BACKGROUND: Fragmented QRS (fQRS) complexes are defined as various RSR' patterns (≥1 R' or notching of S wave or R wave) in two contiguous leads corresponding to a major coronary artery territory. In previous studies, fQRS has been associated with increased morbidity and mortality, sudden cardiac death and recurrent cardiovascular events (CVEs). The causative relationship between fQRS and cardiac fibrosis has been shown in prior studies. The association between inadequate (poor) coronary collaterals and presence of fQRS has not comprehensively been studied in patients with chronic total occlusion (CTO) until now. We tested the hypothesis that the presence of fQRS is associated with inadequate coronary collateral growth. METHODS: This study had a cross-sectional observational design. The study population consisted of patients who underwent coronary angiography with the suspicion of coronary artery disease at our institution in an outpatient manner. Patients who had CTO in at least one major epicardial coronary artery were included. Coronary angiograms of 148 eligible patients from our database were analyzed again. Ninety-three patients had good and 55 had poor collateral development according to the Cohen-Rentrop method. RESULTS: Patients with poor collateral development had higher plasma glucose (130 ± 54 vs. 116 ± 33 mg/dl, P = 0.047) and an older age (65 ± 10 vs. 61 ± 10 years, P = 0.042) in comparison to patients with good collateral growth. The presence and number of fQRS were higher in the poor collateral group than the good collateral group (64 vs. 32%, P < 0.001 and 2.3 ± 2.4 vs. 1.2 ± 2.0, P = 0.002, respectively). Left ventricular ejection fraction was significantly lower in the poor collateral group than the good collateral group (45 ± 11 vs. 51 ± 13, P = 0.014). There was a significant correlation between number of fQRSs and the echocardiographic wall-motion abnormality score (r = 0.662, P < 0.001). In multivariate analysis, only the presence of fQRS was independently related to poor collateral development (odds ratio, 3.559; 95% confidence interval, 1.708-7.415, P = 0.001). CONCLUSION: We found that fQRS was independently related to inadequate coronary collaterals in patients with CTO. fQRS, which may be derived from the effects of myocardial ischemia or scar on myocardial electricity at the cellular level, can represent inadequate coronary collateral development in patients with CTO.
BACKGROUND: Fragmented QRS (fQRS) complexes are defined as various RSR' patterns (≥1 R' or notching of S wave or R wave) in two contiguous leads corresponding to a major coronary artery territory. In previous studies, fQRS has been associated with increased morbidity and mortality, sudden cardiac death and recurrent cardiovascular events (CVEs). The causative relationship between fQRS and cardiac fibrosis has been shown in prior studies. The association between inadequate (poor) coronary collaterals and presence of fQRS has not comprehensively been studied in patients with chronic total occlusion (CTO) until now. We tested the hypothesis that the presence of fQRS is associated with inadequate coronary collateral growth. METHODS: This study had a cross-sectional observational design. The study population consisted of patients who underwent coronary angiography with the suspicion of coronary artery disease at our institution in an outpatient manner. Patients who had CTO in at least one major epicardial coronary artery were included. Coronary angiograms of 148 eligible patients from our database were analyzed again. Ninety-three patients had good and 55 had poor collateral development according to the Cohen-Rentrop method. RESULTS:Patients with poor collateral development had higher plasma glucose (130 ± 54 vs. 116 ± 33 mg/dl, P = 0.047) and an older age (65 ± 10 vs. 61 ± 10 years, P = 0.042) in comparison to patients with good collateral growth. The presence and number of fQRS were higher in the poor collateral group than the good collateral group (64 vs. 32%, P < 0.001 and 2.3 ± 2.4 vs. 1.2 ± 2.0, P = 0.002, respectively). Left ventricular ejection fraction was significantly lower in the poor collateral group than the good collateral group (45 ± 11 vs. 51 ± 13, P = 0.014). There was a significant correlation between number of fQRSs and the echocardiographic wall-motion abnormality score (r = 0.662, P < 0.001). In multivariate analysis, only the presence of fQRS was independently related to poor collateral development (odds ratio, 3.559; 95% confidence interval, 1.708-7.415, P = 0.001). CONCLUSION: We found that fQRS was independently related to inadequate coronary collaterals in patients with CTO. fQRS, which may be derived from the effects of myocardial ischemia or scar on myocardial electricity at the cellular level, can represent inadequate coronary collateral development in patients with CTO.