Patients who temporarily or permanently rely on left ventricular assist devices (LVADs) for end-stage heart failure face complex psychological, emotional, and relational problems. We conducted a mixed-method study to investigate quality of life, psychological symptoms, and emotional and cognitive reactions after LVAD implant. Twenty-six patients admitted to cardiac rehabilitation were administered quality of life questionnaires (Short Form 36 of the Medical Outcomes Study and Minnesota Living with Heart Failure Questionnaire), the Hospital Anxiety and Depression Scale, and the Coping Orientation for Problem Experiences inventory, and underwent three in-depth unstructured interviews within 2 months after LVAD implant. Quality of life assessment (Short Form 36) documented persistently low physical scores whereas mental component scores almost achieved normative values. Clinically relevant depression and anxiety were observed in 18 and 18% of patients, respectively; avoidant coping scores correlated significantly with both depression and anxiety (Pearson correlation coefficients 0.732, P < 0.001 and 0.764, P < 0.001, respectively). From qualitative interviews, factors that impacted on LVAD acceptance included: device type, disease experience during transplant waiting, nature of the assisted organ, quality of patient-doctor communication, the opportunity of sharing the experience, and recipient's psychological characteristics. Quality of life improves early after LVAD implant, but emotional distress may remain high. A multidimensional approach that takes into account patients' psychological characteristics should be pursued to enhance LVAD acceptance.

High arterial CO(2) pressure (P(a)CO(2)) measured in athletes during exercise suggests inadequate hyperventilation. End-tidal CO(2) pressure (P (ET)CO(2)) is used to estimate P(a)CO(2.) However, P(ET)CO(2) also depends on exercise intensity (CO(2) production, .VCO2) and ventilation efficiency (being P(ET)CO(2) function of respiratory rate). We evaluated P(ET)CO(2) as a marker, which combines efficiency of ventilation and performance. A total of 45 well-trained volunteers underwent cardiopulmonary tests and were grouped according to P(ET)CO(2) at respiratory compensation (RC): Group 1 (P(ET)CO(2) 35.1-41.5 mmHg), Group 2 (41.6-45.7) and Group 3 (45.8-62.6). At anaerobic threshold, RC and peak exercise, ventilation (.VE) was similar, but in Group 3, a greater tidal volume (Vt) and lower respiratory rate (RR) were observed. Peak exercise workload and .VO2 were lowest in Group 1 and similar between Group 2 and 3. Group 3 subjects also showed high peak .VCO2 suggesting a greater glycolytic metabolism. In conclusion, a high P(ET)CO(2) during exercise is useful in identifying a specific respiratory pattern characterized by high tidal volume and low respiratory rate. This respiratory pattern may belong to subjects with potential high performance.

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Inflammation is associated with atrial fibrillation (AF), but little is known about the association of AF with the inflammatory serum cytokines after the acute postoperative phase. Thus, we aimed to explore how plasma cytokines concentrations modify during a 3-week cardiac rehabilitation after heart surgery, comparing patients who developed postoperative AF (POAF) and those with permanent AF with patients free from AF (NoAF group). We enrolled 100 consecutive patients and 40 healthy volunteers as a control group. At the beginning of cardiac rehabilitation, 11 days after surgery, serum levels of MPO, PTX3, ADAM17, sST2, IL-25, and IL-33 were dramatically higher, whereas TNFα and IL-37 levels were much lower in NoAF, POAF, and permanent AF patients than in the healthy volunteers. After rehabilitation, most of the cytokines changed tending towards normalization. POAF patients (35% of the total) had higher body mass index and abdominal adiposity than NoAF patients, but similar general characteristics and risk factors for POAF. However, ADAM-17 and IL-25 were always lower in POAF than in NoAF patients, suggesting a protective role of IL-25 and ADAM 17 against POAF occurrence. This finding could impact on therapeutic strategies focusing on the postoperative prophylactic antiarrhythmic interventions. Cardiac surgery is frequently complicated by postoperative atrial fibrillation (POAF), which is associated with increased morbidity and costs 1,2. POAF occurs in a third of patients undergoing cardiac bypass surgery 3 and up to 40% of patients undergoing valvular surgery 4 , usually within the first three days after the intervention. Post-operative atrial arrhythmias can also occur after non-cardiac surgery, especially after thoracic and large abdominal surgery, but with lower incidence 5. Previous studies have demonstrated that inflammation is closely related to the pathogenesis of atrial fibrillation (AF) 6 and there is strong evidence supporting an association between inflammation and AF. The inflammatory cardiac diseases, such as myocarditis, are known to be associated with an increased incidence of arrhythmia, including AF 7. Cardiac surgery is an acute stressful event generating a chain of inflammatory reactions, as a consequence of the aortic clamp, the organ reperfusion injury during cardiopulmonary bypass for extracorporeal circulation and the surgical injury itself. The underlying inflammatory pathway involves leukocyte activation 8. The inflammatory cascade after the surgery, represented by many circulating cytokines, may play a prominent role in initiating POAF. In fact, the cytokines, a network of intracellular proteins produced by lymphocytes, monocytes, and macrophages in response to inflammatory stimuli, have been assessed as potential mediators in the occurrence of AF 9. While a few studies evaluated the concentrations of biohumoral markers of inflammation perioperatively, very little is known about the serum levels of cytokines after the acute post-operative phase, i.e. some days after surgery when the pat...

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