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PubMed1989

Dipyridamole inhibits red cell-induced platelet activation.

We have recently shown that red blood cells can induce spontaneous platelet aggregation (SPA) in whole blood ex vivo, which could be inhibited by dipyridamole. Since this drug, at therapeutic doses is not an effective inhibitor of platelet aggregation in platelet rich plasma, the inhibition of platelet interaction with the red cell was thought to be the mechanism of its action. Values for the percentage fall in the single platelet count due to SPA in whole blood after 3 and 6 min rollermixing were: control 15 +/- 2.2 and 42 +/- 2.9; 6 microM dipyridamole 6 +/- 1.1 (P less than 0.001) and 31 +/- 2.6 (P less than 0.01); 12 microM dipyridamole 2 +/- 0.9 (P less than 0.0005) and 22 +/- 2.3 (P less than 0.0005) (mean +/- SEM, n = 10). Electron microscopic observation revealed that the aggregation involves an initial platelet adhesion to the red blood cell; the adherent platelets then become activated and serve as foci for the growing aggregates. Dipyridamole appeared to inhibit the initial platelet adhesion to the red cell (the principal trigger mechanism for SPA) which may mimic the initiation of thrombosis in some situations in vivo. The inhibitory effect of dipyridamole on the platelet-red cell interaction suggests that this drug has antithrombotic potential in situations where red blood cells have a trigger role in platelet activation and may explain why the drug has been more effective in some situations than in others.

Adult↗
PubMed1987

Dipyridamole reduced myocardial platelet and leukocyte deposition following ischemia and cardioplegia.

Urgent coronary revascularization for acute myocardial ischemia results in an increased mortality and morbidity. Deposition of activated platelets and leukocytes into the ischemic myocardium during reperfusion may augment perioperative ischemic injury. Dipyridamole reduces platelet activation and may reduce myocardial deposition and prevent ischemic injury during reperfusion. The effects of dipyridamole on myocardial platelet and leukocyte deposition were evaluated in a canine model of acute regional myocardial ischemia with reperfusion during cardioplegia on cardiopulmonary bypass. Eight dogs underwent left anterior descending (LAD) coronary artery ligation for 45 min followed by cardiopulmonary bypass and release of the ligature during 60 min of cold crystalloid cardioplegic arrest to simulate urgent revascularization. Four dogs were randomized to receive an infusion of dipyridamole perioperatively (50 mg/hr) and 4 dogs served as controls. Autologous platelets were labeled with 111In, leukocytes with 99mTc, and erythrocytes with 51Cr. The labeled cells were infused immediately after cross-clamp release and myocardial biopsies were obtained at 10, 20, 30, and 60 min of reperfusion. Platelets were deposited in the myocardium during reperfusion and four times more platelets were found in the LAD region than the circumflex region. Leukocyte deposition was similar in the LAD and circumflex regions. Dipyridamole reduced both platelet and leukocyte deposition and the reduction was greater in the LAD than in the circumflex region. Myocardial platelet and leukocyte deposition was found after regional ischemia, cardioplegia, and cardiopulmonary bypass. Dipyridamole reduced myocardial platelet and leukocyte deposition and may reduce perioperative ischemic injury.

Animals↗
PubMed1987

Evidence for an anti-aggregatory effect of adenosine at physiological concentrations and for its role in the action of dipyridamole.

The effects of physiological adenosine concentrations on platelet aggregation in vitro were studied. Furthermore, we evaluated the effect of elevated adenosine levels in vivo, produced by the administration of dipyridamole, on platelet aggregation in whole blood. Platelet aggregation in plasma was significantly inhibited in vitro by adenosine at all concentrations tested in the physiological range (0.1-1.0 microM, 14-63% inhibition). Dipyridamole by itself had no effect at a therapeutic plasma concentration in vitro. Ten patients with ischaemic cerebrovascular disease were given 100 mg dipyridamole orally, and the level of adenosine increased from 0.22 to 0.29 microM (p less than 0.05). This was accompanied by a decrease in ADP-induced platelet aggregation in whole blood (17 to 15 ohms, p less than 0.05). When dipyridamole was infused in 11 healthy subjects, the adenosine level was not significantly elevated but the platelet aggregation was inhibited (from 13 to 11 ohms, p less than 0.05). It is concluded that adenosine may be of importance in the physiological regulation of platelet aggregation. Furthermore, dipyridamole treatment is associated with an anti-aggregatory effect that is probably mediated by its effect on endogenous adenosine levels.

