206 Coronary endothelial dysfunction in patients with chest pain and normal coronary arteriograms is explained by factors known to affect endothelial function

1999 ◽  
Vol 1 ◽  
pp. S38-S38
Author(s):  
B KRISTENSEN ◽  
H SONNE ◽  
H BOTKER ◽  
N ANDERSEN
Keyword(s):  
Chest Pain ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Coronary Endothelial Dysfunction

Prognostic Impact of Coronary Endothelial Dysfunction on Long-Term Adverse Outcome in Patients with Chest Pain and Non-Obstructive Coronary Artery Disease

2013 ◽  
Vol 23 (1) ◽  
pp. 114-119
Author(s):  
Dalia Jarašūnienė ◽  
Ernesta Susekaitė ◽  
Nerijus Klimas
Keyword(s):  
Chest Pain ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Adverse Outcome ◽  
Obstructive Coronary Artery Disease ◽  
Coronary Intervention ◽  
Cardiovascular Death ◽  
Prognostic Impact ◽  
Coronary Endothelial Dysfunction

Coronary endothelial dysfunction is known to be related with adverse cardiovascular outcome. We obtained a long-term follow-up of patients without significant coronary atherosclerosis, complaining of chest pain, in whom intra-coronary acetylene testing was performed in order to assess endothelial function. The study included 41 patient (35 with endothelial dysfunction, 6 with preserved endothelial function). Events considered as adverse outcome were cardiovascular death, acute myocardium-dial infarction, unstable angina pectoris, percutaneous coronary intervention, coronary-aortic by-pass grafting, ischemic stroke and peripheral artery re-vascularization. A high cardiovascular event rate was observed in patients with and without endothelial dysfunction, 34,3% and 50% respectively. Adverse outcome was related not only to endothelial dysfunction but also to traditional cardiovascular risk factors. Thus, evaluation of endothelial function or its determinants seems to be helpful in identifying a subgroup of patients at high risk.

Abstract 17182: Coronary Endothelial Dysfunction in Humans is Associated With Elevated Expression of Clonal Hematopoiesis of Indeterminate Potential

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Morsaleh Ganji ◽  
Terra Lasho ◽  
Takumi Toya ◽  
Ali Ahmed ◽  
Michel Corban ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Dna Methyltransferase ◽  
Early Stage ◽  
Gene Mutations ◽  
Control Group ◽  
Clonal Hematopoiesis ◽  
Cytokine Analysis ◽  
Coronary Endothelial Dysfunction

Introduction: Recent evidence has demonstrated that Clonal Hematopoiesis of Indeterminate Potential (CHIP) increases the risk of cardiovascular events. However, the exact role played by CHIP in early stages of coronary atherosclerosis, characterized by coronary endothelial dysfunction remains to be elucidated. Hypothesis: The current study was designed to test the hypothesis that the presence of CHIP in peripheral blood cells is associated with coronary endothelial dysfunction and increased levels of inflammatory markers. Methods: Next generation sequencing was used to detect mutations among patients who had coronary endothelial dysfunction and control group (normal coronary endothelial function). Endothelial dysfunction was defined by ≥ 20% decrease in coronary artery diameter or ≤50% increase in blood flow in response to acetylcholine injection compared to baseline. Plasma cytokine levels of Interleukin (IL)-6 and IL-8 were also assessed. Results: Clonal hematopoiesis relevant gene mutations were found in 1 out of 64 patients with normal endothelial function (1.5%) and 11 out of 119 cases in the endothelial dysfunction group (9.2%) (P = 0.04) with ASXL1 (Additional sex combs-like 1) being the most frequent gene (4.2%) mutated. Cytokine analysis demonstrated that mutations in ASXL1, DNMT3A (DNA methyltransferase 3A) and TET2 (Ten-eleven-translocation-2) in the endothelial dysfunction group were associated with increased levels of IL-6 and IL-8 (P = 0.001, P = 0.003; respectively). Conclusions: The current study supports a potential role for CHIP in mechanisms of coronary artery disease starting at early stage of atherosclerosis. Furthermore, enhanced expression levels of IL-6 and IL-8 seem to be related to mutations in DNMT3A, ASXL1 and TET2 genes, more than other gene mutations relevant CHIP.

Coronary endothelial function

2021 ◽  
pp. 13-16
Author(s):  
R. Jay Widmer ◽  
Amir Lerman
Keyword(s):  
Coronary Artery Disease ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Obstructive Coronary Artery Disease ◽  
Prognostic Significance ◽  
Vascular Responses ◽  
Catheterization Laboratory ◽  
Coronary Endothelial Function ◽  
Artery Disease ◽  
Coronary Endothelial Dysfunction

The assessment of coronary endothelial function has profound importance in terms of diagnostic and prognostic significance in patients with both obstructive and non-obstructive coronary artery disease. Endothelial dysfunction may take place in both epicardial coronary arteries as well as in the coronary microcirculation. Epicardial coronary endothelial dysfunction can be detected in the catheterization laboratory with abnormal vascular responses to endothelial-dependent physiological or pharmacological stimuli, and is characteristically a precursor to the initial processes of atherosclerotic coronary disease. This chapter discusses coronary endothelial physiology, the prevalence of endothelial dysfunction, how to evaluate coronary endothelial function, and the prognosis for patients with endothelial dysfunction.

Rosuvastatin provides pleiotropic protection against pulmonary hypertension, right ventricular hypertrophy, and coronary endothelial dysfunction in rats

2008 ◽  
Vol 294 (2) ◽  
pp. H801-H809 ◽  
Author(s):  
Xiaowei Sun ◽  
David D. Ku
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Right Ventricular Hypertrophy ◽  
Coronary Endothelial Function ◽  
Novel Approach ◽  
Endothelial Nitric Oxide ◽  
Coronary Endothelial Dysfunction

We recently reported that increased vascular endothelial nitric oxide production could protect against the development of monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH) and right ventricular hypertrophy (RVH) in rats ( 32 ). The present study investigated whether the pleiotropic action of 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors in upregulating endothelial function could also protect against the MCT-induced end-organ damages. Rosuvastatin (2 mg·kg−1·day−1 via oral gavage) or placebo was initiated 1 wk before or 1 wk after MCT (60 mg/kg ip) administration. One month after MCT, significant PAH developed in the placebo rats, which were accompanied by histological evidence of pulmonary vascular thickening and right ventricular hypertrophy. The coronary endothelial vasodilatory function, assessed with endothelial/nitric oxide-dependent responses to acetylcholine and NG-nitro-l-arginine methyl ester (l-NAME), was depressed, while the constrictory responses to known coronary constrictors was enhanced. In rats that received rosuvastatin treatment 1 wk before MCT administration, a significantly reduced PAH and RVH was observed, as well as reduced pulmonary vascular and right ventricular remodelings. Rosuvastatin 1-wk posttreatment had no effect on PAH, but inhibited RVH. Right coronary endothelial dysfunction, which was shown in placebo rats, was effectively prevented by both pre- and postrosuvastatin treatment, while this effect was more dramatic in the pretreated group. Left coronary endothelial function, which was not affected by MCT, also showed an upregulation by rosuvastatin. Taken together, our results demonstrated the pleiotropic protection of rosuvastatin against the development of PAH and RVH and confirmed our previous finding that the targeted preservation of coronary endothelial function and vasoactivity may provide a novel approach to protect against cardiac remodeling.

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