1.The Independent Relationship of Systemic Inflammation With Fragmented QRS Complexes in Patients With Acute Coronary Syndromes.
Mustafa CETIN ; Sinan Altan KOCAMAN ; Turan ERDOGAN ; Aytun CANGA ; Murtaza Emre DURAKOGLUGIL ; Omer SATIROGLU ; Ozgur AKGUL ; Tuncay KIRIS ; Yuksel CICEK ; Baris YAYLAK ; Sitki DOGAN ; Ismail SAHIN ; Mehmet BOSTAN
Korean Circulation Journal 2012;42(7):449-457
BACKGROUND AND OBJECTIVES: QRS complex fragmentations are frequently seen on routine electrocardiograms with narrow or wide QRS complex. Fragmented QRS complex (fQRS) is associated with increased morbidity and mortality, sudden cardiac death and recurrent cardiovascular events. In this study, we aimed to interrogate the relationship of systemic inflammation with the presence of fQRS in patients with acute coronary syndromes (ACS). SUBJECTS AND METHODS: Two-hundred and twenty eligible patients with ACS that underwent coronary angiography were enrolled consecutively in this study. Patients with significant organic valve disease and those with any QRS morphology that had a QRS duration > or =120 ms as well as patients with permanent pacemakers were excluded from this study. RESULTS: Patients with fQRS were of a higher age (p=0.02), had increased C-reactive protein (CRP) levels (p<0.001), prolonged QRS time (p<0.001), extent of coronary artery disease (CAD) (p<0.001), creatine kinase-MB (CK-MB) levels (p=0.006) and Q wave on admission electrocardiography (p<0.001) in comparison to patients with non-fragmented QRS. When we performed multiple logistic regression analysis, fQRS was found to be related to increased CRP levels {odds ratio (OR): 1.2, 95% confidence interval (CI): 1.045-1.316, p=0.007}, QRS duration (OR: 1.1, 95% CI: 1.033-1.098, p<0.001), extent of CAD (OR: 1.5, 95% CI: 1.023-2.144, p=0.037), Q wave (OR: 2.2, 95% CI: 1.084-4.598, p=0.03) and CK-MB levels (OR: 1.0, 95% CI: 1.001-1.037, p=0.04) independently. CONCLUSION: In our study, we found that fQRS was independently related to increased CRP. Fragmented QRS that may result as an end effect of inflammation at cellular level can represent increased cardiac risk by different causative mechanisms in patients with ACS.
Acute Coronary Syndrome
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C-Reactive Protein
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Coronary Angiography
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Coronary Artery Disease
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Creatine
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Death, Sudden, Cardiac
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Electrocardiography
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Humans
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Inflammation
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Logistic Models
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Risk Assessment