Author + information
- Received November 15, 1982
- Revision received January 24, 1983
- Accepted February 9, 1983
- Published online June 1, 1983.
- Richard O. Cannon III, MD*,
- Rita M. Watson, MD,
- Douglas R. Rosing, MD, FACC and
- Stephen E. Epstein, MD, FACC
- ↵*Address for reprints: Richard O. Cannon III, MD, Room 7B-15, Building 10, National Institutes of Health, 9000 Rockville Pike, Bethesda, Maryland 20205.
To study the mechanism of chest pain in patients vvith insignificant large vessel coronary artery disease, 22 patients underwent great cardiac vein flow, coronary resistance and lactate determinations at rest and with coronary sinus pacing followed by coronary arteriography. Nine patients experiencing chest pain with pacing demonstrated significantly lesser increase in flow from base-line values (45 ± 30versus86 ± 50% [mean ± standard deviation], p < 0.025), lesser decrease from baseline in resistance (-28 ± 18 versus -44 ± 11%, p < 0.001) and less lactate consumption (25.0 ± 23.6 versus 45.6 ± 19.0 mmol ml/min, p < 0.025) compared with the 13 patients without pacing-induced chest pain. Pacing conducted during the cold pressor test elicited similar abnormalities in those patients experiencing chest pain and those who did not: four of eight patients experiencing chest pain demonstrated a lowered or new anginal threshold compared with that of the control pacing study. Coronary arteriography during the cold pressor test revealed no significant change in epicardial coronary artery dimension.
After administration of ergonovine, 0.15 mg intravenously, 2 of 20 patients experienced spontaneous chest pain, which was associated with the greatest decrease in flow ( - 13 and -21%, respectively) and increase in resistance ( + 26 and +39%, respectively) of any patient. Pacing resulted in chest pain in 10 of the remaining 18 patients, including 5 patients who had not experienced chest pain during the control pacing study. Although none of these patients exhibited significant epicardial coronary artery narrowing on arteriography, their flow increased less (38 ± 12 versus 126 ± 68%, p < 0.001), resistance decreased less ( -18 ± 4 versus -50 ± 13%, p < 0.001) and was associated with less lactate consumption (32.7 ± 25.2 versus 70.1 ± 29.4mmolml/min, p < 0.01) than in patients not experiencing chest pain. Eight of the 12 patients developing chest pain demonstrated a decreased or new anginal threshold compared with that elicited by pacing during the control study.
These findings suggest that some patients with atypical chest pain have inappropriate coronary arteriolar or small coronary artery constriction with abnormal vasodilator reserve in response to atrial pacing. The abnormality can be unmasked or exacerbated in some patients by vasoconstrictor stimuli, but cannot be identified with standard angiographic assessment of “spasm” because abnormal vasoconstriction occurs in vessels too small to be visualized by angiography.
- Received November 15, 1982.
- Revision received January 24, 1983.
- Accepted February 9, 1983.
- American College of Cardiology Foundation