Key result
Coronary slow flow was independently associated with a significantly higher prevalence of fragmented QRS on 12-lead ECG compared to normal coronary flow (31.7% vs 6.8%, OR 10.848).
Why the study?
Does coronary slow flow increase the presence of fragmented QRS on 12-lead ECG in patients with normal epicardial coronary arteries?
Observational (n=104)
Single-blind
No
Does coronary slow flow increase the presence of fragmented QRS on 12-lead ECG in patients with normal epicardial coronary arteries?
Odds Ratio: 10.848 (95% CI 2.385–49.347)
Absolute Event Rate: 31.7% vs 6.8%
p-value: p=0.002
Coronary slow flow is independently associated with the presence of fragmented QRS on 12-lead ECG, suggesting potential subclinical myocardial damage or altered depolarization in these patients.
BACKGROUND: Coronary slow flow (CSF) is characterised by delayed opacification of coronary arteries in the absence of epicardial occlusive disease. It has been reported that CSF may cause angina, myocardial ischaemia, and infarction. Fragmentation of QRS complex (fQRS) is an easily evaluated non-invasive electrocardiographic parameter. It has been associated with alternation of myocardial activation due to myocardial scar and/or ischaemia. Whether CSF is associated with fQRS is unknown. The presence of fQRS on ECG may be an indicator of myocardial damage in patients with CSF. AIM: To investigate the presence of fQRS in patients with CSF. METHODS: Sixty patients (mean age 55.5 ± 10.5 years) with CSF and 44 patients with normal coronary arteries without associated CSF (mean age 53 ± 8.4 years) were included in this study. The fQRS was defined as the presence of an additional R wave or notching of R or S wave or the presence of fragmentation in two contiguous leads corresponding to a major coronary artery territory. RESULTS: The presence of fQRS was higher in the CSF group than in the controls (p = 0.005). Hypertension was significantly more common in the CSF group (p < 0.001). There was no significant association between the presence of fQRS and an increasing number of vessel involvements. Logistic regression analysis demonstrated that the presence of CSF was the independent determinant of fQRS (OR = 10.848; 95% CI 2.385-49.347; p = 0.002). CONCLUSIONS: Fragmented QRS, indicating increased risk for arrhythmias and cardiovascular mortality, was found to be significantly higher in patients with CSF. We have not found an association between the presence of fragmented QRS and the degree of CSF. Further prospective studies are needed to establish the significance as a possible new risk factor in patients with CSF.
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Yılmaz et al. (2014) conducted an observational in Coronary slow flow (n=104). Coronary slow flow vs. Normal coronary flow was evaluated on Presence of fragmented QRS (fQRS) (OR 10.848, 95% CI 2.385-49.347, p=0.002). Coronary slow flow was independently associated with a significantly higher prevalence of fragmented QRS on 12-lead ECG compared to normal coronary flow (31.7% vs 6.8%, OR 10.848).
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