Comparison of Cardiac Troponin I versus T and Creatine Kinase MB after Coronary Artery Bypass Grafting in Patients with and without Perioperative Myocardial Infarction

Peivandi, AA; Dahm, Manfred; Opfermann, Ulrich T.; Peetz, D.; Doerr, Felix; Loos, Anja H.; Oelert, H.

doi:10.1007/s00059-004-2543-y

Cited by 36 publications

(30 citation statements)

References 18 publications

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“…Previous in vitro studies of cTnT release have defined a fixed minor free early releasable fraction and a major bound fraction of cTnT in cardiomyocytes (4,7,17,18 ). According to the current model, release of the 5%-10% of cTnT that is free is responsible for cTnT increases early after an AMI.…”

Section: Discussionmentioning

confidence: 95%

Revision of the Troponin T Release Mechanism from Damaged Human Myocardium

Starnberg¹,

Jeppsson

Lindahl

et al. 2014

Clinical Chemistry

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BACKGROUND Cardiac troponin T (cTnT) is released from damaged heart tissue in patients with acute myocardial infarction. It is presumed that most cTnT is tightly bound and released following the degradation of myofibrils in necrotic cardiomyocytes, resulting in sustained increases in circulating cTnT. Evidence of a large irreversibly bound fraction is based on the inability to extract most cTnT from cardiac tissue in cold low-salt extraction buffers. METHODS Here we examined in vitro extraction of cTnT from human cardiac tissue in serum at 37 °C. RESULTS We found that over 80% of the cTnT can be extracted from human cardiac tissue in 90 min using large volumes of human serum at 37 °C. The release ratio was highly dependent on the extraction volume and was only 3% if an equal volume of serum and heart tissue was used. In contrast, extraction of the cytoplasmic cardiac damage markers myoglobin and creatinine kinase was much less affected by changing these conditions. Purified cTnT was poorly soluble in a low-salt extraction buffer at 0 °C, previously used to define the free cTnT fraction. CONCLUSIONS Our data indicate that the diffusible fraction of cTnT is likely substantially larger in vivo than previously reported and likely is not fixed but dependent on local plasma flow. It is therefore possible that the sustained increase in circulating cTnT after myocardial infarction is at least in part due to a slow washout of cTnT that interacts reversibly with tropomyosin in myofibrils.

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Section: Discussionmentioning

confidence: 95%

Revision of the Troponin T Release Mechanism from Damaged Human Myocardium

Starnberg¹,

Jeppsson

Lindahl

et al. 2014

Clinical Chemistry

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“…Given that troponin T serum levels can be influenced by renal function, we chose to consider only relevant (greater than 25 %) increases in serum troponin T levels to reflect myocardial cell damage. In cardiac surgery patients, this was done 48 h after surgery, a time interval during which troponin usually decreases [37]. Indeed, troponin T levels increased by a median percentage of 52 % (95 % CI, 28-99 %) in patients with detectable troponin T at study enrollment (n = 8).…”

Section: Discussionmentioning

confidence: 99%

Adverse cardiac events during catecholamine vasopressor therapy: a prospective observational study

et al. 2012

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“…Details of the duration of mechanical ventilation and intensive care unit and hospital length of stay (from the operative day) were collected. Postoperative morbidity was collected including death, myocardial infarction (at least two of the following criteria: cardiac enzyme level elevation with either troponin I > 20 lg.l )1 or CK-MB > 30 lg.l )1 , serial ECG with new Q waves in two or more leads, or new wall motion abnormality on echocardiography [22,23]), ventricular or supraventricular arrhythmia, inotrope use to support low cardiac output, mechanical cardiac support; a bleeding rate of > 200 ml.h .............................................................................................................................................................................................................. oedema, respiratory failure requiring re-intubation of the patient's trachea; superficial wound or skin requiring treatment, deep sternal, chest, urinary or abdominal infection requiring treatment; stroke, transient ischaemic attack, coma, agitation or delirium; serum creatinine increase > 1.5 times baseline value, haemofiltration; and homologous blood product transfusion. Finally, depression was assessed using the cardiac depression index score [24].…”

Section: Methodsmentioning

confidence: 99%

The influence of propofol or desflurane on postoperative cognitive dysfunction in patients undergoing coronary artery bypass surgery*

et al. 2011

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SummaryWe investigated the influence of either propofol or desflurane on the incidence of postoperative cognitive dysfunction in a randomised trial of 180 patients undergoing coronary artery bypass surgery. The primary outcome was incidence of postoperative cognitive dysfunction at 3 months, defined as ‡ 1 SD deterioration in two or more of 12 neurocognitive tests. Secondary outcomes included early postoperative cognitive dysfunction (between days three and seven), delirium on day one, morbidity and length of hospital stay. Early postoperative cognitive dysfunction was significantly higher with propofol compared with desflurane (56 ⁄ 84 (67.5%) vs 41 ⁄ 83 (49.4%), respectively, p = 0.018), but this effect was not seen at 3 months (10 ⁄ 87 (11.2%) vs 9 ⁄ 90 (10.0%), respectively. There was no difference in delirium (7 ⁄ 89 (7.9%) vs 12 ⁄ 91 (13.2%), respectively, length of hospital stay (median (IQR [range]) 7 (6-9 [4-15]) vs 6 (5-7 [5-16) days, respectively or other morbidities. Desflurane was associated with reduced early cognitive dysfunction. Postoperative cognitive dysfunction (POCD) is a common morbidity associated with coronary artery bypass surgery, ranging in frequency from 20% to 60% for between 6 weeks to 3 months after surgery [1][2][3]. It can be an enduring problem for patients, as the presence of POCD at 3 months after surgery has a high chance of persisting into the long term [3,4]. Much research has been devoted to investigating aspects of cardiopulmonary bypass that have been considered to be the most likely cause of POCD, with conflicting results. The focus on cardiopulmonary bypass, and consequent aortic manipulation required for aortic

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Comparison of Cardiac Troponin I versus T and Creatine Kinase MB after Coronary Artery Bypass Grafting in Patients with and without Perioperative Myocardial Infarction

Cited by 36 publications

References 18 publications

Revision of the Troponin T Release Mechanism from Damaged Human Myocardium

Revision of the Troponin T Release Mechanism from Damaged Human Myocardium

Adverse cardiac events during catecholamine vasopressor therapy: a prospective observational study

The influence of propofol or desflurane on postoperative cognitive dysfunction in patients undergoing coronary artery bypass surgery*

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