Publications by authors named "Johannes Mair"

108 Publications

A case report on the successful interventional treatment of a rare cause of left heart failure in a 69-year-old woman.

Eur Heart J Case Rep 2020 Dec 30;4(6):1-5. Epub 2020 Nov 30.

Department of Internal Medicine III - Cardiology and Angiology, Medical University Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria.

Background : Dyspnoea is very common in elderly patients and can be caused by a variety of different diseases. However, the initial diagnosis of patent ductus arteriosus (PDA) as a cause of left heart failure is very rare in this patient population.

Case Summary : A 69-year-old physically active woman with known hypertension presented with worsening exertional dyspnoea. Echocardiography showed a dilated left ventricle with moderately reduced left ventricular ejection fraction, and evidence for PDA. The PDA was confirmed by computed tomography angiography and successfully closed by implantation of an Amplatzer PDA occluder II 06-06 mm. As a result, the heart failure symptoms receded completely.

Discussion : Congenital heart diseases should be considered as heart failure causes even in older adults. In addition to the standard medical therapy, there may be effective interventional treatment options to reverse the symptoms of heart failure in such patients.
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http://dx.doi.org/10.1093/ehjcr/ytaa440DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7891253PMC
December 2020

Biomarkers of coagulation and fibrinolysis in acute myocardial infarction: a joint position paper of the Association for Acute CardioVascular Care and the European Society of Cardiology Working Group on Thrombosis.

Eur Heart J Acute Cardiovasc Care 2020 Nov 7. Epub 2020 Nov 7.

Department of Cardiology, Aarhus University Hospital, Palle Juul-Jensens Blvd. 161, 8200 Aarhus N, Denmark.

The formation of a thrombus in an epicardial artery may result in an acute myocardial infarction (AMI). Despite major advances in acute treatment using network approaches to allocate patients to timely reperfusion and optimal antithrombotic treatment, patients remain at high risk for thrombotic complications. Ongoing activation of the coagulation system as well as thrombin-mediated platelet activation may both play a crucial role in this context. Whether measurement of circulating biomarkers of coagulation and fibrinolysis could be useful for risk stratification in secondary prevention is currently not fully understood. In addition, measurement of such biomarkers could be helpful to identify thrombus formation as the leading mechanism for AMI. The introduction of biomarkers of myocardial injury such as high-sensitivity cardiac troponins made rule-out of AMI even more precise. However, elevated markers of myocardial injury cannot provide proof of a type 1 AMI, let alone thrombus formation. The combined measurement of markers of myocardial injury with biomarkers reflecting ongoing thrombus formation might be helpful for the fast and correct diagnosis of an atherothrombotic type 1 AMI. This position paper gives an overview of the current knowledge and possible role of biomarkers of coagulation and fibrinolysis for the diagnosis of AMI, risk stratification, and individualized treatment strategies in patients with AMI.
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http://dx.doi.org/10.1093/ehjacc/zuaa025DOI Listing
November 2020

Exposing the High Heterogeneity of Circulating Pro B-Type Natriuretic Peptide Fragments in Healthy Individuals and Heart Failure Patients.

Clin Chem 2020 09;66(9):1200-1209

Institute of Clinical Biochemistry, Innsbruck Medical University, Innsbruck , Austria.

Background: The high molecular complexity of variably O-glycosylated and degraded pro B-type natriuretic peptide (proBNP) derived molecular forms challenges current immunoassays. Antibodies used show pronounced differences in cross-reactivities with these circulating fragments, which still need to be better characterized on a molecular level. To pave the way for advanced quantitative assays in the future, it is critical to fully understand these circulating forms.

Methods: Plasma samples were collected from 8 heart failure (HF) patients and 2 healthy controls. NT-proBNP and proBNP were purified by immunoprecipitation and analyzed by nano-flow liquid chromatography coupled to high-resolution mass spectrometry. Fragments formed during proteolysis in solution digestion were distinguished from naturally occurring peptides by using an 18O stable isotope labeling strategy.

Results: We detected 16 previously unknown circulating fragments of proBNP peptides (9 of which are located in the N-terminal and 7 in the C-terminal region), revealing a more advanced state of degradation than previously known. Two of these fragments are indicative of either unidentified processing modes or a far-reaching C-terminal degradation (or a combination thereof) of the precursor proBNP.

Conclusions: Our results further restrict ideal target epitopes for immunoassay antibodies and expand the current thinking of diversity, degradation, and processing of proBNP, as well as the distribution of circulating forms.
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http://dx.doi.org/10.1093/clinchem/hvaa130DOI Listing
September 2020

Application of the fourth universal definition of myocardial infarction in clinical practice.

Biomarkers 2020 Jun 14;25(4):322-330. Epub 2020 May 14.

Department of Medical Sciences, Uppsala University and Uppsala Clinical Research Center, Uppsala University, Sweden.

