Stress-Induced ST-Segment Elevation Following Myocardial Infarction and Its Role in Wall Motion Abnormality, Myocardial Ischemia and Viability. Comparison of Response to Exercise, Dobutamine and Dipyridamole.

Abstract

tress-induced ST-segment elevation is a common finding in patients after myocardial infarction (MI), but its mechanism is still controversial. It has been interpreted as a sign of myocardial ischemia, 1,2 left ventricular wall motion abnormality (WMA) 3,4 or both, 5,6 and recent studies have suggested that ST-segment elevation during stress reflects myocardial viability. [7][8][9][10][11] Stress echocardiography has been proposed as a useful technique for the assessment of myocardial ischemia, left ventricular dysfunction and myocardial viability, but although exercise and pharmacological stress, such as dobutamine and dipyridamole, are widely used in stress echocardiography, there has not been a comparative study of the significance of the stressinduced ST-segment elevation of exercise, dobutamine and dipyridamole in identical patients. Dobutamine and dipyridamole differ in their mechanism of inducing myocardial ischemia: dobutamine is a -receptor agonist that increases myocardial oxygen consumption, whereas dipyridamole causes vasodilation and induces vertical and horizontal blood steals. 12 The purpose of the present study was to determine the relationship between ST-segment elevation Japanese Circulation Journal Vol. 65, December 2001 and wall motion response during exercise, dobutamine and dipyridamole stresses, and to examine the mechanism of stress-induced ST-segment elevation following MI. MethodsTwenty-five consecutive patients, 24 men and 1 woman, aged 53±10 years, were prospectively enrolled. The criteria for recruitment were (1) admission to hospital with a diagnosis of first anterior acute MI and (2) abnormal Q wave in at least 2 leads on the electrocardiogram (ECG) performed in conjunction with stress echocardiography. Patients with bundle branch block (n=2), left ventricular hypertrophy (n=2), unstable angina (n=1), left ventricular failure (n=1), bronchial asthma (n=1), and those unable to exercise adequately (n=3) were excluded. One patient developed serious ventricular arrhythmia during a low dose dobutamine test (10 g·kg -1 ·min -1 ) was also excluded. Sixteen patients were treated with thrombolytic agents within 24 h from the beginning of symptoms and 5 patients underwent coronary angioplasty within 48 h from the onset of MI. None of the patients had a coronary stent implanted. Each patient underwent, in random order, exercise, dobutamine and dipyridamole echocardiography on different days and under the same medication. All stress tests were performed 4-6 weeks after the onset of MI. All antianginal drugs, such as -adrenergic blocking agents, nitrates and calcium antagonists, were discontinued on the day before the stress Stress-induced ST-segment elevation following myocardial infarction (MI) has been correlated with myocardial ischemia, viability and wall motion abnormality, but its mechanism is still unclear, so the present study compared ST-segment elevation and wall motion response during exercise, dobutamine and dipyridamole stresses. Twentyfive patients with their first anterior MI ...

The quantification of dipyridamole induced changes in regional deformation in normal, stunned or infarcted myocardium as measured by strain and strain rate: an experimental study

“…However, others have shown that in contrast to exercise and dobutamine, DIP did not induce ST segment elevation in similar patients [28].…”