Cardiac function can be normalized in selected patients with end-stage IDC by MCSS. The degree of preoperative myocardial fibrosis may be an indicator for outcome; A-beta1-AABs can be used to monitor myocyte recovery. Weaning from MCSS offers an alternative to cardiac transplantation in certain patients.

Background —Idiopathic dilated cardiomyopathy (IDC) frequently is a progressive disease without causative therapy options. Following the hypothesis that in certain patients autoantibodies against cardiac structures may induce, maintain, or promote the progression of the disease, we investigated whether the elimination of these autoantibodies through immunoadsorption would improve cardiac function. Methods and Results —This prospective case-control study included 34 patients with IDC. Each patient presented with moderate to severe heart failure and evidence of autoantibodies directed against β 1 -adrenoceptors (β 1 -AABs). Seventeen patients received standard medical therapy (control group), whereas 17 were also treated with immunoadsorption (treatment group) to eliminate β 1 -AABs. A 1-year follow-up included echocardiographic assessment of left ventricular ejection fraction and internal diameters, β 1 -AAB levels, and clinical status every 3 months. Within 1 year, the mean±SD left ventricular ejection fraction rose from 22.3±3.3% to 37.9±7.9% ( P =0.0001) in the treatment group, with a relative increase of 69.9%. However, in the control group, no overall increase was seen (from 23.8±3.0% to 25.2±5.9%, P =0.3154). Left ventricular diameter in diastole decreased by 14.5% from 74.5±7.1 to 63.7±6.0 mm in the treatment group ( P =0.0001) and by 3.8% ( P =0.2342) in the control group. In the treatment group, the NYHA functional rating improved after immunoadsorption ( P =0.0001). β 1 -AABs did not increase anew. Conclusions —In IDC, the use of immunoadsorption is superior to the use of standard medical therapy. It significantly improves cardiac performance and clinical status.

Impairment of health after overcoming the acute phase of COVID-19 is being observed more and more frequently. Here different symptoms of neurological and/or cardiological origin have been reported. With symptoms, which are very similar to the ones reported but are not caused by SARS-CoV-2, the occurrence of functionally active autoantibodies ( f AABs) targeting G-protein coupled receptors (GPCR- f AABs) has been discussed to be involved. We, therefore investigated, whether GPCR- f AABs are detectable in 31 patients suffering from different Long-COVID-19 symptoms after recovery from the acute phase of the disease. The spectrum of symptoms was mostly of neurological origin (29/31 patients), including post-COVID-19 fatigue, alopecia, attention deficit, tremor and others. Combined neurological and cardiovascular disorders were reported in 17 of the 31 patients. Two recovered COVID-19 patients were free of follow-up symptoms. All 31 former COVID-19 patients had between 2 and 7 different GPCR- f AABs that acted as receptor agonists. Some of those GPCR- f AABs activate their target receptors which cause a positive chronotropic effect in neonatal rat cardiomyocytes, the read-out in the test system for their detection (bioassay for GPCR- f AAB detection). Other GPCR- f AABs, in opposite, cause a negative chronotropic effect on those cells. The positive chronotropic GPCR- f AABs identified in the blood of Long-COVID patients targeted the β 2 -adrenoceptor (β 2 - f AAB), the α 1 -adrenoceptor (α 1 - f AAB), the angiotensin II AT1-receptor (AT1- f AAB), and the nociceptin—like opioid receptor (NOC- f AAB). The negative chronotropic GPCR- f AABs identified targeted the muscarinic M 2 -receptor (M 2 - f AAB), the MAS-receptor (MAS- f AAB), and the ETA-receptor (ETA- f AAB). It was analysed which of the extracellular receptor loops was targeted by the autoantibodies.

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The effect of acute and repeated treatment (seven days) with a valerian extract (Valdispert forte, 405 mg t.i.d.) on objective and subjective measures of sleep was studied. Polysomnography was conducted in 14 elderly poor sleepers on three nights, at one-week intervals (N0, N1, N2). N0 was an adaptation night, N1 and N2 the first and last night under treatment. Six subjects received placebo and eight subjects valerian. Subjects in the valerian group showed an increase in slow-wave sleep (SWS) and a decrease in sleep stage 1. Density of K-complexes was increased under active treatment. There was no effect on sleep onset time or time awake after sleep onset. REM sleep was unaltered. There was also no effect on self-rated sleep quality. We hypothesize that valerian increases SWS in subjects with low baseline values.