The Fourth Universal Definition of Myocardial Infarction (MI) has highlighted the different pathophysiological mechanisms that may lead to ischaemic and non-ischaemic myocardial injury and has emphasised that the diagnosis of myocardial infarction requires the presence of acute myocardial ischaemia in the setting of acute myocardial injury. This case based review intends to illustrate basic principles on how to apply this new, revised definition in clinical practice. The distinction between different types of MIs (type 1 or type 2) and the delineation of MI from acute non-ischaemic myocardial injury may be challenging in individual patients, which is illustrated by presenting and discussing real-life routine cases. Type 1 MI is a consequence of coronary plaque rupture or erosion with intracoronary thrombus formation that is usually apparent on coronary angiography. Plausible triggering mechanisms causing myocardial oxygen supply/demand mismatch must be identified for the diagnosis of type 2 MI and its treatment should focus initially on management of the underlying disease attributable to acute myocardial ischaemia.
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http://dx.doi.org/10.1080/1354750X.2020.1764108DOI Listing
June 2020

Clinical evaluation of capillary B-type natriuretic peptide testing.

Clin Chem Lab Med 2020 03;58(4):618-624

Department of Internal Medicine III - Cardiology and Angiology, Medical University Innsbruck, Innsbruck, Austria.

Background Capillary B-type natriuretic peptide (BNP) testing is attractive in outpatient and emergency settings. The aim of this study was to perform an evaluation of the clinical performances of capillary BNP testing as compared with venous whole blood and plasma point-of-care (POC) BNP as well as plasma N-terminal (NT) proBNP central laboratory testing. Methods BNP was measured with a novel single epitope POC assay (Minicare® BV, Eindhoven, The Netherlands) and NT-proBNP with a central laboratory assay (Roche Diagnostics®, Vienna, Austria). Results BNP and NT-proBNP were measured in 269 patients of a Department of Cardiology (mean age 67.9 ± 13 years, 26.4% females). Capillary BNP very closely correlated with whole blood venous BNP (r = 0.99, p < 0.001). There was also a close correlation of plasma BNP and NT-proBNP concentrations (r = 0.79, p < 0.001). The diagnostic performances of capillary BNP, whole blood venous BNP, plasma BNP and plasma NT-proBNP for acute heart failure (areas under receiver operating characteristic curves [AUC ROC]: 0.73-0.77) or systolic left ventricular dysfunction in the whole study population (AUC ROC: 0.72-0.76) did not differ significantly. All were significant independent predictors of cardiovascular death during follow-up of the whole study population. Conclusions Our study for the first time demonstrated a very close correlation of capillary and venous whole blood or plasma BNP concentrations using the same BNP assay in a large patient cohort. The diagnostic performances of different BNP specimens did not differ significantly, and no significant differences between BNP and NT-proBNP were found either.
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http://dx.doi.org/10.1515/cclm-2019-0672DOI Listing
March 2020

Analytical performance of a single epitope B-type natriuretic peptide sandwich immunoassay on the Minicare platform for point-of-care diagnostics.

Pract Lab Med 2019 May 17;15:e00119. Epub 2019 Mar 17.

Department of Internal Medicine III - Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria.

Point-of-care B-type natriuretic peptide (BNP) testing with adequate analytical performance has the potential to improve patient flow and provide primary care givers with easy-to-use advanced diagnostic tools in the management of heart failure. We present the analytical evaluation of the Minicare BNP immunoassay under development on the Minicare I-20 platform for point-of-care testing. Analytical performance was evaluated using EDTA venous whole blood, EDTA plasma and capillary whole blood. Method comparison with a lab-testing system was performed using samples from 187 patients. Normal values were determined based on 160 healthy adults, aging from 19 to 70 years. Limit of blank (LoB), limit of detection (LoD) were determined to be 3.3 ng/L, 5.8 ng/L. Limit of quantitation (LoQ) in whole blood at 20% and 10% coefficient of variation (CV) was found < 9 ng/L and <30 ng/L respectively without significant differences between EDTA whole blood and EDTA plasma. Total CV was found to be from 6.7% to 9.7% for BNP concentrations between 92.6 and 3984 ng/L. The sample type comparison study demonstrated correlation coefficients between 0.97 and 0.99 with slopes between 1.03 and 1.09 between the different samples. Method comparison between Minicare BNP and Siemens ADVIA Centaur BNP demonstrated a correlation coefficient of 0.92 with a slope of 1.06. The 97.5% URL of a healthy population was calculated to be 72.6 ng/L. The Minicare BNP assay is a robust, easy-to-use and sensitive test for rapid determination of BNP concentrations that can be used in a near-patient setting.
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http://dx.doi.org/10.1016/j.plabm.2019.e00119DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6444177PMC
May 2019

Possible mechanisms behind cardiac troponin elevations.

Biomarkers 2018 Dec 23;23(8):725-734. Epub 2018 Aug 23.

e Department of Cardiovascular Medicine, Mayo Clinic and Medical School , Rochester , MN , USA.

