Hemodynamic and metabolic correlates of dipyridamole-induced myocardial thallium-201 perfusion abnormalities in multivessel coronary artery disease

David P. McLaughlin, George A. Beller, Joel Linden, Carlos R. Ayers, Marcia L. Ripley, Heidi Taylor, Denny D. Watson, Marc D Feldman

Research output: Contribution to journalArticle

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Abstract

The mechanisms responsible for the development of reversible thallium-201 (Tl-201) defects with dipyridamole stress in patients with coronary artery disease (CAD) is not well understood. Previous experimental animal studies have demonstrated coronary steal characterized by an absolute decrease in subendocardial flow distal to a stenosis in response to dipyridamole infusion. Accordingly, the purpose of this study was to determine if reversible Tl-201 defects in response to dipyridamole infusion are reflective of myocardial ischemia or secondary to regional differences in flow reserve. Dipyridamole (0.56 mg/kg) Tl-201 imaging was performed in 23 patients in whom serial electrocardiographic, hemodynamic, aortic and coronary sinus lactate, and coronary sinus adenosine measurements were obtained. All patients with CAD had Tl-201 redistribution (3.8 ± 2.0 defects/patient), and all patients without CAD had normal scans. Mean aortic pressure was similar in both groups and did not change in response to dipyridamole (non-CAD 103 ± 11 vs CAD 99 ± 15 mm Hg, p = NS). Pulmonary capillary wedge pressure was similar at baseline (non-CAD 11 ± 4 vs CAD 13 ± 5 mm Hg, p = NS) and did not change in response to the drug (non-CAD 14 ± 3 vs CAD 15 ± 7 mm Hg, p = NS). Lactate extraction fraction was similar at baseline (non-CAD 0.22 ± 0.09 vs CAD 0.17 ± 0.14, p = NS) and decreased similarly in both groups (non-CAD 0.08 ± 0.06 vs CAD 0.05 ± 0.12, p = NS). Coronary sinus adenosine concentration was significantly higher at baseline in patients with CAD (non-CAD 16 ± 4 vs CAD 35 ± 13 ng/ml, p = 0.034), presumably to maintain resting coronary blood flow, and increased significantly with a comparable percent increase in both groups after dipyridamole (non-CAD 35 ± 10 vs CAD 69 ± 35 ng/ml, p = 0.0001). In this group of patients with multivessel CAD, dipyridamole-induced Tl-201 perfusion abnormalities were not associated with significant myocardial ischemia by hemodynamic and metabolic criteria and appeared to be more indicative of abnormal flow reserve.

Original languageEnglish (US)
Pages (from-to)1159-1164
Number of pages6
JournalThe American Journal of Cardiology
Volume73
Issue number16
DOIs
StatePublished - Jun 15 1994
Externally publishedYes

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Dipyridamole
Thallium
Coronary Artery Disease
Perfusion
Hemodynamics
Arteries
Coronary Sinus
Adenosine
Myocardial Ischemia
Lactic Acid
Sinus of Valsalva
Pulmonary Wedge Pressure
Arterial Pressure
Pathologic Constriction

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Hemodynamic and metabolic correlates of dipyridamole-induced myocardial thallium-201 perfusion abnormalities in multivessel coronary artery disease. / McLaughlin, David P.; Beller, George A.; Linden, Joel; Ayers, Carlos R.; Ripley, Marcia L.; Taylor, Heidi; Watson, Denny D.; Feldman, Marc D.

In: The American Journal of Cardiology, Vol. 73, No. 16, 15.06.1994, p. 1159-1164.

