Optic Neuritis in Multiple Sclerosis-A Review of Molecular Mechanisms Involved in the Degenerative Process.

Multiple sclerosis is a central nervous system inflammatory demyelinating disease with a wide range of clinical symptoms, ocular involvement being frequently marked by the presence of optic neuritis (ON). The emergence and progression of ON in multiple sclerosis is based on various pathophysiological mechanisms, disease progression being secondary to inflammation, demyelination, or axonal degeneration. Early identification of changes associated with axonal degeneration or further investigation of the molecular processes underlying remyelination are current concerns of researchers in the field in view of the associated therapeutic potential. This article aims to review and summarize the scientific literature related to the main molecular mechanisms involved in defining ON as well as to analyze existing data in the literature on remyelination strategies in ON and their impact on long-term prognosis.

Novel Biomarkers of Atherosclerotic Vascular Disease-Latest Insights in the Research Field.

The atherosclerotic vascular disease is a cardiovascular continuum in which the main role is attributed to atherosclerosis, from its appearance to its associated complications. The increasing prevalence of cardiovascular risk factors, population ageing, and burden on both the economy and the healthcare system have led to the development of new diagnostic and therapeutic strategies in the field. The better understanding or discovery of new pathophysiological mechanisms and molecules modulating various signaling pathways involved in atherosclerosis have led to the development of potential new biomarkers, with key role in early, subclinical diagnosis. The evolution of technological processes in medicine has shifted the attention of researchers from the profiling of classical risk factors to the identification of new biomarkers such as midregional pro-adrenomedullin, midkine, stromelysin-2, pentraxin 3, inflammasomes, or endothelial cell-derived extracellular vesicles. These molecules are seen as future therapeutic targets associated with decreased morbidity and mortality through early diagnosis of atherosclerotic lesions and future research directions.

Beta-Blocker-Related Atrioventricular Conduction Disorders-A Single Tertiary Referral Center Experience.

Background and Objectives: Drug-related bradyarrhythmia is a well-documented major adverse event among beta-blocker users and a potential cause for hospitalization or additional interventions. Whether beta-blocker use is associated with specific bradyarrhythmia presentations, and how this relates to other predisposing factors, is not well known. We aim to evaluate the association between beta-blocker use and the type of atrioventricular (AV) conduction disorder in patients with symptomatic bradycardia. Materials and Methods: We conducted a retrospective cohort study on 596 patients with a primary diagnosis of symptomatic bradyarrhythmia admitted to a single tertiary referral center. Of the cases analyzed, 253 patients were on beta-blocker treatment at presentation and 343 had no bradycardic treatment. We analyzed demographics, clinical and paraclinical parameters in relation to the identified AV conduction disorder. A multivariate regression analysis was performed to explore factors associated with beta-blocker use. Results: Of the 596 patients (mean age 73.9 ± 8.8 years, 49.2% male), 261 (43.8%) had a third-degree AV block, 92 (15.4%) had a second-degree AV block, 128 (21.5%) had slow atrial fibrillation, 93 (15.6%) had sick sinus syndrome and 21 (3.5%) had sinus bradycardia/sinus pauses. Beta-blocker use was associated with the female gender (p < 0.001), emergency admission (p < 0.001), dilated cardiomyopathy (p = 0.003), the lower left ventricular ejection fraction (p = 0.02), mitral stenosis (p = 0.009), chronic kidney disease (p = 0.02), higher potassium levels (p = 0.04) and QRS duration > 120 ms (p = 0.02). Slow atrial fibrillation (OR = 4.2, p < 0.001), sick sinus syndrome (OR = 2.8, p = 0.001) and sinus bradycardia/pauses (OR = 32.9, p < 0.001) were more likely to be associated with beta-blocker use compared to the most common presentation (third-degree AV block), after adjusting for other patient characteristics. Conclusions: Beta-blocker use is more likely to be associated with slow atrial fibrillation, sick sinus syndrome and sinus bradycardia/pauses, compared to a second- or third-degree AV block, after adjusting for other patient factors such as gender, admission type, ECG, comorbidities, cardiac function and lab testing.

