PROLONGED IMPAIRMENT OF REGIONAL CONTRACTILE FUNCTION AFTER RESOLUTION OF EXERCISE-INDUCED ANGINA - EVIDENCE OF MYOCARDIAL STUNNING IN PATIENTS WITH CORONARY-ARTERY DISEASE

Background Delayed recovery of contractile function in spite of normal perfusion tie, ''stunning'') has been described in animal models of e xercise-induced myocardial ischemia. Therefore, we investigated whethe r stunning may result from effort angina in patients. Methods and Resu lts Patients with coronary artery disease underwent exercise testing c ombined with quantitative measurements of contractile function for up to 240 minutes after exercise determined by either measurement of regi onal ejection fraction ((TC)-T-99m radionuclide angiography; n=17, gro up A) or computer-assisted measurement of systolic wall thickening (n= 14, group B). In the latter group, myocardial perfusion was also evalu ated by Tc-99m-sestamibi tomographic imaging. Angina induced marked co ntractile dysfunction. Hemodynamic and ECG changes brought about by is chemia were promptly normalized. Furthermore, no perfusion defects cou ld be detected in group B patients 30 minutes after exercise, yet cont ractile function remained impaired well after cessation of exercise. T hirty minutes into recovery, regional ejection fraction of previously ischemic areas was still 82.6+/-4.6% of baseline in group A (P<.05). S imilarly, in group B patients, systolic thickening of previously ische mic segments was still significantly impaired 60 minutes after exercis e, averaging 33.8+/-2.8% versus 40.5+/-2.7% at baseline (P<.05). Contr actile impairment was fully reversible, as the functioning of previous ly ischemic segments normalized between 60 and 120 minutes of recovery . Conclusions Prolonged yet ultimately reversible impairment of region al myocardial function may occur in patients after exercise-induced an gina in the absence of perfusion abnormalities. These findings indicat e that myocardial stunning may ensue after effort angina in patients w ith severe coronary artery disease.