Fragmented QRS on a 12-lead ECG: a predictor of mortality and cardiac events in patients with coronary artery disease.
ABSTRACT Fragmented QRS (fQRS) on a 12-lead electrocardiogram (ECG) is associated with myocardial scar in patients with coronary artery disease (CAD).
We postulated that fQRS is a predictor of cardiac events and mortality in patients who have known CAD or who are being evaluated for CAD.
The cardiac events (myocardial infarction, need for revascularization, or cardiac death) and all-cause mortality were retrospectively reviewed in 998 patients (mean age 65.5 +/- 11.9 years, male 967) who underwent nuclear stress test. The fQRS on a 12-lead ECG included various RSR' patterns (> or =1 R' prime or notching of S wave or R wave) without typical bundle branch block in 2 contiguous leads corresponding to a major coronary artery territory.
All-cause mortality (93 [34.1%] vs 188 [25.9%]) and cardiac event rate (135 [49.5%] vs 200 [27.6%]) were higher in the fQRS group compared with the non-fQRS group during a mean follow-up of 57 +/- 23 months. A Kaplan-Meier survival analysis revealed significantly lower event-free survival for cardiac events (P <.001) and all-cause mortality (P = .02). Multivariate Cox regression analysis revealed that significant fQRS was an independent significant predictor for cardiac events but not for all-cause mortality. The Kaplan-Meier survival analysis showed no significant difference between fQRS and Q waves groups for cardiac events (P = .48) and all-cause mortality (P = .08).
The fQRS is an independent predictor of cardiac events in patients with CAD. It is associated with significantly lower event-free survival for a cardiac event on long-term follow-up.
- Journal of Electrocardiology - J ELECTROCARDIOL. 01/1988; 21.
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ABSTRACT: To report the prevalence of abnormal treadmill test responses and their association with mortality in a large consecutive series of patients referred for standard exercise tests, with testing performed and reported in a standardized fashion. Exercise testing is widely performed, but few databases exist of large numbers of consecutive tests performed on patients referred for routine clinical purposes using standardized methods. Even fewer of the available databases have information regarding all-cause mortality as an outcome. All patients referred for evaluation at two university-affiliated Veterans Affairs medical centers who underwent exercise treadmill testing for clinical indications between 1987 and 2000 were determined to be dead or alive using the Social Security death index after a mean 6.2 years (median, 7 years) of follow-up. Clinical and exercise test variables were collected prospectively according to standard definitions; testing and data management were performed in a standardized fashion using a computer-assisted protocol. All-cause mortality was utilized as the end point for follow-up. Standard survival analysis was performed, including Kaplan-Meier curves and a Cox hazard model. There were 6,213 male patients (mean +/- SD age, 59 +/- 11 years) who underwent standard exercise ECG treadmill testing over the study period with a mean follow-up duration of 6.2 +/- 3.7 years. There were no complications of testing in this clinically referred population, 78% of whom were referred for chest pain, or risk factors or signs or symptoms of ischemic heart disease. Overlapping thirds had typical angina or history of myocardial infarction (MI). Five hundred seventy-nine patients had prior coronary artery bypass surgery, and 522 patients had a history of congestive heart failure (CHF). Indications for testing were in accordance with published guidelines. Twenty percent died over the follow-up period, for an average annual mortality rate of 2.6%. Cox hazard function chose the following variables in rank order as independently and significantly associated with time to death: exercise capacity (metabolic equivalents < 5, age > 65 years, history of CHF, and history of MI. A score based on these variables (summing up the four variables [if yes = 1 point]) classified patients into low-risk, medium-risk, and high-risk groups. The high-risk group (score > or = 3) has a hazard ratio of 5.0 (95% confidence interval, 4.7 to 5.3) and a 5-year mortality rate of 31%. This comprehensive analysis provides rates of various abnormal responses that can be expected in patients referred for exercise testing at a typical medical center. Four simple variables combined as a score powerfully stratified patients according to prognosis.Chest 09/2001; 120(3):1003-13. · 5.85 Impact Factor
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ABSTRACT: We sought to investigate the origin of the fractionated electrogram and its relations to abnormal conduction in cardiomyopathic myocardium. Patients with dilated cardiomyopathy have a high incidence of ventricular tachycardias. Electrograms recorded in these patients are often fractionated. High resolution mapping (200-microM interelectrode distance) of the electrical activity was carried out in 11 superfused papillary muscles and 6 trabeculae from 7 patients who underwent heart transplantation because of dilated cardiomyopathy. Similar measurements were taken in four papillary muscles from dog hearts in which electrical barriers had been artificially made. Ten human preparations were studied histologically. All preparations revealed sites with fractionated electrograms. In three human preparations, activation patterns showed a discernible line of activation block running parallel to the fiber direction. Fractionated electrograms were recorded at sites contiguous to the line of block. In five preparations, fractionated electrograms were recorded at sites where lines of block were not identified. In these preparations, electrical barriers consisted of short stretches of fibrous tissue. In the remaining nine preparations, fractionated electrograms were recorded, both from sites contiguous to distinct obstacles and sites without evidence of a barrier. Our observations showed that fractionated electrograms recorded in myocardium damaged by cardiomyopathy were due to both distinct, long strands and short stretches of fibrous tissue. Delayed conduction was caused by curvation of activation around the distinct lines of block and by the wavy course of activation between the short barriers. The latter reflects extreme nonuniform anisotropy.Journal of the American College of Cardiology 05/1996; 27(5):1071-8. · 14.09 Impact Factor