Background Weaning-induced cardiac pulmonary edema (WiPO) is one of the main mechanisms of weaning failure during mechanical ventilation. We hypothesized that weaning-induced cardiac ischemia (WiCI) may contribute to weaning failure from cardiac origin. Methods A prospective cohort study of patients mechanically ventilated for at least 24 h who failed a first spontaneous breathing trial (SBT) was conducted in four intensive care units. Patients were explored during a second SBT using multiple tools (echocardiography, continuous 12-lead ST monitoring, biomarkers) to scrutinize the mechanisms of weaning failure. WiPO definition was based on three criteria (echocardiographic signs of increased left atrial pressure, increase in B-type natriuretic peptides, or increase in protein concentration during SBT) according to a conservative definition (at least two criteria) and a liberal definition (at least one criterion). WiCI was diagnosed according to the third universal definition of myocardial infarction proposed by the European Society of Cardiology (ESC) and the American Heart Association (AHA) statement for exercise testing. Results Among patients who failed a first SBT, WiPO occurred in 124/208 (59.6%) and 44/208 (21.2%) patients, according to the liberal and conservative definition, respectively. Among patients with ST monitoring, WiCI was diagnosed in 36/177 (20.3%) and 12/177 (6.8%) of them, according to the ESC and AHA definitions, respectively. WiCI was not associated with WiPO and was not associated with weaning outcomes. Only two patients of the cohort were treated for an acute coronary syndrome after the second SBT, and seven other patients required coronary angiography during the weaning period. Conclusions This observational study showed the common occurrence of pulmonary edema in mechanically ventilated patients who failed a first SBT, but the association with cardiac ischemia and weaning outcomes was weak.

BackgroundNecrotizing skin and soft tissue infections (NSTIs) require both prompt medical and surgical treatment. The coordination of multiple urgent interventions by care bundles has improved outcome in other settings. This study aimed to assess the impact of a multidisciplinary care bundle on management and outcome of patients with NSTIs.MethodsPatients with NSTIs admitted between 2006 and 2017 were compared according to admission before or after bundle implementation (2012–2013). This bundle consisted mainly in (1) the creation of a multidisciplinary task force; (2) management guidelines on empirical antibiotics, intensive care unit admission criteria, a triage algorithm to accelerate operating room access; and (3) an active communication policy. Patient recruitment and management were compared between pre- and post-implementation periods. Main outcome was day 60-censored hospital survival.ResultsOverall, 224 patients were admitted: 60 before, 35 during, and 129 after bundle implementation. Admission after implementation was associated with increased yearly admissions (10 [8–13] vs 30 [24–43] patients/year, p = 0.014) and decreased mortality (30 vs 15%, HR = 0.49 [0.26–0.92]; p = 0.026) but was no longer a protective factor for mortality after adjustment on confounding factors (adjusted HR = 0.90 [0.43–1.88], p = 0.780). There was no significant difference regarding time to surgery (0 [0–1] vs 0 [0–1] days, p = 0.192) or rate of antibiotic treatment within 24 h (98% vs 99%, p > 0.99).ConclusionsImplementation of a multidisciplinary care bundle for NSTIs was feasible, but in a retrospective study from an already experienced center was not associated with significantly increased survival after adjustment.

Background Current understanding of the lifetime mortality of patients with hypertrophic cardiomyopathy (HCM) has been extrapolated from cohorts with 8–10 years follow-up. Real survival rates and long-term burden of HCM are largely unresolved. Objective To describe HCM lifetime mortality over 28-years of observation. Methods We analyzed clinical/instrumental data of the historic cohort of 202 patients diagnosed from 1970s. ECG, echocardiographic, clinical records until last follow-up were recorded. Reasons for death were classified as HCM related (Sudden Death (SD), Heart Failure related (HF)) and non-HCM related deaths. Results Patients were followed-up for 28±6 years (41±17 to 69±14 years), 63% were males. Patients progressively dilated the Left Atrium (40±6 to 50±9mm, p<0.01), depressed ejection fraction (65±9 to 54±12, p<0.01), developed diastolic restrictive pattern and decreased LV wall thickness (23±5 to 19±4mm, p<0.01). One-hundred-eighteen deaths occurred at 66±12 years. HCM accounted for 69 deaths, 53 due to HF-related complications and 16 for SD. Annual HCM mortality rate increased from 0.6% at 10 years following diagnosis to 1.4% during 11–28 years of follow-up (p<0.01): HF yearly burden increased from 0.6% to 1.3%, p<0.01, SD remained similar in the two periods (0.1%, 0.4% respectively). Conclusions HCM-related mortality at 10 years significantly underestimated the lifetime rates of HF death, which doubled in the second/third decade of observation. Conversely, SD rates remained constantly low. Real burden of HCM is time dependent and can be appreciated only after prolonged exposure to the disease. Funding Acknowledgement Type of funding source: None