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Recently, much attention has been paid to chronic neuro-inflammatory condition underlying neuropathic pain. It is generally linked with thermal hyperalgesia and tactile allodynia. It results due to injury or infection in the nervous system. The neuropathic pain spectrum covers a variety of pathophysiological states, mostly involved are ischemic injury viral infections associated neuropathies, chemotherapy-induced peripheral neuropathies, autoimmune disorders, traumatic origin, hereditary neuropathies, inflammatory disorders, and channelopathies. In CNS, angiogenesis is evident in inflammation of neurons and pain in bone cancer. The role of chemokines and cytokines is dualistic; their aggressive secretion produces detrimental effects, leading to neuropathic pain. However, whether the angiogenesis contributes and exists in neuropathic pain remains doubtful. In the present review, we elucidated summary of diverse mechanisms of neuropathic pain associated with angiogenesis. Moreover, an overview of multiple targets that have provided insights on the VEGF signaling, signaling through Tie-1 and Tie-2 receptor, erythropoietin pathway promoting axonal growth are also discussed. Because angiogenesis as a result of these signaling, results in inflammation, we focused on the mechanisms of neuropathic pain. These factors are mainly responsible for the activation of post-traumatic regeneration of the PNS and CNS. Furthermore, we also reviewed synthetic and herbal treatments targeting angiogenesis in neuropathic pain.

Imaging is an important tool in the diagnosis and management of infective endocarditis (IE). Echocardiography is an essential examination, especially in native valve endocarditis (NVE), but its diagnostic accuracy is reduced in prosthetic valve endocarditis (PVE). The diagnostic ability is superior for transoesophageal echocardiography (TEE), but a negative test cannot exclude PVE. Both transthoracic echocardiography (TTE) and TEE can provide normal or inconclusive findings in up to 30% of cases, especially in patients with prosthetic devices. New advanced non-invasive imaging tests are increasingly used in the diagnosis of IE. Nuclear medicine imaging techniques have demonstrated their superiority over TEE for the diagnosis of PVE and cardiac implantable electronic device infective endocarditis (CIED-IE). Cardiac computed tomography angiography imaging is useful in PVE cases with inconclusive TTE and TEE investigations and for the evaluation of paravalvular complications. In the present review, imaging tools are described with their values and limitations for improving diagnosis in NVE, PVE and CIED-IE. Current knowledge about multimodality imaging approaches in IE and imaging methods to assess the local and distant complications of IE is also reviewed. Furthermore, a potential diagnostic work-up for different clinical scenarios is described. However, further studies are essential for refining diagnostic and management approaches in infective endocarditis, addressing limitations and optimizing advanced imaging techniques across different clinical scenarios.

Oxidative stress is a complex biological process characterized by the excessive production of reactive oxygen species (ROS) that act as destroyers of the REDOX balance in the body and, implicitly, inducing oxidative damage. All the metabolisms are impaired in oxidative stress and even nucleic acid balance is influenced. ROS will promote structural changes of the tissues and organs due to interaction with proteins and phospholipids. The constellation of the cardiovascular risk factors (CVRFs) will usually develop in subjects with predisposition to cardiac disorders. Oxidative stress is usually related with hypertension (HTN), diabetes mellitus (DM), obesity and cardiovascular diseases (CVDs) like coronary artery disease (CAD), cardiomyopathy or heart failure (HF), that can develop in subjects with the above-mentioned diseases. Elements describing the complex relationship between CVD and oxidative stress should be properly explored and described because prevention may be the optimal approach. Our paper aims to expose in detail the complex physiopathology of oxidative stress in CVD occurrence and novelties regarding the phenomenon. Biomarkers assessing oxidative stress or therapy targeting specific pathways represent a major progress that actually change the outcome of subjects with CVD. New antioxidants therapy specific for each CVD represents a captivating and interesting future perspective with tremendous benefits on subject’s outcome.

