Historically, cardiovascular disease (CVD) has often been regarded as a primarily cardiac condition. Nevertheless, recent research data suggests that this disease should be considered a multifactorial and multisystem one. In this narrative review, available evidence related to inflammatory processes, metabolic disorders, neurohormonal signaling, endothelial dysfunction, and communication between organs will be summarized to illustrate the pathophysiology of CVD. A structured search of available literature was performed using the PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar databases. Only articles from 2010 to 2025 were considered to ensure that the latest developments were accounted for. The selected literature includes clinical trials, observational studies, and reviews. The analysis suggests, that all cardiovascular disorders, including heart failure, coronary artery disease, atrial fibrillation, and hypertension, have common systemic mechanisms, namely, chronic inflammation, immunological dysregulation, insulin resistance, and neurohormonal stimulation. Moreover, complex relationships exist between the heart, kidneys, liver, gastrointestinal tract, adipose tissue, and the brain, and they can lead to the aggravation of disease course. Despite promising results obtained within an integrated approach, several difficulties need to be acknowledged, among which, clinical translational issues and lack of systems-level clinical trials are of primary importance.

Pulmonary embolism (PE) remains a major cause of cardiovascular mortality, and early identification of high-risk patients is essential. The uric acid-to-albumin ratio (UAR) has emerged as a marker reflecting systemic inflammation. This study aimed to evaluate the prognostic value of UAR for in-hospital mortality in patients with acute PE. This single-center, retrospective study included 1052 consecutive patients diagnosed with acute PE. Clinical characteristics, laboratory parameters, echocardiographic findings, and pulmonary imaging results were obtained from hospital records. Multivariable logistic regression analyses were performed to identify independent predictors of in-hospital mortality. The discriminative performance of UAR was assessed using receiver operating characteristic (ROC) curve analysis. Overall, 70 patients (6.7%) died during hospitalization. Non-survivors had significantly higher UAR values compared with survivors (2.33 vs 1.57, P < .001). In multivariable analysis, UAR C-Reactive Protein, and Pulmonary artery severity index (PESI) score independently predicted in-hospital mortality. UAR demonstrated acceptable discriminative ability (Area under the curve .728; 95% CI: .649-.807; P < .001), with an optimal cut-off of 2.12. The combined use of UAR and PESI demonstrated a modest improvement in predictive performance. UAR is an independent predictor of in-hospital mortality in patients with acute PE. Its combination with the PESI score may provide incremental value for early risk stratification.