Nature, health and climate.

The importance of nature for human health has received increasing attention in recent years and is at the focus of this review. Research has shown benefits for physical, mental, and social health as well as for the climate. Nature-based health interventions have already been partly implemented in social care and in the healthcare system. However, more research is needed to support the systematic development and evaluation of nature-based interventions. We need to identify which interventions are most effective for whom, with the goal of providing evidence-based, sustainable, and climate-friendly health improvements.

Heatwaves and association with comorbidities, pharmacotherapy, and mortality.

Heatwaves are getting more common and is the largest weather-related cause of death in high-income countries. A summary of some of the implications is given in this review. Most of the excess mortality is preventable. However, there is need for increased preparedness and awareness. Common non-communicable diseases increase the risk of unfavorable outcome in relation to heatwave, and many commonly prescribed medications affect the heat regulatory system with increasing evidence for increased hospitalisation and mortality. There is an urgent need for further research on heatwaves effect on prescribed medication and mortality.

Sustainable research.

Research, like any other sector, has an effect on climate and is exposed for waste both societal and economic. There is evidence for possible improvements when keeping focus on study design, patient inclusion, transport, and reporting. However, there is a need for further national and international research. Sustainability is incorporated as a quality domaine in the United Kingdom and we will probably see the same development in Denmark, as argued in this review.

Temporal Release of High-Sensitivity Cardiac Troponin T and I and Copeptin After Brief Induced Coronary Artery Balloon Occlusion in Humans.

BACKGROUND: Cardiac troponins (cTns) are the cornerstone of diagnosing acute myocardial infarction. There is limited knowledge on the duration of ischemia necessary to induce a measurable release of cTns or the very-early-release kinetics of cTns after an ischemic event. Copeptin may have a supplementary role in ruling out myocardial infarction early. We investigated the release of cTns and copeptin in the first hours after experimental balloon-induced ischemia in humans. METHODS: Thirty-four patients (median age, 60 years [interquartile range, 51-64]; 15 men, 43%) with angiographically normal coronary arteries were randomly assigned into 4 groups with different durations of induced myocardial ischemia (0, 30, 60, 90 s). Ischemia was induced by inflating a balloon in the left anterior descending artery between the first and second diagonal branch. Blood was collected before balloon inflation (baseline) every 15 minutes for the first 3 hours, and every 30 minutes for the next 3 hours. The cTns were analyzed by 3 high-sensitivity (hs) cTn assays: hs-cTnT (Roche), hs-cTnI (Siemens), and hs-cTnI (Abbott). Copeptin was analyzed by a sandwich immunoluminometric assay. RESULTS: None of the patients had any complications. Increased cTn concentrations were detected by all 3 assays, and the magnitude of the increase was associated with the duration of ischemia. Increased hs-cTnI (Siemens) concentrations were first detectable 15 minutes after 90-s ischemia (median 43.7% increase) and increased more steeply and had a higher peak than the other assays. Copeptin levels did not significantly change. Using the cTnT, hs-cTnI (Siemens), and hs-cTnI (Abbott) concentrations at 0 and 180 minutes, 1 (11%), 0, and 0 patients from the 60-s ischemia group and 5 (63%), 2 (25%), and 1 (11%) from the 90-s ischemia group, respectively, fulfilled criteria for a biochemical myocardial infarction. CONCLUSIONS: This study is the first to report the early-release kinetics of cTn concentrations after different durations of experimental coronary balloon occlusion in humans. All assays detected a cTn increase after only 30 s of ischemia. hs-cTnI (Siemens) rose faster and reached a higher peak. Copeptin levels did not change significantly. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03203057.

Prediction of coronary heart disease or heart failure using high-sensitivity cardiac troponin T: A pilot study.