Cardiac-specific troponins are elevated in blood following cardiac injury and are the preferred diagnostic biomarkers when acute myocardial infarction is suspected clinically. Cardiac troponin (cTn) elevations are also observed in clinical conditions without obvious connection to cardiac injury. Irrespective of the underlying condition, cTn elevation is linked to a poor prognosis, even if the elevation is stable over time. Here, we explore mechanisms that may lead to cTn elevations, including necrosis, apoptosis, necroptosis, cell wounds and decreased clearance. The aim is to broaden the perspective of how we interpret unexpected cTn elevations in patients. The cTn elevations may not be able to serve as direct proof of myocardial necrosis especially in the absence of a clear-cut reason for its release. Abbreviations: AMI: acute myocardial infarction; cTn: cardiac troponin; cTnI: cardiac troponin I; cTnT: cardiac troponin T; MLKL: mixed lineage kinase domain-like; TUNEL: terminal deoxynucleotidyl transferase nick end labeling.
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http://dx.doi.org/10.1080/1354750X.2018.1490969DOI Listing
December 2018

Thyroid-stimulating hormone and adverse left ventricular remodeling following ST-segment elevation myocardial infarction.

Eur Heart J Acute Cardiovasc Care 2019 Dec 11;8(8):717-726. Epub 2018 Apr 11.

University Clinic of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Austria.

Background: Adverse left ventricular remodeling is one of the major determinants of heart failure and mortality in patients surviving ST-segment elevation myocardial infarction (STEMI). The hypothalamic-pituitary-thyroid axis is a key cardiovascular regulator; however, the relationship between hypothalamic-pituitary-thyroid status and post-STEMI left ventricular remodeling is unclear. We aimed to investigate the association between thyroid-stimulating hormone concentrations and the development of left ventricular remodeling following reperfused STEMI.

Methods: In this prospective observational study of 102 consecutive STEMI patients, thyroid-stimulating hormone levels were measured at the first day after infarction and 4 months thereafter. Cardiac magnetic resonance scans were performed within the first week as well as at 4 months follow-up to determine infarct characteristics, myocardial function and as primary endpoint left ventricular remodeling, defined as a 20% or greater increase in left ventricular end-diastolic volume.

Results: Patients with left ventricular remodeling (=15, 15%) showed significantly lower concentrations of baseline (1.20 [0.92-1.91] vs. 1.73 [1.30-2.60] mU/l; =0.02) and follow-up (1.11 [0.86-1.28] vs. 1.51 [1.15-2.02] mU/l; =0.002) thyroid-stimulating hormone. The association between baseline thyroid-stimulating hormone and left ventricular remodeling remained significant after adjustment for major clinical (peak high-sensitivity cardiac troponin T and C-reactive protein, heart rate; odds ratio (OR) 5.33, 95% confidence interval (CI) 1.52-18.63; =0.01) and cardiac magnetic resonance predictors of left ventricular remodeling (infarct size, microvascular obstruction, ejection fraction; OR 4.59, 95% CI 1.36-15.55; =0.01). Furthermore, chronic thyroid-stimulating hormone was related to left ventricular remodeling independently of chronic left ventricular remodeling correlates (infarct size, ejection fraction, left ventricular end-diastolic volume, left ventricular end-systolic volume; OR 9.22, 95% CI 1.69-50.22; =0.01).

Conclusions: Baseline and chronic thyroid-stimulating hormone concentrations following STEMI were independently associated with left ventricular remodeling, proposing a novel pathophysiological axis in the development of post-STEMI left ventricular remodeling.
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http://dx.doi.org/10.1177/2048872618770600DOI Listing
December 2019

Clinical performance of a new point-of-care cardiac troponin I test.

Clin Chem Lab Med 2018 07;56(8):1336-1344

Emergency Department, Hôpital Pitié-Salpêtrière, AP-HP, Paris, France.

Background: We evaluated the clinical performance of the Minicare cardiac troponin-I (cTnI), a new point-of-care (POC) cTnI test for the diagnosis of acute myocardial infarction (AMI) in a prospective, multicentre study (ISRCTN77371338).

Methods: Of 474 patients (≥18 years) admitted to an emergency department (ED) or chest pain unit (CPU) with symptoms suggestive of acute coronary syndrome (ACS; ≤12 h from symptom onset), 465 were eligible. Minicare cTnI was tested immediately, 3 h and 6 h after presentation. AMI diagnoses were adjudicated independently based on current guidelines.

Results: The diagnostic performance of the Minicare cTnI test at 3 h was similar for whole blood and in plasma: sensitivity 0.92 vs. 0.90; specificity 0.91 vs. 0.90; positive predictive value (PPV) 0.68 vs. 0.66; negative predictive value (NPV) 0.98 vs. 0.98; positive likelihood ratio (LR+) 10.18 vs. 9.41; negative likelihood ratio (LR-) 0.09 vs. 0.11. The optimal diagnostic performance was obtained at 3 h using cut-offs cTnI >43 ng/L plus cTnI change from admission ≥18.5 ng/L: sensitivity 0.90, specificity 0.96, PPV 0.81, NPV 0.98, and LR+ 21.54. The area under the receiver operating characteristics (ROC) curve for cTnI whole blood baseline value and absolute change after 3 h curve was 0.93.

Conclusions: These data support the clinical usefulness of Minicare cTnI within a 0 h/3 h-blood sampling protocol supported by current guidelines for the evaluation of suspected ACS.
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http://dx.doi.org/10.1515/cclm-2017-0693DOI Listing
July 2018

Elevated Cardiac Troponin T in Patients With Skeletal Myopathies.

