after procedures. Myocardial infarction was defined as more than ten times the upper reference limit of the 99th percentile for troponin I and for creatine kinase isoform (CK-MB) and by the findings of new late gadolinium enhancement on cardiac magnetic resonance. We assessed the release of cardiac biomarkers in patients with no evidence of myocardial infarction on cardiac magnetic resonance. Results Of 75 patients referred for on-pump coronary bypass surgery, 54 (100%) did not have evidence of myocardial infarction on cardiac magnetic resonance. However, all had a peak troponin I above the 99th percentile; 52 (96%) had an elevation 10 times higher than the 99th percentile. Regarding CK-MB, 54 (100%) patients had a peak CK-MB above the 99th percentile limit, and only 13 (24%) had an elevation greater than 10 times the 99th percentile. The median value of troponin I peak was 3.15 (1.2 to 3.9) ng/mL, which represented 78.7 times the 99th percentile. Conclusion In this study, different from CK-MB findings, troponin was significantly increased in the absence of myocardial infarction on cardiac magnetic resonance. Thus, CK-MB was more accurate than troponin I for excluding procedure-related myocardial infarction. These data suggest a higher troponin cutoff for the diagnosis of coronary bypass surgery related myocardial infarction. Clinical trial registration http://www.isrctn.com/ISRCTN09454308 . Registered 08 May 2012
Journal of Cardiothoracic Surgery
São PauloMyocardial necrosis biomarkers are frequently elevated after cardiac revascularization procedures. However, the diagnosis of acute myocardial infarction (MI) after a revascularization procedure is still a controversial issue. This inability to diagnose MI makes it more difficult to establish a specific therapeutic strategy. With the appearance of high-sensitivity troponins, a myriad of false-positive diagnoses for myocardial infarction have emerged. In 2000
and 2007 in an attempt to standardize the criteria for diagnosing MI, the European Society of Cardiology, the American College of Cardiology, the American Heart Association, and the World Heart Federation formed a
joint task force to address this issue, but the task force was unable to make a satisfactory decision. Therefore, the problem still remained. To reduce diagnostic mistakes, in 2012, this same group arbitrarily raised the cutoff point to 10 times the 99th percentile, but with no solid scientific basis for doing so [1]. Troponin (cTnI) and the creatine kinase isoform (CK-MB) do not reflect, alone, the occurrence of MI related to occlusion of the graft or native artery or varying degrees of myocardial injury. Release of myocardial necrosis markers may be related to incomplete myocardial protection; reperfusion injury; a systemic inflammatory state, including inevitable postsurgical trauma; the handling of intramyocardial vessels; and cardiac defibrillator use [2, 3]. Cardiac troponin may also be increased when nonsurgical damage is present, such as sepsis and
thromboembolic phenomena [1]. cTnIs have also been found elevated in athletes after marathons [4]. This makes the identification of small areas of injury very difficult to assess in clinical practice [5].
Parallel to the increased sensitivity of troponin assays, imaging methods have achieved better accuracy for exclusion of the diagnosis of myocardial infarction.
Thus, due to the limitations on the interpretation of biomarkers after coronary artery bypass grafting (CABG) and the difficulty of excluding MI, cardiac magnetic resonance imaging (CMR) has enabled a more detailed evaluation of the myocardium. Therefore, in this study, we aimed to examine the
release of biomarkers after CABG in patients with no evidence of late enhancement on CMR
The Annals of Thoracic Surgery
São Paulodial necrosis biomarkers and electrocardiographic abnormalities after revascularization procedures has resulted in a change in the myocardial infarction (MI) definition.
Methods. Patients with stable multivessel disease who underwent percutaneous or surgical revascularization were included. Electrocardiograms and concentrations of high-sensitive cardiac troponin I (cTnI) and creatine kinase (CK)-MB were assessed before and after procedures. Cardiac magnetic resonance and late gadolinium enhancement were performed before and after procedures. MI was defined as more than five times the 99th percentile upper reference limit for cTnI and 10 times for CK-MB in percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG), respectively, and new late gadolinium enhancement for cardiac magnetic resonance.
