Radionuclide studies in patients with stress-induced ST-segment elevation after acute myocardial infarction

Coma-Canella, Isabel; Gómez, M. del Val; Terol, Ignacio; Rodrigo, Francisco José Rodríguez; Castro, JoséManuel

doi:10.1016/0002-8703(94)90617-3

Cited by 27 publications

(17 citation statements)

References 26 publications

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“…14 Exercise or the dobutamine stress test can also induce ST-segment elevation in patients with old anteroseptal myocardial infarction, possibly due to asynergy. 15,16 These experimental and clinical results support our hypothesis.…”

Section: St-segment Elevation and Sacsupporting

confidence: 84%

Stretch-Activated Ion Channel Blocker Gadolinium Attenuates Ischemic ST-Segment Elevation in Canine Myocardium

Shimada

Nakamura

Iwanaga³

et al. 1999

Jpn Circ J

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yocardial stretch alters the electrophysiological properties of the cardiac myocyte: modulation of phase 2 and 3 of the action potential 1 and activation of the stretch-activated ion channels (SAC). This phenomenon, reported as mechanoelectrical feedback, is thought to contribute to arrhythmogenesis. 2 After the ischemic myocardium ceases its contraction, the nonischemic myocardium stretches and lengthens the ischemic segment during systole. This segmental abnormality of myocardial contraction may alter the transmembrane potential and action potential duration. 3 Our previous study demonstrated that regional ventricular dyskinesia produced by intracoronary injection of negative inotropic agents induced ST-segment elevation without myocardial ischemia, and suggested that regional ventricular dyskinesia may alter the transmembrane potential and action potential duration. 4 The role of the SAC on ischemic STsegment elevation is not yet fully understood. We, therefore, planned to clarify whether the intracoronary administration of a SAC blocker, gadolinium (Gd), would affect the ST-segment elevation during brief coronary occlusion in the in-vivo canine heart. Methods Experimental PreparationsSix mongrel dogs of both sexes weighing 15-20 kg, were sedated with intramuscular injection of 1.0-1.5 mg/kg of droperidol and anesthetized with 25-30 mg/kg of pentobarbital sodium intravenously. Respiration was controlled using a Harvard pump (Harvard Apparatus Inc, South Natick MS, USA), which provided a mixture of room air and 1.0 L/min of oxygen. Thoracotomy was performed through the fifth left intercostal space, and the epicardium was opened. The left anterior descending artery (LAD) was isolated just distal to the first diagonal branch and perfused through a bypass circuit, made of silicone tubing with anticoagulant properties, from the left subclavian artery. Using an electromagnetic flow probe (Nihon Kohden Co, Tokyo, Japan) in the bypass circuit, we measured bypass blood flow (coronary blood flow). A catheter was inserted through the right femoral vein for intravenous infusion. Aortic blood pressure was monitored using a catheter inserted through the right femoral artery. Left ventricular (LV) pressure was measured through a short catheter inserted into the LV cavity from the apex. A pair of ultrasonic dimension crystals (Nihon Kohden Co) was inserted into the subendocardium perfused through the bypass circuit to measure serial changes of regional myocardial contraction in the plane of the LV minor axis. An epicardial electrocardiogram (ECG) was monitored using a contact electrode placed at the center of the region perfused via the bypass circuit, and using a Wilson central terminal as the indifferent electrode. The data were recorded on a polygraph (Nihon Kohden Co) at paper speeds of 25 and 100 mm/s. The hearts were allowed to beat at their spontaneous rate.Experimental Protocol (Fig 1) After stabilization of hemodynamics and documentation of sufficient reactive hyperemia, the coronary bypass was occluded for 5 min be...

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Section: St-segment Elevation and Sacsupporting

confidence: 84%

Stretch-Activated Ion Channel Blocker Gadolinium Attenuates Ischemic ST-Segment Elevation in Canine Myocardium

Shimada

Nakamura

Iwanaga³

et al. 1999

Jpn Circ J

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“…However, persistent STsegment elevation is sometimes observed in patients with ventricular aneurysm, 3 and exercise or dobutamine stressinduced ST-segment elevation has been observed after MI, possibly due to ventricular asynergy. 4,5 Thus, it is important to determine whether myocardial ischemia is present in these patients. The present results showed that nonischemic ST-segment elevation was induced by regional ventricular dyskinesia, indicating that regional wall motion abnormalities can cause ST-segment elevation in the absence of coronary stenotic lesions and that ST-segment elevation is not always a good marker of myocardial ischemia.…”

Section: Discussionmentioning

confidence: 99%

“…3 In addition, an exercise or dobutamine stress-test sometimes induces ST-segment elevation in patients with an old anteroseptal MI, probably due to asynergy. 4,5 These findings suggest that regional ventricular dyskinesia is a possible mechanism for ST-segment elevation unrelated to myocardial ischemia.We investigated the role of regional ventricular dyskinesia in ST-segment elevation not associated with ischemia in a canine model of regional ventricular dyskinesia produced with negative inotropic agents. …”

