| 1. |
- Eggers, Kai M., et al.
(author)
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Cardiac troponin I levels in an elderly population from the community - The implications of sex
- 2015
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In: Clinical Biochemistry. - : Elsevier BV. - 0009-9120 .- 1873-2933. ; 48:12, s. 751-756
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Journal article (peer-reviewed)abstract
- Objectives: The importance of sex on cardiac troponin levels is increasingly recognized. We investigated whether the entities associated with troponin leakage and the prognostic consequences thereof would differ between elderly men and women from the community. Design and methods: Cardiac troponin I (cTnI) levels were measured using a high-sensitivity assay (Abbott Laboratories) in 70-year old men (n = 502) and women (n = 502) from the PIVUS study. All study participants were followed up for 10 years regarding all-cause mortality and incident cardiovascular (CV) disease. Results: Median cTnI levels were 4.1 and 3.0 ng/L in men and women, respectively (p < 0.001). By multiple linear regression, the relative contribution of lower left-ventricular ejection fraction and ischemic ECG changes to cTnI levels was greater in men compared to women. For other clinical and echocardiographic variables, similar associations were found. cTnI independently predicted all-cause mortality in men (n = 93 [18.5%]; hazard ratio [HR] 1.38 [1.12-1.70]) and women (n = 62 [12.4%]; HR 1.59 [1.11-2.28]) but not incident CV disease in subjects being CV healthy at baseline (n = 163/857). The interaction terms of sex on the associations of cTnI with both outcomes were non-significant. Sex-specific cut-offs did not improve prognostication. Variations in the pattern of entities associated with cTnI leakage had no impact on event rates. Conclusions: We found some differences in the entities associated with higher cTnI levels in elderly community-dwelling men and women. However, this did not translate into differences in the associations of cTnI with adverse outcome.
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| 2. |
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| 3. |
- Lindahl, Olof, et al.
(author)
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An electromechanical breathing device for minimal particle loss while inhaling aerosols
- 1993
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In: Journal of Medical Engineering & Technology. - : Informa UK Limited. - 0309-1902 .- 1464-522X. ; 17:4, s. 138-140
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Journal article (peer-reviewed)abstract
- The design of an electromechanical breathing mask that minimizes particle loss during inhalation of aerosols from a provocation box is described. The device measures air flow by means of an anemometer. A provocation example is depicted and the possibility of measuring the provocation dose is discussed. The breathing device here described has been shown to be easy to use and to give reliable results
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| 4. |
- Savukoski, Tanja, et al.
(author)
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Elevation of cardiac troponins measured after recreational resistance training
- 2015
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In: Clinical Biochemistry. - : Elsevier BV. - 0009-9120 .- 1873-2933. ; 48:12, s. 803-806
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Journal article (peer-reviewed)abstract
- Background: Whereas elevated cardiac troponin (cTn) concentrations i.e. above the 99th percentile of healthy reference population (recommended cutoff for the diagnosis of myocardial infarction) are well-documented in healthy individuals after prolonged and/or intensive exercises such as marathons, data on less-strenuous sports are scarce. Therefore, our aim was to investigate cTnI and cTnT release in response to recreational resistance training, here a single-bout of 1-h kettlebell workout. Methods: Serum samples were collected from 11 apparently healthy volunteers the previous day (pre-exercise), three hours after the kettlebell class (post-exercise), the next day and three days later. The aliquoted samples were analyzed with Abbott Laboratories' Architect high-sensitivity (hs)-cTnI assay (limit of detection, LoD = 2 ng/L), our 3 + 1-type cTnI assay free from cTn-specific autoantibody interference (LoD = 3 ng/L) and Roche Diagnostics' hs-cTnT assay CLOD = 5 ng/L). Results: The post-exercise cTn concentrations were significantly higher than the pre-exercise values (median 5.5-9.6 ng/L vs. 26 ng/L, n = 2) and/or hs-cTnT (>14 ng/L, n = 4). The cTn concentrations returned to baseline during the three days of follow-up. Conclusions: Our study demonstrates abnormally elevated cTns with well-validated sensitive cTn assays after resistance training. This confirms that different kinds of recreational physical activity are yet another confounder that may affect the determination and use of 99th percentile reference values. Therefore, exercise-associated changes should be carefully addressed as part of the evaluation what is "normal cTn".
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| 5. |
- Starnberg, Karin, et al.
(author)
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A Possible Mechanism behind Faster Clearance and Higher Peak Concentrations of Cardiac Troponin I Compared with Troponin T in Acute Myocardial Infarction
- 2020
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In: Clinical Chemistry. - : Oxford University Press (OUP). - 0009-9147 .- 1530-8561. ; 66:2, s. 333-341
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Journal article (peer-reviewed)abstract
- BACKGROUND: Although cardiac troponin I (cTnI) and troponin T (cTnT) form a complex in the human myocardium and bind to thin filaments in the sarcomere, cTnI often reaches higher concentrations and returns to normal concentrations faster than cTnT in patients with acute myocardial infarction (MI). METHODS: We compared the overall clearance of cTnT and cTnI in rats and in patients with heart failure and examined the release of cTnT and cTnI from damaged human cardiac tissue in vitro. RESULTS: Ground rat heart tissue was injected into the quadriceps muscle in rats to simulate myocardial damage with a defined onset. cTnT and cTnI peaked at the same time after injection. cTnI returned to baseline concentrations after 54 h, compared with 168 h for cTnT. There was no difference in the rate of clearance of solubilized cTnT or cTnI after intravenous or intramuscular injection. Renal clearance of cTnT and cTnI was similar in 7 heart failure patients. cTnI was degraded and released faster and reached higher concentrations than cTnT when human cardiac tissue was incubated in 37 degrees C plasma. CONCLUSION: Once cTnI and cTnT are released to the circulation, there seems to be no difference in clearance. However, cTnI is degraded and released faster than cTnT from necrotic cardiac tissue. Faster degradation and release may be the main reason why cTnI reaches higher peak concentrations and returns to normal concentrations faster in patients with MI.
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| 6. |
- Starnberg, Karin, et al.
(author)
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Revision of the troponin T release mechanism from damaged human myocardium.
- 2014
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In: Clinical chemistry. - : Oxford University Press (OUP). - 1530-8561 .- 0009-9147. ; 60:8, s. 1098-104
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Journal article (peer-reviewed)abstract
- 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.
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