The association of coronary flow changes and inflammatory indices to ischaemia–reperfusion microvascular damage and left ventricular remodelling

Bramos, Dimitris; Ikonomidis, Ignatios; Tsirikos, Nikolaos; Kottis, G. K.; Kostopoulou, Vasiliki; Pamboucas, Constantinos; Papadopoulou, Elektra; Venetsanou, Kyriaki; Γιατράκος, Νικόλαος; Yang, Guang‐Zhong; Nihoyannopoulos, Petros; Toumanidis, Savvas

doi:10.1007/s00395-008-0720-5

Cited by 21 publications

(16 citation statements)

References 49 publications

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“…In the case of hypovolemic shock (caused, e.g., by a significant blood loss, and accompanied by pronounced hypotension), the changes in microcirculation are, at least, not completely independent from the hemodynamic parameters. The hemodynamic parameters are correlated with the “no-reflow” phenomenon [17, 18]. One of the definitions of the “no-reflow” phenomenon is incomplete and nonunified reperfusion at the microcirculatory level, despite an adequate reopening of the proximal artery after a period of transient ischemia [19].…”

Section: Disturbances Of Microcirculation No-reflow Phenomenonmentioning

confidence: 99%

No-Reflow Phenomenon and Endothelial Glycocalyx of Microcirculation

Maksimenko

Турашев

2012

Biochemistry Research International

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The progress in reperfusion therapy dictated the necessity for developing new tools and procedures for adjacent/additional therapy of acute cardiovascular disorders. The adjacent therapy is targeted on the damage of the microcirculation, leading to the unfavorable prognosis for the patients. The no-reflow phenomenon holds special place in the multifactorial etiology of the microcirculation disorders, offering a new challenge in treating the patients associated with ST-segment elevation on ECG at myocardial infarction. One of the numerous causes of no-reflow, the influence of the endothelial glycocalyx of the microcirculation, is analyzed. The results obtained in the studies of the endothelial glycocalyx ultrastructure are generalized, the effect that the fragments of the glycocalyx glycosaminoglycans have on the function of the vascular wall is demonstrated. The trends in searching for correlations between the thickness of the capillary glycocalyx and the cardiovascular disease risk are noted.

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Section: Disturbances Of Microcirculation No-reflow Phenomenonmentioning

confidence: 99%

No-Reflow Phenomenon and Endothelial Glycocalyx of Microcirculation

Maksimenko

Турашев

2012

Biochemistry Research International

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“…Cytokines [e.g., tumor necrosis factor-α (TNF), interlukin-1 (IL-1) and IL-2] are postulated as mediators of ischemia/reperfusion (I/R) [5, 21, 34, 42, 45]. These factors are of direct relevance to endothelial dysfunction, since cytokines exert a prominent anti-endothelium-derived relaxing factor effect in blood vessels [2, 21].…”

Section: Introductionmentioning

confidence: 99%

Direct relationship between levels of TNF-α expression and endothelial dysfunction in reperfusion injury

Zhang

et al. 2010

Basic Res Cardiol

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We previously found that myocardial ischemia/reperfusion (I/R) initiates expression of tumor necrosis factor-α (TNF) leading to coronary endothelial dysfunction. However, it is not clear whether there is a direct relationship between levels of TNF expression and endothelial dysfunction in reperfusion injury. We studied levels of TNF expression by using different transgenic animals expressing varying amounts of TNF in I/R. We crossed TNF overexpression (TNF ++/++ ) with TNF knockout (TNF −/− ) mice; thus we have a heterozygote population of mice with the expression of TNF "in between" the TNF −/− and TNF ++/++ mice. Mouse hearts were subjected to 30 min of global ischemia followed by 90 min of reperfusion and their vasoactivity before and after I/R was examined in wild type (WT), TNF −/− , TNF ++/++ and TNF heterozygote (TNF −/++ , cross between TNF −/− and TNF ++/++ ) mice. In heterozygote TNF −/++ mice with intermediate cardiac-specific expression of TNF, acetylcholine-induced or flow-induced endothelial-dependent vasodilation following I/R was between TNF ++/++ and TNF −/− following I/R. Neutralizing antibodies to TNF administered immediately before the onset of reperfusion-preserved endothelial-dependent dilation following I/R in WT, TNF −/++ and TNF ++/++ mice. In WT, TNF −/++ and TNF ++/++ mice, I/R-induced endothelial dysfunction was progressively lessened by administration of free-radical scavenger TEMPOL immediately before initiating reperfusion. During I/R, production of superoxide (O 2 ·− ) was greatest in TNF ++/++ mice as compared to WT, TNF −/++ and TNF −/− mice. Following I/R, arginase mRNA expression was elevated in the WT, substantially elevated in the TNF −/++ and TNF ++/++ mice and not affected in the TNF −/− mice. These results suggest that the level of TNF expression determines arginase expression in endothelial cells during myocardial I/R, which is one of the mechanisms by which TNF compromises coronary endothelial function in reperfusion injury.

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“…We have previously shown in experimental AMI, that the greater the increase of coronary flow during reperfusion the greater the microvascular injury, as assessed by MCE 10. Additionally, the adverse effects of excessive hyperaemia during coronary reflow were associated with adverse LV remodelling 10.…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, the adverse effects of excessive hyperaemia during coronary reflow were associated with adverse LV remodelling 10. Thus, an intervention aiming to reduce the excessive hyperaemia during reperfusion may contribute to the reduction of microvascular injury leading to preservation of myocardial function in patients with AMI or unstable angina 16.…”

Section: Discussionmentioning

confidence: 99%

Staccato reperfusion improves myocardial microcirculatory function and long-term left ventricular remodelling: a randomised contrast echocardiography study

Ikonomidis

Iliodromitis

Tzortzis

et al. 2010

Heart

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The association of coronary flow changes and inflammatory indices to ischaemia–reperfusion microvascular damage and left ventricular remodelling

Abstract: Changes of mean diastolic CF and IL-6 cs are associated with alterations in myocardial microvascular integrity after ischaemia-reperfusion and may be used as a predictor of myocardial dysfunction.

Cited by 21 publications

References 49 publications

No-Reflow Phenomenon and Endothelial Glycocalyx of Microcirculation

No-Reflow Phenomenon and Endothelial Glycocalyx of Microcirculation

Direct relationship between levels of TNF-α expression and endothelial dysfunction in reperfusion injury

Staccato reperfusion improves myocardial microcirculatory function and long-term left ventricular remodelling: a randomised contrast echocardiography study

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