Author + information
- Received November 18, 1992
- Revision received February 22, 1993
- Accepted February 24, 1993
- Published online September 1, 1993.
- Neal G. Uren, BSc, MRCP∗,1,
- Paolo Marraccini, MD∗,†,
- Roberto Gistri, MD†,
- Ranil de Silva, BSc∗ and
- Paolo G. Camici, MD, FESC, FACC∗,†
- ↵∗Address for correspondence: Paolo G. Camici, MD, MRC Cyclotron Unit, Hammersmith Hospital, Du Cane Road, London W12 0HS, UKUnited Kingdom.
Objectives. The aim of this study was to investigate coronary vasodilator reserve and metabolism in myocardium subtended by angiographically normal arteries remote from ischemia.
Background. After infarction, structural and functional changes occur in remote myocardium often subtended by normal arteries. Whether changes occur in regions remote from ischemic but noninfarcted myocardium is unknown.
Methods. Coronary vasodilator reserve was measured with positron emission tomography in 12 patients with single-vessel disease using intravenous dipyridamole (0.56 mg/kg for 4 min). In another 10 patients, simultaneous arterial/great cardiac vein catheterization was performed during atrial pacing to measure myocardial metabolism in regions subtended by diseased or normal arteries.
Results. Basal myocardial blood flow in stenosis-related regions was comparable to that in remote regions but was lower after dipyridamole administration (1.73 ± 0.91 vs. 2.89 ± 0.93 ml/min per g, p < 0.01), giving coronary vasodilator reserve values of 1.80 ± 0.82 and 2.73 ± 0.89 (p < 0.01). In normal control subjects, basal myocardial blood flow was 0.92 ± 0.13 and 3.67 ±0.94 ml/min per g in the basal state and after dipyridamole (both p < 0.05 vs. values in remote regions), and coronary vasodilator reserve was 4.07 ± 0.98 (p < 0.01 vs. values in remote regions). During pacing there was net lactate release in diseased regions (−18 ± 27%, p < 0.05 vs. values in remote regions and control subjects) and extraction in remote regions (38 ± 17%) and in normal control subjects (26 ± 11%). Glucose and alanine extraction were increased in diseased (8 ± 6% and 6 ± 6%) and remote regions (6 ± 3% and 4 ± 3%), compared with values in normal control subjects (2 ± 3% and −1 ± 3%, both p < 0.05 vs. diseased and remote regions).
Conclusions. Coronary vasodilator reserve is reduced and glucose and alanine metabolism is abnormal in regions subtended by normal arteries remote from ischemic but noninfarcted myocardium.
↵1 Neal G. Uren is a Junior Fellow of the British Heart Foundation.
☆ This study was presented in part at the 41st Annual Scientific Session of the American College of Cardiology. This work was partly supported by the European Economic Community (EEC) Concerted Action on PET Investigations of Cellular Regeneration and Degeneration.
- Received November 18, 1992.
- Revision received February 22, 1993.
- Accepted February 24, 1993.