Left ventricular non-compaction (LVNC) is a rare disease defined by morphological criteria, consisting of a two-layered ventricular wall, a thin compacted epicardial layer, and a thick hyper-trabeculated myocardium layer with deep recesses. Controversies still exist regarding whether it is a distinct cardiomyopathy (CM) or a morphological trait of different conditions. This review analyzes data from the literature regarding diagnosis, treatment, and prognosis in LVNC and the current knowledge regarding reverse remodeling in this form of CM. Furthermore, for clear exemplification, we report a case of a 41-year-old male who presented symptoms of heart failure (HF). LVNC CM was suspected at the time of transthoracic echocardiography and was subsequently confirmed upon cardiac magnetic resonance imaging. A favorable remodeling and clinical outcome were registered after including an angiotensin receptor neprilysin inhibitor in the HF treatment. LVNC remains a heterogenous CM, and although a favorable outcome is not commonly encountered, some patients respond well to therapy.

Anticoagulant therapy represents a pivotal element that strongly influences the thromboembolic risk of non-valvular atrial fibrillation (NVAF) subjects. The main purpose of this review was to identify issues and suggest strategies to improve the oral anticoagulants (OACs) treatment adherence, which is the most important predictor of NVAF outcome. Advantages, efficacy, and impact of these drugs on patients’ prognosis were revealed in important clinical trials on large cohorts of patients and are often prescribed nowadays. A real-life data registry, the Global Anticoagulant Registry in the Field-Atrial Fibrillation (GARFIELD-AF) analyzed the profile and outcome of patients diagnosed with NVAF receiving oral antithrombotic treatment. The observations gathered in the registry were crucial for identifying relevant elements that clinicians must improve, such as adherence strategies and predisposing factors that correlated with stroke. Adherence to OACs in AF patients is essential from the viewpoint of clinical efficacy and safety. Major adverse events and negative outcome are correlated with a weak anticoagulation control caused by an ineffective treatment adherence strategy. Solving the issue of oral anticoagulation adherence is possible using new technologies, but future directions should be explored. Mobile phone applications centered on patients’ needs, telemedicine programs that evaluate patients’ evolution and detect adverse reactions or events, encouraging an adequate management of the event without interruption of OACs, represent perspectives with a major impact on treatment adherence.

Recurrent hospitalization after acute coronary syndromes (ACS) is common. Identifying risk factors associated with subsequent cardiovascular events and hospitalization is essential for the management of these patients. Our research consisted in observing the outcomes of subjects after they suffered an acute coronary event and identifying the factors that can predict rehospitalization in the first 12 months and the recurrence of another acute coronary episode. Data from 362 patients admitted with ACS during 2013 were studied. Recurrent hospitalizations were retrospectively reviewed from medical charts and electronic hospital archives over a period of seven years. The mean age of the studied population was 64.57 ± 11.79 years, 64.36% of them being males. The diagnosis of ACS without ST elevation was registered in 53.87% of the patients at index hospitalization. More than half had recurrent hospitalization in the first year after the first ACS episode. Patients with lower ejection fraction (39.20 ± 6.85 vs. 42.24 ± 6.26, p < 0.001), acute pulmonary edema during the first hospitalization (6.47% vs. 1.24%, p = 0.022), coexistent valvular heart disease (69.15% vs. 55.90%, p = 0.017), and three-vessel disease (18.90% vs. 7.45%, p = 0.002) were more frequently readmitted in the following twelve months after their first acute coronary event, while those with complete revascularization were less frequently admitted (24.87% vs. 34.78%, p = 0.005). In multiple regression, complete revascularization during the index event (HR = 0.58, 95% CI 0.35–0.95, p = 0.03) and a higher LVEF (left ventricular ejection fraction) (HR = 0.95, 95% CI 0.92–0.988, p = 0.009) remained independent predictors of fewer early readmissions. Complete revascularization of the coronary lesions at the time of the first event and a preserved LVEF were found to be the predictors of reduced hospitalizations in the first year after an acute coronary event.

