Continuous recording of coronary sinus oxygen saturation during atrial pacing in patients with coronary artery disease or with syndrome X

Coronary sinus oxygen saturation was measured continuously during incremental atrial pacing in 34 patients undergoing cardiac catheterisation. In eleven patients with normal coronary arteriograms, negative exercise tests, and no ST segment depression on the electrocardiogram, an increase in the rate of atrial pacing transiently decreased coronary sinus oxygen saturation but within 20 s oxygen saturation returned to the control value. In six patients with coronary artery disease ST segment depression developed during atrial pacing. The coronary sinus oxygen saturation fell and remained reduced until pacing was discontinued. The size of the fall of coronary sinus oxygen saturation increased with increasing heart rate. In seven patients with coronary artery disease the ST segments were unaltered during atrial pacing and coronary sinus oxygen saturation did not fall. Ten patients with syndrome X were studied. In six ST segment depression developed on atrial pacing. In five, three of whom developed ST segment depression, the changes in coronary sinus oxygen saturation during atrial pacing were similar to those observed in patients without any evidence of coronary artery disease. In three, all of whom developed ST segment depression, coronary sinus oxygen saturation gradually increased throughout the period of atrial pacing. In two patients coronary sinus oxygen saturation fell in a manner similar to that observed in patients with obstructive coronary artery disease who developed ST segment depression on pacing. Thus regulation of coronary blood flow in normal persons in response to an increase of heart rate is rapid. Oxygen extraction across the coronary bed can increase by up to 30% and a persistent increase in oxygen extraction is an indicator of myocardial ischaemia. The term "syndrome X" does not describe a homogeneous group of patients but in the majority coronary sinus oxygen saturation does not fall despite symptoms and changes on the electrocardiogram, indicating that inadequate coronary blood flow is not the dominant mechanism.     

Potassium exchange in the human heart during atrial pacing and myocardial ischaemia

Potassium homoeostasis in the heart was studied during atrial pacing in 20 patients undergoing diagnostic coronary angiography. The potassium concentrations in the coronary sinus and a systemic artery were recorded continuously by means of catheter tip potassium electrodes. Ten patients with coronary artery disease and a positive exercise test developed chest pain and ST segment depression on the electrocardiogram during atrial pacing. Potassium concentrations in the coronary sinus rose initially and increased further when myocardial ischaemia developed. Ten patients including five with normal coronary arteries remained symptom free during atrial pacing with no electrocardiographic changes. In these patients coronary sinus potassium concentration increased at the onset of pacing, but returned to near control values despite continued pacing. In both groups arterial potassium concentration remained constant. Immediately after the end of pacing there was an abrupt transient fall in potassium concentrations in the coronary sinus to below control values. These results indicate that in man, as in other species, an increase in heart rate causes the transient movement of potassium out of the cell into the extracellular space. The onset of myocardial ischaemia is associated with a further loss of potassium from the cell. The end of pacing or ischaemia is accompanied by a re-uptake of potassium by heart muscle.     

Potassium exchange in the human heart during atrial pacing and myocardial ischaemia.

Potassium homoeostasis in the heart was studied during atrial pacing in 20 patients undergoing diagnostic coronary angiography. The potassium concentrations in the coronary sinus and a systemic artery were recorded continuously by means of catheter tip potassium electrodes. Ten patients with coronary artery disease and a positive exercise test developed chest pain and ST segment depression on the electrocardiogram during atrial pacing. Potassium concentrations in the coronary sinus rose initially and increased further when myocardial ischaemia developed. Ten patients including five with normal coronary arteries remained symptom free during atrial pacing with no electrocardiographic changes. In these patients coronary sinus potassium concentration increased at the onset of pacing, but returned to near control values despite continued pacing. In both groups arterial potassium concentration remained constant. Immediately after the end of pacing there was an abrupt transient fall in potassium concentrations in the coronary sinus to below control values. These results indicate that in man, as in other species, an increase in heart rate causes the transient movement of potassium out of the cell into the extracellular space. The onset of myocardial ischaemia is associated with a further loss of potassium from the cell. The end of pacing or ischaemia is accompanied by a re-uptake of potassium by heart muscle.     

Angina pectoris with normal coronary arteriograms: hemodynamic and metabolic response to atrial pacing.

