Author + information
- Received June 4, 2002
- Revision received August 29, 2002
- Accepted September 20, 2002
- Published online February 19, 2003.
- Rosa Sicari, MD, PhD*,* (, )
- Emilio Pasanisi, MD*,
- Lucia Venneri, MD*,
- Patrizia Landi, BSc*,
- Lauro Cortigiani, MD*,
- Eugenio Picano, MD, PhD*,
- Echo Persantine International Cooperative (EPIC) and Echo Dobutamine International Cooperative (EDIC) Study Groups
- ↵*Reprint requests and correspondence:
Dr. Rosa Sicari, CNR, Institute of Clinical Physiology, Via G. Moruzzi, 1, 56125 Pisa, Italy.
Objectives The purpose of this study was to assess the long-term value of pharmacologic stress echocardiography with either dipyridamole or dobutamine (DET) for prediction of cardiac death in patients with proven or suspected coronary artery disease (CAD).
Background Stress echocardiography is an established, cost-effective technique for the detection of CAD.
Methods From the Echo Persantine International Cooperative–Echo Dobutamine International Cooperative data bank, 7,333 patients (5,452 males; 59 ± 10 years) underwent pharmacologic stress echocardiography with either high-dose dipyridamole (0.84 mg/kg over 10 min) (n = 4,984) or high-dose dobutamine (up to 40 μg/kg/3 min) (n = 2,349) for diagnostic purposes. Patients were followed up for a mean of 2.6 years (range 1 to 206 months).
Results The DET was positive for myocardial ischemia in 2,854 (35%) patients and negative in 4,479 (61%) patients. During the follow-up there were 161 cardiac deaths (sudden death and fatal myocardial infarction) (2.1% of the total population). Kaplan-Meier survival estimates showed a significantly better outcome for those patients with a negative pharmacologic stress echocardiography test compared with those with a positive test (92 vs. 71.2%, p = 0.0000).
Conclusions Pharmacologic stress echocardiography with either dipyridamole or dobutamine is effective in predicting cardiac death during a long-term follow-up. A negative stress echocardiography test result is related to a favorable outcome.
☆ Financial support for the present study was received from the National Council of Research, Institute of Clinical Physiology, Pisa, Italy.
- Received June 4, 2002.
- Revision received August 29, 2002.
- Accepted September 20, 2002.
- American College of Cardiology Foundation