Author + information
- Received July 22, 1996
- Revision received December 2, 1996
- Accepted December 4, 1996
- Published online March 15, 1997.
- John J. Mahmarian, MD, FACCA,*,
- Richard M. Steingart, MD, FACCB,
- Sandra FormanC,
- Barry L. Sharaf, MD, FACCD,
- Mary Ellen CoglianeseB,
- D. Douglas Miller, MD, FACCE,
- Carl J. Pepine, MD, FACCF,
- A. David Goldberg, MD, FACCG,
- Marilyn F. Bloom, RNA,
- Sheila ByersE,
- Laurel DvorakG,
- Craig M. Pratt, MD, FACCA,1,2,
- Asymptomatic Cardiac Ischemia Pilot (ACIP) Investigators
- ↵*Dr. John J. Mahmarian, Baylor College of Medicine, 6550 Fannin, SM-1246, Houston, Texas 77030-2716.
Objectives. This study sought to explore the relation between markers of ischemia detected by ambulatory electrocardiographic (AECG) monitoring and stress myocardial perfusion single-photon emission computed tomography (SPECT).
Background. Stress myocardial SPECT and AECG monitoring are both utilized in evaluating patients with coronary artery disease. However, information is limited regarding the relation between the presence and extent of ischemia as detected by these two modalities.
Methods. This was an ancillary study of the Asymptomatic Cardiac Ischemia Pilot (ACIP) trial. One hundred six patients with previous coronary angiography underwent AECG monitoring and stress SPECT within a close temporal time period. The frequency and duration of ischemia as assessed by AECG monitoring and the total and ischemic stress-induced myocardial perfusion defect sizes as assessed by SPECT were quantified in separate core laboratories. Multivariate logistic regression and linear regression analysis were used to determine associations between AECG and SPECT abnormalities with regard to angiographic, demographic and treadmill exercise variables.
Results. Seventy-four percent of patients with significant (≥50%) coronary artery stenosis had SPECT abnormalities, whereas 61% had ischemia by AECG monitoring. The most important predictors of SPECT abnormalities were severity (p < 0.001) of coronary artery stenosis, followed by total exercise duration (p = 0.016) and patient age (p = 0.04). The only predictor of AECG abnormalities was the presence of ST segment depression on the initial exercise treadmill test (p = 0.021). Only a 50% concordance for normalcy or abnormalcy was observed between the SPECT and AECG results, and no relation was observed between the frequency or duration of AECG ischemia and the quantified total or ischemic myocardial perfusion defect size as assessed by SPECT.
Conclusions. Ischemia as detected by AECG monitoring does not correlate with the presence and extent of ischemia as quantified by stress SPECT. Because these techniques appear to detect different pathophysiologic manifestations of ischemia, they may be complementary in more fully defining the functional significance of coronary artery disease and, in particular, which patients are at highest risk for adverse cardiac events.
(J Am Coll Cardiol 1997;29:764–9)
↵1 A complete list of the ACIP investigators and participating centers appears in J Am Coll Cardiol 1995;26:594–605.
↵2 Address for reprints: ACIP Clinical Coordinating Center, Maryland Medical Research Institute, 600 Wyndhurst Avenue, Baltimore, Maryland 21210.
This study was presented in part at the 46th Annual Scientific Session of the American College of Cardiology, Orlando, Florida, March 1996 and was funded by the National Heart, Lung, and Blood Institute, Cardiac Diseases Branch, Division of Heart and Vascular Disease, National Institutes of Health, Bethesda, Maryland by Research Contracts HV-90-07, HV-90-08, HV-91-05 to HV-91-14. Study medications and placebo were donated by Zeneca Pharmaceuticals Group, Wilmington, Delaware; Hoechst Marion Roussel, Kansas City, Missouri; and Pfizer, New York, New York.
↵fn1 Support for electro cardiographic data collection was provided in part by Applied Cardiac Systems, Laguna Hills, California; Marquette Electronics, Milwaukee, Wisconsin; Mortara Instrument, Milwaukee, Wisconsin; and Quinton Instruments, Seattle, Washington. Some centers had partial support from General Clinical Research Center grants.
- Received July 22, 1996.
- Revision received December 2, 1996.
- Accepted December 4, 1996.
- The American College of Cardiology