Equivalent early sensitivities of myoglobin, creatine kinase MB mass, creatine kinase isoform ratios, and cardiac troponins I and T for acute myocardial infarction

Mair, Johannes; Morandell, Doris; Genser, Norbert; Lechleitner, Peter; Dienstl, F; Puschendorf, Bernd

doi:10.1093/clinchem/41.9.1266

Cited by 234 publications

(44 citation statements)

References 29 publications

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“…Soluble cytosolic proteins may be released before insoluble structurally bound proteins (Adams, 1999;Mair, 1999). In skeletal muscle, there are cytosolic and structurally bound pools of sTnI (Sorichter et al 1997) similar to those for cTnI (Mair et al 1995). Although a change in level of cTnI is not detected within the first few hours after onset of symptoms of myocardial infarction (Wu et al 1999), we could detect an increase in fast sTnI as early as 1 h after load onset.…”

Section: Time Course Of Fast Stni Releasementioning

confidence: 75%

Respiratory muscle injury, fatigue and serum skeletal troponin I in rat

Simpson

Eyk

Iscoe

2004

The Journal of Physiology

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To evaluate injury to respiratory muscles of rats breathing against an inspiratory resistive load, we measured the release into blood of a myofilament protein, skeletal troponin I (sTnI), and related this release to the time course of changes in arterial blood gases, respiratory drive (phrenic activity), and pressure generation. After ∼1.5 h of loading, hypercapnic ventilatory failure occurred, coincident with a decrease in the ratio of transdiaphragmatic pressure to integrated phrenic activity (P di / Phr) during sighs. This was followed at ∼1.9 h by a decrease in the P di / Phr ratio during normal loaded breaths (diaphragmatic fatigue). Loading was terminated at pump failure (a decline of P di to half of steady-state loaded values), ∼2.4 h after load onset. During 30 s occlusions post loading, rats generated pressure profiles similar to those during occlusions before loading, with comparable blood gases, but at a higher neural drive. In a second series of rats, we tested for sTnI release using Western blot-direct serum analysis of blood samples taken before and during loading to pump failure. We detected only the fast isoform of sTnI, release beginning midway through loading. Differential detection with various monoclonal antibodies indicated the presence of modified forms of fast sTnI. The release of fast sTnI is consistent with load-induced injury of fast glycolytic fibres of inspiratory muscles, probably the diaphragm. Characterization of released fast sTnI may provide insights into the molecular basis of respiratory muscle dysfunction; fast sTnI may also prove useful as a marker of impending respiratory muscle fatigue.

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Section: Time Course Of Fast Stni Releasementioning

confidence: 75%

Respiratory muscle injury, fatigue and serum skeletal troponin I in rat

Simpson

Eyk

Iscoe

2004

The Journal of Physiology

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“…farction. 20,21 Troponin I is more specific than alpha hydroxy butyrate dehydrogenase and is more sensitive than the cardiac isoform of creatine kinase for detection of myocardial cellular injury in humans, and therefore has been found to be useful in human medicine for the detection of myocardial infarcts, doxorubicin toxicity, and severe congestive heart failure. [22][23][24] Activity of serum creatine kinase in 2 affected puppies was found to be within the reference range 2 days before euthanasia (compared to the clinical laboratory reference range at the Veterinary Hospital of the University of Pennsylvania).…”

Section: Discussionmentioning

confidence: 99%

Dilated Cardiomyopathy in Juvenile Portuguese Water Dogs

Sleeper

Henthorn

Vijayasarathy

et al. 2002

Veterinary Internal Medicne

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Dilated cardiomyopathy recently has been recognized in juvenile Portuguese Water Dogs. The purpose of this study was to evaluate unaffected and affected puppies by physical examination, electrocardiogram (ECG), echocardiogram, specific biochemical assays, and ultrastructure to document disease progression and to develop a method of early detection. Results of segregation analysis were consistent with autosomal recessive inheritance. Of 124 puppies evaluated clinically and echocardiographically, 10 were affected. No significant differences were found between unaffected and affected puppies for blood and myocardial carnitine or taurine concentrations, serum chemical variables, results of ophthalmological examinations, ECGs, or measurement of urine metabolites. Ultrastructural examination of myocardium from affected dogs revealed myofibrillar atrophy and small regions of myofibrillar degeneration, most prominently at the region of the intercalated discs. Only echocardiography allowed detection of affected puppies before clinical signs became evident. Echocardiography revealed a significant difference in the shortening fraction, E point to septal separation, and the end systolic and diastolic left ventricular internal diameters. Affected puppies were detected 1-4 weeks before the development of acute congestive heart failure.

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“…To fill this gap, in the current study, we investigated the relationship between Type D personality and disease severity as indicated by troponin-I. We also measured myoglobin, a complementary early marker of acute myocardial infarction (Mair et al, 1995;de Winter, Koster, Sturk, & Sanders, 1995).…”

Section: Statement Of Contributionmentioning

confidence: 99%

Type D personality is related to severity of acute coronary syndrome in patients with recurrent cardiovascular disease

García‐Retamero

Petrova

Arrebola-Moreno

et al. 2016

British J Health Psychol

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Type D personality was related to a worse lipid profile and more severe acute coronary syndrome in patients with previous history of CVD. Given the strong relationship between disease severity and subsequent mortality, these results suggest that severity of the myocardial infarction may be a potential mechanism explaining increased mortality in Type D patients with recurrent CVD. Statement of contribution What is already known on this subject? Type D personality has been related to worse outcomes in cardiac patients. However, recent studies show mixed results, suggesting the need to clarify potential mechanisms. What does this study add? Type D personality is related to severity of acute coronary syndrome in patients with previous history of cardiovascular disease. This effect is partially accounted for by lower HDL levels in Type D patients. Disease severity is a potential mechanism by which Type D personality may affect cardiovascular health of patients with recurrent CVD.

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Equivalent early sensitivities of myoglobin, creatine kinase MB mass, creatine kinase isoform ratios, and cardiac troponins I and T for acute myocardial infarction

Cited by 234 publications

References 29 publications

Respiratory muscle injury, fatigue and serum skeletal troponin I in rat

Respiratory muscle injury, fatigue and serum skeletal troponin I in rat

Dilated Cardiomyopathy in Juvenile Portuguese Water Dogs

Type D personality is related to severity of acute coronary syndrome in patients with recurrent cardiovascular disease

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