We conducted a three-week randomized trial comparing the improvement of functional capacity by exercise training in chronic heart failure by the steady-state (EF 27.3%, n = 20) and the interval modus (EF 29.3%, n = 20) with a control group (EF = 26.6%, n = 10). Minimal EF was 10%, the lowest maximal oxygen consumption was 9.3 ml/kg/min and the lowest cardiac output was 1.9 l/min; 9 patients had been evaluated for HTX. VO2 at the anaerobic threshold and at maximal exercise increased in the continuous exercise group by 1.4 or 1.6 ml/kg/min, respectively, corresponding to an increase of 13.7% (p < 0.05) and 9.3% (p < 0.05). In the interval training group the increase was 1.3 and 1.5 ml/kg/min corresponding to 14% (p < 0.05) and 8.1% (p < 0.05). Continuous short-term exercise had no impact to central hemodynamics as pulmonary artery pressure (PA), capillary wedge pressure (pc), cardiac index (CI) or stroke volume index (SVI), whereas after interval training a significant increase at maximal exercise could be seen in CI (p < 0.05) and SVI (p < 0.01) with a concomitant drop in systemic peripheral resistance (p < 0.05) compared to the steady-state modus. Interval training was further characterized by a higher short-term but lower mean work load with a significantly smaller increase in lactate. Quality of life was improved according to the SF-36 questionnaire in both training groups but the psychologic sum factor was three times as high, increasing to 24.2% in the steady-state exercise group. It can be concluded that clinically stable patients with heart failure and even those already having been evaluated for cardiac transplantation profit from short-term physical training. Both training modalities seem equally suited to improve functional capacity. However interval training leads to more pronounced improvement in hemodynamics compared to the steady-state exercise, whereas the later had a greater impact on psychological well-being and quality of life. Patients with heart failure and severe peripheral deconditioning tolerate higher workloads with more peripheral stress by an interval training modus. Long-term training modalities need to be established to further improve and stabilize functional status.

BackgroundIdiopathic portal hypertension (IPH) is a disorder of unknown etiology and is characterized clinically by portal hypertension, splenomegaly, and hypersplenism accompanied by pancytopenia. This study evaluates the pathogenic concept of the disease by a systematic review of the literature and illustrates novel pathologic and laboratory findings.Case PresentationWe report the first case of uncontrolled splenic hyperperfusion and enlargement with subsequent hypersplenism leading to life-threatening complications of IPH in infancy and emergent splenectomy.ConclusionsOur results suggest that splenic NO and VCAM-1, rather than ET-1, have a significant impact on the development of IPH, even at a very early stage of disease. The success of surgical interventions targeting the splenic hyperperfusion suggests that the primary defect in the regulation of splenic blood flow seems to be crucial for the development of IPH. Thus, beside other treatment options splenectomy needs to be considered as a prime therapeutic option for IPH.

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