The apelin–ELABELA–APJ axis, collectively known as the apelinergic system, has emerged as a key regulator of cardiovascular homeostasis. Acting through G-protein-coupled mechanisms, it modulates vascular tone, cardiac contractility, angiogenesis, fluid balance, and metabolism. Growing evidence indicates that dysregulation of apelinergic signaling contributes to the development and progression of atherosclerosis, hypertension, and heart failure. Experimental studies demonstrate cardioprotective actions of apelin and ELABELA, including anti-fibrotic, anti-inflammatory, vasodilatory, and pro-angiogenic effects, whereas some findings suggest context-dependent pro-atherogenic or vasoconstrictive roles. Clinical data show that circulating apelinergic peptides vary across cardiovascular conditions, being upregulated in acute coronary syndromes and diminished in chronic ischemic or hypertensive disease. In heart failure, early compensatory activation is followed by progressive depletion, and low ELABELA levels correlate with disease severity. Moreover, the apelinergic system may exert anti-arrhythmic effects through modulation of myocardial electrophysiology and structural remodeling. Novel synthetic APJ agonists and stabilized peptide analogs show promising preclinical efficacy in reducing cardiac remodeling, improving contractility, and lowering blood pressure. Altogether, the apelinergic pathway represents a multifaceted modulator and a promising therapeutic target in cardiovascular medicine, warranting further translational studies to elucidate its diagnostic and treatment potential.

Background/Objectives: The ageing population has heightened interest in the prognostic role of geriatric conditions, notably frailty syndrome (FS) and cognitive impairment (CI). Evidence indicates a significant link between cardiovascular disease, FS, and CI. However, limited research has explored the impact of impaired functional and cognitive performance on outcomes in acute coronary syndrome (ACS) patients. This study aimed to evaluate the effect of coexisting FS and CI (FSxCI) on early and 6-month complications in older adults with ACS. Methods: This study included 196 ACS patients (119 men) aged 65 and over (mean = 74.7 years), with 90.8% undergoing invasive treatment (PCI in 81.6%, CABG in 9.2%). FS and CI were assessed on the third hospital day using the Tilburg Frailty Indicator (TFI) and Mini Mental State Examination (MMSE). Early (in-hospital) complications included major bleeding, ventricular arrhythmia (VT), conduction disturbances, cardiac arrest, stent thrombosis, acute heart failure (Killip–Kimball class III/IV), stroke, prolonged stay, and in-hospital death. Six-month follow-up recorded major adverse cardiovascular and cerebrovascular events (MACCEs). Results: Patients with FSxCI (n = 107, 54.6%) were older and had higher hypertension prevalence and lower nicotine dependence. FSxCI patients faced over twice the risk of prolonged hospital stays (OR 2.39; p = 0.01) and nearly three times the risk of early complications (OR 2.73; p < 0.001). At 6 months, FSxCI tripled the risk of MACCEs (OR 2.8; p = 0.007). Kaplan–Meier analysis confirmed a worse 6-month prognosis for FSxCI patients. Conclusions: Elderly patients with ACS and concomitant FSxCI had significantly higher rates of early (in-hospital) and 6-month complications. FSxCI was associated with a worse 6-month prognosis. This highlights its significance for clinical decision-making, as identifying FSxCI in ACS patients can help prioritize high-risk individuals for tailored interventions, optimize resource allocation, and improve outcomes.

DOI: 10.20452/pamw.16862, Published online: October 15, 2024, Authors: Radosław Wontor, Bogusława Ołpińska, Maria Łoboz-Rudnicka, Rafał Wyderka, Krzysztof Dudek, Krystyna Łoboz-Grudzień, Joanna Jaroch

Background: Despite a growing evidence from the animal models of the cardioprotective function of the apelinergic system in the setting of myocardial infarction, little is known on the role of apelinergic system in the development of post- infarction adverse left ventricle remodeling in humans. Methods: The study group consisted of 49 patients with first-time ST-segment elevation myocardial infarction of anterior wall treated invasively. Echocardiography was performed on index hospitalization and on one-year check-up, with categorizing the study population into group with adverse LV remodeling defined as an increase of LV end diastolic volume by > 20% (n = 12) and the group without adverse remodeling (n = 29). ELA, AP-17, AP-13 and APJ receptor levels were measured on one-year follow-up. Results: Patients with adverse LV remodeling presented significantly higher plasma level of apelin-13 (85.63 [75.43– 96.13] vs 65.43 [57.35– 69.35], p = 0.001) and apelin-17 (69.36 [42.61– 77.04] vs 30.04 [25.97– 41.95], p = 0.004). In a univariable logistic regression analysis, higher LVEDV and LVEDV1, higher LVESV and LVESVi, lower LVEF, higher WMSI score, higher SYNTAX score, higher levels of hs-CRP during index hospitalization and higher levels of AP-13 and AP-17 on the one-year check-up were associated with adverse LV remodeling. In multivariable logistic regression analysis, only AP-17 level was independently associated with adverse LV remodeling (p = 0.050). Conclusion: Apelinergic system may be involved in the development of post- infarction adverse left ventricle remodeling.

Background: Little is known about the effect of cardiac rehabilitation (CR) on carotid arterial stiffness (CAS) in patients with myocardial infarction (MI). Patients and Methods: Rehabilitation group (B) included 90 patients with MI subjected to CR, control group (K) consisted of 30 patients with MI not participating in CR, and healthy group comprised 38 persons without cardiovascular risk factors. CAS was determined using echo-tracking before and after CR. Results: At baseline, patients with MI (B+K) presented with significantly higher mean values of CAS parameters: beta-stiffness index (7.1 vs 6.4, p = 0.004), Peterson’s elastic modulus (96 kPa vs 77 kPa, p < 0.001) and PWV-beta (6.1 m/s vs 5.2 m/s, p < 0.001) than healthy persons. Age (beta: r = 0.242, p = 0.008; EP: r = 0.250, p = 0.006; PWV-beta: r = 0.224, p = 0.014) and blood pressure: SBP (EP: r = 0.388, PWV-beta: r = 0.360), DBP (AC: r = 0.225) and PP (PWV-beta: r = 0.221) correlated positively with the initial parameters of CAS. Beta-stiffness index (Rho=− 0.26, p = 0.04) and PWV-beta (Rho = 0.29, p = 0.03) correlated inversely with peak exercise capacity expressed in METs. After CR, mean values of beta-stiffness index (6.2 vs 7.1, p = 0.016), EP (78 kPa vs 101 kPa, p = 0.001) and PWV-beta (5.4 m/s vs 6.2 m/s, p = 0.001) in group B were significantly lower than in group K. In group B, CAS parameters decreased significantly after CR. Univariate analysis demonstrated that the likelihood of an improvement in CAS after CR was significantly higher in patients with baseline systolic blood pressure < 120 mm Hg (OR = 2.74, p = 0.009) and left ventricular ejection fraction < 43% (OR = 5.05, p = 0.005). Conclusion: In patients with MI, CR exerted a beneficial effect on CAS parameters. The improvement in CAS was predicted by lower SBP and LVEF at baseline.