mentioning

confidence: 91%

Nonischemic ST-Segment Elevation Induced by Negative Inotropic Agents

Shimada¹,

Nakamura

Iwanaga³

et al. 1999

Jpn Circ J

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ince the publication of Pardee's study, 1 ST-segment elevation on an electrocardiogram (ECG) has been considered one of the most useful markers of acute myocardial infarction (MI). During myocardial ischemia, electrical changes, such as shortening of the action potential duration, depolarization of the resting membrane potential and a decrease in the amplitude of the action potential, cause an abnormal injury current from the normal to the ischemic myocardium, resulting in ST-segment elevation. 2 However, persistent ST-segment elevation after the infarcted myocardium heals is thought to be a sign of left ventricular aneurysm. 3 In addition, an exercise or dobutamine stress-test sometimes induces ST-segment elevation in patients with an old anteroseptal MI, probably due to asynergy. 4,5 These findings suggest that regional ventricular dyskinesia is a possible mechanism for ST-segment elevation unrelated to myocardial ischemia.We investigated the role of regional ventricular dyskinesia in ST-segment elevation not associated with ischemia in a canine model of regional ventricular dyskinesia produced with negative inotropic agents. Methods Surgical PreparationsThirty-three mongrel dogs of either sex weighing 15-25 kg were sedated with an intramuscular injection of 1.0-1.5 mg/kg of body weight of droperidol and anesthetized with intravenous injection of 25-30 mg/kg of pentobarbital.Respiration was controlled with a Harvard pump (Harvard Apparatus Inc, South Natick, MA, USA) using a mixture of room air and 1.0 L/min of oxygen. A thoracotomy was performed via the left fifth intercostal space, and the pericardium was opened. The left anterior descending artery (LAD) isolated just distal to the first diagonal branch was cannulated and perfused with autologous arterial blood from the left subclavian artery through a bypass circuit made of silicone tubing with anticoagulant properties. An electromagnetic flow probe (Nihon Kohden Co, Tokyo, Japan) was placed in the bypass circuit to measure bypass blood flow (coronary blood flow). A catheter was inserted through the right femoral vein for intravenous infusions. Aortic pressure was monitored using a catheter inserted via the right femoral artery. Left ventricular (LV) pressure was measured through a short catheter inserted into the LV cavity from the apex. A pair of ultrasonic dimension crystals (Nihon Kohden Co) was inserted into the subendocardium perfused via the bypass circuit to measure serial changes of regional myocardial contraction. The epicardial ECG was monitored using a contact electrode placed at the center of the region perfused via the bypass circuit, and using Wilson central terminal as the indifferent electrode (Fig 1). The data were recorded on a polygraph (Nihon Kohden Co) at a paper speed of 25 and 100 mm/s. The heart was allowed to beat at its spontaneous rate without pacing. Experimental ProtocolAfter documentation of sufficient reactive hyperemia and stabilization of hemodynamic parameters, we administered a continous intracoronary infusion of adenosin...

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“…In 34 patients with recent myocardial infarction, a specificity of 56% of the ST-segment elevation during stress testing for myocardial ischemia assessed by myocardial perfusion scintigraphy was found by Elhendy et al [13]. Coma-Canella et al [14]comparing stress-induced ischemia by dobutamine thallium-201 scintigraphy and stress-induced asynergy by dobutamine radionuclide ventriculography concluded that stress-induced ST-segment elevation in patients with myocardial infarction is not related to ischemia but to stress-induced left ventricular asynergy. In the present study, although 50% of the patients with stress-induced ST-segment elevation in Q wave leads showed ischemia on thallium-201 scintigraphy, there was no overall agreement between ST shifts and myocardial perfusion in the infarct area (ĸ = –0.33; p = NS, fig.…”

Section: Discussionmentioning

confidence: 99%

Role of Myocardial Ischemia and Left Ventricular Wall Motion Abnormalities as Contributory Factors in the Genesis of Exercise-Induced ST-Segment Elevation in Q-Wave Myocardial Infarction

Macieira-Coelho¹,

Garcia-Alves²,

Dionísio³

et al. 1999

Cardiology

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In patients with a previous myocardial infarction, controversy exists regarding the significance of postexercise ST-segment elevation in the infarct-related leads. Although usually admitted to be a sign of left ventricular dysfunction or myocardial aneurysm, other studies however have related this finding to transient myocardial ischemia and to the presence of jeopardized but viable myocardium in the infarct area. The aim of the present study was to assess the significance of postexercise ST-segment elevation in Q-wave leads as a marker of transmural ischemia or left ventricular dysfunction in 36 consecutive patients, 16 with exercise-induced ST-segment elevation in infarct-related leads. Patients were evaluated by treadmill exercise testing, coronary angiography and ventriculography, thallium-201 tomographic scintigraphy and radionuclide ventriculography within 3 months of the first myocardial infarction. Sixteen patients (group I) had exercise-induced ST segment elevation and 20 (group II) postexercise inversion, no change or pseudonormalization of the T wave in infarct-related leads. The study showed no difference in infarct-related artery, vessel disease or luminal diameter stenosis in groups I and II. The overall agreement between ST shifts and myocardial perfusion in the infarct area was 30.56% with a κ coefficient of –0.33 (p = NS). The overall agreement between ST shifts and wall motion abnormalities was 69.44% with a κ coefficient of 0.39 (p < 0.01), stress-induced ST-segment elevation being associated with severe wall contractile disorders in 85% of the patients. In conclusion stress-induced ST-segment elevation in Q wave leads, although not a marker of wall motion abnormalities, is associated with akinesia or dyskinesia of the left ventricular wall.

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Radionuclide studies in patients with stress-induced ST-segment elevation after acute myocardial infarction

Cited by 27 publications

References 26 publications

Stretch-Activated Ion Channel Blocker Gadolinium Attenuates Ischemic ST-Segment Elevation in Canine Myocardium

Stretch-Activated Ion Channel Blocker Gadolinium Attenuates Ischemic ST-Segment Elevation in Canine Myocardium

Nonischemic ST-Segment Elevation Induced by Negative Inotropic Agents

Role of Myocardial Ischemia and Left Ventricular Wall Motion Abnormalities as Contributory Factors in the Genesis of Exercise-Induced ST-Segment Elevation in Q-Wave Myocardial Infarction

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