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Purpose of Review In this article, we review a range of digital technologies for possible application in heart failure patients, with a focus on lessons learned. We also discuss a future model of heart failure management, as digital technologies continue to become part of standard care. Recent Findings Digital technologies are increasingly used by healthcare professionals and those living with heart failure to support more personalised and timely shared decision-making, earlier identification of problems, and an improved experience of care. The COVID-19 pandemic has accelerated the acceptability and implementation of a range of digital technologies, including remote monitoring and health tracking, mobile health (wearable technology and smartphone-based applications), and the use of machine learning to augment data interpretation and decision-making. Much has been learned over recent decades on the challenges and opportunities of technology development, including how best to evaluate the impact of digital health interventions on health and healthcare, the human factors involved in implementation and how best to integrate dataflows into the clinical pathway. Summary Supporting patients with heart failure as well as healthcare professionals (both with a broad range of health and digital literacy skills) is crucial to success. Access to digital technologies and the internet remains a challenge for some patients. The aim should be to identify the right technology for the right patient at the right time, in a process of co-design and co-implementation with patients.

Heart failure (HF) is highly prevalent and associated with adverse outcomes and high costs. Compared with the general population, depression is up to five times more common in HF patients. Comorbid depression increases morbidity and mortality risk and health-care expenditures even further and decreases quality of life. Possible, often interrelated, mediators of these effects include biological, behavioral, and psychosocial factors. Screening instruments such as the self-administered PHQ-2 facilitate detection of patients at risk. Although antidepressants may improve psychological well-being, no positive effects on hard clinical endpoints have been demonstrated to date.

ObjectiveDeficiency of anabolic sex steroids is common in heart failure (HF). The pathophysiological implications of this phenomenon, however, have not been fully elucidated. This clinical study investigated the significance of low serum androgen levels in HF.DesignProspective cohort study.Patients and MethodsIn 191 consecutively recruited men with HF (mean age 64 years; New York Heart Association (NYHA) class I–IV 24%/35%/35%/6%) and reduced (ejection fraction (EF) ≤40%, n=96) or preserved (EF >40%, n=95) left ventricular function total and free serum testosterone, dehydroepiandrosterone sulfate (DHEAS) and sex hormone binding globulin (SHBG) were measured. The median observation period was 859 days.ResultsDuring follow-up 53 patients (28%) died. Whereas total serum testosterone was normal in most patients (91%), free testosterone and DHEAS were reduced in 79% and 23%, respectively. DHEAS and free testosterone, but not total testosterone, were inversely associated with NYHA class (both p<0.01). Lower free testosterone and DHEAS and higher SHBG predicted all-cause mortality risk (hazard ratio (HR) 0.89, 95% CI 0.82 to 0.96 per 1 ng/dl free testosterone, p=0.004; HR 0.95, 95% CI 0.89 to 1.00 per 10 μg/dl DHEAS, p=0.058; and HR 1.18, 95% CI 1.05 to 1.33 per 10 nmol/l SHBG, p=0.006, respectively; adjusted for age and NYHA class). However, further adjustment for carefully selected confounding factors abolished these associations.ConclusionIn male HF patients, low serum levels of androgens are associated with adverse prognosis, but this relation is confounded by indicators of a poor health state. The results suggest that low serum androgens develop as a sequel of this progressive multifaceted systemic disorder.

Heart failure and depression are widespread diseases and of particular clinical and economic relevance. Compared with the general population depression is up to 5‑times more common in patients with heart failure, with adverse effects on morbidity, mortality, quality of life and treatment costs. Depressive symptoms overlap with those of heart failure which renders diagnosis difficult. Simple screening tools, e. g. the two-item patient health questionnaire, help to recognize depression in the clinical routine. To date, there is no evidence that antidepressant pharmacotherapy improves mood and clinical outcomes in patients with heart failure and comorbid depression and antidepressant pharmacotherapy remains to be decided on a case by case basis; however, physical training, cognitive behavioral therapy and multidisciplinary comprehensive disease management improved symptoms and/or prognosis in a limited number of randomized studies.

A total of 52 pharmacologically untreated subjects with essential hypertension were randomly allocated to either 8 weeks of contemplative meditation combined with breathing techniques (CMBT) or no intervention in this observer-blind controlled pilot trial. CMBT induced clinically relevant and consistent decreases in heart rate, systolic and diastolic blood pressure if measured during office readings, 24-h ambulatory monitoring and mental stress test. Longer-term studies should evaluate CMBT as an antihypertensive strategy.

Background Peripartum cardiomyopathy (PPCM) is an idiopathic heart disease that develops in the last month of pregnancy and/or the first months following delivery in previously healthy women and may lead to acute heart failure. A cleaved fragment of the nursing hormone prolactin is considered essential in the pathophysiology of PPCM. To date, no specific therapy has been tested for PPCM in a randomized controlled trial of adequate size. Aims The purpose of this trial is to investigate the safety of the dopamin-D2-receptor agonist bromocriptine and its effects on left ventricular (LV) function in women with PPCM. Methods This is an 11 center German trial with a prospective randomized controlled open-label design. The trial enrolls females with newly diagnosed PPCM according to European Society of Cardiology criteria with a LV ejection fraction (LVEF) <35 %. Patients are randomized 1:1 to either best supportive care (BSC) including standard heart failure therapy plus 8 weeks of bromocriptine therapy (2.5 mg b.i.d. for 14 days and 2.5 mg q.d. from day 15 to 56) or to BSC plus 1 week of low-dose bromocriptine (2.5 mg q.d.) with anticoagulant therapy at a prophylactic dose administered during the period of bromocriptine treatment in both groups. The primary endpoint is change in LVEF from baseline to 6 months follow-up as assessed by cardiac magnetic resonance imaging (or echocardiography if CMR is not tolerated). The secondary endpoints are hospitalization for worsening heart failure, heart transplantation, and all-cause mortality during follow-up or a combination of these endpoints. A total of 60 patients will be recruited (including 6 potential dropouts) giving a power of 0.9 for an expected LVEF change of 10.8 % between treatment groups at 6 months. Perspective This trial will provide important knowledge on potential benefits and safety of prolonged inhibition of prolactin release with bromocriptine in addition to standard heart failure therapy in newly diagnosed PPCM. Trial registration: ClinicalTrials.gov Identifier: NCT00998556.

