Acute hemodynamic changes during intravenous dipyridamole thallium imaging early after infarction

Donald D Miller, Ronald A. Scott, Jeffrey S. Riesmeyer, Tuhin K. Chaudhuri, Ralph Blumhardt, Charles A. Boucher, Robert A. O'Rourke

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

In order to determine the safety and hemodynamic effects of intravenous dipyridamole infusion for thallium-201 scintigraphy in patients with acute ischemic syndromes, 10 patients with recent uncomplicated myocardial infarction (7 ± 2 days pre-test) had central pressures and cardiac output values measured serially in a coronary care unit during and after the administration of dipyridamole (0.56 mg/kg over 4 minutes) and following aminophylline reversal (50 to 150 mg intravenously) of dipyridamole effect. Cardiac medications were not discontinued. Double product did not change significantly (8522 ± 1811 versus 9044 ± 1701; p = NS). Serious ischemic events did not occur, although 20% of patients had noncardiac side effects and 30% developed ≥ 1 mm ST segment depression with associated angina in one-third of these cases. The peripheral blood pressure and heart rate response did not predict the occurrence of myocardial ischemia. Dipyridamole significantly reduced systemic vascular resistance (1218 ± 302 to 739 ± 166 dyne/sec-1/cm-5; p < 0.05) and increased cardiac index (3.1 ± 0.7 to 4.7 ± 1.0 L/min/m2; p < 0.05) within approximately 10 minutes, in association with a significant increase in pulmonary capillary wedge pressure (13 ± 5 to 17 ± 6 mm Hg; p < 0.05). Three patients developed silent new "V" waves in their pulmonary capillary wedge pressure tracing, associated with anterior thallium redistribution. All three patients with newly elevated wedge pressures (>15 mm Hg) had both thallium-201 redistribution and multivessel coronary disease. A ≥3 mm Hg increase in wedge pressure (mean increase = 6 ± 3 mm Hg) occurred in five of eight (63%) patients with multivessel disease and in five of six (83%) patients with thallium-201 redistribution, while patients with single-vessel disease and no thallium-201 redistribution had a mean wedge increase of 2 ± 1 mm Hg. Aminophylline promptly reversed the hemodynamic effects of dipyridamole to baseline values, including new "V" waves. In summary, dipyridamole induces important hemodynamic changes similar to those occurring in spontaneous or exercise-induced angina that are not blunted by autonomically active drugs or reflexes in this early post-infarction setting. Early (≤7 day) post-infarction testing provides time- and cost-effective risk stratification, saving an average of 4 hospital days and $1843 ± $1181 per patient. As with any diagnostic intervention with the potential to induce myocardial ischemia during risk stratification, this test should be cautiously monitored, especially in patients with recent acute ischemic syndromes.

Original languageEnglish (US)
Pages (from-to)686-694
Number of pages9
JournalAmerican Heart Journal
Volume118
Issue number4
DOIs
StatePublished - Jan 1 1989
Externally publishedYes

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Dipyridamole
Thallium
Infarction
Hemodynamics
Aminophylline
Myocardial Ischemia
Coronary Care Units
Pulmonary Wedge Pressure
Intravenous Infusions
Radionuclide Imaging
Cardiac Output
Vascular Resistance
Coronary Disease
Reflex
Heart Rate
Myocardial Infarction
Exercise
Blood Pressure
Safety
Pressure

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Miller, D. D., Scott, R. A., Riesmeyer, J. S., Chaudhuri, T. K., Blumhardt, R., Boucher, C. A., & O'Rourke, R. A. (1989). Acute hemodynamic changes during intravenous dipyridamole thallium imaging early after infarction. American Heart Journal, 118(4), 686-694. https://doi.org/10.1016/0002-8703(89)90580-2

Acute hemodynamic changes during intravenous dipyridamole thallium imaging early after infarction. / Miller, Donald D; Scott, Ronald A.; Riesmeyer, Jeffrey S.; Chaudhuri, Tuhin K.; Blumhardt, Ralph; Boucher, Charles A.; O'Rourke, Robert A.

In: American Heart Journal, Vol. 118, No. 4, 01.01.1989, p. 686-694.