J Am Coll Cardiol 2018 04;71(14):1540-1549

Division of Cardiology, Department of Internal Medicine, Medical University of Graz, Graz, Austria. Electronic address:

Background: Cardiac troponins are often elevated in patients with skeletal muscle disease who have no evidence of cardiac disease.

Objectives: The goal of this study was to characterize cardiac troponin concentrations in patients with myopathies and derive insights regarding the source of elevated troponin T measurements.

Methods: Cardiac troponin T (cTnT) and cardiac troponin I (cTnI) concentrations were determined by using high sensitivity assays in 74 patients with hereditary and acquired skeletal myopathies. Patients underwent comprehensive cardiac evaluation, including 12-lead electrocardiogram, 24-h electrocardiogram, cardiac magnetic resonance imaging, and coronary artery computed tomography. cTnT and cTnI protein expression was determined in skeletal muscle samples of 9 patients and in control tissues derived from autopsy using antibodies that are used in commercial assays. Relevant Western blot bands were subjected to liquid chromatography tandem mass spectrometry for protein identification.

Results: Levels of cTnT (median: 24 ng/l; interquartile range: 11 to 54 ng/l) were elevated (>14 ng/l) in 68.9% of patients; cTnI was elevated (>26 ng/l) in 4.1% of patients. Serum cTnT levels significantly correlated with creatine kinase and myoglobin (r = 0.679 and 0.786, respectively; both p < 0.001). Based on cTnT serial testing, 30.1% would have fulfilled current rule-in criteria for myocardial infarction. Noncoronary cardiac disease was present in 23%. Using cTnT antibodies, positive bands were found in both diseased and healthy skeletal muscle at molecular weights approximately 5 kDa below cTnT. Liquid chromatography tandem mass spectrometry identified the presence of skeletal troponin T isoforms in these bands.

Conclusions: Measured cTnT concentrations were chronically elevated in the majority of patients with skeletal myopathies, whereas cTnI elevation was rare. Our data indicate that cross-reaction of the cTnT immunoassay with skeletal muscle troponin isoforms was the likely cause.
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http://dx.doi.org/10.1016/j.jacc.2018.01.070DOI Listing
April 2018

How is cardiac troponin released from injured myocardium?

Eur Heart J Acute Cardiovasc Care 2018 Sep 27;7(6):553-560. Epub 2017 Dec 27.

11 Mayo Clinic and Medical School, Rochester, USA.

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.
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http://dx.doi.org/10.1177/2048872617748553DOI Listing
September 2018

Relation of Low-Density Lipoprotein Cholesterol With Microvascular Injury and Clinical Outcome in Revascularized ST-Elevation Myocardial Infarction.

J Am Heart Assoc 2017 Oct 10;6(10). Epub 2017 Oct 10.

University Clinic of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Austria

Background: Microvascular injury (MVI) after primary percutaneous coronary intervention for ST-elevation myocardial infarction (STEMI) is a major determinant of adverse clinical outcome. Experimental data indicate an impact of hypercholesterolemia on MVI; however, there is a lack of clinical studies confirming this relation. We aimed to investigate the association of cholesterol concentrations on admission with MVI visualized by cardiac magnetic resonance imaging and clinical outcome in STEMI patients treated by primary percutaneous coronary intervention.

Methods And Results: In this prospective, observational study, we included 235 consecutive revascularized STEMI patients. Cholesterol (total cholesterol, low-density lipoprotein [LDL], and high-density lipoprotein cholesterol) and triglyceride concentrations were determined at presentation. Cardiac magnetic resonance scans were performed 2 (2-4) days after infarction to assess infarct characteristics, including MVI. Clinical end point was the occurrence of major adverse cardiac events (MACE) comprising all-cause mortality, nonfatal reinfarction, and new congestive heart failure. Patients with MVI (n=129; 55%) showed higher levels of total cholesterol (204 [172-226] versus 185 [168-212] mg/dL; =0.01) and LDL cholesterol (142 [113-166] versus 118 [103-149] mg/dL; =0.001), whereas high-density lipoprotein cholesterol and triglycerides did not differ significantly. In multivariable analysis, including all significant clinical and cardiac magnetic resonance determinants of MVI, LDL concentration emerged as an independent predictor of MVI (odds ratio, 1.02 [95% confidence interval, 1.01-1.02]; =0.002). Furthermore, increased LDL cholesterol (>150 mg/dL) significantly predicted the occurrence of major adverse cardiac events (hazard ratio, 3.09 [95% confidence interval, 1.22-7.87]; =0.01).

Conclusions: In STEMI patients undergoing primary percutaneous coronary intervention, baseline LDL cholesterol concentrations were independently associated with MVI, revealing a clinically relevant link between LDL metabolism and MVI in acute STEMI.
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http://dx.doi.org/10.1161/JAHA.117.006957DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5721881PMC
October 2017

Use of copeptin for rapid rule-out of acute myocardial infarction.

Eur Heart J Acute Cardiovasc Care 2018 Sep 8;7(6):570-576. Epub 2017 Jun 8.