Adenosine↗
PubMed1990

Dipyridamole combined with anticoagulant in prevention of early postoperative thromboembolism after cardiac valve replacement.

The preventive effect of 300 mg/day dipyridamole, plus warfarin, on the development of thromboembolism after cardiac valve replacement was evaluated. Study 1 involved 71 patients receiving dipyridamole, 100 mg t.i.d., plus warfarin and resulted in a 2.8% incidence of thromboembolism. Study 2 involved 179 patients and compared the effectiveness of slow release capsules with tablet form dipyridamole at the same dosage, both plus warfarin. No thromboembolic episodes occurred in either group. No serious side-effects of dipyridamole were seen in either study. The results suggest that both slow release and tablet form dipyridamole in combination with warfarin are useful in the postoperative management of heart valve replacement.

Adolescent↗
PubMed1996

The pyrimido-pyrimidine derivatives, dipyridamole, mopidamol and RA-642, prevent from retinal vascular defects in experimental diabetes mellitus.

We compared the effects of dipyridamole, RA-642, and mopidamol on platelet activity and thromboxane/prostacyclin balance in relation to the degree of retinal vascularization in a model of experimental streptozotocin-induced diabetes in rats. After 3 months, collagen-induced platelet aggregation in whole blood was 25% higher in diabetic animals than in nondiabetics. Dipyridamole inhibited 43% platelet aggregation, mopidamol 39%, and RA-642 36%. Platelet production of thromboxane B2 was 87% higher in untreated diabetic rats. Mopidamol and RA-642 produced a 46% and 41% inhibition of thromboxane B2. Dipyridamole did not inhibited thromboxane B2 synthesis. Aortic production of 6-keto-PGF1 alpha was 43% lower in untreated diabetic animals and showed no change after treatment with either mopidamol or RA-642. In contrast, dipyridamole caused a 90% increase in aortic production of prostacyclin. Computerized analysis of retinal vascularization showed that untreated diabetic rats had a 81% decrease in the area occupied by peroxidase-labelled vessels as compared with nondiabetics. Treatment with dipyridamole, mopidamol, and RA-642 caused 2.5-fold, 2.8-fold and four-fold increases, respectively, in the percentage of retinal surface occupied by peroxidase-labelled vessels. Differences in retinal vascularization between diabetic animals given RA-642 and nondiabetic controls were negligible.

Animals↗
PubMed1983

Salvage capacity of hepatoma 3924A and action of dipyridamole.

The role and behavior of the salvage enzymes in the biosynthesis of purines (adenine and hypoxanthine-guanine phosphoribosyltransferases) and pyrimidines (uridine-cytidine, deoxycytidine and thymidine kinases) were elucidated. In liver purine metabolism the transferase activities were orders of magnitude higher than the activities of the enzymes of de novo biosynthesis. In both purine and pyrimidine biosynthesis the activities of the enzymes of the de novo pathways were low (23 pmol to 70 nmol/hr/mg protein), whereas those of salvage synthetic pathways ranged from 0.8 to 1,470 nmol/hr/mg protein. In purine metabolism the salvage enzymes had markedly higher affinity to the shared substrate PRPP (4 to 40 microM) than the rate-limiting enzyme of de novo synthesis, amidophosphoribosyltransferase (900 microM). In rapidly growing hepatoma 3924A the activities of the enzymes of de novo purine biosynthesis increased, whereas those of the salvage pathway changed little. However, the activities of the enzymes of the salvage pathways remained much higher than those of the enzymes of de novo purine production. In pyrimidine production in the hepatomas the activities of both de novo and salvage enzymes markedly increased. However, the activities of the salvage enzymes far outstripped those of the enzymes of the de novo pathways. To inhibit the operation of the salvage pathways, the action of the transport inhibitor, dipyridamole, was examined. In tissue culture, dipyridamole inhibited the transport of purine and pyrimidine nucleosides with an IC50 of 10(-6) or 10(-7) M. As measured by colony-forming assay, dipyridamole killed hepatoma cells with an IC50 of 20 microM. Dipyridamole markedly depressed the pools of ATP, GTP, CTP and UTP; in combination chemotherapy with acivicin, an anti-glutamine agent, synergistic action was observed on the pools of nucleotides in hepatoma 3924A in vivo. These investigations emphasize the importance of the capacity to utilize precursors by the salvage enzymes and may explain, in part at least, the failure of inhibitors of the de novo pathways to yield lasting chemotherapeutic results. Combination chemotherapy of inhibitors of the de novo pathways with an inhibitor of the salvage pathways (dipyridamole) should impact on our understanding of the contribution of salvage pathways and provide a rational basis for successful combination chemotherapy of neoplastic diseases.

