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Abstract This study aimed to investigate the effects of chronic sympathoinhibition on glucose uptake by the myocardium and by the skeletal muscle in an animal model of obesity associated with leptin signaling deficiency. 6 obese Zucker rats (OZR) and 6 control Lean Zucker rats (LZR) were studied during basal conditions, chronic clonidine administration (30 days, 300 µg/kg), and washout recovery period. Glucose uptake in the myocardium and in the skeletal muscle was measured using positron emission tomography (PET) and 2-[18F] fluoro-2-deoxy-D-glucose ([18F]FDG). The standardized uptake value (SUV) corrected for blood glucose was used for the semi-quantitative analysis. Body weight, food and water intake, blood glucose concentration, blood pressure variability as an index of sympathetic activity and hemodynamic parameters such as mean arterial blood pressure (MAP), systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) were analyzed. Myocardial glucose uptake was significantly lower during basal conditions in OZR versus LZR. In both OZR and LZR, chronic clonidine significantly reduced myocardial glucose uptake and hemodynamic variables (such as MAP, SBP, DBP, HR), and sympathetic activity (SA). [18F]FDG skeletal muscle uptake did not significantly differ in OZR versus LZR. Our findings indicate that cardiac glucose metabolism is reduced in obesity presumably in relation with the level of sympathetic activation.

Background: Acute pulmonary embolism (PE) is a condition with increased morbidity and mortality. It is important to identify patients with high mortality risk. Inflammation and thrombosis are interconnected in the pathophysiology of PE. The aim of the study was to investigate the prognostic value of multiple blood cellular indices such as neutrophil-to-lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR), platelet-to-lymphocyte ratio (PLR), neutrophil-to-lymphocyte platelet ratio (NLPR), systemic immune–inflammation index (SII), systemic inflammation response index (SIRI) and aggregate index of systemic inflammation (AISI) in acute PE. Methods: A total of 157 patients with acute PE confirmed by chest computed tomographic angiography (CTPA) were enrolled. These patients were divided into two categories according to the simplified pulmonary embolism severity index (sPESI): high risk and low risk. Results: Univariate logistic regression analysis showed that right ventricle dysfunction, NLR, SII and SIRI were significantly associated with high risk of acute PE. NLR of 4.32 was associated with high-risk PE with a sensitivity of 57.4% and specificity of 65.7% (AUC = 0.635). SII of 1086.55 was associated with high-risk PE with a sensitivity of 55.7% and specificity of 71.4% (AUC = 0.614). SIRI of 2.87 was associated with high-risk PE with a sensitivity of 59% and specificity of 62.9% (AUC = 0.624). Multivariate logistic regression analysis demonstrated that right ventricle dysfunction, NLR, PLR and NLPR are independent predictors of high-risk acute PE. Secondly, NLR, NLPR, SII and SIRI were significantly correlated with in-hospital mortality of acute PE. Based on receiver-operating characteristic (ROC) curve values of 7.66 for NLR (AUC 0.911, sensitivity of 85.7% and sensibility of 83%), 0.02 for NLPR (AUC 0.871, sensitivity of 85.7% and sensibility of 70%), 1542.71 for SII (AUC 0.782, sensitivity of 71.4% and sensibility of 72%) and 5.72 for SIRI (AUC 0.788, sensitivity of 71.4% and sensibility of 73%) could predict in-hospital mortality. Conclusions: The blood cellular indices (NLR, NLPR, SII and SIRI) are associated with high-risk acute PE and in-hospital mortality. Right ventricular dysfunction, NLR and NLPR are independent predictors for high-risk acute PE.

Background and Objectives: Chronic heart failure (CHF) caused by ischemic heart disease (IHD) is the leading cause of death worldwide and presents significant health challenges. Effective management of IHD requires prevention, early detection, and treatment to improve patient outcomes. This study aims to expand the diagnostic utility of various 24 h Holter ECG parameters, such as T-wave alternans (TWA), late ventricular potentials (LVPs), and heart rate variability (HRV) in patients with CHF caused by IHD. Additionally, we seek to explore the association between these parameters and other comorbid conditions affecting the prognosis of CHF patients. Materials and Methods: We conducted a prospective case–control study with 150 patients divided into two subgroups: 100 patients with CHF caused by IHD, and 50 patients in the control group. Data included medical history, physical examination, laboratory tests, echocardiography, and 24 h Holter monitoring. Results: Our comparative analysis demonstrated that both TWA and LVPs were significantly higher in patients with CHF compared to the control group (p < 0.01), indicating increased myocardial electrical vulnerability in CHF patients. Both time and frequency-domain HRV parameters were significantly lower in the CHF group. However, the ratio of NN50 to the total count of NN intervals (PNN50) showed a borderline significance (p = 0.06). While the low-frequency (LF) domain was significantly lower in CHF patients, the high-frequency (HF) domain did not differ significantly between groups. Acceleration and deceleration capacities were also significantly altered in CHF patients. Categorizing CHF patients by left ventricular ejection fraction (LVEF) revealed that the mean of the 5-min normal-to-normal intervals over the complete recording (SDNN Index) was significantly higher in patients with LVEF ≥ 50% compared to those with CHF with reduced EF and CHF with mildly reduced EF (p < 0.001), whereas the other HRV parameters showed no significant differences among the groups. Conclusions: Holter ECG parameters can become a reliable tool in the assessment of patients with CHF. The integration of multiple Holter ECG parameters, such as TWA, LVPs, and HRV, can significantly enhance the diagnostic assessment of CHF caused by IHD. This comprehensive approach allows for a more nuanced understanding of the patient’s condition and potential outcomes.

