Increase of serum troponin I and ST-segment depression are objective markers of myocardial ischemia/injury. Abnormalities of the 2 indicators have been associated with supraventricular tachycardia (SVT) but their relevance for diagnosing acute coronary syndrome and the presence of coronary artery disease (CAD) in this setting have not been clarified. Therefore, we sought to evaluate the frequency of CAD based on increased troponin I and ST-segment depression during SVT. During a 5-year period, 104 patients were admitted with a diagnosis of SVT, 80 of whom had troponin I testing, and 70 of these patients could be assessed for ST-segment changes. Thirty-seven patients (48%) had increased troponin I (mean 1.54 ± 2.7 ng/dl, normal ≤0.07 ng/dl) and 46 patients (57%) had ST-segment depression ≥1.0 mm. There were no significant differences in baseline characteristics and clinical presentation of patients with and without troponin I increase or ST-segment depression. There was no difference in the diagnosis of CAD by noninvasive or invasive testing in patients with and without increased troponin I. More patients with than without ST-segment depression had evidence of CAD (22% vs none, p = 0.01), but after adjusting for covariates, ST-segment depression was not a significant predictor of CAD. In conclusion, increased troponin I and ST-segment depression are not significant markers of acute coronary syndrome in patients with SVT.
Increase of serum troponin I and ST-segment depression are objective markers of myocardial ischemia/injury and these 2 findings have been reported in patients during supraventricular tachycardia (SVT). Evidence of these abnormalities in patients with SVT often prompts evaluation to exclude coronary artery disease (CAD). Most studies of this problem have been limited to case reports and small numbers of patients. We reported a case of a 29-year-old man with SVT associated with markedly increased troponin and severely ischemic electrocardiographic changes associated with normal coronary arteries. In the largest study of this problem, Dorenkamp et al found a 4% prevalence of CAD with no relation to troponin I increase or ST-segment depression. We sought to evaluate this syndrome further to identify predictors of CAD in a large cohort of patients presenting with SVT.
Methods
We queried the University of California (Davis) Medical Center database for patients admitted from 2002 to 2007 with an International Classification of Diseases, Ninth Revision code for SVT. The following data were collected: age, gender, smoking status, cardiac history, diabetes, hypertension, hyperlipidemia, chronic kidney disease, and chest pain at time of presentation with SVT. SVT was defined as narrow complex regular tachycardia with a rate ≥140 beats/min. Troponin I was considered increased if higher than our laboratory standard value (≥0.07 ng/ml). ST-segment depression was defined as ≥1.0-mm horizontal or downsloping depression 0.08 second after the J-point on 12-lead electrocardiogram. Electrocardiographic characteristics assessed included rate of SVT and presence and degree of ST-segment depression. We assessed evidence of CAD by noninvasive studies (myocardial stress scintigraphy, stress echocardiography, and treadmill exercise testing) or coronary angiography.
CAD was defined by a positive myocardial stress scintigraphic finding (stress-induced perfusion defect, stress-induced left ventricular wall motion abnormality), horizontal ST-segment depression ≥1.0 mm 0.08 second after the J-point, or >60% luminal diameter stenosis in ≥1 major coronary artery. History of CAD was defined as previous myocardial infarction, abnormal noninvasive stress test finding, or CAD by angiogram. We determined the relation of ST-segment depression and troponin I increase to the diagnosis of CAD and we evaluated the relation of the following selected clinical variables to CAD in the setting of SVT: age ≥45 years, male gender, history of CAD, hypertension, diabetes, hyperlipidemia, and smoking.
All patients ≥18 years of age were included in the analysis. Exclusion criteria were narrow complex tachyarrhythmias other than SVT (sinus tachycardia, atrial fibrillation, atrial tachycardia, and atrial flutter). The study was approved by our institutional review board.
We used descriptive statistics for demographic and clinical variables. Continuous variables are presented as means ± SDs and categorical variables as proportions. Two-sample tests ( t tests for continuous variables and chi-square tests for proportions) were applied to identify significant differences in the 2 groups of patients with and without troponin I increase and those with and without ST-segment depression. Multivariate exact logistic regression analysis was performed to identify variables independently associated with CAD (primary end point). A p value <0.05 was considered statistically significant. All data analyses were performed with STATA 10 software (STATA Corp., College Station, Texas).