Animals↗
PubMed1982

Pulmonary uptake of PGE2 is inhibited by dipyridamole in rat isolated lungs.

The metabolism of prostaglandin E2 (PGE2) is decreased by dipyridamole (20 microM) in rat isolated perfused lungs. The inhibition of the metabolism is reversible as the decreased metabolism returned to the control level when pulmonary infusion of dipyridamole was abolished. After pulmonary injection of 14C-PGE2 (10 nmol) the radioactivity appeared more rapidly in the effluent when dipyridamole was infused into pulmonary circulation. Dipyridamole in vitro did not change the activity of 15-hydroxyprostaglandin dehydrogenase (15-OH-PGDH) in the 100,000 x g supernatant fraction of homogenized lungs. Thus, the decreased metabolism seems to be due to the inhibition of the uptake of PGE2 into the lungs. When the rats were pretreated with dipyridamole in drinking water for one week the activity of 15-OH-PGDH in the 100,000 x g supernatant fraction of the lungs was not changed significantly.

Animals↗
PubMed1983

Dipyridamole interferes with the incorporation of arachidonic acid and stimulates prostacyclin production in rat lungs.

Following the injection of 4 nmol of 14C-arachidonic acid into the pulmonary circulation of rat isolated lungs more than 90% of the radioactivity was retained by the lung tissue. When dipyridamole (20 microM) was infused into the pulmonary circulation during 14C-arachidonate injection the amount of radiolabel was increased in diacylglycerols as well as in phosphatidylinositol and phosphatidylserine of the perfused lungs whereas the amount of radioactivity was decreased in phosphatidylethanolamine. When dipyridamole was infused into the lungs prelabelled with 14C-arachidonic acid the distribution of radiolabel in different lung lipid fractions was not changed significantly. However, dipyridamole seemed to stimulate the formation of prostacyclin in rat lungs as the amount of 6-keto-PGF1 alpha was increased in the perfusion effluent. The present study indicates that dipyridamole interferes with the incorporation of arachidonic acid into different lipids in rat lungs. In addition, the release of prostacyclin seems to be stimulated by dipyridamole.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Determination of dipyridamole by modified extraction-gravimetry with a surface acoustic wave resonator sensor.

A simple and sensitive extraction-gravimetric method for the determination of dipyridamole is presented. The method is based on the extraction of free dipyridamole with chloroform, after neutralization with a basic agent, followed by measurement of the frequency shift response of the specially designed surface acoustic wave resonator sensor after evaporation of the extractant from the surface of the resonator. The frequency shift response was proportional to the amount of dipyridamole in the range 0.065-1.12 micrograms. Experimental parameters and the effect of interfering substances on the assay of dipyridamole were also examined in this study. The method was applied to the determination of dipyridamole in tablets.

Chloroform↗
PubMed1991

Accuracy and safety of technetium-99m hexakis 2-methoxy-2-isobutyl isonitrile (Sestamibi) myocardial scintigraphy with high dose dipyridamole test in patients with effort angina pectoris: a multicenter study. Italian Group of Nuclear Cardiology.

Clinical and physiologic evidence indicates that maximal coronary vasodilation is not achieved in a large number of patients with use of the standard dose of dipyridamole (0.56 mg/kg body weight over 4 min). The feasibility, safety and accuracy of technetium-99m hexakis 2-methoxy-2-isobutyl isonitrile (Sestamibi) scintigraphy associated with intravenous high dose dipyridamole (0.56 mg/kg over 4 min followed 4 min later by an additional 0.28 mg/kg over 2 min) were evaluated in a multicenter study. Planar myocardial perfusion images were obtained at rest and after dipyridamole in 101 patients with effort chest pain and no prior myocardial infarction. High dose dipyridamole (62 patients) was used when typical chest pain or electrocardiographic (ECG) signs of ischemia, or both, did not occur during or after the standard dose (39 patients). With high dose dipyridamole, 34 patients had pain (18 patients) or ECG signs of ischemia (ST depression greater than or equal to 2 mm) (8 patients), or both (8 patients), whereas the other 28 patients had Sestamibi injection in the absence of symptoms or ECG changes. All patients underwent coronary angiography: 81 had significant coronary artery disease (greater than or equal to 50% reduction of lumen diameter) (affecting one vessel in 38, two vessels in 19 and three vessels in 24 patients) and 20 patients had normal coronary arteries. The overall sensitivity, specificity and predictive accuracy of Sestamibi scintigraphy were 81%, 90% and 83%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

Coronary flow velocity changes after intravenous dipyridamole infusion: measurements using intravascular Doppler guide wire. A documentation of flow inhomogeneity.