Seventeen subjects ranging from 36 to 58 years of age presented with chest pain suggestive of myocardial ischemia. Each patient had a positive double Master's two-step test with ST segment depression of 0.5 mm. or more in the postexercise ECG. In each case coronary angiography and left ventriculography were normal. Hemodynamic and metabolic investigations were carried out during sinus rhythm and atrial pacing. Thirteen patients experienced pain during pacing but only one showed an abnormal hemodynamic response. Two patients showed abnormal myocardial lactate metabolism during the control period and four during pacing-induced tachycardia. The increase in ejection fractions in this group suggests hyperdynamic ventricular contraction which could result in increased oxygen requirements and thus induce ischemic pain in the absence of arteriographically demonstrable coronary artery disease.     

The pacing stress test: thallium-201 myocardial imaging after atrial pacing. Diagnostic value in detecting coronary artery disease compared with exercise testing

Many patients suspected of having coronary artery disease are unable to undergo adequate exercise testing. An alternate stress, pacing tachycardia, has been shown to produce electrocardiographic changes that are as sensitive and specific as those observed during exercise testing. To compare thallium-201 imaging after atrial pacing stress with thallium imaging after exercise stress, 22 patients undergoing cardiac catheterization were studied with both standard exercise thallium imaging and pacing thallium imaging. Positive ischemic electrocardiographic changes (greater than 1 mm ST segment depression) were noted in 11 of 16 patients with coronary artery disease during exercise, and in 15 of the 16 patients during atrial pacing. One of six patients with normal or trivial coronary artery disease had a positive electrocardiogram with each test. Exercise thallium imaging was positive in 13 of 16 patients with coronary artery disease compared with 15 of 16 patients during atrial pacing. Three of six patients without coronary artery disease had a positive scan with exercise testing, and two of these same patients developed a positive scan with atrial pacing. Of those patients with coronary artery disease and an abnormal scan, 85% showed redistribution with exercise testing compared with 87% during atrial pacing. Segment by segment comparison of thallium imaging after either atrial pacing or exercise showed that there was a good correlation of the location and severity of the thallium defects (r = 0.83, p = 0.0001, Spearman rank correlation). It is concluded that the location and presence of both fixed and transient thallium defects after atrial pacing are closely correlated with the findings after exercise testing.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of indomethacin on coronary hemodynamics, myocardial metabolism and anginal threshold in coronary artery disease

The effects of orally administered indomethacin or placebo on coronary hemodynamics were studied in 23 patients with coronary artery disease. After indomethacin administration the systemic arterial pressure increased by 12 +/- 4% and the myocardial oxygen consumption by 24 +/- 11%. Coronary sinus flow did not change and coronary vascular resistance increased slightly. Oxygen saturation of the arterial blood did not change, but coronary sinus saturation decreased substantially. Hemodynamic values returned to normal 150 minutes after administration of indomethacin. During rapid atrial pacing, coronary sinus flow increased 79 +/- 14% above the rest value when pacing was done before indomethacin administration; only a 56 +/- 12% increase was seen when pacing was repeated after indomethacin. Peak heart rate achieved during atrial pacing, severity of angina and the degree of ST-segment depression were not altered by indomethacin treatment. Orally administered indomethacin has a mild coronary vasoconstrictive effect that does not interfere substantially with the expected increase in myocardial blood flow during rapid atrial pacing. Anginal threshold is not altered by orally administered indomethacin.     

Nocturnal angina: precipitating factors in patients with coronary artery disease and those with variant angina

Factors precipitating nocturnal myocardial ischaemia were investigated in 10 patients with frequent daytime and nocturnal angina pectoris. Eight patients had fixed obstructive coronary artery disease or a low exercise threshold or both before the onset of ischaemia. Two patients had variant angina with normal coronary arteries and negative exercise tests. During sleep the electrocardiogram, electroencephalogram, electro-oculogram, electromyogram, chest wall movements, nasal airflow, and oxygen saturation were continuously measured. Forty two episodes of transient ST segment depression were recorded in the eight patients with coronary artery disease and 26 episodes of ST segment depression and elevation in the two patients with variant angina and normal coronary arteries. All episodes of ST segment depression in the former group of patients were preceded by an increase in heart rate as a result of arousal and lightening of sleep, bodily movements, rapid eye movement sleep, or sleep apnoea (one episode). In contrast, in the variant angina group no increase in heart rate, arousal, or apnoea preceded 23 of the 26 episodes of ST segment change. Thus increase in myocardial oxygen demand was important in precipitating nocturnal angina in patients with coronary artery disease and reduced coronary reserve. In the patients with coronary spasm these factors did not often precede the onset of nocturnal myocardial ischaemia.     