9 Department of Medical Sciences, Uppsala University and Uppsala Clinical Research Centre, Uppsala University, Sweden.

Copeptin is currently understood as a quantitative marker of endogenous stress. It rises rapidly in multiple acute disorders including acute myocardial infarction. As a single variable, it has only modest diagnostic accuracy for acute myocardial infarction. However, the use of copeptin within a dual-marker strategy together with conventional cardiac troponin increases the diagnostic accuracy and particularly the negative predictive value of cardiac troponin alone for acute myocardial infarction. The rapid rule-out of acute myocardial infarction is the only application in acute cardiac care mature enough to merit consideration for routine clinical care. However, the dual-marker approach seems to provide only very small incremental value when used in combination with sensitive or high-sensitivity cardiac troponin assays. This review aims to update and educate regarding the potential and the procedural details, as well as the caveats and challenges of using copeptin in clinical practice.
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http://dx.doi.org/10.1177/2048872617710791DOI Listing
September 2018

What to do when you question cardiac troponin values.

Eur Heart J Acute Cardiovasc Care 2018 Sep 9;7(6):577-586. Epub 2017 May 9.

10 Mayo Clinic and Medical School, Rochester, MN, USA.

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.
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http://dx.doi.org/10.1177/2048872617708973DOI Listing
September 2018

Equal clinical performance of a novel point-of-care cardiac troponin I (cTnI) assay with a commonly used high-sensitivity cTnI assay.

Clin Chim Acta 2017 Jun 25;469:119-125. Epub 2017 Mar 25.

Philips Handheld Diagnostics, Eindhoven, The Netherlands.

Background: Efficient rule-out of acute myocardial infarction (MI) facilitates early disposition of chest pain patients in emergency departments (ED). Point-of-care (POC) cardiac troponin (cTn) may improve patient throughput. We compared the diagnostic accuracy of a novel cTnI test (Minicare cTnI, Philips), with current POC cTnI (I-Stat, Abbott) and high-sensitivity central laboratory cTnI (hs-cTnI; Architect, Abbott) assays.

Methods: The clinical performance of the assays were compared in samples from 450 patients from a previous clinical evaluation of Minicare cTnI.

Results: Minicare cTnI correlated with Architect hs-cTnI (r=0.85, p<0.0001) and I-Stat cTnI (r=0.93, p<0.0001). Areas under the receiver operating characteristics curves were 0.87-0.91 at admission (p=ns) and 0.96-0.97 3h after admission (p=ns). The negative predictive values (NPV) at admission were 95% ((92-97%, 95% CI) for Minicare cTnI and increased to 99% (97-100%) at 2-4h, and similar to Architect hs-cTnI (98%, 96-100%), but higher than I-Stat cTnI (95%, 92-97%; p<0.01). Negative likelihood ratios (LR-) after 2-4h were 0.06 (0.02-0.17, 95% CI) for Minicare cTnI, 0.11 (0.05-0.24) for Architect hs-cTnI (p=0.02) and 0.28 (0.18-0.43) for I-Stat cTnI (p<0.0001). The clinical concordances between Minicare cTnI and Architect hs-cTnI were 92% (admission) and 95% (2-4h), with lower concordances between Minicare cTnI and I-Stat cTnI (83% and 78%, respectively; p=0.007).

Conclusions: The Minicare cTnI POC assay may become useful for prompt and safe ruling-out of AMI in ED patients with suspected AMI using a guideline supported 0/3h sampling protocol.
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http://dx.doi.org/10.1016/j.cca.2017.03.023DOI Listing
June 2017

Open surgical retrieval of an embolized PFO occluder system.

Vasa 2017 Jul 20;46(4):310-312. Epub 2017 Feb 20.

1 Department of Vascular Surgery, Innsbruck Medical University, Innsbruck, Austria.

Device migration after intervention for persistent foramen ovale occlusion is a rare complication. In case of failure of endovascular device retrieval, open surgical removal is indicated, safe, and reliable.
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http://dx.doi.org/10.1024/0301-1526/a000620DOI Listing
July 2017

Increased Cardiac Troponin T and N-Terminal B-Type Natriuretic Peptide in a 78-Year-Old Woman Admitted for Dizziness.

Authors:
Johannes M Mair

Clin Chem 2017 01;63(1):435-436

Department of Internal Medicine III, Cardiology and Angiology, Innsbruck Medical University, Innsbruck, Austria.

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http://dx.doi.org/10.1373/clinchem.2016.265603DOI Listing
January 2017

Multimarker approach for the prediction of microvascular obstruction after acute ST-segment elevation myocardial infarction: a prospective, observational study.

BMC Cardiovasc Disord 2016 11 28;16(1):239. Epub 2016 Nov 28.

University Clinic of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Anichstraße 35, A-6020, Innsbruck, Austria.

Background: Presence of microvascular obstruction (MVO) derived from cardiac magnetic resonance (CMR) imaging is among the strongest outcome predictors after ST-segment elevation myocardial infarction (STEMI). We aimed to investigate the comparative predictive values of different biomarkers for the occurrence of MVO in a large cohort of reperfused STEMI patients.

