Changes in sleep-disordered breathing from the acute to the stable phase of pulmonary embolism: The ESAET study.

BACKGROUND: /Objective: Sleep-disordered breathing (SDB) may change from the acute to stable phase of some cardiovascular disorders, but little is known whether these dynamic changes also exist in pulmonary embolism (PE). This study aimed to analyze the changes in the apnea-hypopnea index (AHI) from the acute to stable phase of PE as well as the factors associated. PATIENTS/METHODS: We conducted a prospective, longitudinal and multicenter study of consecutive adults requiring hospitalization for non-hypotensive acute PE, with a protocol including clinical, imaging (transthoracic echocardiography [TTE] and computed tomography), blood tests and a sleep study within 48 h of diagnosis of PE. After 3 months of follow-up, the sleep study was repeated. Right ventricular (RV) dysfunction was defined according to TTE criteria. RESULTS: One hundred and eleven patients (mean age [SD]: 63 [15] years; body mass index: 28.4 [4.7] kg/m2) were included. The initial AHI was 24.4 (21.8) events/h (AHI≥5: 82.8 %; AHI≥30: 33.3 %). Seventy-seven patients (69.4 %) had RV dysfunction. In the overall cohort, the AHI decreased by 8.7 events/h from the acute to stable phase (24.4/h vs. 15.7/h; p=0.013). Patients with RV dysfunction showed a greater decrease in AHI (mean decrease 12.3/h vs. 0.43/h). In the multivariable analysis a drop of an AHI≥5 events/hour was independently associated with the presence of initial RV dysfunction (hazard ratio 3.9; 95%CI 1.3 to 12.1). CONCLUSIONS: In hemodynamically stable patients with acute PE, there is a transient but clinically significant decrease in the AHI from the acute to stable phase, particularly when initially presenting with RV dysfunction.

SMAD4 Expression in Monocytes as a Potential Biomarker for Atherosclerosis Risk in Patients with Obstructive Sleep Apnea.

Obstructive sleep apnea (OSA) patients are at special risk of suffering atherosclerosis, leading to major cardiovascular diseases. Notably, the transforming growth factor (TGF-ß) plays a crucial role in the development and progression of atherosclerosis. In this context, the central regulator of TGF-ß pathway, SMAD4 (small mother against decapentaplegic homolog 4), has been previously reported to be augmented in OSA patients, which levels were even higher in patients with concomitant cardiometabolic diseases. Here, we analyzed soluble and intracellular SMAD4 levels in plasma and monocytes from OSA patients and non-apneic subjects, with or without early subclinical atherosclerosis (eSA). In addition, we used in vitro and ex vivo models to explore the mechanisms underlying SMAD4 upregulation and release. Our study confirmed elevated sSMAD4 levels in OSA patients and identified that its levels were even higher in those OSA patients with eSA. Moreover, we demonstrated that SMAD4 is overexpressed in OSA monocytes and that intermittent hypoxia contributes to SMAD4 upregulation and release in a process mediated by NLRP3. In conclusion, this study highlights the potential role of sSMAD4 as a biomarker for atherosclerosis risk in OSA patients and provides new insights into the mechanisms underlying its upregulation and release to the extracellular space.

Idiopathic fibrosing mediastinitis: spectrum of imaging findings with emphasis on its association with IgG4-related disease.

PURPOSE: The purpose of this study was to review the clinicoradiological features of idiopathic fibrosing mediastinitis (FM). METHODS: The records of six patients with idiopathic FM were retrospectively reviewed. RESULTS: The most common presenting symptom was cough. There were three localized forms and three diffuse forms. Definitive histological diagnosis was most commonly made with mediastinoscopy. Interestingly, three of our patients had disease manifestations of IgG4-related disease (IgG4-RD) outside the mediastinum. CONCLUSION: The imaging findings of idiopathic FM vary depending on the involved mediastinal structures. Therapeutic options include medical treatment, stenting, or surgery. Radiologists should pay attention to the possible association of idiopathic FM with extrathoracic manifestations of the IgG4-RD spectrum.

Parada cardiorrespiratoria en un paciente con SAHS / No disponible

El Síndrome de apnea hipopnea del sueño (SAHS) se contempla como una enfermedad crónica. Sin embargo, algunos pacientes con SAHS pueden presentar episodios agudos, en relación con alteraciones en la repolarización ventricular, como arritmias potencialmente mortales, parada cardiorrespiratoria e incluso muerte súbita. La repolarización ventricular se ha evaluado mediante mediciones de la onda T y el intervalo QT. El incremento de mortalidad en pacientes con SAHS, especialmente durante la noche, obliga a identificar parámetros predictores de trastornos de la repolarización miocárdica, así como evaluar un tratamiento eficaz en este tipo de pacientes donde la parada cardiorrespiratoria, puede ser el primer síntoma de esta enfermedad (AU)

Obstructive sleep apnea syndrome (OSAS) is a common chronic respiratory sleep disorder; however, patients with OSAS may occasionally present with severe cardiac arrhythmias and sudden cardiac death caused by electrical disturbances during ventricular repolarization. The assessment of ventricular repolarization has been evaluated by using T wave and QT interval measurements. Increased mortality in patients with OSAS, particularly at night, emphasizes the importance of identifying possible parameters by which OSAS could affect myocardial electrical stability and requires the study of an effective treatment in this kind of patients where the cardiac arrest, could be the first symptom of this disease (AU)