Cardiovascular disease, particularly coronary artery disease (CAD), remains a predominant cause of mortality globally. Factors such as atherosclerosis and inflammation play significant roles in the pathogenesis of CAD. The nexus between inflammation and CAD is underscored by the role of immune cells, such as neutrophils, lymphocytes, monocytes, and macrophages. These cells orchestrate the inflammatory process, a core component in the initiation and progression of atherosclerosis. The activation of these pathways and the subsequent lipid, fibrous element, and calcification accumulation can result in vessel narrowing. Hematological parameters derived from routine blood tests offer insights into the underlying inflammatory state. Recent studies have highlighted the potential of inflammatory hematological ratios, such as the neutrophil/lymphocyte ratio, platelet/lymphocyte ratio, monocyte/lymphocyte ratio and lymphocyte/monocyte ratio. These parameters are not only accessible and cost-effective but also mirror the degree of systemic inflammation. Several studies have indicated a correlation between these markers and the severity, prognosis, and presence of CAD. Despite the burgeoning interest in the relationship between inflammatory markers and CAD, there remains a paucity of data exploring these parameters in young patients with acute myocardial infarction. Such data could offer valuable insights into the unique pathophysiology of early-onset CAD and improve risk assessment and predictive strategies.

Hypertrophic cardiomyopathy (HCM) is the most prevalent genetically inherited cardiomyopathy that follows an autosomal dominant inheritance pattern. The majority of HCM cases can be attributed to mutation of the MYBPC3 gene, which encodes cMyBP-C, a crucial structural protein of the cardiac muscle. The manifestation of HCM’s morphological, histological, and clinical symptoms is subject to the complex interplay of various determinants, including genetic mutation and environmental factors. Approximately half of MYBPC3 mutations give rise to truncated protein products, while the remaining mutations cause insertion/deletion, frameshift, or missense mutations of single amino acids. In addition, the onset of HCM may be attributed to disturbances in the protein and transcript quality control systems, namely, the ubiquitin–proteasome system and nonsense-mediated RNA dysfunctions. The aforementioned genetic modifications, which appear to be associated with unfavorable lifelong outcomes and are largely influenced by the type of mutation, exhibit a unique array of clinical manifestations ranging from asymptomatic to arrhythmic syncope and even sudden cardiac death. Although the current understanding of the MYBPC3 mutation does not comprehensively explain the varied phenotypic manifestations witnessed in patients with HCM, patients with pathogenic MYBPC3 mutations can exhibit an array of clinical manifestations ranging from asymptomatic to advanced heart failure and sudden cardiac death, leading to a higher rate of adverse clinical outcomes. This review focuses on MYBPC3 mutation and its characteristics as a prognostic determinant for disease onset and related clinical consequences in HCM.

Venous thrombosis is a common and potentially fatal disease, because of its high morbidity and mortality, especially in hospitalized patients. To establish the diagnosis of venous thrombosis, in the last years, a multi-modality approach that involves not only imaging modalities but also serology has been evolving. Multiple studies have demonstrated the use of some biomarkers, such as D-dimer, selectins, microparticles or inflammatory cytokines, for the diagnosis and treatment of venous thrombosis, but there is no single biomarker available to exclusively confirm the diagnosis of venous thrombosis. Considering the fact that there are some issues surrounding the management of patients with venous thrombosis and the duration of treatment, recent studies support the idea that these biomarkers may help guide the length of appropriate anticoagulation treatment, by identifying patients at high risk of recurrence. At the same time, biomarkers may help predict thrombus evolution, potentially identifying patients that would benefit from more aggressive therapies. This review focuses on classic and novel biomarkers currently under investigation, discussing their diagnostic performance and potential benefit in guiding the therapy for venous thrombosis.

Studies in recent years have shown increased interest in developing new methods of evaluation, but also in limiting post infarction ventricular remodeling, hoping to improve ventricular function and the further evolution of the patient. This is the point where biomarkers have proven effective in early detection of remodeling phenomena. There are six main processes that promote the remodeling and each of them has specific biomarkers that can be used in predicting the evolution (myocardial necrosis, neurohormonal activation, inflammatory reaction, hypertrophy and fibrosis, apoptosis, mixed processes). Some of the biomarkers such as creatine kinase–myocardial band (CK-MB), troponin, and N-terminal-pro type B natriuretic peptide (NT-proBNP) were so convincing that they immediately found their place in the post infarction patient evaluation protocol. Others that are related to more complex processes such as inflammatory biomarkers, atheroma plaque destabilization biomarkers, and microRNA are still being studied, but the results so far are promising. This article aims to review the markers used so far, but also the existing data on new markers that could be considered, taking into consideration the most important studies that have been conducted so far.

Despite all the important advances in its diagnosis and treatment, acute myocardial infarction (AMI) is still one of the most prominent causes of morbidity and mortality worldwide. Early identification of patients at high risk of poor outcomes through the measurement of various biomarker concentrations might contribute to more accurate risk stratification and help to guide more individualized therapeutic strategies, thus improving prognoses. The aim of this article is to provide an overview of the role and applications of cardiac biomarkers in risk stratification and prognostic assessment for patients with myocardial infarction. Although there is no ideal biomarker that can provide prognostic information for risk assessment in patients with AMI, the results obtained in recent years are promising. Several novel biomarkers related to the pathophysiological processes found in patients with myocardial infarction, such as inflammation, neurohormonal activation, myocardial stress, myocardial necrosis, cardiac remodeling and vasoactive processes, have been identified; they may bring additional value for AMI prognosis when included in multi-biomarker strategies. Furthermore, the use of artificial intelligence algorithms for risk stratification and prognostic assessment in these patients may have an extremely important role in improving outcomes.

At the end of 2019, a variation of a coronavirus, named SARS-CoV-2, has been identified as being responsible for a respiratory illness disease (COVID-19). Since ventilation is an important factor that influences airborne transmission, we proposed to study the impact of heating, ventilation and air-conditioning (HVAC) with a variable air volume (VAV) primary air system, on the dispersion of infectious aerosols, in a cardiac intensive care unit, using a transient simulation with computational fluid dynamics (CFD), based on the finite element method (FEM). We analyzed three scenarios that followed the dispersion of pathogen carrying expiratory droplets particles from coughing, from patients possibly infected with COVID-19, depending on the location of the patients in the intensive care unit. Our study provides the mechanism for spread of infectious aerosols, and possibly of COVID-19 infection, by air conditioning systems and also highlights important recommendations for disease control and optimization of ventilation in intensive care units, by increasing the use of outdoor air and the rate of air change, decreasing the recirculation of air and using high-efficiency particulate air (HEPA) filters. The CFD-FEM simulation approach that was applied in our study could also be extended to other targets, such as public transport, theaters, philharmonics and amphitheaters from educational units.