Methods: This study included 128 STEMI patients. CMR imaging was performed within the first week after infarction to assess infarct characteristics, including MVO. Admission and peak concentrations of high-sensitivity cardiac troponin T (hs-cTnT), creatine kinase (CK), N-terminal pro-B-type natriuretic peptide (NT-proBNP), high-sensitivity C-reactive protein (hs-CRP), lactate dehydrogenase (LDH), aspartate transaminase (AST) and alanine transaminase (ALT) were measured.

Results: MVO was detected in 69 patients (54%). hs-cTnT, CK, hs-CRP, LDH, AST and ALT peak concentrations showed similar prognostic value for the prediction of MVO (area under the curve (AUC) = 0.77, 0.77, 0.68, 0.79, 0.78 and 0.73, all p > 0.05), whereas the prognostic utility of NT-proBNP was weakly lower (AUC = 0.64, p < 0.05). Combination of these biomarkers did not increase predictive utility compared to hs-cTnT alone (p = 0.349).

Conclusions: hs-cTnT, CK, hs-CRP, LDH, AST and ALT peak concentrations provided similar prognostic value for the prediction of MVO. The prognostic utility of NT-proBNP was lower. Combining these biomarkers could not further improve predictive utility compared to hs-cTnT alone.
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http://dx.doi.org/10.1186/s12872-016-0415-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5126989PMC
November 2016

Circulating micro ribonucleic acids in cardiovascular disease: a look beyond myocardial injury.

Authors:
Johannes Mair

Ann Transl Med 2016 Oct;4(Suppl 1):S30

Department of Internal Medicine III - Cardiology and Angiology, Innsbruck Medical University, A-6020 Innsbruck, Austria.

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http://dx.doi.org/10.21037/atm.2016.10.67DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5104598PMC
October 2016

Analytical evaluation of a new point of care system for measuring cardiac Troponin I.

Clin Biochem 2017 Mar 12;50(4-5):174-180. Epub 2016 Nov 12.

Philips Handheld Diagnostics, Eindhoven, The Netherlands.

Objectives: Point-of-care cardiac troponin testing with adequate analytical performances has the potential to improve chest pain patients flow in the emergency department. We present the analytical evaluation of the newly developed Philips Minicare cTnI point-of-care immunoassay.

Design & Methods: Li-heparin whole blood and plasma were used to perform analytical studies. The sample type comparison study was performed at 4 different hospitals. The 99th percentile upper reference limit (URL) study was performed using Li-heparin plasma, Li-heparin whole blood and capillary blood samples from 750 healthy adults, aging from 18 to 86years.

Results: Limit of the blank, limit of detection and limit of quantitation at 20% coefficient of variation (CV) were determined to be 8.5ng/L, 18ng/L and 38ng/L respectively without significant differences between whole blood and plasma for LoQ. Cross-reactivity and interferences were minimal and no high-dose hook was observed. Total CV was found to be from 7.3% to 12% for cTnI concentrations between 109.6 and 6135.4ng/L. CV at the 99th percentile URL was 18.6%. The sample type comparison study between capillary blood, Li-heparin whole blood and Li-heparin plasma samples demonstrated correlation coefficients between 0.99 and 1.00 with slopes between 1.03 and 1.08. The method comparison between Minicare cTnI and Beckman Coulter Access, AccuTnI+3 demonstrated a correlation coefficient of 0.973 with a slope of 1.09. The 99th percentile URL of a healthy population was calculated to be 43ng/L with no significant difference between genders or sample types.

Conclusions: The Minicare cTnI assay is a sensitive and precise, clinical usable test for determination of cTnI concentration that can be used in a near-patient setting as an aid in the diagnosis of acute myocardial infarction.
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http://dx.doi.org/10.1016/j.clinbiochem.2016.11.011DOI Listing
March 2017

Combined biomarker testing for the prediction of left ventricular remodelling in ST-elevation myocardial infarction.

Open Heart 2016;3(2):e000485. Epub 2016 Sep 20.

Department of Cardiology and Angiology , University Clinic of Internal Medicine III, Medical University of Innsbruck , Innsbruck , Austria.

Objective: The utility of different biomarkers for the prediction of left ventricular remodelling (LVR) following ST-elevation myocardial infarction (STEMI) has been evaluated in several studies. However, very few data exist on the prognostic value of combined biomarkers. The aim of this study was to comprehensively investigate the prognostic value for LVR of routinely available biomarkers measured after reperfused STEMI.

Methods: Serial measurements of N-terminal pro-B-type natriuretic peptide (NT-proBNP), high-sensitivity cardiac troponin T (hs-cTnT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) and high-sensitivity C reactive protein (hs-CRP) were performed in 123 patients with STEMI treated with primary percutaneous coronary intervention in this prospective observational study. Patients underwent cardiac MRI at 2 (1-4) and 125 (121-146) days after infarction. An increase in end-diastolic volume of ≥20% was defined as LVR.

