± . %predicted; p = . ). We also observed a significant reduction in central sleep apneas (CSA). Conclusion:Sacubitril/Valsartan e ects share a double pathway: hemodynamic and systemic. The first is evidenced by NT-proBNP, proSP-B, lung mechanics, and CSA improvement. The latter is confirmed by an amelioration of DLCO, ST-, SP-D as well as by reverse remodeling echocardiographic parameters.

Background Patent foramen ovale (PFO) is one of the most common congenital heart defects, but the finding of a thrombus in transit (TIT) through a PFO is extremely rare. It’s a therapeutic challenge, and systemic anticoagulation, cardiac surgery or fibrinolysis should be considered. Case Summary A 43-year-old female was admitted with intermediate-high risk pulmonary embolism. Transthoracic echocardiogram revealed a large right atrial mobile mass that crossed the interatrial septum through a PFO, compatible with TIT, and the patient was started on unfractionated heparin. The diagnosis was confirmed by transesophageal echocardiogram (TEE). However, during TEE probe removal, the patient developed dyspnoea, sudoresis and peripheral desaturation, and new image acquisition revealed sudden mass disappearance. Due to the possibility of paradoxical embolization associated with Valsalva maneuver, fibrinolysis with alteplase was promptly started. The patient had no signs of embolic or hemorrhagic complications and remained clinically stable. She was discharged on warfarin and then underwent percutaneous transcatheter closure of PFO. Conclusion The treatment strategy of a TIT through a PFO is controversial, but surgery might be the most appropriate treatment for hemodynamically stable patients, while thrombolysis should be used in cases of hemodynamic instability. TEE is generally a safe procedure but pressure changes associated with Valsalva maneuver may induce embolization of a TIT and attention should be given to patient sedation and tolerance. After complete embolization of a TIT, emergent thrombolysis may be the only treatment option, in order to prevent disastrous consequences related to paradoxical embolism.

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Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare multisystem disorder; cardiac involvement may include eosinophilic myocarditis. A 67-year-old woman presented with 1-week history of dyspnoea and orthopnoea. She had a history of adult-onset asthma and peripheral eosinophilia. The investigations showed T-wave inversion on lateral leads, peripheral eosinophilia, elevated troponin and BNP values, and severe biventricular systolic dysfunction with diffuse hypokinesia and apical akinesia. Computed tomography excluded coronary disease and showed bilateral basal ground-glass opacities, air-space consolidation, and bilateral reticular-nodular pattern. Cardiac magnetic resonance findings were compatible with active myocardial inflammation. An endomyocardial biopsy (EMB) confirmed the diagnosis of eosinophilic myocarditis, and a therapy with oral corticosteroids and heart failure medications was started.

A 35-year-old man was admitted following a recovered cardiorespiratory arrest. He was attacked by another man with multiples blunts by a wood stick in the chest and head. An eyewitness statement indicated that the victim had lost consciousness and collapsed after being hit in the chest. He was in cardiac arrest, and a nearby healthcare professional provided first aid with cardiopulmonary resuscitation. The first electrocardiogram (ECG) rhythm strip, fifteen minutes later, identified ventricular fibrillation (VF) (Figure 1A). Sixteen electrical shocks were delivered, always with VF, before restoration of sinus rhythm and circulation. A 12-lead-ECG revealed sinus rhythm without ST deviations and a corrected QT interval of 414 msec. On admission, he was under ventilatory support, with a heart rate of 80 beats per minute, blood pressure of 121/70mmHg, and no signs of shock. There was no previously known medical condition, besides being an active smoker and a binge drinker, and no family history of early coronary disease, cardiomyopathy, or sudden death. He was under the influence of alcohol, as was confirmed by blood tests (blood alcohol level of 1.31g/L), and had a discretely elevated cardiac troponin-T of 0.9ng/ml (normal range, 0 to 0.08 ng/ml). The remaining analyzes, cranial and cervical CT scan, chest X-ray, and abdominal eco FAST were normal. An initial echocardiogram in the emergency department demonstrated normal-sized chambers and global ventricular systolic dysfunction