uu.seUppsala University Publications
Change search
Link to record
Permanent link

Direct link
BETA
Alternative names
Publications (10 of 284) Show all publications
Boeckel, J.-N., Palapies, L., Klotsche, J., Zeller, T., von Jeinsen, B., Perret, M. F., . . . Keller, T. (2018). Adjusted Troponin I for Improved Evaluation of Patients with Chest Pain. Scientific Reports, 8, Article ID 8087.
Open this publication in new window or tab >>Adjusted Troponin I for Improved Evaluation of Patients with Chest Pain
Show others...
2018 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 8, article id 8087Article in journal (Refereed) Published
Abstract [en]

The use of cardiac troponins (cTn) is the gold standard for diagnosing myocardial infarction. Independent of myocardial infarction (MI), however, sex, age and kidney function affect cTn levels. Here we developed a method to adjust cTnI levels for age, sex, and renal function, maintaining a unified cut-off value such as the 99th percentile. A total of 4587 individuals enrolled in a prospective longitudinal study were used to develop a model for adjustment of cTn. cTnI levels correlated with age and estimated glomerular filtration rate (eGFR) in males/females with r(age) = 0.436/0.518 and with (r)(eGFR) = -0.142/-0.207. For adjustment, these variables served as covariates in a linear regression model with cTnl as dependent variable. This adjustment model was then applied to a real-world cohort of 1789 patients with suspected acute MI (AMI) (N = 407). Adjusting cTnI showed no relevant loss of diagnostic information, as evidenced by comparable areas under the receiver operator characteristic curves, to identify AMI in males and females for adjusted and unadjusted cTnI. In specific patients groups such as in elderly females, adjusting cTnI improved specificity for AMI compared with unadjusted cTnI. Specificity was also improved in patients with renal dysfunction by using the adjusted cTnI values. Thus, the adjustments improved the diagnostic ability of cTnI to identify AMI in elderly patients and in patients with renal dysfunction. Interpretation of cTnI values in complex emergency cases is facilitated by our method, which maintains a single diagnostic cut-off value in all patients.

Place, publisher, year, edition, pages
NATURE PUBLISHING GROUP, 2018
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:uu:diva-357270 (URN)10.1038/s41598-018-26120-l (DOI)000432928200012 ()29799020 (PubMedID)
Available from: 2018-08-17 Created: 2018-08-17 Last updated: 2018-08-17Bibliographically approved
Mair, J., Lindahl, B., Müller, C., Giannitsis, E., Huber, K., Möckel, M., . . . Jaffe, A. S. (2018). Editor's Choice-What to do when you question cardiac troponin values. European heart journal. Acute cardiovascular care., 7(6), 577-586
Open this publication in new window or tab >>Editor's Choice-What to do when you question cardiac troponin values
Show others...
2018 (English)In: European heart journal. Acute cardiovascular care., ISSN 2048-8726, Vol. 7, no 6, p. 577-586Article in journal (Refereed) Published
Abstract [en]

High-sensitivity cardiac troponin assays enable cardiac troponin measurement with a high degree of analytical sensitivity and a low level of analytical imprecision at the low measuring range. One of the most important advantages of these new assays is that they allow novel, more rapid approaches for ruling in or ruling out acute myocardial infarctions. The increase in the early diagnostic sensitivity of high-sensitivity cardiac troponin assays comes at the cost of a reduced acute myocardial infarction specificity of the biomarker, because more patients with other causes of acute or chronic myocardial injury without overt myocardial ischaemia are detected than with previous cardiac troponin assays. Increased troponin concentrations that do not fit with the clinical presentation are seen in the daily routine, mainly as a result of a variety of pathologies, and if tested in the same sample, even discrepancies between high-sensitivity cardiac troponin I and troponin T test results may sometimes be found as well. In addition, analytically false-positive test results occasionally may occur since no assay is perfect. In this review, we summarise the biochemical, pathophysiological and analytical background of the work-up for such a clinical setting.

