Serotonin acts solely via 5-HT₄-receptors to control human cardiac contractile function. The effects of serotonin via 5-HT₄-receptors lead to positive inotropic and chronotropic effects, as well as arrhythmias, in the human heart. In addition, 5-HT₄-receptors may play a role in sepsis, ischaemia, and reperfusion. These presumptive effects of 5-HT₄-receptors are the focus of the present review. We also discuss the formation and inactivation of serotonin in the body, namely, in the heart. We identify cardiovascular diseases where serotonin might play a causative or additional role. We address the mechanisms which 5-HT₄-receptors can use for cardiac signal transduction and their possible roles in cardiac diseases. We define areas where further research in this regard should be directed in the future, and identify animal models that might be generated to this end. Finally, we discuss in what regard 5-HT₄-receptor agonists or antagonists might be useful drugs that could enter clinical practice. Serotonin has been the target of many studies for decades; thus, we found it timely to summarise our current knowledge here.

Dopamine has effects on the mammalian heart. These effects can include an increase in the force of contraction, and an elevation of the beating rate and the constriction of coronary arteries. Depending on the species studied, positive inotropic effects were strong, very modest, or absent, or even negative inotropic effects occurred. We can discern five dopamine receptors. In addition, the signal transduction by dopamine receptors and the regulation of the expression of cardiac dopamine receptors will be of interest to us, because this might be a tempting area of drug development. Dopamine acts in a species-dependent fashion on these cardiac dopamine receptors, but also on cardiac adrenergic receptors. We will discuss the utility of drugs that are currently available as tools to understand cardiac dopamine receptors. The molecule dopamine itself is present in the mammalian heart. Therefore, cardiac dopamine might act as an autocrine or paracrine compound in the mammalian heart. Dopamine itself might cause cardiac diseases. Moreover, the cardiac function of dopamine and the expression of dopamine receptors in the heart can be altered in diseases such as sepsis. Various drugs for cardiac and non-cardiac diseases are currently in the clinic that are, at least in part, agonists or antagonists at dopamine receptors. We define the research needs in order to understand dopamine receptors in the heart better. All in all, an update on the role of dopamine receptors in the human heart appears to be clinically relevant, and is thus presented here.

Adult cardiac surgery with extracorporeal circulation is known to be associated with increased risk of blood transfusion leading to adverse outcomes. Procedures like retrograde autologous priming (RAP) may reduce these negative side effects. This randomized prospective study was initiated to assess whether RAP using specifically designed RAP bag (Terumo) has immediate effects on patient outcome. One hundred eighteen adults undergoing elective CABG or elective aortic valve replacement were randomly assigned by a computer program into two groups: the RAP group (n = 54) in which the retrograde autologous priming was applied and the non-RAP (n = 64) group in which the same setting was used without the possibility to save priming volume. Patient demographics, preoperative characteristics and postoperative outcomes were analyzed for both groups. The primary endpoint defined as rate of intraoperative blood transfusion was significantly reduced in the RAP-group (p = 0.04). The absolute risk reduction for RAP managed patients was 13.5 percent points. There were no significant differences in operation time and blood loss. No deaths and no myocardial infarctions were observed. The number of patients needed to treat to prevent at least one red blood cell transfusion was around 8 (NNT = 7.42). Retrograde autologous priming is a safe and less invasive procedure which achieves clear benefits for adult cardiac surgery patients. In the light of increasing red blood cell transfusion risks and costs and the wish of patients to avoid a transfusion implementation of retrograde autologous priming is an interesting option. German Clinical Trials Register ID: DRKS00013512 , registered 04 December 2017.

Background: Patients with severely reduced LV-EF ≤ 30% undergoing CABG have a high risk for postoperative cardiogenic shock. The optimal timing of an adequate hemodynamic support has an impact on short- and midterm mortality after CABG. This study aimed to assess the prophylactic use of the Impella pump in high-risk patients undergoing elective cardiac surgery. Methods: In this single-center retrospective study, 14 patients with LV-EF (≤30%) undergoing cardiac surgery received a prophylactic, perioperative Impella (5.0, 5.5) support between 2020 and 2022. Results: The mean age at surgery was 64.2 ± 2.6 years, the mean preoperative LV-EF was 20.7% ± 1.56%. The duration of Impella support was 4 (3–7.8) days and the 30-day survival rate was 92.85%. Acute renal failure occurred in four patients who were dialyzed on average for 1.2 ± 0.7 days. Mechanical ventilation was needed for 1.75 (0.9–2.7) days. Time to inotrope/vasopressor independence was 2 (0.97–7.25) days with a highest lactate level (24 h postoperatively) of 3.8 ± 0.6 mmol/l. Postoperative LV-EF showed a significant improvement when compared to preoperative LV-EF (29.1% ± 2.6% vs. 20.7% ± 1.56% (p = 0.022)). Conclusion: The prophylactic Impella application seems to be a safe approach to improve the outcomes of this patient population.

Glucagon exerts effects on the mammalian heart. These effects include alterations in the force of contraction, beating rate, and changes in the cardiac conduction system axis. The cardiac effects of glucagon vary according to species, region, age, and concomitant disease. Depending on the species and region studied, the contractile effects of glucagon can be robust, modest, or even absent. Glucagon is detected in the mammalian heart and might act with an autocrine or paracrine effect on the cardiac glucagon receptors. The glucagon levels in the blood and glucagon receptor levels in the heart can change with disease or simultaneous drug application. Glucagon might signal via the glucagon receptors but, albeit less potently, glucagon might also signal via glucagon-like-peptide-1-receptors (GLP1-receptors). Glucagon receptors signal in a species- and region-dependent fashion. Small molecules or antibodies act as antagonists to glucagon receptors, which may become an additional treatment option for diabetes mellitus. Hence, a novel review of the role of glucagon and the glucagon receptors in the mammalian heart, with an eye on the mouse and human heart, appears relevant. Mouse hearts are addressed here because they can be easily genetically modified to generate mice that may serve as models for better studying the human glucagon receptor.