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J Am Coll Cardiol, 2004; 43:1236-1240, doi:10.1016/j.jacc.2003.10.054 © 2004 by the American College of Cardiology Foundation |






,*
* Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota, USA
Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota, USA
Division of Biostatistics, Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota., USA
Manuscript received September 5, 2003; revised manuscript received October 20, 2003, accepted October 28, 2003.
* Reprint requests and correspondence: Dr. Patricia A. Pellikka, Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic, Mayo Foundation, 200 First Street SW, Rochester, Minnesota 55905, USA.
pellikka.patricia{at}mayo.edu
OBJECTIVES: The purpose of the study was to determine if atrial ectopy (AE) or atrial arrhythmias during exercise are predictive of an increased risk of cardiac events and death.
BACKGROUND: Although stress-induced atrial arrhythmias are common during exercise testing, there is a paucity of data regarding the correlation with underlying heart disease and cardiovascular outcomes. Atrial arrhythmias may reflect underlying left atrial enlargement and diastolic dysfunction, which are prognostic of mortality. We hypothesized that these stress-induced arrhythmias are associated with long-term adverse cardiac events.
METHODS: Exercise echocardiography was performed in 5,375 patients (age 61 ± 12 years) with known or suspected coronary artery disease. An abnormal result was defined as exercise-induced atrial fibrillation (AF)/atrial flutter, supraventricular tachycardia (SVT), or AE.
RESULTS: A total of 311 (5.8%) patients died (132 [2.5%] from cardiac causes) over a period of 3.1 ± 1.7 years. In addition, 193 (3.6%) patients experienced a myocardial infarction (MI) and 531 (9.9%) patients required revascularization. During exercise testing, 1,272 (24%) patients developed AE, 185 (3.4%) developed SVT, and 43 (0.8%) developed AF. The five-year cardiac death rate was not statistically different between groups (none [3.8%], AE [4.3%], SVT [3.7%], AF [0%], p = 0.43). The five-year rate of MI was significantly different between groups (none [5.7%], AE [8.3%], SVT [0%], AF [9.0%], p = 0.005). The five-year rate of revascularization between groups was not significantly different (none [14.2%], AE [17.0%], SVT [11.8%], AF [14.8%], p = 0.50). A composite of all five-year adverse end points was similar between groups (none [22.7%], AE [27.8%], SVT [17.7%], AF [25.7%], p = 0.10). In stepwise multivariate analysis, AE was not predictive of myocardial infarction when taking into account traditional clinical variables and exercise test results.
CONCLUSIONS: In this large cohort of patients, the occurrence of AE was predictive of an increased risk of MI. However, the association did not persist after adjustment for clinical and exercise variables known to predict adverse long-term cardiovascular outcomes. The rate of long-term cardiac death or revascularization was not influenced by the development of stress-induced atrial arrhythmias.
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