Elsevier

Atherosclerosis

Volume 233, Issue 2, April 2014, Pages 636-640
Atherosclerosis

Coronary artery ectasia is related to coronary slow flow and inflammatory activation

https://doi.org/10.1016/j.atherosclerosis.2014.01.018Get rights and content

Highlights

  • Coronary artery ectasia extension is related to impairment of coronary flow.

  • Coronary artery ectasia extension is related to inflammatory activation.

  • Inflammatory response is related to impaired coronary flow in coronary ectasia.

Abstract

Aim

To evaluate possible links between coronary flow anomalies, inflammatory activation and coronary artery ectasia (CAE).

Methods

Fourteen consecutive patients with CAE diagnosed at coronary angiography were enrolled in the study and compared with 17 patients with coronary atherosclerosis without CAE and 15 controls with normal coronary angiography. All patients underwent blood assay with evaluation of circulating levels of interleukin (IL)-1b, IL-2, IL-8, IL-10 and tumor-necrosis-factor(TNF)-α. The number of coronary segments showing CAE at coronary angiography, the Markis class, and coronary flow assessed with TIMI frame count (TFC) were also assessed.

Results

Subjects with CAE showed higher levels of IL-1b, TNF-α, and IL-10 (p < 0.05).

The number of coronary segments showing CAE was related to TFC both in left anterior descending (LAD) coronary artery (p < 0.01) and in right coronary artery (RCA) (p < 0.001), and to circulating levels of IL-1b and IL-10 (p < 0.01). TFC on LAD (p < 0.05) and on RCA (p < 0.001), circulating IL-1b levels (p < 0.01), IL-8 (p < 0.05), and IL-10 (p < 0.01) were proportionally increased comparing controls, subjects with coronary atherosclerosis without CAE, and with decreasing Markis class.

In subjects with CAE involving LAD, TFC on LAD was related to IL-8 and TNF-α levels (p < 0.05); subjects with IL-1b levels above median showed higher TFC values on LAD (p < 0.01),

Conclusions

In subjects with CAE, the extension of disease is related to the impairment of coronary circulation and to inflammatory activation. The inflammatory response is also related to an impaired coronary circulation.

Section snippets

Background

Etiology and progression of atherosclerosis are characterized by the activation of inflammatory mechanisms [1], [2]; also coronary complications of atherosclerosis may present with an inflammatory activation [3], [4], [5]. Increased levels of C-reactive protein (CRP) and acute phase proteins are detectable in the acute phase of acute myocardial infarction (AMI) and may predict the risk of future adverse events [3], [6].

Coronary artery ectasia (CAE), a variant of coronary atherosclerosis

Methods

Fourteen consecutive patients with CAE diagnosed at coronary angiography were enrolled in the study and compared with 17 patients with coronary atherosclerosis without CAE and 15 controls with normal coronary angiography.

CAE was defined as the diameter of the ectatic segment being more than 1.5 times larger compared with an adjacent healthy reference segment [7], [13], as in prior studies.

All patients underwent blood assay with evaluation of circulating levels of interleukin (IL)-1b, IL-2,

Statistical analysis

The results were expressed as mean value ± standard deviation for continuous variable or percentage for dichotomic variable. Variables were tested for normality with Kolmogorov–Smirnov and Lilliefors and compared with Student's t test, Mann–Whitney U-test, or χ2 test as required.

Correlations were analyzed using Pearson's or Spearman correlation test as required. Entered and stepwise multiple regression analysis was used to analyze variables affecting cytokines levels, including confounding

Results

Population's characteristics are given in Table 1. Markis class IV CAE was found in 42.9% of subjects with CAE, class III in 21.4%, class II in 28.6%, and class I in 7.1%.

The CAE group showed higher rates of subjects with circulating levels of IL-1b (r = 0.36, p for trend < 0.05, Fig. 1) and TNF-α (r = 0.30, p < 0.05, Fig. 1) above upper level of normal (ULN) and higher circulating levels of IL-10 (p < 0.05, Fig. 2) in comparison to coronary atherosclerosis without CAE group and controls: the number of

Discussion

We showed in this study several links between CAE presence and severity, anomalies in coronary flow and inflammatory response.

Our findings provide further evidence that subjects with CAE are characterized by increased circulating levels of inflammatory markers. Turban et al. previously found increased CRP levels in subjects with CAE [8].

In a study by Turhan et al. patients with isolated CAE showed higher expression of plasma soluble adhesion molecules, intercellular adhesion molecule-1 and

Limitations

Principal limitation of our study is the small number of patients enrolled; further studies involving a larger number of subjects are needed in order to confirm these preliminary data and define a possible prognostic role of inflammatory activation. All the subjects in the CAE group were male: further data are required also from female populations.

Most subjects with CAE enrolled in the study showed ectasia on RCA: a more balanced population with more cases of CAE on left coronary artery is

Conclusions

In subjects with CAE, the extension of disease is related to the impairment of coronary circulation and inflammatory activation. The inflammatory response is also related to an impaired coronary circulation.

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