Abstract Current therapies for Parkinson’s disease (PD) are palliative, of which the levodopa/carbidopa therapy remains the primary choice but is unable to modulate the progression of neurodegeneration. Due to the complication of such a multifactorial disorder and significant limitations of the therapy, numerous genetic approaches have been proved effective in finding out genes and mechanisms implicated in this disease. Following the observation of a higher frequency of PD in Gaucher’s disease (GD), a lysosomal storage condition, mutations of glycosylceramidase beta (GBA) encoding glucocerebrosidase (GCase) have been shown to be involved and have been explored in the context of PD. GBA mutations are the most common genetic risk factor of PD. Various studies have revealed the relationships between PD and GBA gene mutations, facilitating a better understanding of this disorder. Various hypotheses delineate that the pathological mutations of GBA minimize the enzymatic activity of GCase, which affects the proliferation and clearance of α-synuclein; this affects the lysosomal homeostasis, exacerbating the endoplasmic reticulum stress or encouraging the mitochondrial dysfunction. Identification of the pathological mechanisms underlying the GBA-associated parkinsonism (GBA + PD) advances our understanding of PD. This review based on current literature aims to elucidate various genetic and clinical characteristics correlated with GBA mutations and to identify the numerous pathological processes underlying GBA + PD. We also delineate the therapeutic strategies to interfere with the mutant GCase function for further improvement of the related α-synuclein–GCase crosstalks. Moreover, the various therapeutic approaches such as gene therapy, chaperone proteins, and histone deacetylase inhibitors for the treatment of GBA + PD are discussed.

Diabetes exacerbates the progression of atherosclerosis and is associated with increased risk of developing acute coronary syndrome (ACS). Approximatively 25–30% of patients admitted for ACS have diabetes. ACS occurs earlier in diabetics and is associated with increased mortality and a higher risk of recurrent ischemic events. An increased proinflammatory and prothrombotic state is involved in the poorer outcomes of diabetic patients. In the past decade advancement in both percutaneous coronary intervention (PCI) and coronary artery by-pass graft (CABG) techniques and more potent antiplatelet drugs like prasugrel and ticagrelor improved outcomes of diabetic patients with ACS, but this population still experiences worse outcomes compared to non-diabetic patients. While in ST elevation myocardial infarction urgent PCI is the method of choice for revascularization, in patients with non-ST elevation ACS an early invasive approach is suggested by the guidelines, but in the setting of multivessel (MV) or complex coronary artery disease (CAD) the revascularization strategy is less clear. This review describes the accumulating evidence regarding factors involved in promoting increased incidence and poor prognosis of ACS in patients with diabetes, the evolution over time of prognosis and outcomes, revascularization strategies and antithrombotic therapy studied until now.

Although major advances have occurred lately in medical therapy, ischemic heart failure remains an important cause of death and disability. Viable myocardium represents a cause of reversible ischemic left ventricular dysfunction. Coronary revascularization may improve left ventricular function and prognosis in patients with viable myocardium. Although patients with impaired left ventricular function and multi-vessel coronary artery disease benefit the most from revascularization, they are at high risk of complications related to revascularization procedure. An important element in selecting the patients for myocardial revascularization is the presence of the viable myocardium. Multiple imaging modalities can assess myocardial viability and predict functional improvement after revascularization, with dobutamine stress echocardiography, nuclear imaging tests and magnetic resonance imaging being the most frequently used. However, the role of myocardial viability testing in the management of patients with ischemic heart failure is still controversial due to the failure of randomized controlled trials of revascularization to reveal clear benefits of viability testing. This review summarizes the current knowledge regarding the concept of viable myocardium, depicts the role and tools for viability testing, discusses the research involving this topic and the controversies related to the utility of myocardial viability testing and provides a patient-centered approach for clinical practice.