Research output: Contribution to journalArticle

McLaughlin, David P. ; Beller, George A. ; Linden, Joel ; Ayers, Carlos R. ; Ripley, Marcia L. ; Taylor, Heidi ; Watson, Denny D. ; Feldman, Marc D. / Hemodynamic and metabolic correlates of dipyridamole-induced myocardial thallium-201 perfusion abnormalities in multivessel coronary artery disease. In: The American Journal of Cardiology. 1994 ; Vol. 73, No. 16. pp. 1159-1164.
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abstract = "The mechanisms responsible for the development of reversible thallium-201 (Tl-201) defects with dipyridamole stress in patients with coronary artery disease (CAD) is not well understood. Previous experimental animal studies have demonstrated coronary steal characterized by an absolute decrease in subendocardial flow distal to a stenosis in response to dipyridamole infusion. Accordingly, the purpose of this study was to determine if reversible Tl-201 defects in response to dipyridamole infusion are reflective of myocardial ischemia or secondary to regional differences in flow reserve. Dipyridamole (0.56 mg/kg) Tl-201 imaging was performed in 23 patients in whom serial electrocardiographic, hemodynamic, aortic and coronary sinus lactate, and coronary sinus adenosine measurements were obtained. All patients with CAD had Tl-201 redistribution (3.8 ± 2.0 defects/patient), and all patients without CAD had normal scans. Mean aortic pressure was similar in both groups and did not change in response to dipyridamole (non-CAD 103 ± 11 vs CAD 99 ± 15 mm Hg, p = NS). Pulmonary capillary wedge pressure was similar at baseline (non-CAD 11 ± 4 vs CAD 13 ± 5 mm Hg, p = NS) and did not change in response to the drug (non-CAD 14 ± 3 vs CAD 15 ± 7 mm Hg, p = NS). Lactate extraction fraction was similar at baseline (non-CAD 0.22 ± 0.09 vs CAD 0.17 ± 0.14, p = NS) and decreased similarly in both groups (non-CAD 0.08 ± 0.06 vs CAD 0.05 ± 0.12, p = NS). Coronary sinus adenosine concentration was significantly higher at baseline in patients with CAD (non-CAD 16 ± 4 vs CAD 35 ± 13 ng/ml, p = 0.034), presumably to maintain resting coronary blood flow, and increased significantly with a comparable percent increase in both groups after dipyridamole (non-CAD 35 ± 10 vs CAD 69 ± 35 ng/ml, p = 0.0001). In this group of patients with multivessel CAD, dipyridamole-induced Tl-201 perfusion abnormalities were not associated with significant myocardial ischemia by hemodynamic and metabolic criteria and appeared to be more indicative of abnormal flow reserve.",
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AU - Ayers, Carlos R.

AU - Ripley, Marcia L.

AU - Taylor, Heidi

AU - Watson, Denny D.

AU - Feldman, Marc D

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N2 - The mechanisms responsible for the development of reversible thallium-201 (Tl-201) defects with dipyridamole stress in patients with coronary artery disease (CAD) is not well understood. Previous experimental animal studies have demonstrated coronary steal characterized by an absolute decrease in subendocardial flow distal to a stenosis in response to dipyridamole infusion. Accordingly, the purpose of this study was to determine if reversible Tl-201 defects in response to dipyridamole infusion are reflective of myocardial ischemia or secondary to regional differences in flow reserve. Dipyridamole (0.56 mg/kg) Tl-201 imaging was performed in 23 patients in whom serial electrocardiographic, hemodynamic, aortic and coronary sinus lactate, and coronary sinus adenosine measurements were obtained. All patients with CAD had Tl-201 redistribution (3.8 ± 2.0 defects/patient), and all patients without CAD had normal scans. Mean aortic pressure was similar in both groups and did not change in response to dipyridamole (non-CAD 103 ± 11 vs CAD 99 ± 15 mm Hg, p = NS). Pulmonary capillary wedge pressure was similar at baseline (non-CAD 11 ± 4 vs CAD 13 ± 5 mm Hg, p = NS) and did not change in response to the drug (non-CAD 14 ± 3 vs CAD 15 ± 7 mm Hg, p = NS). Lactate extraction fraction was similar at baseline (non-CAD 0.22 ± 0.09 vs CAD 0.17 ± 0.14, p = NS) and decreased similarly in both groups (non-CAD 0.08 ± 0.06 vs CAD 0.05 ± 0.12, p = NS). Coronary sinus adenosine concentration was significantly higher at baseline in patients with CAD (non-CAD 16 ± 4 vs CAD 35 ± 13 ng/ml, p = 0.034), presumably to maintain resting coronary blood flow, and increased significantly with a comparable percent increase in both groups after dipyridamole (non-CAD 35 ± 10 vs CAD 69 ± 35 ng/ml, p = 0.0001). In this group of patients with multivessel CAD, dipyridamole-induced Tl-201 perfusion abnormalities were not associated with significant myocardial ischemia by hemodynamic and metabolic criteria and appeared to be more indicative of abnormal flow reserve.

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