Place, publisher, year, edition, pages
SAGE PUBLICATIONS LTD, 2018
Keywords
Cardiac troponin I, cardiac troponin T, high sensitivity, discrepancy, interference, mismatch
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:uu:diva-366277 (URN)10.1177/2048872617708973 (DOI)000444973300011 ()28485179 (PubMedID)
Available from: 2018-11-26 Created: 2018-11-26 Last updated: 2018-11-26Bibliographically approved
Eggers, K. M., Jernberg, T. & Lindahl, B. (2018). High-sensitivity cardiac troponin T, left ventricular function, and outcome in non-ST elevation acute coronary syndrome. American Heart Journal, 197, 70-76
Open this publication in new window or tab >>High-sensitivity cardiac troponin T, left ventricular function, and outcome in non-ST elevation acute coronary syndrome
2018 (English)In: American Heart Journal, ISSN 0002-8703, E-ISSN 1097-6744, Vol. 197, p. 70-76Article in journal (Refereed) Published
Abstract [en]

Background Cardiac troponin (cTn) levels reflect infarct size and depressed left ventricular ejection fraction (LVEF) in patients with non-ST elevation acute coronary syndrome (NSTE-ACS). However, there is very limited information on whether cTn measured with a high-sensitivity (hs) assay would provide incremental prognostic information to the LVEF in NSTE-ACS patients. Methods This was a registry-based study (SWEDEHEART registry) investigating 20,652 NSTE-ACS patients with available information on hs-cTnT (highest level recorded during the hospitalization) and the LVEF estimated using echocardiography. All patients had been followed for 1 year. Results Hs-cTnT levels independently predicted major cardiovascular events (MACE) in cohorts with normal, slightly depressed, moderately depressed, and severely depressed LVEF. The adjusted hazard ratios in these cohorts were 1.18 (95% CI 1.13-1.23), 1.12 (95% CI 1.06-1.18), 1.12 (95% CI 1.06-1.19), and 1.21 (95% CI 1.13-1.30), respectively. Hs-cTnT levels were particularly predictive for cardiovascular mortality and readmission for heart failure. Excluding patients with previous cardiac disease did not affect the overall interrelations of hs-cTnT and LVEF with MACE. Conclusions Hs-cTnT levels provide incremental prognostic value independent of the LVEF in patients with NSTE-ACS. Hs-cTnT is particularly predictive for MACE in patients with severely depressed LVEF but also in those with a normal LVEF. Accordingly, a normal LVEF should not be used as an argument not to target patients to thorough workup.

Place, publisher, year, edition, pages
MOSBY-ELSEVIER, 2018
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:uu:diva-348973 (URN)10.1016/j.ahj.2017.11.012 (DOI)000425723700009 ()29447786 (PubMedID)
Available from: 2018-05-03 Created: 2018-05-03 Last updated: 2018-05-03Bibliographically approved
Eggers, K. M., Jernberg, T., Lindhagen, L. & Lindahl, B. (2018). High-Sensitivity Cardiac Troponin T Levels Identify Patients With Non-ST-Segment Elevation Acute Coronary Syndrome Who Benefit From Invasive Assessment [Letter to the editor]. JACC: Cardiovascular Interventions, 11(16), 1665-1667
Open this publication in new window or tab >>High-Sensitivity Cardiac Troponin T Levels Identify Patients With Non-ST-Segment Elevation Acute Coronary Syndrome Who Benefit From Invasive Assessment
2018 (English)In: JACC: Cardiovascular Interventions, ISSN 1936-8798, E-ISSN 1876-7605, Vol. 11, no 16, p. 1665-1667Article in journal, Letter (Other academic) Published
Place, publisher, year, edition, pages
ELSEVIER SCIENCE INC, 2018
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:uu:diva-363868 (URN)10.1016/j.jcin.2018.03.027 (DOI)000442425900029 ()30139480 (PubMedID)
Funder
Swedish Foundation for Strategic Research
Available from: 2018-11-14 Created: 2018-11-14 Last updated: 2018-11-14Bibliographically approved
Mair, J., Lindahl, B., Hammarsten, O., Mueller, C., Giannitsis, E., Huber, K., . . . Jaffe, A. S. (2018). How is cardiac troponin released from injured myocardium?. European heart journal. Acute cardiovascular care., 7(6), 553-560
Open this publication in new window or tab >>How is cardiac troponin released from injured myocardium?
Show others...
2018 (English)In: European heart journal. Acute cardiovascular care., ISSN 2048-8726, Vol. 7, no 6, p. 553-560Article in journal (Refereed) Published
Abstract [en]