BACKGROUND: High-sensitivity cardiac troponin T (hs-cTnT) is a good prognostic marker for mortality. However, it is uncertain if hs-cTnT can be used to detect sub-clinical cardiac disease. METHOD: Pilot study in patients without known heart disease and elevated hs-cTnT measured at presentation to the emergency department. Hs-cTnT was measure with Roche Diagnostics. Echocardiography was used to assess structural heart disease and the participants underwent computed tomography angiography for assessment of coronary artery disease and agatston score. RESULTS: Ten patients were included in the final cohort. Median age was 68 years IQR (57-78) and 80% were female (n = 8). Six patients had a history of chronic obstructive lung disease and five patients had history of hypertension. The median level of hs-cTnT was 26 ng/L and values ranged from 19 ng/L to 495 ng/L. The median calcium score was 12. Three patients had signs of coronary artery disease. All patients had normal left ventricular ejection fraction with a median LVEF at 54.5%. Two patients were noted to have increased left ventricular mass index (LVMI). CONCLUSION: The majority of patients with hs-cTnT above the 99th percentile did not have structural heart disease or ischaemic coronary disease. However, 30% of the patient did have signs of coronary disease and might benefit from preventive medical treatment. Measuring hs-cTnT in the absence of acute illness might be a better approach for evaluation for sub-clinical cardiac disease.

Can copeptin and troponin T ratio predict final infarct size and myocardial salvage index in patients with ST-elevation myocardial infarction: A sub-study of the DANAMI-3 trial.

BACKGROUND: Primary percutaneous coronary intervention (pPCI) is recommended in patients presenting with ST-elevation myocardial infarction (STEMI) within <12 h of symptom onset. However, patients-reported symptom duration is not always reliable. Cardiac specific troponin T (cTnT) and the endogenous stress marker copeptin have different temporal release patterns for myocardial infarction MI. We hypothesized that copeptin/troponin-ratio is associated to the duration of coronary occlusion and therefore inversely proportional to myocardial salvage. METHOD: Patients older than 18 years with first time STEMI referred to pPCI were eligible. cTnT and copeptin values were measured at admission. A cardiac magnetic resonance scanning (CMR) was done during the index admission for assessment of area at risk (AAR), and later 3 months to assess final infarct size (FIS). Myocardial salvage index (MSI) was calculated based on these measurements. RESULTS: A total of 468 patients were included. The median time from patient-reported onset of symptoms to pPCI was 192 min (IQR 150 min - 290 min). At presentation 416 (89%) patients had hs-cTnT values above the 99th percentile, median hs-cTnT was 53 ng/l (IQR 24 ng/l-146 ng/l) and 318 (68%) patients had copeptin values above the 99th percentile (18.9 pmol/l), median copeptin was 50 pmol/l (IQR 14 pmol/l-131 pmol/l). Symptom duration showed a weak but significant association with AAR (R2 = 0.02, p = .04), FIS (R2 = 0.03, p < .01) and MSI (R2 = 0.04, p < .01). Copeptin/troponin-ratio was significantly associated with symptom duration (R2 = 0.19, p < .01), but not AAR (R2 = 0.02, p = .19), FIS (R2 = 0.02, p = .12), or MSI (R2 = 0.01, p = .25). CONCLUSION: Copeptin/troponin-ratio is associated with patient-reported symptom duration, but there was no association with area at risk, final infarct size or myocardial salvage index.

High-sensitivity cardiac troponin T is superior to troponin I in the prediction of mortality in patients without acute coronary syndrome.

BACKGROUND: Differences in prevalence and prognostic information of cardiac troponin T (cTnT) and I (cTnI) concentrations in patients without acute coronary syndrome (ACS) are insufficiently investigated. High-sensitivity assays (hs-cTn) have led to an increased interest in hs-cTn for risk stratification. Here, we compare hs-cTnT and hs-cTnI in prediction of mortality patients without ACS. METHOD AND RESULTS: Patients aged >18 years, consecutively admitted to an emergency department (ED) were included. Blood was collected at admission and later analyzed with high-sensitivity assays for cTnT (Roche) and cTnI (Siemens). Troponin concentrations were reported as normal or increased according to the clinical cut-off value of 99th percentile as defined by the manufacturer. The primary outcome was all-cause mortality. Of the 822 participants (median, 65 years [48-77]; 428 female [52%]), 239 patients died. Median follow-up time was 3.0 years [2.1-3.0]. Elevation of hs-cTn was observed in 40% (n = 345) for hs-cTnT and 8% (n = 64) for hs-cTnI, p < 0.001. The relationship between elevated hs-cTn and mortality was strong for both hs-cTnT and hs-cTnI [HR 6.0 (95%CI: 2.9-12.6) vs. 5.1 (95%CI: 1.9-13.6)].There was no difference in prognostic accuracy for short-term mortality (30 days) between hs-cTnT and hs-cTnI. However, the prognostic accuracy for long-term mortality (1080 days) was superior for hs-cTnT than for hs-cTnI [area under the receivers operating curve (AUC) 0.81 vs 0.74, p < 0.001]. CONCLUSION: Both hs-cTnI and hs-cTnT were predictive for all-cause mortality. Notably, hs-cTnT measurement showed superior prognostic performance in predicting long-term all-cause mortality compared with hs-cTnI.

