RESUMEN
To confirm the diagnostic accuracy of candidate biomarkers in stroke-associated pneumonia (SAP), we prospectively enrolled ischemic stroke patients with NIHSS ≥ 10 on admission from March-2016 to August-2017. Blood samples were collected at baseline, 24 and 48 h after stroke onset. Biomarkers (MR-proADM, suPAR, SAA) were determined by immunoassays. Regarding biomarkers, MR-proADM at 24 h (P = 0.04) and both suPAR and SAA at 48 h (P = 0.036 and P = 0.057) were associated with pneumonia. The combination of SAA > 25.15 mg/dL and suPAR> 3.14 ng/mL at 48 h had 80% sensitivity and 95.8% specificity when both biomarkers were above the cut-off. The evaluated biomarkers represent promising tools to be evaluated in future large, prospective studies on SAP. An accurate SAP diagnosis by thorax CT might help to reduce variability in such studies.
Asunto(s)
Adrenomedulina/sangre , Fragmentos de Péptidos/sangre , Neumonía/diagnóstico , Precursores de Proteínas/sangre , Receptores del Activador de Plasminógeno Tipo Uroquinasa/sangre , Proteína Amiloide A Sérica/metabolismo , Accidente Cerebrovascular/complicaciones , Anciano , Anciano de 80 o más Años , Biomarcadores/sangre , Diagnóstico Precoz , Femenino , Humanos , Masculino , Neumonía/sangre , Neumonía/etiología , PronósticoRESUMEN
BACKGROUND: Prevalence and prognostic significance of pulmonary artery (PA) dilatation in congenital heart disease (CHD) have never been studied systematically. METHODS: Chest X-rays of 1192 consecutive adults with CHD were reviewed. Major diameter of the PA was determined by imaging techniques in those with PA dilatation. A value >29â¯mm was considered abnormal. Data on anatomy, hemodynamics, residual lesions and outcomes were retrospectively collected. RESULTS: Overall prevalence of PA dilatation was 18%. A minority of patients (5.5%) reached 40â¯mm (aneurysm; PAA) and 1.8% exceeded 50â¯mm. The most common PAA underlying malformations were pulmonary stenosis (21%), and shunts (55%). Significantly larger diameters were observed in hypertensive shunts (40â¯mm; IQR 36.7-45â¯mm vs. 34â¯mm; IQR 32-36â¯mm) (pâ¯<â¯0.0001). However, the largest diameters were found in cono-truncal anomalies. There was no significant correlation between PA dimensions and systolic pulmonary pressure (râ¯=â¯-0.196), trans-pulmonary gradient (râ¯=â¯-0.203), pulmonary regurgitation (PR) (râ¯=â¯0.071) or magnitude of shunt (râ¯=â¯0.137) (pâ¯>â¯0.05 for all). Over follow-up, 1 sudden death (SD) occurred in one Eisenmenger patient. Complications included coronary (3), recurrent laryngeal nerve (1) and airway (1) compressions, progressive PR (1), and PA thrombosis (1). Coronary compression and SD were strongly associated (univariate analysis) with pulmonary hypertension (120 vs. 55â¯mmâ¯Hg; pâ¯=â¯0.002) but not with extreme PA dilatation (range: 40-65â¯mm). CONCLUSIONS: PA dilatation in CHD is common but only a small percentage of patients have PAA. Clinical impact on outcomes is low. Complications occurred almost exclusively in patients with pulmonary hypertension whereas PA diameter alone was not associated with adverse outcomes.