Cardiac troponin I and cardiac troponin T are nowadays the criterion biomarkers for the laboratory diagnosis of acute myocardial infarction due to their very high sensitivities and specificities for myocardial injury. However, still many aspects of their degradation, tissue release and elimination from the human circulation are incompletely understood. Myocardial injury may be caused by a variety of different mechanisms, for example, myocardial ischaemia, inflammatory and immunological processes, trauma, drugs and toxins, and myocardial necrosis is preceded by a substantial reversible prelethal phase. Recent experimental data in a pig model of myocardial ischaemia demonstrated cardiac troponin release into the circulation from apoptotic cardiomyocytes as an alternative explanation for clinical situations with increased cardiac troponin without any other evidence for myocardial necrosis. However, the comparably lower sensitivities of all currently available imaging modalities, including cardiac magnetic resonance imaging for the detection of particularly non-focal myocardial necrosis in patients, has to be considered for cardiac troponin test result interpretation in clinical settings without any other evidence for myocardial necrosis apart from increased cardiac troponin concentrations as well.

Place, publisher, year, edition, pages
SAGE PUBLICATIONS LTD, 2018
Keywords
Cardiac troponin I, cardiac troponin T, myocardial injury, release, reversible, necrosis, apoptosis
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:uu:diva-366275 (URN)10.1177/2048872617748553 (DOI)000444973300008 ()29278915 (PubMedID)
Available from: 2018-11-26 Created: 2018-11-26 Last updated: 2018-11-26Bibliographically approved
Gard, A., Lindahl, B., Batra, G., Hadziosmanovic, N., Hjort, M., Szummer, K. E. & Baron, T. (2018). Interphysician agreement on subclassification of myocardial infarction.. Heart, 104(15), 1284-1291
Open this publication in new window or tab >>Interphysician agreement on subclassification of myocardial infarction.
Show others...
2018 (English)In: Heart, ISSN 1355-6037, E-ISSN 1468-201X, Vol. 104, no 15, p. 1284-1291Article in journal (Refereed) Published
Abstract [en]

OBJECTIVE: The universal definition of myocardial infarction (MI) differentiates MI due to oxygen supply/demand mismatch (type 2) from MI due to plaque rupture (type 1) as well as from myocardial injuries of non-ischaemic or multifactorial nature. The purpose of this study was to investigate how often physicians agree in this classification and what factors lead to agreement or disagreement.

METHODS: A total of 1328 patients diagnosed with MI at eight different Swedish hospitals 2011 were included. All patients were retrospectively reclassified into different MI or myocardial injury subtypes by two independent specially trained physicians, strictly adhering to the third universal definition of MI.

RESULTS: Overall, there was a moderate interobserver agreement with a kappa coefficient (κ) of 0.55 in this classification. There was substantial agreement when distinguishing type 1 MI (κ: 0.61), compared with moderate agreement when distinguishing type 2 MI (κ: 0.54). In multivariate logistic regression analyses, ST elevation MI (P<0.001), performed coronary angiography (P<0.001) and larger changes in troponin levels (P=0.023) independently made the physicians agree significantly more often, while they disagreed more often with symptoms of dyspnoea (P<0.001), higher systolic blood pressure (P=0.001) and higher C reactive protein levels on admission (P=0.016).

CONCLUSION: Distinguishing MI types is challenging also for trained adjudicators. Although strictly adhering to the third universal definition of MI, differentiation between type 1 MI, type 2 MI and myocardial injury only gave a moderate rate of interobserver agreement. More precise and clinically applicable criteria for the current classification, particularly for type 2 MI diagnosis, are urgently needed.

