Endothelial Dysfunction and Damage in Congestive Heart Failure

Abstract

Background-Congestive heart failure (CHF) is associated with endothelial perturbation (as defined by flow-mediated endothelial-dependent vasodilation [FMD, an index of endothelial dysfunction], circulating endothelial cells [CECs, an index of endothelial damage], or plasma indexes of endothelial damage/dysfunction [eg, von Willebrand factor (vWf) and soluble thrombomodulin (sTM)]) and raised plasma levels of brain natriuretic peptide (BNP, a peptide hormone associated with left ventricular systolic dysfunction and prognosis). However, the relations between these parameters are unclear. Methods and Results-To test the hypothesis that there is a relation between endothelial perturbation (defined by FMD, CECs, vWf, and sTM) and BNP in CHF, we studied these indexes in 30 patients with CHF who were compared with 20 age-matched control subjects. FMD, CECs, plasma vWf, and BNP levels (but not sTM) were all abnormal in patients with CHF. There were significant inverse correlations between FMD and vWf (Pϭ0.001), CECs (Pϭ0.002) and BNP (Pϭ0.006) as well as a positive correlation between CECs and vWf (Pϭ0.032). In multivariate analysis, BNP (PϽ0.001) and FMD (PϽ0.001) were both independently associated with CHF. Conclusions-Ample evidence of endothelial cell damage/dysfunction in CHF cannot be fully explained by the variance in plasma BNP per se. Therefore, the routes by which these indexes influence the pathophysiology of CHF as well as predict adverse outcomes may be independent.

Circulating Endothelial Cells and Endothelial Progenitor Cells in Obstructive Sleep Apnea

“…First, the numbers of CECs and circulating EPCs that can be identified from peripheral blood samples are small, even in patients with cardiovascular disease [19]. The number of CECs in control subjects is similar to that reported by others [7][8][9]. Thus, due to the relatively rare event analysis, the sample sizes in this study may have been too small to detect differences.…”

“…There is growing evidence that patients with obstructive sleep apnea (OSA) have evidence of endothelial dysfunction, as assessed by functional measures such as endothelial-dependent vasodilation [5,6]. Circulating endothelial cells (CECs) have been reported to be increased in a variety of conditions in which vascular injury might be expected, such as sickle cell anemia with crisis [7], acute coronary syndrome [8], congestive heart failure [9], both primary and secondary pulmonary hypertension [10], and systemic sclerosis [11]. It is possible that detached circulating endothelial cells are a marker for vascular endothelial cell damage and thus might be elevated in patients with OSA.…”

Relation of Brain Natriuretic Peptide Levels to Cognitive Dysfunction in Adults >55 Years of Age With Cardiovascular Disease

“…High levels of BNP are associated with reduced endothelial function, particularly in patients with heart failure. 15 In turn, endothelial abnormalities have recently been linked to cerebrovascular disease and reduced cognitive function. 9,16,17 Further research is needed to clarify the relation between BNP and these possible mechanisms.…”

Ambient particulate matter exposure and cardiovascular diseases: a focus on progenitor and stem cells

“…Endothelial dysfunction or injury is considered one of the major factors that contribute to the development of cardiovascular diseases like atherosclerosis 11, coronary heart disease 12, congestive heart failure 40, 41, 42 and periphery artery disease 43. Bone marrow‐derived EPCs play a critical role in vascular re‐endothelialization, angiogenesis and prevention of neointima formation after vascular injury 13, 15, 44.…”

“…Thus, the level of circulating EPCs has been an important and independent predictor for cardiovascular outcome in CAD patients 45, and it is crucial to preserve the number and function of EPCs at a healthy level for the normal functionality of vasculature in patients with cardiovascular diseases. A variety of factors are critically involved in the regulation of the in vivo dynamics of EPC number and function, including (but not limited to) cytokines and growth factors like granulocyte‐stimulating colony stimulating factor and VEGF 40, 41, 42, nitric oxide, pharmacological agents like statins 49 and environmental factors like air pollution 19, 50. Some disease states like hyperlipidaemia, DM, inflammation, oxidative stress, ischaemia and chronic heart failure are also important for the dynamic changes of EPCs in vivo 19, 51, 52, 53, 54.…”