Accurate estimation of risk with both imaging and biochemical parameters in intermediate risk pulmonary embolism (PE) remains challenging. The aim of the study was to evaluate echocardiographic parameters that reflect right and left heart hemodynamic as predictors of adverse events in intermediate risk PE. This was a retrospective observational study on patients with computed tomography pulmonary angiography diagnosis of PE admitted at Cardiology department of the Clinical Emergency Hospital of Oradea, Romania between January 2018—December 2021. Echocardiographic parameters obtained at admission were studied as predictors of in hospital adverse events. The following adverse outcomes were registered: death, resuscitated cardiac arrest, hemodynamic deterioration and need of rescue thrombolysis. An adverse outcome was present in 50 patients (12.62%). PE related death was registered in 17 patients (4.3%), resuscitated cardiac arrest occurred in 6 patients (1.51%). Another 20 patients (5.05%) required escalation of therapy with thrombolysis and 7 (1.76%) patients developed haemodynamic instability. Echocardiographic independent predictors for in hospital adverse outcome were RV/LV ≥ 1 (HR = 3.599, 95% CI 1.378–9.400, p = 0.009) and VTI ≤ 15 mm (HR = 11.711, 95% CI 4.336–31.633, p < 0.001). The receiver operator curve renders an area under curve for LVOT VTI ≤ 15 mm of 0.792 (95% CI 0.719–0.864, p < 0.001) and for a RV/LV ≥ 1 of 0.746 (95% CI 0.671–0.821, p < 0.001). A combined criterion (LVOT VTI ≤ 15 and RV/LV ≥ 1) showed a positive predictive value of 75% and a negative predictive value of 95% regarding in hospital adverse outcomes. Low LVOT VTI and increased RV/LV are useful for identifying normotensive patients with PE at risk for short term adverse outcomes. Combining an LVOT VTI ≤ 15 cm with a RV/LV ≥ 1 can identify with increased accuracy PE patients with impending risk of clinical deterioration.

A well-functioning immune system of the host body plays pivotal role in the maintenance of ordinary physiological and immunological functions as well as internal environment. Balanced immunity enhances defense mechanism against infection, diseases and unwanted pathogens to avoid hypersensitivity reactions and immune related diseases. The ideal immune responses are the results of corrective interaction between the innate immune cells and acquired components of the immune system. Recently, the interest towards the immune system increased as significant target of toxicity due to exposure of chemicals, drugs and environmental pollutants. Numerous factors are involved in altering the immune responses of the host such as sex, age, stress, malnutrition, alcohol, genetic variability, life styles, environmental-pollutants and chemotherapy exposure. Immunomodulation is any modification of immune responses, often involved induction, amplification, attenuation or inhibition of immune responses. Several synthetic or traditional medicines are available in the market which promptly have many serious adverse effects and create pathogenic resistance. Phytochemicals are naturally occurring molecules, which significantly play an imperative role in modulating favorable immune responses. The present review emphasizes on the risk factors associated with alterations in immune responses, and immunomodulatory activity of phytochemicals specifically, glycosides, alkaloids, phenolic acids, flavonoids, saponins, tannins and sterols and sterolins.

The incidence of the no-reflow (NR) phenomenon varies depending on the diagnostic criteria used. If just the angiographic criteria are considered (i.e., a degree of thrombolysis in myocardial infarction ≤2), it will be found that the incidence of NR is quite low; on the other hand, when the myocardial NR is taken into account (i.e., a decrease in the quality of myocardial reperfusion expressed by the degree of myocardial blush), the real incidence is higher. Thus, the early establishment of a diagnosis of NR and the administration of specific treatment can lead to its reversibility. Otherwise, regardless of the follow-up period, patients with NR have a poor prognosis. In the present work, we offer a comprehensive perspective on diagnostic tools for NR detection, for improving the global management of patients with arterial microvasculature damage, which is a topic of major interest in the cardiology field, due to its complexity and its link with severe clinical outcomes.

Rheumatoid arthritis (RA) is a chronic, systemic, autoimmune disorder, predominantly symmetric, which causes joint inflammation, cartilage degeneration and bone erosion, resulting in deformity and the loss of physical function. Although the management of RA has steadily improved, the pathophysiological mechanism is incompletely elucidated, and therapeutic options are still limited. Due to shortcomings in the efficacy or safety profiles of conventional RA therapies, therapeutic alternatives have been considered. Therefore, natural extracts containing polyphenolic compounds can become promising adjuvant agents for RA global management, due to their antioxidant, anti-inflammatory and apoptotic properties. Polyphenols can regulate intracellular signaling pathways in RA and can generate different immune responses through some key factors (i.e., MAPK, interleukins (ILs 1 and 6), tumor necrosis factor (TNF), nuclear factor light k chain promoter of activated receptor (NF-κB), and c-Jun N-terminal kinases (JNK)). The critical function of the Toll like-receptor (TLR)-dependent mitogen-activating protein kinase (MAPK) signaling pathway in mediating the pathogenic characteristics of RA has been briefly discussed. Oxidative stress can trigger a change in transcription factors, which leads to the different expression of some genes involved in the inflammatory process. This review aims to provide a comprehensive perspective on the efficacy of polyphenols in mitigating RA by inhibiting signaling pathways, suggesting future research perspectives in order to validate their use.