Keywords
acute coronary syndromes, acute myocardial infarction
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:uu:diva-343488 (URN)10.1136/heartjnl-2017-312409 (DOI)000442379200013 ()29453330 (PubMedID)
Funder
Swedish Foundation for Strategic Research Swedish Association of Local Authorities and Regions
Available from: 2018-02-27 Created: 2018-02-27 Last updated: 2018-10-22Bibliographically approved
Eggers, K. M., Hadziosmanovic, N., Baron, T., Hambraeus, K., Jernberg, T., Nordenskjöld, A., . . . Lindahl, B. (2018). Myocardial Infarction with Nonobstructive Coronary Arteries: The Importance of Achieving Secondary Prevention Targets. American Journal of Medicine, 131(5), 524-531.e6
Open this publication in new window or tab >>Myocardial Infarction with Nonobstructive Coronary Arteries: The Importance of Achieving Secondary Prevention Targets
Show others...
2018 (English)In: American Journal of Medicine, ISSN 0002-9343, E-ISSN 1555-7162, Vol. 131, no 5, p. 524-531.e6Article in journal (Refereed) Published
Abstract [en]

BACKGROUND:

Approximately 5% to 10% of all patients with myocardial infarction have nonobstructive coronary arteries. Studies investigating the importance of follow-up and achievement of conventional secondary prevention targets in these patients are lacking.

METHODS:

In this analysis from the Swedish Web-system for Enhancement and Development of Evidence-based care in Heart disease Evaluated According to Recommended Therapies (SWEDEHEART) registry, we investigated 5830 patients with myocardial infarction with nonobstructive coronary arteries (group 1) and 54,637 patients with myocardial infarction with significant coronary artery disease (≥50% stenosis; group 2). Multivariable- and propensity score-adjusted statistics were used to assess the reduction in the 1-year risk of major adverse events associated with prespecified secondary preventive measures: participation in follow-up at 6 to 10 weeks after the hospitalization and achievement of secondary prevention targets (blood pressure and low-density lipoprotein cholesterol levels in the target ranges, nonsmoking, and participation in exercise training).

RESULTS:

Patients in group 1 were less often followed up compared with patients in group 2 and less often achieved any of the secondary prevention targets. Participation in the 6- to 10-week follow-up was associated with a 3% to 20% risk reduction in group 1, similar as for group 2 according to interaction analysis. The improvement in outcome in group 1 was mainly mediated by achieving target range low-density lipoprotein cholesterol levels (24%-32% risk reduction) and, to a smaller extent, by participation in exercise training (10%-23% risk reduction).

CONCLUSIONS:

Selected secondary preventive measures are associated with prognostic benefit in patients with myocardial infarction with nonobstructive coronary arteries, in particular achieving target range low-density lipoprotein cholesterol levels. Our results indicate that these patients should receive similar follow-up as myocardial infarction patients with significant coronary stenoses.

Keywords
Follow-up, Myocardial infarction, Myocardial infarction with nonobstructive coronary arteries, Prognosis, Secondary prevention
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:uu:diva-343494 (URN)10.1016/j.amjmed.2017.12.008 (DOI)000430269500039 ()29287973 (PubMedID)
Funder
Swedish Foundation for Strategic Research
Available from: 2018-02-27 Created: 2018-02-27 Last updated: 2018-06-19Bibliographically approved
Hofmann, R., Witt, N., Lagerqvist, B., Jernberg, T., Lindahl, B., Erlinge, D., . . . James, S. K. (2018). Oxygen therapy in ST-elevation myocardial infarction. European Heart Journal, 39(29), 2730-2739
Open this publication in new window or tab >>Oxygen therapy in ST-elevation myocardial infarction
Show others...
2018 (English)In: European Heart Journal, ISSN 0195-668X, E-ISSN 1522-9645, Vol. 39, no 29, p. 2730-2739Article in journal (Refereed) Published
Abstract [en]

Aims

To determine whether supplemental oxygen in patients with ST-elevation myocardial infarction (STEMI) impacts on procedure-related and clinical outcomes.

