Postoperative atrial fibrillation (POAF) is the most common arrhythmia following cardiac surgery. This review critically explores the interplay between cardiopulmonary bypass (CPB) and aortic cross-clamping (ACC) times in POAF development. CPB disrupts systemic homeostasis by inducing inflammatory cascades, oxidative stress, and ischemia–reperfusion injury. Prolonged ACC times further exacerbate myocardial ischemia and structural remodeling, with durations exceeding 60–75 min consistently linked to an increased POAF risk. However, variability in outcomes across studies reveals the complex, multifactorial nature of POAF pathogenesis. Patient-specific variables, such as baseline comorbidities and myocardial protection strategies, modulate these risks, emphasizing the need for personalized surgical approaches. Despite advancements in myocardial protection techniques and anti-inflammatory strategies, the incidence of POAF remains persistently high, indicating a gap in translating mechanistic insights into effective interventions. Emerging biomarkers, including microRNAs (e.g., miR-21, miR-483-5p, etc.) and markers of myocardial injury like troponin I, offer potential for enhanced risk stratification and targeted prevention. However, their clinical applicability requires further validation in diverse patient populations. This review underscores the critical need for integrative research that combines clinical, molecular, and procedural variables to elucidate the nuanced interplay of factors driving POAF. Future directions include leveraging advanced intraoperative monitoring tools, refining thresholds for CPB and ACC times, and developing individualized perioperative protocols.

Echocardiographic markers of right ventricular dysfunction or pressure overload (RV_d/PO) have been used in risk assessment of patients with acute pulmonary embolism (APE). Nevertheless, the role of echocardiography in these patients is incompletely determined. We evaluated the right ventricular function using 'non-conventional' markers of RV_d/PO in patients with APE. This was a prospective, single-arm, single-centre study. Consecutive adult patients hospitalised for APE were included. The RV free wall longitudinal strain (RV-FWLS), the fractional area change (FAC), the ratio tricuspid annular plane systolic excursion (TAPSE)/pulmonary arterial systolic pressure (PASP), and the pulmonary vascular resistance (PVR) were evaluated. One hundred patients (mean age 70.0 ± 13.9 years, female 48%) were screened and 73 had adequate RV-FWLS images. The most common abnormal echocardiographic marker was RV-FWLS (44/73; p < 0.001, for all other echocardiographic indices). Thirty-one patients had either PASP ≥ 36 mmHg or PVR > 2 WU (49.2% of the patients with both indices available). There were significant correlations between RV-FWLS, TAPSE/PASP and PVR with both D-Dimers and B-type natriuretic peptide (BNP), and between FAC and BNP. RF-FWLS differed significantly between patients with a simplified pulmonary embolism severity index (sPESI) score 0 and those with a score ≥1 (p < 0.001). RV_d/PO coexists with APE in a large proportion of patients. RV-FWLS is the most abnormal echocardiographic sign and is related to clinical and biochemical prognostic indices.

Background/Objectives: Patients with acute myeloid leukemia (AML) have a higher propensity for adverse cardiovascular outcomes, primarily due to the toxic effects of chemotherapeutic agents. The purpose of this systematic review is to explore the association of acute myeloid leukemia treatment with adverse cardiovascular events. Methods: We systematically screened the literature for studies providing comparative data on cardiovascular toxicities in patients treated for acute myeloid leukemia. After the initial search, 3649 papers were screened and a final total number of 46 were included for the review process. Results: Common chemotherapeutic agents used in AML may cause cardiovascular (CV) toxicities. A plethora of pathophysiological mechanisms are incriminated for these effects. Drug combinations may increase the risk in a synergistic way. In addition, common mutations of AML, personal history of previous cardiovascular disease and impaired heart function carry an increased complication risk. Biomarkers, as well as multimodality imaging, may be used for the early detection of cardiovascular toxicities. Conclusions: Increased risks of CV toxicity and comorbidities are observed among AML patients. With all the available diagnostic modalities, early detection and CV prevention strategies can improve the patient’s prognosis and quality of life.

Background: A significant proportion of pulmonary embolisms (PEs) occurs in patients during hospitalisation for another reason. However, limited data regarding differences between out-of-hospital PE (OHPE) and in-hospital PE (IHPE) is available. We aimed to compare these groups regarding their clinical characteristics, biochemical markers, and echocardiographic indices. Methods: This was a prospective, single-arm, single-centre study. Adult consecutive patients with non-COVID-related PE from September 2019 to March 2022 were included and followed up for 12 months. Results: The study included 180 (84 women) patients, with 89 (49.4%) suffering from IHPE. IHPE patients were older, they more often had cancer, were diagnosed earlier after the onset of symptoms, they had less frequent pain and higher values of high sensitivity troponin I and brain natriuretic peptide levels compared to OHPE patients. Echocardiographic right ventricular (RV) dysfunction was detected in similar proportions in the 2 groups. IHPE had increased in-hospital mortality (14.6% vs. 3.3%, p = 0.008) and similar post-discharge to 12-month mortality with OHPE patients. Conclusions: In this prospective cohort study, IHPE differed from OHPE patients regarding age, comorbidities, symptoms, and levels of biomarkers associated with RV dysfunction. IHPE patients had higher in-hospital mortality compared to OHPE patients and a similar risk of death after discharge.

This review explores the advantages of ivabradine in the management of cardiac surgery patients, particularly highlighting its heart rate (HR)-reducing properties, its role in minimizing the impact of atrial fibrillation, and its contributions to improving left ventricular diastolic function, as well as reducing pain, stress, and anxiety. In parallel, studies provide evidence that ivabradine influences endothelial inflammatory responses through mechanisms such as biomechanical modulation. Unlike traditional beta-blockers that may induce hypotension, ivabradine selectively inhibits hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, allowing for effective HR reduction without compromising blood pressure stability. This characteristic is particularly beneficial for patients at risk of atrial fibrillation post-surgery, where HR control is crucial for cardiovascular stability. This is an area in which ivabradine appears to play a role prophylactically, possibly in combination with beta-blockers. Furthermore, ivabradine has been associated with enhanced diastolic parameters in left ventricular function, reflecting its potential to improve surgical outcomes in patients with compromised heart function. In addition to its cardiovascular benefits, it appears to alleviate psychological stress and anxiety, common in postoperative settings, by moderating the neuroendocrine response to stress, thereby reducing stress-induced hormone levels. Furthermore, it has notable analgesic properties, contributing to pain management through its action on HCN channels in both the peripheral and central nervous systems. Collectively, these findings indicate that ivabradine may serve as a valuable therapeutic agent in the perioperative care of cardiac surgery patients, addressing both physiological and psychological challenges during recovery.