The importance of fragmented QRS complexes in prediction of myocardial infarction and reperfusion parameters in patients undergoing primary percutaneous coronary intervention.

OZET RS complex fragmentations are frequently seen on surface electrocardiograms with narrow or wide QRS complex including paced rhythm, bundle branch block or ventricular premature beats.[1] These fragmentations on surface ECG have been associated with increased adverse cardiovascular events in previous studies.[2-5] Fragmented QRS may be important for stratifying patients at high risk for CVEs on admission and after ST elevation myocardial infarction. fQRS on a 12-lead resting ECG are defined as various RSR′ patterns (≥1 R′ or notching of S wave or R wave) with or without Q waves without a typical bundle-branch block in 2 contiguous leads corresponding to a major coronary artery territory. Sometimes fQRS may be the only electrocardiographic marker of myocardial damage in patients with non-Q myocardial infarction and in patients with resolved Q wave.[6] The reasons for documented association between fQRS and increased morbidity and mortality, sudden cardiac death and recurrent adverse cardiac events have been investigated in previous studies.[4,5,7-10] In these studies, the main causative mechanism of fQRS was cardiac fibrosis.[11,12] Additionally, fQRS may represent altered ventricular depolarization, which can be derived from mechanisms such as non-homogeneous activation of ischemic ventricles in the setting of STEMI. The causative relationship between fQRS and cardiac fibrosis is known, but the dynamic effects of primary percutaneous coronary intervention on fQRS and their association with MI and reperfusion parameters have not been studied until now. In this study, we investigated the effect of p-PCI on fQRS and the relationship between the presence of fQRS on preand post-PCI ECG and reperfusion parameters in patients with STEMI. PATIENTS AND METHODS Patient population and study protocol The study was conducted in the cardiology clinics at Rize Education and Research Hospital, Rize, Turkey and Ordu State Hospital in Ordu, Turkey. The sample size of our study was determined by patients admitted to our clinic at diagnosis of STErolled consecutively. All patients were examined by an experienced cardiologist immediately after hospitalization. Clinical characteristics, which consisted of multiple descriptors from each patient’s history and physical examination, were collected by physicians from cardiology clinics for each patient and were stored in the database of coronary angiography laboratory at each institute. We recorded the baseline characteristics, including hypertension, diabetes mellitus, smoking status, family history for CAD, and lipid parameters. Killip score was used for used for risk stratification.[13] Patients with significant organic valvular heart disease (3 patients) and bundle branch block (LBBB) (4 patients), incomplete or complete RBBB (3 patients) or duration of QRS ≥120 ms (7 patients with intra-ventricular conduction delay), known history of prior MI (10 patients), and patients with permanent pacemakers (1 patient) were excluded from the study. These exclusion criterions were used in to protect the study data from confounding factors other than STEMI origin and location. In the current study, data was retrospectively collected after exclusion of ineligible patients. Informed consent was obtained from all patients prior to the study. The study was performed in accordance with the principles stated in the Declaration of Helsinki. Laboratory measurements Cardiac biomarkers levels including creatine kinase (CK), creatine kinase-MB fraction (CK-MB) and Troponin-I and inflammatory markers including leukocyte counts were measured at our emergency department and used in the analyses as admission values. The lipid samples were drawn by venipuncture to perform routine blood chemistry after fasting for at least 8 hours. Glucose, creatinine, and Turk Kardiyol Dern Ars 214