Methods and results The DETermination of the role of Oxygen in suspected Acute Myocardial Infarction (DETO2X-AMI) trial randomized patients with suspected myocardial infarction (MI) to receive oxygen at 6 L/min for 6-12 h or ambient air. In this pre-specified analysis, we included only STEMI patients who underwent percutaneous coronary intervention (PCI). In total, 2807 patients were included, 1361 assigned to receive oxygen, and 1446 assigned to ambient air. The pre-specified primary composite endpoint of all-cause death, rehospitalization with MI, cardiogenic shock, or stent thrombosis at 1 year occurred in 6.3% (86 of 1361) of patients allocated to oxygen compared to 7.5% (108 of 1446) allocated to ambient air [hazard ratio (HR) 0.85, 95% confidence interval (95% CI) 0.64-1.13; P = 0.27]. There was no difference in the rate of death from any cause (HR 0.86, 95% CI 0.61-1.22; P = 0.41), rate of rehospitalization for MI (HR 0.92, 95% CI 0.57-1.48; P = 0.73), rehospitalization for cardiogenic shock (HR 1.05, 95% CI 0.21-5.22; P = 0.95), or stent thrombosis (HR 1.27, 95% CI 0.46-3.51; P = 0.64). The primary composite endpoint was consistent across all subgroups, as well as at different time points, such as during hospital stay, at 30 days and the total duration of follow-up up to 1356 days.

Conclusions Routine use of supplemental oxygen in normoxemic patients with STEMI undergoing primary PCI did not significantly affect 1-year all-cause death, rehospitalization with MI, cardiogenic shock, or stent thrombosis.

Place, publisher, year, edition, pages
OXFORD UNIV PRESS, 2018
Keywords
Oxygen, ST-elevation myocardial infarction, Percutaneous coronary intervention, Registry-based randomized clinical trial, Reactive oxygen species, Reperfusion injury
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:uu:diva-363057 (URN)10.1093/eurheartj/ehy326 (DOI)000441009100012 ()29912429 (PubMedID)
Funder
Swedish Research Council, VR20130307Swedish Foundation for Strategic Research , SFF KF10-0024Swedish Heart Lung Foundation
Available from: 2018-10-18 Created: 2018-10-18 Last updated: 2018-10-18Bibliographically approved
Eggers, K. M., Lindahl, B., Venge, P. & Lind, L. (2018). Predictors of 10-year changes in levels of N-terminal pro B-type natriuretic peptide and cardiac troponin I in the elderly. International Journal of Cardiology, 257, 300-305
Open this publication in new window or tab >>Predictors of 10-year changes in levels of N-terminal pro B-type natriuretic peptide and cardiac troponin I in the elderly
2018 (English)In: International Journal of Cardiology, ISSN 0167-5273, E-ISSN 1874-1754, Vol. 257, p. 300-305Article in journal (Refereed) Published
Abstract [en]

Background: Measurement of N-terminal pro B-type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) might be useful for monitoring of cardiovascular disease in the elderly. However, it is not clear whether changes in these biomarkers are associated with changes in the cardiovascular risk profile and if this pattern could be modified by changes in lifestyle habits or medications.

Methods: We measured levels of NT-proBNP and cTnI in community-dwelling subjects (PIVUS study) upon visits scheduled at age 70 (n = 1007), 75 (n = 825) and 80 (n = 602). The associations of these biomarkers with repeated measurements of clinical variables (risk factors, lifestyle habits, echocardiographic data and medications) were investigated using sex-adjusted linear mixed random effect models.

Results: NT-proBNP and cTnI were positively associated with increasing age. NT-proBNP, but not cTnI, was affected by changes of renal function and the degree of obesity. NT-proBNP was more closely related than cTnI to changes in echocardiographic estimates of cardiac geometry and function. Biomarker levels and/or their changes were inversely associated with a physically more active lifestyle (both NT-proBNP and cTnI) and statin treatment at age 70 (only cTnI). Changes in smoking status or antihypertensive treatment had no effect on biomarker levels.