Results
One hundred four subjects were admitted with a diagnosis of SVT. Group mean heart rate during SVT was 174 ± 27 beats/min, during which 1/2 of patients had ST-segment depression and >1/3 had chest pain. Eighty patients had testing, of whom 46% had increased troponin I ( Table 1 ). ). Seventy of these patients could have their ST segment assessed because others had abnormalities on baseline electrocardiogram. The most rapid heart rate was 205 beats/min, highest troponin I was 13.1 ng/ml, and deepest ST-segment depression was 3 mm. There was no significant difference in the characteristics of patients who did and did not have troponin I testing ( Table 1 ). Of these 80 patients, most were middle-aged, 3/5 were women, and there was a high prevalence of cardiac risk factors. More women than men had troponin 1 increase (55% vs 32%) and 62% of patients with a history of CAD had troponin I increase compared to 43% without a history of CAD (p = NS). In patients with and without troponin I increase or ST-segment depression, there were no significant differences in baseline characteristics, SVT rate, or proportion with chest pain ( Tables 1 and 2 ).
| Clinical Characteristics | Troponin Positive | Troponin Negative |
|---|---|---|
| (n = 37) | (n = 43) | |
| Age (years), mean ± SD | 57 ± 18 | 58 ± 17 |
| Women | 27 (73%) | 22 (51%) |
| History of coronary artery disease ⁎ | 8 (22%) | 5 (12%) |
| Diabetes mellitus | 15 (41%) | 10 (23%) |
| Hypertension | 25 (68%) | 23 (53%) |
| Hyperlipidemia | 15 (41%) | 11 (26)% |
| Smoking | 15 (41%) | 13 (30%) |
| Chest pain | 14 (38%) | 15 (35%) |
| ST-segment depression present | 21/28 (75%) | 25/42 (60%) |
⁎ Defined as previous myocardial infarction, abnormal noninvasive stress test finding, or coronary artery disease by angiogram.
| Variable | With ST-Segment Depression | Without ST-Segment Depression |
|---|---|---|
| (n = 46) | (n = 24) | |
| Age (years), mean ± SD | 58 ± 16 | 55 ± 19 |
| Women | 31 (67%) | 12 (50%) |
| Hypertension | 29 (63%) | 12 (50%) |
| Diabetes mellitus | 16 (35%) | 8 (33%) |
| Hyperlipidemia | 17 (37%) | 5 (21%) |
| History of coronary artery disease ⁎ | 9 (20%) | 2 (8%) |
| Smoking | 13 (28%) | 10 (42%) |
| Creatinine (mg/dl), mean ± SD | 1.4 ± 1.6 | 1.1 ± 0.7 |
| Blood pressure (mm Hg), mean ± SD | 123 ± 30 | 114 ± 29 |
| Heart rate (beats/min), mean ± SD | 176 ± 26 | 165 ± 28 |
⁎ Defined as previous myocardial infarction, abnormal noninvasive stress test finding, or coronary artery disease by angiogram.
Thirty-five patients (44%) had cardiac evaluation, which included coronary angiography in >3/4. Characteristics of patients who underwent evaluation for CAD are listed in Table 3 . Compared to patients not receiving further evaluation, patients who did had more chest pain (46% vs 24%, p = 0.04) or history of CAD (26% vs 7%, p = 0.03). Table 4 presents patients with and without CAD demonstrated by coronary angiogram (26%) and positive noninvasive testing (11%).
| Clinical Characteristics | Prevalence in Patients Referred for CAD Evaluation | Prevalence in Patients Not Referred for CAD Evaluation | p Value |
|---|---|---|---|
| (n = 35) | (n = 42) | ||
| Age (years), mean ± SD | 57.1 ± 16 | 57.3 ± 17 | NS |
| Women | 22 (63%) | 27 (64%) | NS |
| History of coronary artery disease ⁎ | 9 (26%) | 3 (7%) | 0.03 † |
| Diabetes mellitus | 10 (29%) | 14 (33%) | NS |
| Hypertension | 25 (71%) | 23 (55%) | NS |
| Hyperlipidemia | 14 (40%) | 11 (26%) | NS |
| Smoking | 13 (37%) | 13 (31%) | NS |
| ST-segment depression | 21/29 (72%) | 24/39 (62%) | NS |
| Elevated troponin | 17 (49%) | 18 (43%) | NS |
| Chest pain | 16 (46%) | 10 (24%) | 0.04 † |
⁎ Defined as previous myocardial infarction, abnormal noninvasive stress test finding, or coronary artery disease by angiogram.
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