ABSTRACT
Objective: To examine changes in concentration, time-to-peak and the ensuing half-life of cardiac biomarkers in patients with myocardial infarction. Methods: Blood sampling was performed every third hour within 24 h after percutaneous coronary intervention (PCI) on a cohort of patients with ST elevation myocardial infarction. Cardiac troponin (cTn) was measured by the Dimension Vista, Vitros, Atellica, and Alinity high-sensitivity (hs) cTnI assays, and the Elecsys hs-cTnT assay. Further, creatine kinase (CK), myoglobin, creatine kinase MB (CKMB) and other biomarkers were analyzed. Results: A total of 36 patients completed blood sampling (median age 60 years, IQR 56.4-66.5 years; seven women, 19.4%). Hs-cTnI measured by the Vitros assay was the first hs-cTn to peak at 9.1 h (95%-CI 6.2-10.1) after PCI and 11.7 h (95%-CI 10.4-14.8) after symptoms onset. There were no notable differences between hs-cTn assays in regard to time-to-peak. Also, Vitros hs-cTnI reached the highest median ratio of concentration to upper reference level of nearly 2,000. The median half-life from peak concentration ranged from 7.6 h for myoglobin (CI 6.8-8.6) to 17.8 h for CK (CI 6.8-8.6). For hs-cTn assays the median T½ ranged from 12.4 h for the Vista hs-cTnI assay (95%-CI 11.0-14.1 h) to 17.3 h for the Elecsys hs-cTnT (95%-CI 14.9-20.8 h). Conclusions: This study updates knowledge on the kinetics of cardiac biomarkers in current clinical use. There was no notable difference in trajectories, time-to-peak or half-life between hs-cTn assays.
ABSTRACT
Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is associated with persistent symptoms ("long COVID"). We assessed the burden of long COVID among nonhospitalized adults with polymerase chain reaction (PCR)-confirmed SARS-CoV-2 infection. Methods: In the fall of 2020, a cross-sectional survey was performed in the adult Danish general population. This included a self-administered point-of-care test for SARS-CoV-2 antibodies, the Short Form Health Survey (SF-12), and coronavirus disease 2019 (COVID-19)-associated symptom questions. Nonhospitalized respondents with a positive SARS-CoV-2 PCR test ≥12 weeks before the survey (cases) were matched (1:10) to seronegative controls on age, sex, and body mass index. Propensity score-weighted odds ratios (ORs) and ORs for risk factors were estimated for each health outcome. Results: In total, 742 cases and 7420 controls were included. The attributable risk of at least 1 long-COVID symptom was 25.0 per 100 cases (95% confidence interval [CI], 22.2-27.4). Compared to controls, cases reported worse general health (OR, 5.9 [95% CI, 5.0-7.0]) and had higher odds for a broad range of symptoms, particularly loss of taste (OR, 11.8 [95% CI, 9.5-14.6]) and smell (OR, 11.2 [95% CI, 9.1-13.9]). Physical and Mental Component Summary scores were also significantly reduced with differences of -2.5 (95% CI, -3.1 to -1.8) and -2.0 (95% CI, -2.7 to -1.2), respectively. Female sex and severity of initial infection were major risk factors for long COVID. Conclusions: Nonhospitalized SARS-CoV-2 PCR-positive individuals had significantly reduced physical and mental health, and 1 in 4 reported persistence of at least 1 long-COVID symptom.
ABSTRACT
BACKGROUND: Fibroblast growth factor 23 (FGF23) is known to cause left ventricular hypertrophy (LVH), but controversy exists concerning its effect in dialysis. This study evaluated associations between FGF23 levels, echocardiography and prognosis in patients on hemodialysis (HD). METHODS: Patients >18 years on chronic HD were included in this cross-sectional study. Plasma C-terminal FGF23 concentration was measured with ELISA and transthoracic echocardiography was performed, both before and after HD treatment. RESULTS: 239 haemodialysis (HD) patients were included in the study. The FGF23 was median 3560 RU/ml (IQR 1447-9952). The mean left ventricular mass index (LVMI) was 110.2 ± 26.7 g/m2 and the left ventricular ejection fraction (LVEF) was 52.7 ± 9.9%. Defined by LVMI, LVH was found in 110 patients (46%), of which 92 (84%) had hypertension (p < 0.01). Patients with LVH had FGF23 levels of 5319 RU/ml (IQR 1858-12,859) and those without 2496 RU/ml (IQR 1141-7028) (p < 0.01). FGF23 was significant positive correlated with LVMI (p < 0.01), and negatively to LVEF (p < 0.01). In a multivariate analysis, FGF23 was correlated with LVEF (p < 0.01), but only marginally to LVMI (p < 0.01). Cardiovascular events in the follow up period was not correlated with FGF23. Furthermore, FGF23 was independently correlated with overall mortality (p< 0.001). CONCLUSION: FGF23 was positively correlated with LVH and negatively to LVEF. FGF23 was an independent predictor for overall mortality
ANTECEDENTES: Se sabe que el factor de crecimiento fibroblástico 23 (FGF23) provoca hipertrofia ventricular izquierda (HVI), pero existe controversia sobre su efecto en la diálisis. Este estudio evaluó las asociaciones entre los niveles del FGF23, la ecocardiografía y el pronóstico en pacientes en hemodiálisis (HD). MÉTODOS: Se incluyeron pacientes >18 años con HD crónica en este estudio transversal. La concentración del FGF23 en el extremo C del plasma se midió con ELISA y se realizó una ecocardiografía transtorácica, antes y después del tratamiento de HD. RESULTADOS: Se incluyeron 239 pacientes en HD en el estudio. El FGF23 tenía una mediana de 3.560 RU/ml (amplitud intercuartílica: 1.447-9.952). El índice de masa ventricular izquierdo (IMVI) medio fue de 110,2 ± 26,7 g/m2 y la fracción de eyección del ventrículo izquierdo (FEVI) fue del 52,7 ± 9,9%. Definida por el IMVI, la HVI se localizó en 110 pacientes (46%), de los cuales 92 (84%) presentaban hipertensión (p < 0,01). Los pacientes con HVI presentaron niveles del FGF23 de 5.319 RU/ml (amplitud intercuartílica: 1.858-12.859) y aquellos sin 2.496RU/ml (amplitud intercuartílica: 1.141-7.028) (p < 0,01). El FGF23 fue considerablemente positivo correlacionado con el IMVI (p < 0,01) y negativo con la FEVI (p < 0,01). En un análisis multivariante, el FGF23 se correlacionó con la FEVI (p <0,01), pero solo marginalmente con el IMVI (p < 0,01). Los episodios cardiovasculares en el período de seguimiento no se correlacionaron con el FGF23. Además, el FGF23 se correlacionó independientemente con la mortalidad general (p < 0,001). CONCLUSIÓN: El FGF23 se correlacionó positivamente con la HVI y negativamente con la FEVI. El FGF23 fue un factor independiente para la mortalidad general