Results: LVR occurred in 16 (13%) patients. Peak concentrations of the following biomarkers showed significant areas under the curves (AUCs) for the prediction of LVR-NT-proBNP: 0.68 (95% CI 0.59 to 0.76, p=0.03), hs-cTnT: 0.75 (95% CI 0.66 to 0.82, p<0.01), AST: 0.72 (95% CI 0.63 to 0.79, p<0.01), ALT: 0.66 (95% CI 0.57 to 0.75, p=0.03), LDH: 0.78 (95% CI 0.70 to 0.85, p<0.01) and hs-CRP: 0.63 (95% CI 0.54 to 0.72, p=0.05). The combination of all biomarkers yielded a significant increase in AUC to 0.85 (95% CI 0.77 to 0.91) (all vs NT-proBNP: p=0.02, all vs hs-cTnT: p=0.02, all vs AST: p<0.01, all vs ALT: p<0.01, all vs hs-CRP: p<0.01 and all vs LDH: p=0.04).

Conclusions: In patients with reperfused STEMI, the combined assessment of peak NT-proBNP, hs-cTnT, AST, ALT, hs-CRP and LDH provide incremental prognostic information for the prediction of LVR when compared with single-biomarker measurement.
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http://dx.doi.org/10.1136/openhrt-2016-000485DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5030543PMC
September 2016

Adult patent ductus arteriosus : An unusual cause of heart failure in an octogenarian female.

Wien Klin Wochenschr 2016 Dec 26;128(23-24):925-927. Epub 2016 Aug 26.

Department of Internal Medicine III - Cardiology and Angiology, Innsbruck Medical University, Anichstrasse 35, 6020, Innsbruck, Austria.

Patent ductus arteriosus (PDA) is the third most common congenital abnormality in which the arterial duct, which normally closes spontaneously after birth within 24-48 h in full-term infants, remains permanently open. Breathlessness is very common in elderly patients and can be caused by several comorbidities, mostly cardiac and pulmonary diseases. PDA as a cause of heart failure in this patient population is very rare and diagnosis depends on high clinical awareness. Here we present a case diagnosed with multimodality imaging including 3‑dimensional (3D) transthoracic and transesophageal echocardiography and 3D-volume rendering technique (VRT) computed tomography.
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http://dx.doi.org/10.1007/s00508-016-1061-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5161762PMC
December 2016

Relation of inflammatory markers with myocardial and microvascular injury in patients with reperfused ST-elevation myocardial infarction.

Eur Heart J Acute Cardiovasc Care 2017 Oct 20;6(7):640-649. Epub 2016 Jul 20.

1 University Clinic of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Austria.

Background: In patients with acute ST-elevation myocardial infarction (STEMI), elevated concentrations of inflammatory markers are correlated with worse clinical outcome. The aim of this study was comprehensively to investigate the relationship of circulating markers of inflammation with myocardial and microvascular damage after STEMI.

Methods: In 111 consecutive STEMI patients, blood samples were obtained on admission and from day 1 to day 4 after primary percutaneous coronary intervention and analysed for high-sensitivity C-reactive protein (hs-CRP), white blood cell count and fibrinogen. Cardiac magnetic resonance imaging was performed within the first week and 4 months after primary percutaneous coronary intervention.

Results: Peak concentrations of hs-CRP (20.5 (9.6-44.4) mg/L), white blood cell count (12.4 (10.5-15.3) G/L) and fibrinogen (3640 (3150-4550) mg/L) showed significant correlations with both infarct size ( r=0.31 to 0.41; P<0.01) and left ventricular ejection fraction ( r=-0.29 to -0.39; P<0.01) assessed in the acute as well as chronic stage following STEMI. Furthermore, peak concentrations of these inflammatory markers were significantly higher in patients with microvascular obstruction compared to patients without microvascular obstruction ( P⩽0.01). C-statistics revealed that the prognostic values of all three biomarkers for the prediction of large chronic infarct size (>8% of left ventricular myocardial mass) were moderate without significant differences (area under the curve: hs-CRP 0.73 (95% confidence interval (CI) 0.63-0.82), white blood cell count 0.67 (95% CI 0.56-0.78) and fibrinogen 0.69 (95% CI 0.59-0.79); all P>0.12). Combination of inflammatory markers did not significantly increase the area under the curve ( P>0.05).

Conclusion: In reperfused STEMI patients, increased levels of hs-CRP, white blood cell count and fibrinogen are associated with decreased left ventricular function and more pronounced myocardial damage at baseline and 4 months after infarction.
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http://dx.doi.org/10.1177/2048872616661691DOI Listing
October 2017

Novel biomarkers predicting cardiac function after acute myocardial infarction.

Br Med Bull 2016 09 14;119(1):63-74. Epub 2016 Jul 14.

Department of Cardiology and Angiology, University Clinic of Internal Medicine III, Medical University of Innsbruck, Anichstraße 35, A-6020 Innsbruck, Austria

Background: Measurement of biomarkers provides a cost-effective and widely available method to estimate cardiac dysfunction and clinical outcome of patients with acute myocardial infarction (AMI).

Sources Of Data: PubMed entries with terms 'myocardial infarction' and the respective biomarker.

Areas Of Agreement: Cardiac troponins and natriuretic peptides are closely related to left ventricular dysfunction and the occurrence of adverse clinical events following AMI.

Areas Of Contention: The incremental value of novel biomarkers is controversial.