OBJECTIVES: This study assessed changes in coronary flow velocity measured distal to a significant stenosis of the left anterior descending coronary artery and at the adjacent normal left circumflex coronary artery, produced by intravenous administration of dipyridamole, in patients undergoing coronary angioplasty with a documented perfusion defect on dipyridamole-thallium-201 scintigraphy. BACKGROUND: Significant flow inhomogeneity is believed to develop during coronary vasodilation induced by dipyridamole, causing a defect in the thallium-201 scintigram. The recently developed intracoronary Doppler guide wire permits assessment of flow velocity variables in normal and stenotic arteries. METHODS: In 17 patients with stable angina we studied changes in time-averaged peak velocity and the diastolic/systolic velocity ratio simultaneously using two 0.014-in. (0.36-mm) Doppler guide wires at baseline and after 4 min of dipyridamole infusion (0.56 mg/kg body weight). Coronary flow velocity reserve and relative flow reserve were correlated with the degree of stenosis on coronary angiography and quantitative analysis of thallium-201 images. RESULTS: No changes in distal flow velocity was observed in the stenotic vessel (5.5 +/- 33.7% [mean +/- SD]), in contrast to a significant increase observed in the adjacent normal vessel (162.4 +/- 39.8%). Poststenotic coronary flow velocity reserve correlated with percent lumen diameter stenosis (r = -0.66, p < 0.05). A correlation was also observed between the relative flow reserve/thallium-201 relative perfusion ratio (r = 0.90, p < 0.001). CONCLUSIONS: To our knowledge, these findings represent the first direct proof of dipyridamole-induced flow inhomogeneity producing a perfusion defect on thallium-201 imaging. The degree of inhomogeneity is related to the extent of the perfusion defect.

Adult↗
PubMed2004

Dipyridamole is neuroprotective for cultured rat embryonic cortical neurons.

The effects of a clinically useful cardiovascular agent, dipyridamole, were examined in a rodent tissue culture model of neuroprotection. Dipyridamole effectively protected rat embryonic day 18 (E18) cortical neurons from either 48 h trophic deprivation or 48 h exposure to the glutathione synthesis inhibitor, L-buthionine (R,S) sulfoximine. The neuron sparing actions of dipyridamole were time- and concentration-dependent and mimicked the actions of exogenously applied glutathione. These results demonstrate that dipyridamole protects primary neuronal cultures against either trophic or chemically mediated insults, and suggest that dipyridamole has a potent antioxidant ability that compensates for glutathione depletion in neuronal cultures.

Animals↗
PubMed2004

Glyburide inhibits dipyridamole-induced forearm vasodilation but not adenosine-induced forearm vasodilation.

BACKGROUND: The mechanism of the vasodilator response to adenosine has not been elucidated in humans. Stimulation of adenosine receptors on endothelial and vascular smooth muscle cells with subsequent endothelial release of nitric oxide and opening of adenosine triphosphate (ATP)-sensitive potassium (K(ATP)) channels has been suggested. AIM: The aim of this study was to investigate the involvement of K(ATP) channels in the vasodilator response to adenosine and the nucleoside transport inhibitor dipyridamole. Methods and results In healthy male volunteers, adenosine (0.6, 1.9, 5.6, 19, 57, and 190 nmol. min(-1). dL(-1)) was infused into the brachial artery, and forearm blood flow (FBF) was measured by use of strain-gauge plethysmography. Adenosine increased the FBF ratio (FBF in experimental arm/FBF in control arm) from 1.3 +/- 0.2 to 1.2 +/- 0.2, 1.5 +/- 0.2, 2.8 +/- 0.4, 7.3 +/- 2.3, 11.1 +/- 4.1, and 12.9 +/- 3.7 for the six increasing adenosine doses, respectively. Simultaneous infusion of glyburide (INN, glibenclamide), a blocker of K(ATP) channels, did not affect this response (from 1.7 +/- 0.4 to 1.5 +/- 0.2, 2.2 +/- 0.3, 4.0 +/- 1.0, 9.3 +/- 4.0, 13.5 +/- 6.4, and 15.9 +/- 5.3 for the 6 increasing doses of adenosine, respectively; P =.439, n = 6). The increase in FBF ratio during infusion of the nucleoside transport inhibitor dipyridamole (20, 60, and 200 nmol. min(-1). dL(-1)) was significantly reduced by glyburide, as follows: from 1.2 +/- 0.1 to 1.7 +/- 0.2, 2.4 +/- 0.5, and 2.9 +/- 0.4, respectively, during saline solution and from 1.6 +/- 0.2 to 1.8 +/- 0.2, 2.1 +/- 0.3, and 2.2 +/- 0.4, respectively, during glyburide (P =.010 for effect of glyburide on response from baseline, ANOVA for repeated measures; n = 8). The vasodilator response to dipyridamole was significantly inhibited by the adenosine receptor antagonist theophylline. CONCLUSION: Opening of vascular K(ATP) channels is involved in the forearm vasodilator response to dipyridamole but not to adenosine. Differences in stimulated cell type (endothelium for adenosine versus smooth muscle cells for dipyridamole) may underlie this divergent pharmacologic profile.

