European Journal of Cardiovascular Medicine

Introduction Heart failure (HF) is as a clinical condition explained by current or previous complaints like breathlessness, ankle swelling, and tiredness, along with signs like elevated JVP, pulmonary crepitation’s, and peripheral oedema, all of which are caused by an anatomical and/ or physiological cardiac abnormality and confirmed by at least 1 of the following: raised BNP levels or verifiable evidence of respiratory, cardiac or systemic congestion Materials And Methods This is a observational study was conducted in the Department of General Medicine, Mahavir Institute of Medical Sciences. Two hundred twenty patients who were admitted to the ICU and who underwent the measurement of serum UA were enrolled in this study. AHF was defined as either new-onset HF or the decompensation of chronic HF with symptoms sufficient to warrant hospitalization. HF was diagnosed according to the Framingham criteria for a clinical diagnosis of HF, based on the fulfilment of two major criteria or one major and two minor criteria. Results  Age was not significantly associated with uric acid levels (P=0.153). However, a trend was observed where patients aged 71-80 years had the highest proportion of high uric acid (75%), while those aged 41-50 years had a lower proportion (28.57%). Men and women had similar uric acid levels (P=0.550). Patients with COPD, dilated cardiomyopathy, and coronary artery disease had slightly higher uric acid levels, but the association was not statistically significant. Among co-morbidities, diabetes, hypertension, smoking, and alcohol consumption were not significantly different between high and low uric acid groups. However, patients with high uric acid had significantly higher rates of ICU admission (93.55%) and mortality (94.40%), suggesting a strong association between elevated uric acid and worse clinical outcomes. Conclusion This study confirms that elevated serum uric acid is an independent predictor of worse clinical outcomes in CHF. Patients with higher UA levels have more severe disease, increased ICU admission, and significantly worse survival rates. Given these findings, uric acid measurement should be integrated into routine CHF risk stratification. Future research should explore whether lowering UA can directly improve patient outcomes and reduce cardiovascular mortality.

              

Angiogenesis research has grown extensively over the past few decades with the recognition that angiogenesis plays a key role in embryonic development, wound healing, and also pathological conditions such as tumor metastasis. Numerous in vitro angiogenesis assays have been designed to mimic in vivo angiogenesis process. The in vitro assays are quick, simple, quantitative, and cost-effective, and have thereby played valuable roles in evaluation of the effects of test compounds on angiogenesis. However, each in vitro assay represents an individual step of a complex angiogenic cascade. Furthermore, significant diversities exist within endothelial cell types and within basement membrane extracts used in the assays. Thus, choosing appropriate cell types and assay conditions that most closely resemble the disease-specific angiogenesis being studied is essential to obtain meaningful results. Performing multiple in vitro assays together should also be considered to get data that is translatable from the preclinical to the clinical stage. For these reasons, increasing our understanding of in vitro assays is necessary for proper assay performance as well as correct interpretation of the results. Here we discuss two main critical factors regarding endothelial cell types and basement membrane extracts that are known to largely affect in vitro angiogenesis assays. We also introduce recent improvements in the most widely-used in vitro angiogenesis assays, which are 2-dimensional (2D) tube formation assays and 3-dimensional (3D) spheroid angiogenesis assay.

Objective: This study was conducted to develop and determine the validity and reliability of a bilingual psychometric instrument for assessment of knowledge, attitude, self-care practice and health-related quality of life (HRQoL) (KAPQ-HF) among Malaysian heart failure (HF) patients.

Over the past decade, molecular details of lymphatic vessels (lymphatics) have been rapidly acquired due to the identification of lymphatic endothelial-specific markers. Separate from the cardiovascular system, the lymphatic system is also an elaborate network of vessels that are important in normal physiology. Lymphatic vessels have the unique task to regulate fluid homeostasis, assist in immune surveillance, and transport dietary lipids. However, dysfunctional lymphatic vessels can cause pathology, while normal lymphatics can exacerbate pathology. This review summarizes the development and growth of lymphatic vessels in addition to highlighting their critical roles in physiology and pathology. Also, we discuss recent work that suggests a connection between lymphatic dysfunction and cardiovascular disease.

Endothelial dysfunction is a key event in the development of vascular disease, and it precedes clinically obvious vascular pathology. Abnormal activation of the RhoA/Rho kinase (ROCK) pathway has been found to elevate vascular tone through unbalancing the production of vasodilating and vasoconstricting substances. Inhibition of the RhoA/ROCK pathway can prevent endothelial dysfunction in a variety of pathological conditions. This review, based on recent molecular, cellular, and animal studies, focuses on the current understanding of the ROCK pathway and its roles in endothelial dysfunction.