Background and Objective: In the landscape of heart failure, non-cardiac comorbidities represent a formidable challenge, imparting adverse prognostic implications. Holter ECG monitoring assumes a supplementary role in delineating myocardial susceptibility and autonomic nervous system dynamics. This study aims to explore the potential correlation between Holter ECG parameters and comorbidities in individuals with ischemic cardiomyopathy experiencing heart failure (HF), with a particular focus on the primary utility of these parameters as prognostic indicators. Materials and Methods: In this prospective inquiry, a cohort of 60 individuals diagnosed with heart failure underwent stratification into subgroups based on the presence of comorbidities, including diabetes, chronic kidney disease, obesity, or hyperuricemia. Upon admission, a thorough evaluation of all participants encompassed echocardiography, laboratory panel analysis, and 24 h Holter monitoring. Results: Significant associations were uncovered between diabetes and unconventional physiological indicators, specifically the Triangular index (p = 0.035) and deceleration capacity (p = 0.002). Pertaining to creatinine clearance, notable correlations surfaced with RMSSD (p = 0.026), PNN50 (p = 0.013), and high-frequency power (p = 0.026). An examination of uric acid levels and distinctive Holter ECG patterns unveiled statistical significance, particularly regarding the deceleration capacity (p = 0.045). Nevertheless, in the evaluation of the Body Mass Index, no statistically significant findings emerged concerning Holter ECG parameters. Conclusions: The identified statistical correlations between non-cardiac comorbidities and patterns elucidated in Holter ECG recordings underscore the heightened diagnostic utility of this investigative modality in the comprehensive evaluation of individuals grappling with HF. Furthermore, we underscore the critical importance of the thorough analysis of Holter ECG recordings, particularly with regard to subtle and emerging parameters that may be overlooked or insufficiently acknowledged.

Exercise-based cardiac rehabilitation (ExCR) programs are essential for patients diagnosed with cardiac diseases. Studies have shown that they aid in the rehabilitation process and may even facilitate a return to previous cardiorespiratory fitness. Also, patients who enroll and follow such programs have shown a lower rate of complications and mortality in the long run. The results vary depending on the type of program followed and the degree of debilitation the disease has caused. Therefore, in order to obtain optimal results, it is ideal to tailor each ExCR program to the individual profile of each patient. At the moment, the two most studied and employed training types are medium-intensity continuous training (MICT) and high-intensity interval training (HIIT). For most of the time, MICT was the first-choice program for patients with cardiovascular disease. In recent years, however, more and more studies have pointed towards the benefits of HIIT and how it better aids patients in recovering their cardiovascular fitness. Generally, MICT is more suited for patients with a severe degradation in functional capacity and who require a higher degree of safety (e.g., elderly, with a high number of comorbidities). On the other hand, while HIIT is more demanding, it appears to offer better outcomes. Therefore, this review aimed to summarize information from different publications on both types of training regimens in ExCR and assess their utility in current clinical practice.

(1) Background: Given its high cardiac specificity and its capacity to directly assess the cardiac function, cardiac myosin-binding protein (MyBP-C) is a promising biomarker in patients with acute heart failure (AHF). The aim of our study was to investigate the clinical utility of this novel marker for diagnosis and short-term prognosis in subjects with AHF. (2) Methods: We measured plasma levels of MyBP-C at admission in 49 subjects (27 patients admitted with AHF and 22 controls). (3) Results: The plasma concentration of MyBP-C was significantly higher in patients with AHF compared to controls (54.88 vs. 0.01 ng/L, p < 0.001). For 30-day prognosis, MyBP-C showed significantly greater AUC (0.972, p < 0.001) than NT-proBNP (0.849, p = 0.001) and hs-TnI (0.714, p = 0.047). In a multivariate logistic regression analysis, an elevated level of MyBP-C was the best independent predictor of 30-day mortality (OR = 1.08, p = 0.039) or combined death/recurrent 30-days rehospitalization (OR = 1.12, p = 0.014). (4) Conclusions: Our data show that circulating MyBP-C is a sensitive and cardiac-specific biomarker with potential utility for the accurate diagnosis and prognosis of AHF.