Haemodynamic response to myocardial ischaemia during unrestricted activity, exercise testing, and atrial pacing assessed by ambulatory pulmonary artery pressure monitoring

Ambulatory pulmonary artery pressure monitoring by means of a transducer tipped catheter with a simultaneous frequency modulated electrocardiogram and a miniaturised tape recorder was used to study the haemodynamic implications of ST segment depression in patients with coronary artery disease. Nineteen male patients (mean (SD) age 58 (11) years) with clinical and angiographic evidence of coronary artery disease were studied together with six controls. Changes in the ST segment and pulmonary artery diastolic pressure during treadmill exercise, atrial pacing, and unrestricted ambulant activity were analysed. During exercise, pulmonary artery diastolic pressure rose significantly in patients with coronary artery disease but not in the controls. One patient with ST depression greater than 1 mm did not have a rise in pulmonary artery diastolic pressure on exercise; two had a rise in pulmonary artery diastolic pressure with no ST segment change despite severe angina. The pulmonary artery diastolic pressure tended to rise before or simultaneously with the onset of ST segment depression. The haemodynamic response to atrial pacing was similar in normal controls and patients with coronary artery disease. During ambulatory monitoring there were 29 episodes of ST segment depression all of which were associated with a rise in pulmonary artery diastolic pressure and chest pain. The onset of ST segment depression occurred before a rise in pulmonary artery diastolic pressure in 11 episodes, was simultaneous with it in 11, and followed it in seven episodes. During exercise and ambulatory monitoring there was a correlation between the magnitude of ST segment depression and the rise in pulmonary artery diastolic pressure. Pain was a late feature during exercise, atrial pacing, and anginal episodes. This technique for the first time allows the relation between ST segment changes and haemodynamic alterations in left ventricular function to be assessed in ambulant patients with coronary artery disease.     

Haemodynamic response to myocardial ischaemia during unrestricted activity, exercise testing, and atrial pacing assessed by ambulatory pulmonary artery pressure monitoring.

Ambulatory pulmonary artery pressure monitoring by means of a transducer tipped catheter with a simultaneous frequency modulated electrocardiogram and a miniaturised tape recorder was used to study the haemodynamic implications of ST segment depression in patients with coronary artery disease. Nineteen male patients (mean (SD) age 58 (11) years) with clinical and angiographic evidence of coronary artery disease were studied together with six controls. Changes in the ST segment and pulmonary artery diastolic pressure during treadmill exercise, atrial pacing, and unrestricted ambulant activity were analysed. During exercise, pulmonary artery diastolic pressure rose significantly in patients with coronary artery disease but not in the controls. One patient with ST depression greater than 1 mm did not have a rise in pulmonary artery diastolic pressure on exercise; two had a rise in pulmonary artery diastolic pressure with no ST segment change despite severe angina. The pulmonary artery diastolic pressure tended to rise before or simultaneously with the onset of ST segment depression. The haemodynamic response to atrial pacing was similar in normal controls and patients with coronary artery disease. During ambulatory monitoring there were 29 episodes of ST segment depression all of which were associated with a rise in pulmonary artery diastolic pressure and chest pain. The onset of ST segment depression occurred before a rise in pulmonary artery diastolic pressure in 11 episodes, was simultaneous with it in 11, and followed it in seven episodes. During exercise and ambulatory monitoring there was a correlation between the magnitude of ST segment depression and the rise in pulmonary artery diastolic pressure. Pain was a late feature during exercise, atrial pacing, and anginal episodes. This technique for the first time allows the relation between ST segment changes and haemodynamic alterations in left ventricular function to be assessed in ambulant patients with coronary artery disease.     

Nocturnal angina: precipitating factors in patients with coronary artery disease and those with variant angina.