Acute myocardial infarction and extensive systemic thrombosis in thrombotic thrombocytopenic purpura: A case report and review of literature.

BACKGROUND: Thrombotic thrombocytopenic purpura (TTP) is a thrombotic microangiopathy characterized by the pentad of hemolytic anemia, fever, thrombocytopenia, renal failure, and neurological dysfunction. The formation of microthrombi in the arterioles and capillaries of various organs is one of the main pathophysiological mechanisms. Clinical manifestations of cardiac involvement in TTP patients are variable. Acute myocardial infarction has been reported as a complication with TTP as the secondary thrombotic event. Its emergence as the initial thrombotic event is extremely rare. CASE SUMMARY: A 49-year-old previously healthy man was admitted for fever, typical angina chest pain 3 d prior to presentation, and newly onset left lower limb pain. The electrocardiogram illustrated ST-elevation acute myocardial infarction of the antero-lateral wall of the left ventricle. Transthoracic echocardiography depicted two large thrombi at the apex of the left ventricle and moderately reduced ejection fraction (40%). Venous Doppler ultrasound showed occlusion of the left popliteal artery. Laboratory tests showed severe thrombocytopenia, mild hemolytic anemia, elevated D-dimers, and high troponin and creatine kinase-MB. Abdominal computed tomography revealed other thrombotic sites (superior mesenteric artery, posterior aortic wall, spleen and renal infarction, and ileum necrosis). He was immediately started on steroids and addressed to surgery for acute abdominal pain. After an initial stabilization of the hematological deficit, he went into general surgery for resection of the necrotic ileum but died soon after the intervention due to multiple organ failure. CONCLUSION: Cardiac involvement in TTP patients is common, challenging and more often fatal, especially when other thrombotic complications coexist.

The Role of High Triglycerides Level in Predicting Cognitive Impairment: A Review of Current Evidence.

The burden of cognitive disorders is huge and still growing, however the etiology and the degree of cognitive impairment vary considerably. Neurodegenerative and vascular mechanisms were most frequently assessed in patients with dementia. Recent studies have shown the possible involvement of triglycerides levels in cognitive function through putative mechanisms such as brain blood barrier dysfunction or amyloid metabolism imbalance, but not all research in the field found this association. Several clinical studies evaluated the relationship between different forms of cognitive decline and levels of serum triglycerides, independent of other cardiovascular risk factors. This review focuses on the role of triglycerides in cognitive decline, cerebral amyloidosis and vascular impairment. Considering that the management of hypertriglyceridemia benefits from lifestyle modification, diet, and specific drug therapy, future studies are requested to appraise the triglycerides-cognitive impairment relationship.

Uric Acid-An Emergent Risk Marker for Thrombosis?

Hyperuricemia is nowadays an established cardiovascular risk factor. Experimental studies linked elevated serum uric acid (SUA) levels with endothelial dysfunction (ED), inflammation, and prothrombotic state. The purpose of this review is to summarize the current evidence that emphasizes the possible role of uric acid as a biomarker for a prothrombotic state. A large number of clinical trials correlated SUA levels with both incident and recurrent cases of venous thromboembolism (VTE), independent of other confounding risk factors. Moreover, increased SUA levels may be an important tool for the risk stratification of patients with pulmonary embolism (PE). Left atrial thrombosis was correlated with high SUA levels in several studies and its addition to classical risk scores improved their predictive abilities. In patients with acute myocardial infarction (MI), hyperuricemia was associated with increased mortality, and the idea that hyperuricemia may be able to act as a surrogate to unstable coronary plaques was advanced. Finally, SUA was correlated with an increased risk of thromboembolic events in different systemic diseases. In conclusion, uric acid has been considered a marker of a thrombotic milieu in several clinical scenarios. However, this causality is still controversial, and more experimental and clinical data is needed.