Heart failure remains a frequent cause of death and is the leading reason for hospitalization in Germany although therapeutic options have significantly increased over the past years particularly in heart failure with reduced ejection fraction. Clinical symptoms are usually preceded by cardiac remodeling, which was originally defined only by left ventricular dilatation and depressed function but is also associated with typical cellular and molecular processes. Healing after acute myocardial infarction is characterized by inflammation, cellular migration and scar formation. Cardiac remodeling is accompanied by adaptive changes of the peripheral cardiovascular system. Since prevention is the primary goal, rapid diagnosis and treatment of myocardial infarction are mandatory. Early reperfusion therapy limits infarct size and enables the best possible preservation of left ventricular function. Standard pharmacotherapy includes angiotensin-converting enzyme inhibitors, angiotensin-1-receptor blockers and beta blockers. In addition, mineralocorticoid receptor antagonists have proven beneficial. Compounds specifically targeting infarct healing processes are currently under development.

Background and purpose: Mitogen‐activated protein kinases (MAPK) are centrally involved in several mechanisms important for heart failure such as apoptosis, activation of inflammatory responses and cell proliferation. We therefore evaluated the effect of the selective p38 MAPK inhibitor SB 239063 on progression of left ventricular remodelling after myocardial infarction (MI) in rats. Experimental approach: Rats were treated for 9 weeks with placebo or SB 239063 by gavage (15mg kg‐1) twice daily starting 7 days after ligation of the left anterior descending artery. Serial transthoracic echocardiography was performed at days 7, 36 and 70. Key results: Over the 9 weeks, mortality was not different between the groups. On echocardiography, animals after myocardial infarction exhibited significant left ventricular dilatation as expected (week 10, end‐systolic diameter, placebo sham 5.21± 0.34 vs. placebo MI 8.44± 0.57 mm). However, there was no difference between placebo and SB 239063‐treated rats (week 10, end‐systolic diameter, SB MI 7.76± 0.74mm, not significantly different from placebo MI). Haemodynamics changed accordingly. Moreover, SB 239063 had no effect on left ventricular hypertrophy. Treatment with SB 239063 significantly reduced cytokine expression of tumour necrosis factor and interleukin‐1β after myocardial infarction. However, collagen content was not influenced by the treatment. Conclusion: Despite a reduction of inflammation, treatment with the p38 inhibitor SB 239063 does not affect cardiac remodelling and cardiac function when treatment is started 7 days after myocardial infarction. British Journal of Pharmacology (2007) 150, 130–135. doi:10.1038/sj.bjp.0706963

Herzinsuffizienz ist mit hoher Sterblichkeit, häufigen Krankenhausaufnahmen, schlechter Lebensqualität und steigenden Kosten assoziiert. Trotz Fortschritten bei medikamentösen und Device-basieren Therapien bleiben Mortalität und Morbidität nach Ersthospitalisierung wegen akuter kardialer Dekompensation (AKD) hoch. In randomisierten Studien, die den Wert verschiedener Formen des nichtinvasiven Telemonitorings prüften, wurden Hospitalisierungen wegen AKD selten vermindert, weil klinische Zeichen und Symptome keine frühen Indikatoren der AKD darstellen, sodass bei ihrem Auftreten stationäre Behandlungen oft schon unvermeidbar sind. Unter verschiedenen implantierbaren Monitoring-Devices erwies sich in den USA das drahtlose Telemonitoring des pulmonalarteriellen Drucks (PAP) mit dem CardioMEMS™-Sensor (Abbott, Sylmar, Kalifornien, USA) als sicher und klinisch effektiv. Bei so überwachten Patienten wurden – unabhängig von der kardialen Pumpfunktion – Hospitalisierungen wegen AKD deutlich reduziert, weil die Früherkennung hämodynamischer Dekompensationen an einem PAP-Anstieg noch vor Auftreten klinischer Symptome eine präventive Therapieanpassung ermöglichte. Derzeit wird diese Technologie auch in Europa erprobt. Die Leitlinie der Europäischen Gesellschaft für Kardiologie empfiehlt, bei Risikopatienten die Implantation eines CardioMEMS™-Sensors zu erwägen (Klasse IIb-B). Technische Weiterentwicklungen implantierbarer Systeme erlauben z. B. die Druckmessung im linken Vorhof, die erweiterte Nutzung hämodynamischer Daten (z. B. kontinuierliche Druckmessung) oder eine Selbstüberwachung durch Patienten mit einem interaktiven Modul. Anwendungsbreite und Bedeutung druckgeführter Therapien werden in Zukunft absehbar weiter wachsen mit der reellen Chance einer effektiveren Vermeidung von klinischen Ereignissen auch in Risikopopulationen.