Factors precipitating nocturnal myocardial ischaemia were investigated in 10 patients with frequent daytime and nocturnal angina pectoris. Eight patients had fixed obstructive coronary artery disease or a low exercise threshold or both before the onset of ischaemia. Two patients had variant angina with normal coronary arteries and negative exercise tests. During sleep the electrocardiogram, electroencephalogram, electro-oculogram, electromyogram, chest wall movements, nasal airflow, and oxygen saturation were continuously measured. Forty two episodes of transient ST segment depression were recorded in the eight patients with coronary artery disease and 26 episodes of ST segment depression and elevation in the two patients with variant angina and normal coronary arteries. All episodes of ST segment depression in the former group of patients were preceded by an increase in heart rate as a result of arousal and lightening of sleep, bodily movements, rapid eye movement sleep, or sleep apnoea (one episode). In contrast, in the variant angina group no increase in heart rate, arousal, or apnoea preceded 23 of the 26 episodes of ST segment change. Thus increase in myocardial oxygen demand was important in precipitating nocturnal angina in patients with coronary artery disease and reduced coronary reserve. In the patients with coronary spasm these factors did not often precede the onset of nocturnal myocardial ischaemia.     

The myocardial oxygen supply/demand ratio in patients with and without coronary artery disease

This study was performed to assess the relationship between coronary sinus blood flow (by thermodilution) and myocardial oxygen demand (heart rate-systolic arterial pressure double product) during atrial pacing in patients with and without coronary artery disease. In 11 individuals with coronary artery disease, pacing was performed to ischemia, as reflected by electrocardiographic changes or lactate production; 8 patients without coronary artery disease served as controls. Coronary sinus blood flow (in ml/min) was similar for the two groups at rest. However, the increase in coronary blood flow from rest to peak pacing was less (P = 0.025) in those with coronary artery disease (50 ± 26 ml/min) than in controls (79 ± 26 ml/min). The ratio of coronary sinus blood flow to double product was the same at rest in both groups (11.1 ± 2.2 × 10^?3 controls, 11.6 ± 2.7 × 10^?3 coronary artery disease; NS). At peak pacing, it was unchanged in the controls (10.4 ± 2.0 × 10^?3) but fell in those with coronary artery disease (9.0 ± 2.5 × 10^?3; P = 0.002). The aortic-coronary sinus oxygen content difference was similar at rest in both groups and did not change in response to pacing in either group. Thus, in response to augmented myocardial oxygen demand, patients without coronary artery disease have an appropriate increase in coronary blood flow and myocardial oxygen supply, while in those with coronary artery disease who develop ischemia the increment in myocardial blood flow (and oxygen supply) is inappropriately low.     

Evaluation of myocardial oxygen extraction dynamics in syndrome X by continuous measurement of coronary sinus oxygen saturation and its relation to clinical features]

We investigated the relation of myocardial oxygen extraction dynamics to pathophysiology and clinical features in syndrome X. In patients with syndrome X who underwent cardiac catheterization, coronary sinus oxygen saturation (n = 21) during rapid atrial pacing loading was continuously measured using a fiberoptic catheter system, and global and regional left ventricular function (n = 14) was evaluated before and immediately after pacing loading. Results were as follows: 1) In 5 of 21 patients with syndrome X, coronary sinus oxygen saturation during pacing loading fell less than 5% below the baseline without any impairments of global and regional left ventricular function. 2) In 16 patients with syndrome X, coronary sinus oxygen saturation during the pacing loading continuously fell over 5% below the baseline accompanied by impairment of both global and regional left ventricular function. The decrease in regional wall motion of the left ventricle was mainly observed in the apical area. These findings imply that changes in myocardial oxygen extraction dynamics in syndrome X during rapid atrial pacing may show the extent of a patchy area where myocardial oxygen demand-supply imbalance occurs due to coronary microcirculatory disturbances.     

Effects of pharmacologically-induced hypertension on myocardial ischemia and coronary hemodynamics in patients with fixed coronary obstruction

Twenty patients with fixed coronary artery obstruction were studied during rapid atrial pacing and methoxamine infusion. During pacing to heart rates of 142 +/- 4 (mean +/- SEM) beats per minute coronary sinus flow increased from 108 +/- 8 to 187 +/- 15 cc/min and myocardial oxygen consumption increased by + 80 +/- 11%. During methoxamine infusion that raised arterial systolic pressure to 196 +/- 5 mm Hg, similar increases in coronary sinus flow (to 179 +/- 13 cc/min) and myocardial oxygen consumption (+ 77 +/- 12%) occurred. Chest pain and ischemic ST segment changes developed in 17 and 14 patients respectively during atrial pacing, an incidence significantly greater (P less than 0.05) than during infusion of methoxamine (6 and 3 patients). Myocardial lactate extraction which averaged 26 +/- 4% during control was decreased to 10 +/- 8% during pacing and to 24 +/- 7% during methoxamine; the difference between decreases was not significant. The data show that at similar increases in myocardial oxygen consumption stress of increased heart rate results in more myocardial ischemia than stress of increased afterload.     

