Adult growth hormone deficiency (AGHD) is considered a rare endocrine disorder involving patients with childhood-onset and adult-onset growth hormone deficiency (AoGHD) and characterized by adverse cardiometabolic risk profile. Besides traditional cardiovascular risk factors, endothelial dysfunction, low-grade inflammation, impaired adipokine profile, oxidative stress and hypovitaminosis D may also contribute to the development of premature atherosclerosis and higher cardiovascular risk in patients with AGHD. Growth hormone replacement has been proved to exert beneficial effects on several cardiovascular risk factors, but it is also apparent that hormone substitution in itself does not eliminate all cardiometabolic abnormalities associated with the disease. Novel biomarkers and diagnostic techniques discussed in this review may help to evaluate individual cardiovascular risk and identify patients with adverse cardiometabolic risk profile. In the absence of disease-specific guidelines detailing how to assess the cardiovascular status of these patients, we generally recommend close follow-up of the cardiovascular status as well as low threshold for a more detailed evaluation.

Obesity is characterized by an excessive accumulation of fat leading to a plethora of medical complications, including coronary artery disease, hypertension, type 2 diabetes mellitus or impaired glucose tolerance and dyslipidemia. Formerly, several physiological roles of organokines, including adipokines, hepatokines, myokines and gut hormones have been described in obesity, especially in the regulation of glucose and lipid metabolism, insulin sensitivity, oxidative stress, and low-grade inflammation. The canonical effect of these biologically active peptides and proteins may serve as an intermediate regulatory level that connects the central nervous system and the endocrine, autocrine, and paracrine actions of organs responsible for metabolic and inflammatory processes. Better understanding of the function of this delicately tuned network may provide an explanation for the wide range of obesity phenotypes with remarkable inter-individual differences regarding comorbidities and therapeutic responses. The aim of this review is to demonstrate the role of organokines in the lipid and glucose metabolism focusing on the obese non-diabetic subgroup. We also discuss the latest findings about sarcopenic obesity, which has recently become one of the most relevant metabolic disturbances in the aging population.

Altered organokine expression contributes to increased cardiometabolic risk in obesity. Our aim was to evaluate the associations of serum afamin with glucose homeostasis, atherogenic dyslipidemia, and other adipokines in severe obesity to clarify the early metabolic alterations. 106 non-diabetic obese (NDO) subjects and 62 obese patients with type 2 diabetes matched for age, gender, and body mass index (BMI) were enrolled in this study. We compared their data with 49 healthy, lean controls. Serum afamin and retinol-binding protein 4 (RBP4), as well as plasma plasminogen activator inhibitor-1 (PAI-1), were measured with ELISA, and lipoprotein subfractions were analyzed using Lipoprint gel electrophoresis. Afamin and PAI-1 found to be significantly higher in the NDO and T2M group (p < 0.001 and p < 0.001, respectively) than in the controls. In contrast, RBP4 was unexpectedly lower in the NDO and T2DM group compared to controls (p < 0.001). Afamin showed negative correlations with mean LDL size and RBP4, but positive correlations with anthropometric, glucose/lipid parameters, and PAI-1 in both the overall patients and the in NDO + T2DM groups. BMI, glucose, intermediate HDL, and small HDL were predictors of afamin. Afamin may serve as a biomarker for the severity of cardiometabolic disturbances in obesity. The complexity of organokine patterns in NDO subjects draws attention to the diverse spectrum of obesity-related comorbidities.

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Sudden cardiac death is a leading cause of death worldwide, whereby myocardial infarction is considered the most frequent underlying condition. Percutaneous coronary intervention (PCI) is an important component of post-resuscitation care, while uninterrupted high-quality chest compressions are key determinants in cardiopulmonary resuscitation (CPR). In our paper, we evaluate a case of a female patient who suffered aborted cardiac arrest due to myocardial infarction. The ambulance crew providing prehospital care for sudden cardiac arrest used a mechanical chest compression device during advanced CPR, which enabled them to deliver ongoing resuscitation during transfer to the PCI laboratory located 20 km away from the scene. Mechanical chest compressions were continued during the primary coronary intervention. The resuscitation, carried out for 2 h and 35 min, and the coronary intervention were successful, as evidenced by the return of spontaneous circulation and by the fact that, after a short rehabilitation, the patient was discharged home with a favorable neurological outcome. Our case can serve as an example for the effective and safe use of a mechanical compression device during primary coronary intervention.