Head-to-head comparison of cardiac troponin T and troponin I in patients without acute coronary syndrome: a systematic review.

BACKGROUND: Cardiac-specific troponin T (cTnT) and troponin I (cTnI) are considered diagnostically equal in patients with acute coronary syndrome (ACS). The aim of this systematic review was to compare the prevalence and prognostic strength of elevations of cTnT and cTnI in patients with other conditions than ACS. METHODS: A systemic review was conducted in concordance with the PRISMA guidelines. The studies were identified by searching PubMed, EMBASE and Cochrane Central Register, from May to August 2016. Studies measuring both cTnT and cTnI in populations without ACS were eligible. RESULTS: Twenty-nine studies were included (n = 25,859). Seventeen studies reported on prognostic information with follow-up time ranging for 30 d-5 years. Elevation above the 99th percentile (reference value for a healthy population) in non-ACS population was reported to be 0-39% for cTnI and 40-100% for cTnT. Elevation of cTnT tends to be a superior predictor for all-cause mortality and elevation of cTnI tends to be a superior predictor for cardiovascular related mortality. DISCUSSION: In the absence of ACS, elevation of cTnT is more frequent than elevation of cTnI. CONCLUSION: Both cTnT and cTnI elevations have important prognostic information regarding morbidity, cardiac mortality and all-cause mortality.

[Acute dyspnoea triggered by spontaneous pneumothorax in a pregnant woman with pulmonary agenesis].

A 29-year-old pregnant woman was admitted to hospital with chest pain and dyspnoea. A thoracal computed tomography (CT) was performed to rule out pulmonary embolism, and it revealed a left-sided pneumothorax, which was treated with tube thoracostomy. Three days after discharge she was readmitted with spontaneous pressure pneumothorax. Her clinical condition did not improve, and a pulmonary scintigraphy and a new thoracal CT showed unilateral right pulmonary agenesis. Pulmonary agenesis is very rare in adulthood, and in this case it was complicated with spontaneous pneumothorax.

Prevalence and significance of troponin elevations in patients without acute coronary disease.

BACKGROUND: Cardiac troponin T and I are important diagnostic and prognostic markers in patients with acute coronary syndrome (ACS). Troponin elevations in various non-ACS scenarios have been documented, but few studies have been conducted on the general hospitalized population, none compared the diagnostic performance of troponin I and T. METHODS AND RESULTS: Patients aged >18years (n=1097), consecutively admitted to a district hospital, were included in the study. Blood samples were collected at admission and analysed with three different troponin assays. Serum was available in 92.2%, giving a study population of 1012 patients (mean age 61.6years, 510 (50.4%) female). ACS was diagnosed among 125 (12.4%) of the patients. Remaining patients were admitted with a broad spectrum of medical and surgical conditions. Of the total population, sc-cTnI was above the 99th percentile in 93 (9.2%), hs-cTnI was above the 99th percentile in 80 (7.9%) and hs-cTnT was above the 99th percentile in 400 (39.5%) of the patients (p<0.001 for all differences). Hs-cTnT was stronger correlated with estimated glomerular filtration rate (r [2]=0.13 vs r [2]=0.06) and haemoglobin (r [2]=0.1 vs r2=0.02) than with hs-cTnI, none were correlated with C-reactive protein (r [2]=0.04 vs r [2]=0.02). The correlation between ln(hs-cTnT) and ln(hs-cTnI) was better in ACS patients than in non-ACS patients (r [2]=0.79 vs r [2]=0.47, p<0.001). CONCLUSION: Hs-cTnT was elevated above the 99th percentile in more than one third of the non-ACS patients, while hs-cTnI and sc-cTnI were elevated in approximately one tenth. The correlation between hs-cTnT and hs-cTnI concentrations was significantly stronger in ACS patients than in non-ACS patients.