Adenosine↗
PubMed2006

Pulmonary hemodynamic effects of dipyridamole infusion in patients with normal and elevated pulmonary artery systolic pressure receiving PB127.

BACKGROUND: Intravenous administration of microspheres used as ultrasound contrast agents may potentially alter pulmonary hemodynamics. PB127 (POINT Biomedical Corp., San Carlos, CA) is an investigational ultrasound perfusion-imaging agent used in conjunction with dipyridamole to diagnose coronary artery disease. The effects of PB127 alone or in combination with dipyridamole on pulmonary hemodynamics have not been described. METHODS: We studied 20 patients, including 10 with elevated screening pulmonary artery systolic pressure (>35 mm Hg). Doppler-derived pulmonary hemodynamics were determined before and after continuous infusion of PB127 (0.175 mg/kg diluted in 5% dextrose) or 5% dextrose. Patients then received dipyridamole (0.56 mg/kg) and hemodynamics were again assessed. RESULTS: During PB127/dextrose infusion, there were no significant changes in pulmonary hemodynamics compared with baseline. After dipyridamole, there were small increases in pulmonary artery systolic pressure and in pulmonary flow and a reduction in pulmonary vascular resistance. These changes occurred in patients with normal and elevated pulmonary artery systolic pressure. CONCLUSION: PB127 infusion does not alter pulmonary hemodynamics. Mild alterations of pulmonary hemodynamics occur after dipyridamole administration.

Aged↗
PubMed2005

The additive prognostic value of restrictive pattern and dipyridamole-induced contractile reserve in idiopathic dilated cardiomyopathy.

BACKGROUND: Diastolic dysfunction and lack of contractile reserve are unfavorable prognostic predictors in patients with dilated cardiomyopathy (DCM). AIMS: This study aims to assess whether diastolic dysfunction and lack of dipyridamole-induced contractile reserve were additive predictors of poor outcome in patients with DCM. METHODS: A total of 116 patients with DCM and ejection fraction (EF<35%) were studied by dipyridamole echo (0.84 mg/kg over 10 min). At rest, a restrictive filling pattern was defined as: E/A ratio >2 and an E-wave deceleration time of <140 ms on transmitral flow velocity profile. RESULTS: Rest wall motion score index (WMSI) was 2.2+/-0.3 and decreased to 1.9+/-0.41 after dipyridamole (p<0.001). During follow-up (median 26.5 months), 22 cardiac deaths occurred. At multivariate analysis, dipyridamole-induced contractile reserve yielded significant incremental prognostic value (RR=0.275, p<0.006) over NYHA class (RR=1.971, p<0.03), angiotensin-converting enzyme inhibitor therapy (RR=0.173, p<0.001), and left ventricular end-diastolic diameter (RR=1.131, p<0.001). The worst prognostic combination was the presence of restrictive pattern at rest and the absence of contractile reserve (deltaWMSI<0.15). CONCLUSION: In patients with DCM, the ominous combination of restrictive transmitral flow pattern and lack of contractile reserve during dipyridamole stress predicts an unfavourable outcome.

Aged↗
PubMed2006

Crystal modification of dipyridamole using different solvents and crystallization conditions.

