New-onset conduction defects and their relationship with in-hospital major cardiac events in unstable angina pectoris.
BACKGROUND
The aim of this prospective cohort study was to describe the incidence and the risk factors for the development of intraventricular conduction defects and the relationship of these defects with in-hospital major cardiac events (MACE) in unstable angina pectoris.


METHODS
Two-hundred-and-seventy consecutive patients presenting with Braunwald class IIIB angina without a conduction defect at admission were included in the study and followed up during the in-hospital period.


RESULTS
Fifty-one patients who developed non-ST-elevation myocardial infarction during the first day were excluded from the study. Of the remaining 219 patients, 40 (18%) had a new permanent conduction defect (group 1) and 179 (82%) did not have a conduction defect (group 2) during the in-hospital period. The patients in group 1 were significantly older (mean age of 63.5 +/- 11 years compared with 59 +/- 10 years, P = 0.01) and a history of previous coronary artery bypass grafting (CABG) was more frequent in this group (12.5% compared with 1.6%, P = 0.004). By logistic regression analysis, age (P = 0.01, odds ratio (OR) = 1.473, 95% confidence interval (CI) = 1.108-2.612) and previous CABG (P = 0.005, OR = 3.995, 95% CI = 1.811-7.383) were also found to be risk factors for the development of a conduction defect. In-hospital total MACE, death and heart failure were more frequently observed in group 1 (P = 0.005, P = 0.02, P = 0.001, respectively). The incidences of recurrent refractory angina, acute myocardial infarction and urgent revascularization were not different between the groups. ST-segment depression at admission (P = 0.009, OR = 1.654, 95% CI = 1.228-2.675) and a new-onset conduction defect (P = 0.02, OR = 1.625, 95% CI = 1.244-2.754) were found to be predictors of the development of in-hospital MACE.


CONCLUSIONS
In unstable angina pectoris, patients with a new-onset conduction defect are relatively older and have more frequently undergone previous CABG. Because in-hospital MACE, death and heart failure are more common in patients with a new conduction defect, they should be considered as high risk and treated more aggressively.
Okmen
Ertan
E
Department of Cardiology, Siyami Ersek Cardiovascular and Thoracic Surgery Center, Istanbul, Turkey. ertanokmen@hotmail.com
Gurol
Tayfun
T
Erdinler
Izzet
I
Sanli
Arda
A
Cam
Nese
N
D000368:Aged; D000789:Angina, Unstable / Q000175:diagnosis*; D001145:Arrhythmias, Cardiac / Q000175:diagnosis*; D015415:Biomarkers / Q000097:blood; D017023:Coronary Angiography; D001026:Coronary Artery Bypass; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form; D003937:Diagnosis, Differential; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006327:Heart Block / Q000175:diagnosis*; D006760:Hospitalization; D006801:Humans; D015994:Incidence; D007527:Isoenzymes / Q000097:blood; D008297:Male; D008875:Middle Aged; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors / Q000627:therapeutic use; D011446:Prospective Studies; D012307:Risk Factors; D013223:Statistics as Topic; D016896:Treatment Outcome; D014336:Troponin / Q000097:blood
D015415:Biomarkers; D007527:Isoenzymes; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D014336:Troponin; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form