Research output: Contribution to journalArticle

Miller, DD, Scott, RA, Riesmeyer, JS, Chaudhuri, TK, Blumhardt, R, Boucher, CA & O'Rourke, RA 1989, 'Acute hemodynamic changes during intravenous dipyridamole thallium imaging early after infarction', American Heart Journal, vol. 118, no. 4, pp. 686-694. https://doi.org/10.1016/0002-8703(89)90580-2
Miller, Donald D ; Scott, Ronald A. ; Riesmeyer, Jeffrey S. ; Chaudhuri, Tuhin K. ; Blumhardt, Ralph ; Boucher, Charles A. ; O'Rourke, Robert A. / Acute hemodynamic changes during intravenous dipyridamole thallium imaging early after infarction. In: American Heart Journal. 1989 ; Vol. 118, No. 4. pp. 686-694.
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abstract = "In order to determine the safety and hemodynamic effects of intravenous dipyridamole infusion for thallium-201 scintigraphy in patients with acute ischemic syndromes, 10 patients with recent uncomplicated myocardial infarction (7 ± 2 days pre-test) had central pressures and cardiac output values measured serially in a coronary care unit during and after the administration of dipyridamole (0.56 mg/kg over 4 minutes) and following aminophylline reversal (50 to 150 mg intravenously) of dipyridamole effect. Cardiac medications were not discontinued. Double product did not change significantly (8522 ± 1811 versus 9044 ± 1701; p = NS). Serious ischemic events did not occur, although 20{\%} of patients had noncardiac side effects and 30{\%} developed ≥ 1 mm ST segment depression with associated angina in one-third of these cases. The peripheral blood pressure and heart rate response did not predict the occurrence of myocardial ischemia. Dipyridamole significantly reduced systemic vascular resistance (1218 ± 302 to 739 ± 166 dyne/sec-1/cm-5; p < 0.05) and increased cardiac index (3.1 ± 0.7 to 4.7 ± 1.0 L/min/m2; p < 0.05) within approximately 10 minutes, in association with a significant increase in pulmonary capillary wedge pressure (13 ± 5 to 17 ± 6 mm Hg; p < 0.05). Three patients developed silent new {"}V{"} waves in their pulmonary capillary wedge pressure tracing, associated with anterior thallium redistribution. All three patients with newly elevated wedge pressures (>15 mm Hg) had both thallium-201 redistribution and multivessel coronary disease. A ≥3 mm Hg increase in wedge pressure (mean increase = 6 ± 3 mm Hg) occurred in five of eight (63{\%}) patients with multivessel disease and in five of six (83{\%}) patients with thallium-201 redistribution, while patients with single-vessel disease and no thallium-201 redistribution had a mean wedge increase of 2 ± 1 mm Hg. Aminophylline promptly reversed the hemodynamic effects of dipyridamole to baseline values, including new {"}V{"} waves. In summary, dipyridamole induces important hemodynamic changes similar to those occurring in spontaneous or exercise-induced angina that are not blunted by autonomically active drugs or reflexes in this early post-infarction setting. Early (≤7 day) post-infarction testing provides time- and cost-effective risk stratification, saving an average of 4 hospital days and $1843 ± $1181 per patient. As with any diagnostic intervention with the potential to induce myocardial ischemia during risk stratification, this test should be cautiously monitored, especially in patients with recent acute ischemic syndromes.",
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N2 - In order to determine the safety and hemodynamic effects of intravenous dipyridamole infusion for thallium-201 scintigraphy in patients with acute ischemic syndromes, 10 patients with recent uncomplicated myocardial infarction (7 ± 2 days pre-test) had central pressures and cardiac output values measured serially in a coronary care unit during and after the administration of dipyridamole (0.56 mg/kg over 4 minutes) and following aminophylline reversal (50 to 150 mg intravenously) of dipyridamole effect. Cardiac medications were not discontinued. Double product did not change significantly (8522 ± 1811 versus 9044 ± 1701; p = NS). Serious ischemic events did not occur, although 20% of patients had noncardiac side effects and 30% developed ≥ 1 mm ST segment depression with associated angina in one-third of these cases. The peripheral blood pressure and heart rate response did not predict the occurrence of myocardial ischemia. Dipyridamole significantly reduced systemic vascular resistance (1218 ± 302 to 739 ± 166 dyne/sec-1/cm-5; p < 0.05) and increased cardiac index (3.1 ± 0.7 to 4.7 ± 1.0 L/min/m2; p < 0.05) within approximately 10 minutes, in association with a significant increase in pulmonary capillary wedge pressure (13 ± 5 to 17 ± 6 mm Hg; p < 0.05). Three patients developed silent new "V" waves in their pulmonary capillary wedge pressure tracing, associated with anterior thallium redistribution. All three patients with newly elevated wedge pressures (>15 mm Hg) had both thallium-201 redistribution and multivessel coronary disease. A ≥3 mm Hg increase in wedge pressure (mean increase = 6 ± 3 mm Hg) occurred in five of eight (63%) patients with multivessel disease and in five of six (83%) patients with thallium-201 redistribution, while patients with single-vessel disease and no thallium-201 redistribution had a mean wedge increase of 2 ± 1 mm Hg. Aminophylline promptly reversed the hemodynamic effects of dipyridamole to baseline values, including new "V" waves. In summary, dipyridamole induces important hemodynamic changes similar to those occurring in spontaneous or exercise-induced angina that are not blunted by autonomically active drugs or reflexes in this early post-infarction setting. Early (≤7 day) post-infarction testing provides time- and cost-effective risk stratification, saving an average of 4 hospital days and $1843 ± $1181 per patient. As with any diagnostic intervention with the potential to induce myocardial ischemia during risk stratification, this test should be cautiously monitored, especially in patients with recent acute ischemic syndromes.

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