Author + information
- Received March 25, 1996
- Revision received October 9, 1996
- Accepted October 25, 1996
- Published online February 1, 1997.
- Julio A Panza, MD, FACCA,*,
- Joy M Laurienzo, RN, BSNA,
- Rodolfo V Curiel, MDA,
- Ellis F Unger, MDA,
- Arshed A Quyyumi, MD, FACCA,
- Vasken Dilsizian, MD, FACCA and
- Richard O Cannon III, MD, FACCA
- ↵*Dr. Julio A. Panza, Director of Echocardiography, National Institutes of Health, Building 10, Room 7B-15, Bethesda, Maryland 20892.
Objectives. The present study sought to determine whether myocardial contractile abnormalities accompany the development of chest pain in patients with normal coronary angiograms.
Background. The mechanism of chest pain in patients with angina despite a normal coronary arteriogram is controversial. Although previous studies postulated the existence of coronary microvascular dysfunction, others failed to find evidence of myocardial ischemia, and recent studies have demonstrated abnormal cardiac sensitivity in these patients that can lead to chest pain on a nonischemic basis.
Methods. Seventy patients (26 men and 44 women, mean age 49 ± 10 years) with angina-like chest pain and angiographically normal coronary arteries underwent exercise treadmill testing, radionuclide angiography at rest and during exercise, thallium stress testing and transesophageal dobutamine stress echocardiography. The results of exercise treadmill testing and stress echocardiography were compared with those obtained in 26 normal control subjects (19 men and 7 women, mean age 56 ± 7 years).
Results. Abnormalities consistent with myocardial ischemia were noted in 31% of the patients during exercise treadmill testing, in 16% during exercise radionuclide angiography and in 18% during thallium stress testing. The findings of the radionuclide studies were not concordant with one another and were not related to the presence of repolarization changes during exercise testing. During infusion of dobutamine, chest pain developed in 59 patients (84%) and in none of the control subjects (p < 0.0001); repolarization changes occurred in 22 patients (34%) and in 2 control subjects (8%) (p < 0.04). None of the patients or the control subjects developed regional wall motion abnormalities with dobutamine. The quantitative myocardial contractile response to dobutamine was similar in patients and control subjects, with an 80% power to detect a 25% difference in systolic wall thickening at the maximal dose of dobutamine.
Conclusions. There was no agreement in the results of noninvasive tests in our patients. Despite the frequent provocation of chest pain and electrocardiographic abnormalities with dobutamine, the patients demonstrated a quantitatively normal myocardial contractile response without development of wall motion abnormalities. These observations strongly suggest that myocardial ischemia is not the cause of chest pain in patients with a normal coronary arteriogram.
(J Am Coll Cardiol 1997;29:293–301)
- Received March 25, 1996.
- Revision received October 9, 1996.
- Accepted October 25, 1996.
- The American College of Cardiology