Results. Of the 202 patients studied, 69 (34.1%) underwent on-pump CABG, 67 (33.2%) off-pump CABG, and 66 (32.7%) PCI. The receiver operating characteristic curve showed the accuracy of cTnI for on-pump CABG, off-pump CABG, and PCI patients was 21.7%, 28.3%, and 52.4% and for CK-MB was 72.5%, 81.2%, and 90.5%, respectively. The specificity of cTnI was 3.6%, 9.4%, and 42.1% and of CK-MB was 73.2%, 86.8%, and 96.4%, respectively. Sensitivity of cTnI was 100%, 100%, and 100% and of CK-MB was 69.2%, 64.3%, and 44.4%, respectively. The best cutoff of cTnI for on-pump CABG,
off-pump CABG, and PCI was 6.5 ng/mL, 4.5 ng/mL, and 4.5 ng/mL (162.5, 112.5, and 112.5 times the 99th percentile upper reference limit) and of CK-MB was 37.5 ng/mL, 22.5 ng/mL, and 11.5 ng/mL (8.5, 5.1, and 2.6 times the 99th percentile upper reference limit), respectively.
Conclusions. Compared with cardiac magnetic resonance, CK-MB was more accurate than cTnI for diagnosing MI. These data suggest a higher troponin cutoff for the diagnosis of procedure-related MI
Biomarker release after percutaneous coronary intervention in patients without established myocardial infarction as assessed by cardiac magnetic resonance with late gadolinium enhancement
Hypotheses, rationale, design, and methods for prognostic evaluation of cardiac biomarker elevation after percutaneous and surgical revascularization in the absence of manifest myocardial infarction. A comparative analysis of biomarkers and cardiac magnetic resonance. The MASS-V Trial
Abstract Background Although the release of cardiac biomarkers after percutaneous (PCI) or surgical revascularization (CABG) is common, its prognostic significance is not known. Questions remain about the mechanisms and degree of correlation between the release, the volume of myocardial tissue loss, and the long-term significance. Delayed-enhancement of cardiac magnetic resonance (CMR) consistently quantifies areas of irreversible myocardial injury. To investigate the quantitative relationship between irreversible injury and cardiac biomarkers, we will evaluate the extent of irreversible injury in patients undergoing PCI and CABG and relate it to postprocedural modifications in cardiac biomarkers and long-term prognosis. Methods/Design The study will include 150 patients with multivessel coronary artery disease (CAD) with left ventricle ejection fraction (LVEF) and a formal indication for CABG; 50 patients will undergo CABG with cardiopulmonary bypass (CPB); 50 patients with the same arterial and ventricular condition indicated for myocardial revascularization will undergo CABG without CPB; and another 50 patients with CAD and preserved ventricular function will undergo PCI using stents. All patients will undergo CMR before and after surgery or PCI. We will also evaluate the release of cardiac markers of necrosis immediately before and after each procedure. Primary outcome considered is overall death in a 5-year follow-up. Secondary outcomes are levels of CK-MB isoenzyme and I-Troponin in association with presence of myocardial fibrosis and systolic left ventricle dysfunction assessed by CMR. Discussion The MASS-V Trial aims to establish reliable values for parameters of enzyme markers of myocardial necrosis in the absence of manifest myocardial infarction after mechanical interventions. The establishments of these indices have diagnostic value and clinical prognosis and therefore require relevant and different therapeutic measures. In daily practice, the inappropriate use of these necrosis markers has led to misdiagnosis and therefore wrong treatment. The appearance of a more sensitive tool such as CMR provides an unprecedented diagnostic accuracy of myocardial damage when correlated with necrosis enzyme markers. We aim to correlate laboratory data with imaging, thereby establishing more refined data on the presence or absence of irreversible myocardial injury after the procedure, either percutaneous or surgical, and this, with or without the use of cardiopulmonary bypass.</p
