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Prolonged impairment of regional contractile function after resolution of exercise-induced angina. Evidence of myocardial stunning in patients with coronary artery disease.
Circulation 1996 November 16
BACKGROUND: Delayed recovery of contractile function in spite of normal perfusion (ie, "stunning") has been described in animal models of exercise-induced myocardial ischemia. Therefore, we investigated whether stunning may result from effort angina in patients.
METHODS AND RESULTS: Patients with coronary artery disease underwent exercise testing combined with quantitative measurements of contractile function for up to 240 minutes after exercise determined by either measurement of regional ejection fraction (99mTc radionuclide angiography; n = 17, group A) or computer-assisted measurement of systolic wall thickening (n = 14, group B). In the latter group, myocardial perfusion was also evaluated by 99mTc-sestamibi tomographic imaging. Angina induced marked contractile dysfunction. Hemodynamic and ECG changes brought about by ischemia were promptly normalized. Furthermore, no perfusion defects could be detected in group B patients 30 minutes after exercise, yet contractile function remained impaired well after cessation of exercise. Thirty minutes into recovery, regional ejection fraction of previously ischemic areas was still 82.6 +/- 4.6% of baseline in group A (P < .05). Similarly, in group B patients, systolic thickening of previously ischemic segments was still significantly impaired 60 minutes after exercise, averaging 33.8 +/- 2.8% versus 40.5 +/- 2.7% at baseline (P < .05). Contractile impairment was fully reversible, as the functioning of previously ischemic segments normalized between 60 and 120 minutes of recovery.
CONCLUSIONS: Prolonged yet ultimately reversible impairment of regional myocardial function may occur in patients after exercise-induced angina in the absence of perfusion abnormalities. These findings indicate that myocardial stunning may ensue after effort angina in patients with severe coronary artery disease.
METHODS AND RESULTS: Patients with coronary artery disease underwent exercise testing combined with quantitative measurements of contractile function for up to 240 minutes after exercise determined by either measurement of regional ejection fraction (99mTc radionuclide angiography; n = 17, group A) or computer-assisted measurement of systolic wall thickening (n = 14, group B). In the latter group, myocardial perfusion was also evaluated by 99mTc-sestamibi tomographic imaging. Angina induced marked contractile dysfunction. Hemodynamic and ECG changes brought about by ischemia were promptly normalized. Furthermore, no perfusion defects could be detected in group B patients 30 minutes after exercise, yet contractile function remained impaired well after cessation of exercise. Thirty minutes into recovery, regional ejection fraction of previously ischemic areas was still 82.6 +/- 4.6% of baseline in group A (P < .05). Similarly, in group B patients, systolic thickening of previously ischemic segments was still significantly impaired 60 minutes after exercise, averaging 33.8 +/- 2.8% versus 40.5 +/- 2.7% at baseline (P < .05). Contractile impairment was fully reversible, as the functioning of previously ischemic segments normalized between 60 and 120 minutes of recovery.
CONCLUSIONS: Prolonged yet ultimately reversible impairment of regional myocardial function may occur in patients after exercise-induced angina in the absence of perfusion abnormalities. These findings indicate that myocardial stunning may ensue after effort angina in patients with severe coronary artery disease.
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