Dipyridamole crystals having different types of habits, improved dissolution rate were prepared by recrystallization from selected solvents, such as acetonitrile, benzene and methanol (Method I); crystals have also been made by solvent change using methanolic solution of dipyridamole in the presence of 2% solutions of Tween-80, Povidone K30 and polyethylene glycol (PEG) 4000 (Method II). Scanning electron microscopy, X-ray powder diffractometry, IR spectrometry and differential scanning calorimetry were used to investigate the physicochemical characteristics of the crystals. The comparative dissolution behavior of the newly developed crystals and that of the untreated dipyridamole were also studied. It was found that the newly developed crystals were different from each other with respect to physical properties but are chemically identical. The crystals, obtained (Method I) from benzene and acetonitrile, produced needle shaped crystals and that obtained from methanol produced rectangular shaped crystals. But the crystals obtained (Method II) with the methanolic solution of the drug in the presence of Tween-80, Povidone K30 and PEG-4000 produced smooth needle shaped crystals. X-ray diffraction spectra and differential scanning calorimetry study of the newly developed crystals, clearly indicate that dipyridamole exist in different crystal modification. The dissolution rate of newly developed crystals was found to be greater than the pure drug dipyridamole. Stability studies at 40 degrees C (75% RH) for 1 month for the modified crystals as well as the pure drug did show some changes in the XRD and DSC but not in IR studies.

Calorimetry, Differential Scanning↗
PubMed2005

Comparison of treadmill exercise versus dipyridamole stress with myocardial perfusion imaging using rubidium-82 positron emission tomography.

OBJECTIVES: This study assessed the feasibility of treadmill exercise rubidium-82 ((82)Rb) positron emission tomography (PET) and compared image quality and diagnostic content with dipyridamole (82)Rb PET in patients referred for evaluation of coronary artery disease (CAD). BACKGROUND: Dipyridamole stress (82)Rb PET myocardial perfusion imaging (MPI) is an accurate imaging modality used to diagnose CAD and determine prognosis. Although pharmacologic stress is used routinely, exercise treadmill stress may be an alternative and provide clinical information helpful to decision making, particularly for patients unwilling or unable to tolerate pharmacologic stress. METHODS: Fifty patients (mean age, 60 +/- 10 years; 47 men) underwent treadmill exercise and dipyridamole (82)Rb PET. Images were assessed: 1) qualitatively using a 17-segment model and a semiquantitative visual score on a five-point scale and with calculation of summed stress score (SSS), summed rest score (SRS), and summed difference score (SDS); and 2) quantitatively with a 70% threshold for abnormal perfusion and expressed as extent of abnormal perfusion (% left ventricular). RESULTS: Treadmill exercise was preferred by 74% of patients (37 of 50, p < 0.001). The exercise and dipyridamole (82)Rb PET summed scores and quantitative extent of abnormal perfusion were very similar and highly correlated. Results of Bland-Altman analysis showed no significant bias. Image quality was superior with exercise stress with greater myocardial uptake and higher target to background ratios. CONCLUSIONS: Treadmill exercise (82)Rb PET is feasible and provides imaging results of similar diagnostic content and superior image quality compared with dipyridamole stress. Treadmill exercise is a reasonable alternative to pharmacologic stress with (82)Rb PET MPI.

Coronary Circulation↗
PubMed2006

Treadmill exercise produces larger perfusion defects than dipyridamole stress N-13 ammonia positron emission tomography.

OBJECTIVES: The aim of this study was to compare treadmill exercise (TEX) and dipyridamole stress on the uptake and retention of N-13 ammonia. BACKGROUND: Size and severity of stress-induced myocardial perfusion defects are clinically important. Because ammonia uptake and retention seems to be related to perfusion, viability, and metabolism, exercise stress might induce larger perfusion defects than dipyridamole stress. METHODS: Twenty-six patients underwent TEX and dipyridamole stress N-13 ammonia positron emission tomography (PET). Images were assessed with a 17-segment model and a five-point score. Summed stress score (SSS), summed rest score (SRS), and summed difference score (SDS) were calculated. Left ventricular (LV) defect sizes were measured quantitatively with a 70% threshold for abnormal perfusion. RESULTS: Compared with dipyridamole stress, TEX yielded larger SSS (9.1 +/- 5.7 vs. 6.9 +/- 5.9; p < 0.01), SDS (5.8 +/- 4.7 vs. 3.7 +/- 4.6; p < 0.02), and percentage of LV stress defect (19.3 +/- 11.5% vs. 13.8 +/- 13.6%; p < 0.02). CONCLUSIONS: In patients achieving adequate exercise, TEX N-13 ammonia PET myocardial perfusion imaging (MPI) yields larger stress perfusion defects than dipyridamole stress and might reflect the true myocardial ischemic burden. Treadmill exercise might be the preferred method of stress for routine N-13 ammonia PET MPI.

Aged↗