Continuous monitoring of coronary sinus oxygen saturation during pacing loading in patients with syndrome X

To determine whether patients with syndrome X suffer from myocardial ischemia, coronary sinus oxygen saturation was continuously measured during pacing loading in 31 patients. Subjects were categorized by groups as syndrome X (11 patients), effort angina (14), and old myocardial infarction and valvular heart disease (6). Pacing loading induced evidence of ischemia in all syndrome X patients and in eight of the 11 patients with effort angina, while there was no such evidence in those with old myocardial infarction and valvular heart disease. Coronary sinus oxygen saturation in syndrome X decreased significantly from 44.2 +/- 5.8% to 33.5 +/- 4.4% (p less than 0.01), and it decreased from 47.0 +/- 4.9% to 31.2 +/- 4.0% (p less than 0.01) in effort angina with induced ischemic evidence, indicating that a significant reduction in coronary sinus oxygen saturation reflects the presence of myocardial ischemia. In the group with old myocardial infarction and valvular heart disease, coronary sinus oxygen saturation remained nearly unchanged during pacing. The pattern of depression of coronary sinus oxygen saturation during pacing was steeper in effort angina than in syndrome X. Therefore, we conclude that, although syndrome-X may not be a homogeneous group of patients, most of them may develop myocardial ischemia due to reduced vasodilator reserves of the small coronary artery.     

Detection of pacing-induced myocardial ischemia by endocardial electrograms recorded during cardiac catheterization

Rapid atrial pacing confirms myocardial ischemia in patients with coronary artery disease when angina is provoked, and is accompanied by an increase in left ventricular end-diastolic pressure. In such cases, abnormalities in the surface electrocardiogram (ECG) are often not apparent. To enhance detection of subendocardial ischemia during rapid atrial pacing, local unipolar electrograms were recorded from the tip of a 0.025 in. (0.064 cm) diameter guidewire positioned against the endocardial surface of potentially ischemic regions. Endocardial electrograms, left ventricular end-diastolic pressure and multiple surface ECG leads were recorded during rapid atrial pacing in 21 patients with coronary artery disease. Before pacing, endocardial electrograms in all 21 patients were free of ST elevation. Marked ST elevation was apparent in 17 of the 21 patients after rapid atrial pacing and could be abolished by nitroglycerin. Moreover, in several patients, endocardial ST elevation after rapid atrial pacing was abolished after successful percutaneous transluminal coronary angioplasty of the critically stenosed artery supplying the ischemic region of myocardium. It is concluded that ST elevation in the endocardial electrogram after rapid atrial pacing is a reflection of myocardial ischemia and may be a sensitive marker of pacing-induced ischemia appearing earlier than angina, postpacing increase in left ventricular end-diastolic pressure or ST depression in the surface ECG.     

Continuous measurement of coronary sinus oxygen saturation in patients with effort angina and vasospastic angina]

Coronary sinus oxygen saturation (CSO2-Sat) was measured continuously using a fiberoptic catheter system during interventional catheterization, i.e., pacing stress test and ergonovine provocation test to determine whether such measurement can detect myocardial ischemia. Subjects consisted of 24 patients who underwent routine cardiac catheterization; 14 patients with effort angina, 3 with old myocardial infarction and 3 with valvular heart disease were assigned to pacing stress test, and 4 with vasospastic angina were assigned to ergonovine provocation test. The results were as follows: 1. Among 14 patients with effort angina, ischemic electrocardiographic changes occurred in 10 patients during pacing stress test. Of these 10 patients, CSO2-Sat decreased in 8 with ischemic electrocardiographic changes. All patients with decrease in CSO2-Sat had significant left coronary artery stenosis. CSO2-Sat continued to decrease throughout intervention and never came back to the baseline. Decrease in CSO2-Sat was more than 5% in most of the cases. 2. In all patients with vasospastic angina, coronary vasospasm was induced by the ergonovine provocation test. CSO2-Sat declined (> 5%) gradually, preceding anginal pain and ischemic ST segment changes. The present study suggests that continuous monitoring of coronary sinus oxygen saturation may be useful in detecting myocardial ischemia at its early stage, except for patients with right coronary artery disease.     

Effects of atrial pacing on QT dispersion in patients with coronary artery disease without angina pectoris and ST segment depression.

