rmance and a reduction in mortality in STEMI management.
Our results indicate that systematic data assessment and regular feedback is a feasible long-term strategy and may be linked to improved performance and a reduction in mortality in STEMI management.
Mucinous adenocarcinoma arising in unresected congenital pulmonary airway malformation (CPAM) is rare. Underlying driver mutations in addition to KRAS gain-of-function mutations in this setting and the long-term outcomes of these patients are unknown.
We report a case of metastatic mucinous adenocarcinoma harboring both KRAS and GNAS mutations arising in a type 1 CPAM of a 14-year-old male. A literature review was performed.
Next-generation sequencing revealed identical KRAS (G12V) mutations in both the CPAM and metastatic adenocarcinoma and a missense mutation in the GNAS (R201C) gene in the metastatic adenocarcinoma only. Median survival was 23 and 4 years for patients with localized (no or limited spread within the same lobe of CPAM) and distant involvement (spread to any different lobe of CPAM) of mucinous cells, respectively (95% confidence interval, 23-23 and 1.5-22 years, respectively; P = .017).
Mucinous cell proliferation associated with type 1 CPAM has exceptionally good long-term outcomes if confined within the same lobe of CPAM. A second oncogenic mutation in the GNAS gene may be necessary for progression to malignancy and distant spread.
Mucinous cell proliferation associated with type 1 CPAM has exceptionally good long-term outcomes if confined within the same lobe of CPAM. A second oncogenic mutation in the GNAS gene may be necessary for progression to malignancy and distant spread.
Infective endocarditis is a severe infection which can occur in adult patients with congenital heart disease. We aimed to determine outcomes and risk factors of death in adult congenital heart disease and to investigate differences with infective endocarditis in non-congenital heart disease.
Between March 2000 and June 2018, 671 consecutive episodes of infective endocarditis in adult patients were retrospectively recorded. Cases were classified according to the modified Duke classification. All adult congenital heart disease cases were managed by infectious disease specialists and adult congenital heart disease cardiologists. During this period, 142 infective endocarditis episodes (21%) occurred in adult congenital heart disease patients with simple (46.5%), moderate (21.1%), or complex (32.4%) congenital heart disease. In-hospital mortality was 12.7%. The strongest predictive factors of in-hospital death in multivariate analysis were complexity of congenital heart disease (odds ratio (OR) 8.02, 95% confi this group.
Although mortality associated with infective endocarditis is lower in adult patients with congenital heart disease than patients without congenital heart disease, infective endocarditis mortality is particularly high in patients with complex congenital heart disease. Education and prevention about the risk of infective endocarditis is essential, especially in this group.
Coronary microvascular dysfunction and obstruction (CMVO) is a strong predictor of a poor prognosis in patients with ST-segment elevation myocardial infarction (STEMI). Although research has suggested that obstructive sleep apnea (OSA) exacerbates CMVO after primary percutaneous coronary intervention, data supporting a correlation between OSA and CMVO are limited. This study was performed to investigate whether OSA is associated with CMVO, detected as microvascular obstruction on cardiovascular magnetic resonance images, in patients with STEMI.
Patients (N = 249) with a first STEMI underwent primary percutaneous coronary intervention. CMVO was evaluated on cardiovascular magnetic resonance images based on the presence of microvascular obstruction. OSA was classified into four levels of severity based on the respiratory event index (REI) absent (REI of <5), mild (REI of ≥5 to <15), moderate (REI of ≥15 to <30) and severe (REI of ≥30).
The REI was significantly higher in the presence of microvascular obstruction (n = 139) than in its absence (n = 110) (REI of 12.8 vs. 10.7, respectively; p = 0.023). Microvascular obstruction was observed in 42%, 58%, 57% and 70% of patients in the absent, mild, moderate and severe OSA groups, respectively. Multiple logistic regression analysis showed that severe OSA was associated with increased odds of microvascular obstruction (odds ratio (OR), 5.10; 95% confidence interval (CI),1.61-16.2; p = 0.006). Mild and moderate OSA were also associated with increased odds of microvascular obstruction (mild OSA OR, 2.88; 95% CI, 1.19-7.00; p = 0.019 and moderate OSA OR, 3.79; 95% CI, 1.43-10.1; p = 0.008).
Severe OSA was associated with CMVO after primary percutaneous coronary intervention in patients with STEMI.
Severe OSA was associated with CMVO after primary percutaneous coronary intervention in patients with STEMI.
Up to 40% of patients with ST-segment elevation myocardial infarction (STEMI) present later than 12 hours after symptom onset. However, data on clinical outcomes in STEMI patients treated with primary percutaneous coronary intervention 12 or more hours after symptom onset are non-existent. We evaluated the association between primary percutaneous coronary intervention performed later than 12 hours after symptom onset and clinical outcomes in a large all-comer contemporary STEMI cohort.
All STEMI patients treated with primary percutaneous coronary intervention in eastern Denmark from November 2009 to November 2016 were included and stratified by timing of the percutaneous coronary intervention. https://www.selleckchem.com/products/CGS-21680-hydrochloride.html The combined clinical endpoint of all-cause mortality and hospitalisation for heart failure was identified from nationwide Danish registries.
We included 6674 patients 6108 (92%) were treated less than 12 hours and 566 (8%) were treated 12 or more hours after symptom onset. During a median follow-up period of 3.8 (interquartile range 2.3-5.6) years, 30-day, one-year and long-term cumulative rates of the combined endpoint were 11%, 17% and 25% in patients treated 12 or fewer hours and 21%, 29% and 37% in patients treated more than 12 hours (P<0.001 for all) after symptom onset. Late presentation was independently associated with an increased risk of an adverse clinical outcome (hazard ratio 1.42, 95% confidence interval 1.22-1.66; P<0.001).
Increasing duration from symptom onset to primary percutaneous coronary intervention was associated with an increased risk of an adverse clinical outcome in patients with STEMI, especially when the delay exceeded 12 hours.
Increasing duration from symptom onset to primary percutaneous coronary intervention was associated with an increased risk of an adverse clinical outcome in patients with STEMI, especially when the delay exceeded 12 hours.