Conclusions: Changes in NT-proBNP and cTnI levels are associated with different patterns of cardiovascular disease burden when using a longitudinal approach. However, levels of both biomarkers and their changes also reflect changes in the cardiovascular risk profile that might be modifiable. This is an important aspect for the use of any cardiovascular biomarker in an elderly population.

Place, publisher, year, edition, pages
ELSEVIER IRELAND LTD, 2018
Keywords
Biomarkers, Cardiovascular risk, Cardiac troponin, NT-pro B-type natriuretic peptide, Longitudinal changes
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:uu:diva-351561 (URN)10.1016/j.ijcard.2017.10.095 (DOI)000427530200074 ()29506712 (PubMedID)
Funder
Swedish Heart Lung Foundation, 20100947Swedish Society of Medicine, SLS-248691
Available from: 2018-05-30 Created: 2018-05-30 Last updated: 2018-05-30Bibliographically approved
Nordenskjöld, A. M., Baron, T., Eggers, K. M., Jernberg, T. & Lindahl, B. (2018). Predictors of adverse outcome in patients with myocardial infarction with non-obstructive coronary artery (MINOCA) disease. International Journal of Cardiology, 261, 18-23
Open this publication in new window or tab >>Predictors of adverse outcome in patients with myocardial infarction with non-obstructive coronary artery (MINOCA) disease
Show others...
2018 (English)In: International Journal of Cardiology, ISSN 0167-5273, E-ISSN 1874-1754, Vol. 261, p. 18-23Article in journal (Refereed) Published
Abstract [en]

Background: Myocardial infarction (MI) with non-obstructive coronary arteries (MINOCAs) is an increasingly recognized entity. No previous study has evaluated predictors for new major adverse cardiacvascular events (MACEs) and death in patients with MINOCA.

Methods: We conducted an observational study of MINOCA patients recorded between July 2003 and June 2013 and followed until December 2013 for outcome events. Out of 199,163 MI admissions, 9092 consecutive unique patients with MINOCA were identified. The mean age was 65.5 years and 62% were women. MACE was defined as all-cause mortality, rehospitalization for acute MI, ischemic stroke and heart failure. Hazard ratio and 95% confidence interval (HR; 95% CI) was calculated using Cox-regression.

Results: A total of 2147 patients (24%) experienced a new MACE and 1254 patients (14%) died during the mean follow-up of 4.5 years. Independent predictors for MACE after adjustment, were older age (1.05; 1.04–1.06), diabetes (1.44; 1.21–1.70), hypertension (1.25; 1.09–1.43), current smoking (1.38; 1.15–1.66), previous myocardial infarction (1.38; 1.04–2.82), previous stroke (1.69; 1.35–2.11), peripheral vascular disease (1.55; 1.97–2.23), chronic obstructive pulmonary disease (1.63; 1.32–2.00), reduced left ventricular ejection fraction (2.00; 1.54–2.60), lower level of total cholesterol (0.88; 0.83–0.94) and higher level of creatinine (1.01; 1.00–1.03). Independent predictors for all cause death were age, current smoking, diabetes, cancer, chronic obstructive pulmonary disease, previous stroke, reduced left ventricular fraction, lower level of total cholesterol and higher levels of creatinine and CRP.

Conclusions: The clinical factors predicting new MACE and death of MINOCA patients seem to be strikingly similar to factors previously shown to predict new cardiovascular events in patients with MI and obstructive coronary artery disease.

Keywords
Myocardial infarction, Myocardial infarction with non-obstructive, coronary arteries, Predictors
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:uu:diva-353356 (URN)10.1016/j.ijcard.2018.03.056 (DOI)000430081000004 ()29563017 (PubMedID)
Funder
Swedish Foundation for Strategic Research
Available from: 2018-06-12 Created: 2018-06-12 Last updated: 2018-06-12Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-5795-0061

Search in DiVA

Show all publications