The occurrence of new-onset AF following CABG and the relationship with FQRS were investigated. They divided the patients into two groups, those with postoperative AF, and those without AF. studied 272 patients who underwent isolated CABG surgery in a prospective observational design. It was demonstrated that the FQRS was as predictor of the occurrence of post-operative atrial fibrillation (AF) in patients after coronary artery by-pass graft (CABG) surgery. It seems reasonable to associate the structural changes of the ventricular myocardium with structural and/or functional alterations in the atrium causing atrial arrhythmias. On the other hand, there was a statistically significant difference in mortality associated to the presence of FQRS in patients with acute coronary syndrome and myocardial necrosis. In patients with LV dysfunction, there is no clear evidence that presence of FQRS could predict arrhythmic events. Myocardial scars from a previous infarction may provide the anatomic substrate for ventricular tachycardia in patients with coronary disease and impaired left ventricular function. The initiation and perpetuation of a circus movement reentrant ventricular arrhythmia depend on the firing of a trigger event such as a premature ventricular complex in the presence of a vulnerable myocardial substrate. The presence of FQRS represents distortion of signal conduction and depolarization process within the ventricles which is related to myocardial scar/myocardial ischemia or myocardial fibrosis. suggested that FQRS complex in infarcted canine heart is caused by slow and inhomogeneous activation associated to healed myocardial scar rather than changes in trans-membrane resting or action potentials. Friedman et al suggested that persistent changes in Purkinje fibers and myocardial fibrosis may cause slow and inhomogeneous myocardial activation in the canine heart with induced myocardial infarction. They named it high-frequency components to the presence of FQRS complexes. showed that the slurring and changes in the morphology of the QRS complex are more common among patients with prior myocardial infarction (MI) and among patients with either right or left ventricular (LV) enlargement. Fragmented wide QRS complex (FWQRS) were defined as various RSR patterns with or without a Q wave, with more than 2 R waves (R’) or more than 2 notches in the R wave, or more than 2 notches in the down-stroke or upstroke of the S wave, in 2 contiguous leads corresponding to a major coronary artery territory. Therefore, several entities associated with the presence of myocardial scar formation such as coronary artery disease, cardiomyopathies, heart failure, and congenital heart diseases influence the finding of FQRS.įQRS is defined as the presence of an additional R wave (R’) or notching in the nadir of the S wave, or the presence of more than 1 R’ in 2 contiguous leads, corresponding to a major coronary artery territory on the resting 12-lead ECG with filter range 0.16–100 Hz, AC filter 60 Hz, paper speed 25 mm/s and 10 mm/mV. The finding of FQRS on a conventional 12-lead electrocardiogram (ECG) is associated to depolarization abnormality which suggests conduction delay from inhomogeneous activation of the ventricles due to myocardial scar. There was a statistically significant difference in mortality associated to the presence of FQRS in patients with acute coronary syndrome and myocardial necrosis. It has been suggested that FQRS is caused by slow and non-homogeneous depolarization associated to healed myocardial scar. On the other hand, in patients with stable coronary artery disease and in patients with acute MI, fragmented QRS complex (FQRS) was found to be a good predictor of cardiac events. Despite the lack of desirable positive predictive value for the risk of cardiovascular events, systolic dysfunction is still widely used in clinical practice. In routine practice and clinical studies, a low left ventricular ejection fraction is routinely utilized for risk stratification in patients with structural heart disease.
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