Extensive experimental, clinical, and epidemiological evidence has explained and proven that products of natural origin are significantly important in preventing and/or ameliorating various disorders, including different types of cancer that researchers are extremely focused on. Among these studies on natural active substances, one can distinguish the emphasis on resveratrol and its properties, especially the potential anticancer role. Resveratrol is a natural product proven for its therapeutic activity, with remarkable anti-inflammatory properties. Various other benefits/actions have also been reported, such as cardioprotective, anti-ageing, antioxidant, etc. and its rapid digestion/absorption as well. This review aims to collect and present the latest published studies on resveratrol and its impact on cancer prevention, molecular signals (especially p53 protein participation), and its therapeutic prospects. The most recent information regarding the healing action of resveratrol is presented and concentrated to create an updated database focused on this topic presented above.

The main causes of death in patients with chronic kidney disease (CKD) are of cardiovascular nature. The interaction between traditional cardiovascular risk factors (CVRF) and non-traditional risk factors (RF) triggers various complex pathophysiological mechanisms that will lead to accelerated atherosclerosis in the context of decreased renal function. In terms of mortality, CKD should be considered equivalent to ischemic coronary artery disease (CAD) and properly monitored. Vascular calcification, endothelial dysfunction, oxidative stress, anemia, and inflammatory syndrome represents the main uremic RF triggered by accumulation of the uremic toxins in CKD subjects. Proteinuria that appears due to kidney function decline may initiate an inflammatory status and alteration of the coagulation—fibrinolysis systems, favorizing acute coronary syndromes (ACS) occurrence. All these factors represent potential targets for future therapy that may improve CKD patient’s survival and prevention of CV events. Once installed, the CAD in CKD population is associated with negative outcome and increased mortality rate, that is the reason why discovering the complex pathophysiological connections between the two conditions and a proper control of the uremic RF are crucial and may represent the solutions for influencing the prognostic. Exclusion of CKD subjects from the important trials dealing with ACS and improper use of the therapeutical options because of the declined kidney functioned are issues that need to be surpassed. New ongoing trials with CKD subjects and platelets reactivity studies offers new perspectives for a better clinical approach and the expected results will clarify many aspects.

Non-alcoholic fatty liver disease (NAFLD) has a growing prevalence in recent years. Its association with cardiovascular disease has been intensively studied, and certain correlations have been identified. The connection between these two entities has lately aroused interest regarding therapeutic management. In order to find the best therapeutic options, a detailed understanding of the pathophysiology that links (NAFLD) to cardiovascular comorbidities is needed. This review focuses on the pathogenic mechanisms that are behind these two diseases and on the therapeutic management available at this time.

Clostridioides difficile (CD) is responsible for nosocomial diarrhea syndrome with possible severe progression. Recurrence of the disease induces higher health system costs, as well as exposes patients to additional health risks. Patients with recurrence of this disease are difficult to identify, so the purpose of this study is to quantify various demographic, clinical, and treatment factors that could prevent further progression to recurrence of the disease. In the period 2018–2019, about 195 patients were diagnosed with more than one episode of CDI in the three months following the first episode. The recurrence rate for CDI was 53.84% (60.95% for one episode and 39.05% for multiple episodes). Most commonly afflicted were 60–69-year-old patients, or those with higher Charlson Comorbidity Index (CCI). Multiple analyses associated cardiovascular (odds ratios (OR) = 3.02, 95% confidence intervals (CI) = 1.23–7.39, p = 0.015), digestive (OR = 3.58, 95% CI = 1.01–12.63, p = 0.047), dementia (OR = 3.26, 95% CI = 1.26–8.41, p = 0.014), immunosuppressive (OR = 3.88, 95% CI = 1.34–11.21, p = 0.012) comorbidities with recurrences. Risk factor identification in the first episode of CDI could lead to the implementation of treatment strategies to improve the patients’ quality of life affected by this disease.