The aim of this study was to investigate QT dispersion during atrial pacing in patients with coronary artery disease (CAD) without clinical ischemia, such as angina pectoris and ST segment depression. Thirteen patients with normal coronary arteries and 42 patients with CAD (12 with single-vessel, 16 with two-vessel and 14 with three-vessel disease) having no angina pectoris or ST segment depression during atrial pacing with maximum rate of 120/minute were enrolled in the study. Twelve-lead surface ECGs were recorded at 100 mm/second paper speed before pacing, at maximum pacing rate, and during the recovery period for measurement of QT interval parameters. Corrected QTd (QTcd) increased from 43.4 +/- 8.1 to 49.3 +/- 9.5 ms (p < 0.05) in the control group, from 46.1 +/- 8.1 to 74.3 +/- 7.7 ms (p < 0.0001) in the single-vessel disease group, from 48.5 +/- 10.4 to 93.8 +/- 22.1 ms in the two-vessel disease group (p < 0.0001), and from 49.7 +/- 13.6 to 128.5 +/- 31 ms (p < 0.0001) in the three-vessel disease group at peak atrial pacing period. A positive correlation was found between the severity of CAD and QTcd (r = 0.49, p < 0.0001). It was found that pacing-induced QTc dispersion identifies coronary disease extent, even when there is no ST depression or T wave inversion during pacing.     

Continuous coronary sinus and arterial pH monitoring during pacing-induced ischaemia in coronary artery disease.

Catheter tip pH electrodes were used for continuous recording of coronary sinus and arterial pH during atrial pacing in 20 patients undergoing coronary arteriography for chest pain. An ischaemic response to atrial pacing was identified by the onset of angina and/or electrocardiographic abnormalities. Technically satisfactory coronary sinus recordings were obtained in 18 patients. Mean coronary sinus pH at the peak pacing rate fell by 0.021 +/- 0.006 units (n = 9) in the ischaemic group, while there was no significant change in the non-ischaemic group. A larger fall in coronary sinus pH (-0.052 +/- 0.009) was found in the ischaemic group in the 30 seconds after the end of atrial pacing, the maximum change occurring after 16.1 +/- 1.5 seconds. A maximum fall of coronary sinus pH greater then 0.02 units identified patients with an ischaemic response. Changes in arterial pH did not account for these results. The sensitivity of coronary sinus pH recording for the detection of ischaemic heart disease is enhanced by sampling during the "washout" phase after the end of pacing.     

Abnormal regional myocardial flow in myocardial bridging of the left anterior descending coronary artery

A patient with angina pectoris, myocardial bridging of the left anterior descending coronary artery and otherwise normal coronary arteries is presented. Regional myocardial blood flow was studied with the thermodilution technique. Atrlal pacing of the heart at a rate of over 140/min reproduced the anginal syndrome, with S-T segment depression in the electrocardiogram. There was a transient decrease in great cardiac vein flow during rapid pacing with a simultaneous increase in total coronary sinus flow. The study demonstrates that in this patient, a myocardial bridge was associated with decreased blood flow to the area perfused by the bridged artery with a concomitant increase in coronary sinus flow as the pacing rate was increased from 96 to 150 and 180/min.After administration of nitroglycerin, the bridging effect was more accentuated on angiography; pacing-induced tachycardia was associated with similar changes in great cardiac vein and coronary sinus flows with less S-T segment depression in the electrocardiogram and chest pain of milder intensity.     

Coronary artery spasm during dobutamine stress echocardiography in a patient with angiographically normal coronary arteries.

Dobutamine stress echocardiography (DSE) has been extensively used for diagnostic and prognostic purposes in patients with suspected or known coronary artery disease. During DSE transitory alterations of myocardial wall mobility can occur in the absence of electrocardiographic alterations, or they can be associated with ST segment depression or even elevation on the electrocardiogram. ST segment elevation during DSE has been reported as an infrequent event, generally associated with previous myocardial infarction or coronary artery disease with critical lesions, since the positive inotropic and chronotropic effects of dobutamine produce an increase in myocardial oxygen demand, causing ischemia and segmental contractility abnormalities in patients with significant coronary stenosis. The present case relates to a patient referred for DSE after an ischemic treadmill exercise test. During DSE she presented ST segment elevation associated with chest pain. Subsequent coronary arteriography showed normal coronary arteries. We speculate that coronary spasm may have occurred in this patient, as a paradoxical response to the dobutamine-induced increase in coronary flow.