Future Directions: The combination of traditional and novel biomarkers might further improve risk stratification of patients with AMI.

Search Strategy: We searched all entries on the PubMed database with the MeSH terms 'myocardial infarction' and 'cardiac troponins', 'natriuretic peptides', 'copeptin', galectin-3', 'corin', 'fetuin-A', 'adiponectin' and 'microRNA'.
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http://dx.doi.org/10.1093/bmb/ldw027DOI Listing
September 2016

Rapid rule out of acute myocardial infarction: novel biomarker-based strategies.

Eur Heart J Acute Cardiovasc Care 2017 Apr 1;6(3):218-222. Epub 2016 Jul 1.

9 Department of Medical Sciences, Uppsala University and Uppsala Clinical Research Center, Sweden.

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http://dx.doi.org/10.1177/2048872616653229DOI Listing
April 2017

Left main occlusion - a classic electrocardiogram.

Wien Klin Wochenschr 2016 Jul 8;128(13-14):521-3. Epub 2016 Jun 8.

Department of Internal Medicine III - Cardiology and Angiology, Medical University Innsbruck, Innsbruck, Austria.

Left main occlusion is associated with a dire prognosis, as the left main supplies blood to >75 % of the left ventricle. This is a case showing a classic electrocardiogram (ECG) together with the echocardiogram videos and images from coronary angiography.
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http://dx.doi.org/10.1007/s00508-016-1007-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4945673PMC
July 2016

Editor's Choice-Rule-in of acute myocardial infarction: Focus on troponin.

Eur Heart J Acute Cardiovasc Care 2017 04 2;6(3):212-217. Epub 2016 Jun 2.

9 Department of Medical Sciences, Uppsala University and Uppsala Clinical Research Centre, Uppsala University, Sweden.

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http://dx.doi.org/10.1177/2048872616653228DOI Listing
April 2017

Will sacubitril-valsartan diminish the clinical utility of B-type natriuretic peptide testing in acute cardiac care?

Eur Heart J Acute Cardiovasc Care 2017 Jun 12;6(4):321-328. Epub 2016 Jan 12.

9 Mayo Clinic and Medical School, USA.

Since the approval of sacubitril-valsartan for the treatment of chronic heart failure with reduced ejection fraction, a commonly raised suspicion is that a wider clinical use of this new drug may diminish the clinical utility of B-type natriuretic peptide testing as sacubitril may interfere with B-type natriuretic peptide clearance. In this education paper we critically assess this hypothesis based on the pathophysiology of the natriuretic peptide system and the limited published data on the effects of neprilysin inhibition on natriuretic peptide plasma concentrations in humans. As the main clinical application of B-type natriuretic peptide testing in acute cardiac care is and will be the rapid rule-out of suspected acute heart failure there is no significant impairment to be expected for B-type natriuretic peptide testing in the acute setting. However, monitoring of chronic heart failure patients on sacubitril-valsartan treatment with B-type natriuretic peptide testing may be impaired. In contrast to N-terminal-proBNP, the current concept that the lower the B-type natriuretic peptide result in chronic heart failure patients, the better the prognosis during treatment monitoring, may no longer be true.
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http://dx.doi.org/10.1177/2048872615626355DOI Listing
June 2017

N-terminal pro-B-type natriuretic peptide is associated with aortic stiffness in patients presenting with acute myocardial infarction.

Eur Heart J Acute Cardiovasc Care 2016 Dec 9;5(8):560-567. Epub 2015 Oct 9.

University Clinic of Internal Medicine III, Medical University of Innsbruck, Austria

Background: Aortic stiffness is associated with increased left ventricular (LV) afterload, a process which is accompanied by a release of natriuretic peptides. Aortic pulse wave velocity (PWV) has been demonstrated to be the functional surrogate of aortic stiffness. We sought to investigate the impact of aortic PWV on N-terminal pro-B-type natriuretic peptide (NT-proBNP) concentrations in patients with acute myocardial infarction (AMI).

Methods: This prospective observational study included 86 consecutive patients undergoing percutaneous coronary intervention for AMI. Aortic PWV was determined 47 h (interquartile range (IQR) 27-64 h) after AMI using an established oscillometric device. NT-proBNP values were measured using a commercially available immunoassay.

Results: The mean age of the study cohort was 60±11 years; 19% were female. Median aortic PWV was 7.8 m/s (IQR 6.8-9.4 m/s). Patients with a PWV above the median showed significantly higher NT-proBNP peak concentrations (median=1330 ng/l, IQR: 729-3180 ng/l vs median=498 ng/l, IQR: 124-1575 ng/l, p=0.001). Aortic PWV (beta=0.373, p=0.014) was independently associated with NT-proBNP peak concentrations even after correction for LV function, cardiac troponin T levels, heart rate, blood pressure, body mass index and the primary prevention European Society of Cardiology (ESC) SCORE (model: R=0.542, p=0.014).

Conclusion: In patients with AMI, aortic PWV is independently associated with NT-proBNP concentrations. This finding suggests an impact of aortic PWV on myocardial wall stress after AMI.
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http://dx.doi.org/10.1177/2048872615610866DOI Listing
December 2016