Increased thrombolysis in myocardial infarction frame count in patients with myocardial infarction and normal coronary arteriogram: a possible link between slow coronary flow and myocardial infarction

Yetkın, Ertan; Turhan, Hasan; Erbay, Ali Rıza; Aksoy, Yüksel; Şenen, Kubilay

doi:10.1016/j.atherosclerosis.2005.01.005

Cited by 31 publications

(27 citation statements)

References 37 publications

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“…Mean age of the smokers with MI was found to be lower than control subjects [13]. Male predominance in smoking patients with myocardial infarction has been reported by several studies [6,13]. Panagiotakos et al…”

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confidence: 73%

“…Since, NO is inactivated by superoxide anions, which are scavenged by EC-SOD, and smokers have lower EC-SOD levels, it is reasonable to suggest that smoking might increase the coronary tone via oxidative stress related pathway [9][10][11]. Decreased plasma extracellular superoxide dismutase level has also been implicated in male smokers with vasospastic angina and slow coronary flow [10,12].Recently we have been reported that smoking might play a triggering role in patents with slow coronary flow [13]. It has also been reported that smoking results in increased thrombolysis in myocardial infarction frame count indicating harmful effects on coronary vasomotion in patients with angiographically normal coronary arteries [13,14].…”

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confidence: 99%

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Effects of smoking on myocardial infarction at early ages

Yetkın

Tekin

Yağmur

et al. 2007

International Journal of Cardiology

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confidence: 73%

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confidence: 99%

Effects of smoking on myocardial infarction at early ages

Yetkın

Tekin

Yağmur

et al. 2007

International Journal of Cardiology

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“…Yetkin et al [24] have found that patients with myocardial infarction and normal coronary arteries have increased TIMI frame count, indicating the slow coronary flow; compared with subjects without myocardial infarction. They have suggested that SCFP might be the underlying cause of myocardial infarction in those patients.…”

Section: Discussionmentioning

confidence: 99%

Increased platelet activation in patients with slow coronary flow

Çelik

Yuksel²,

Buğan

et al. 2009

J Thromb Thrombolysis

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We tested the hypothesis that increased platelet activation may be present in patients with slow coronary flow (SCF) and may contribute to the pathogenesis of slow coronary flow phenomenon (SCFP). Fifty patients angiographically proven normal coronary flow (control group; mean age = 61.3 +/- 7.0 years, 43 male) and 50 patients with angiographically proven SCF in all coronary arteries (patient group; man age = 62.7 +/- 6.7 years, 38 male) were included in the present study. Coronary flow rates of all subjects were documented by Thrombolysis In Myocardial Infarction frame count (TIMI frame count). Patients with a corrected TIMI frame count greater than two standard deviations from normal published range for the particular vessel were considered as having SCF. Complete blood count and mean platelet volume (MPV) was measured from whole blood sample with Abbott Cell-Dyne 4000 cell counter. Plasma sP-selectin concentrations were analyzed with sP-Selectin ELISA kit. There were no statistically significant differences between the two groups with respect to baseline demographic, clinical and lipid parameters. Not only MPV values but also plasma sP-selectin levels were significantly higher in patients with the patients with SCF compared to those of controls (for MPV; 8.2 +/- 0.7 vs. 7.2 +/- 0.6 fl, P < 0.001, for sP-Selectin; 1.5 +/- 0.3 vs. 1.0 +/- 0.2 ng/ml, P < 0.001). Interestingly, significant positive correlations were detected between mean TIMI frame counts and MPV and sP-selectin levels (for MPV; r = 0.56, P < 0.001, for sP-selectin r = 0.67, P < 0.001). The current study demonstrates that platelet activity is increased in the patients with SCF compared to that of the patients with normal coronary flow.

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“…Abnormal CTFCs in the absence of epicardial narrowing in acute coronary syndromes Yetkin et al have demonstrated that the CTFC was significantly higher in patients with acute myocardial infarction and ''normal'' coronary arteries (those without a stenosis) compared to patients without an MI and normal coronary arteries [45]. The CTFC has also been shown to be significantly higher (slower) in patients with aortic stenosis and normal coronary arteries.…”

Section: Insight Into the Pathophysiology Of Acute Coronary Syndromesmentioning

confidence: 99%