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PubMed1993

Prevention of one-year vein-graft occlusion after aortocoronary-bypass surgery: a comparison of low-dose aspirin, low-dose aspirin plus dipyridamole, and oral anticoagulants. The CABADAS Research Group of the Interuniversity Cardiology Institute of The Netherlands.

Aspirin, alone or in combination with dipyridamole, is known to prevent occlusion of aortocoronary vein grafts. The benefit of dipyridamole in addition to aspirin remains controversial, and the efficacy and safety of oral anticoagulants for prevention of vein-graft occlusion have not been established. We assessed one-year angiographic vein-graft patency after aortocoronary-bypass surgery in 948 patients assigned to receive aspirin, aspirin plus dipyridamole, or oral anticoagulants in a prospective, randomised trial. The design was double-blind and placebo-controlled for the aspirin groups, but open for oral anticoagulant treatment. Dipyridamole (5 mg/kg per 24 h intravenously for 28 h, followed by 200 mg twice daily) and oral anticoagulants (desired prothrombin time range 2.8-4.8 international normalised ratio) were started before surgery, and aspirin (50 mg per day) was started after surgery. Clinical outcome was assessed by the incidence of myocardial infarction, thrombosis, major bleeding, or death. Occlusion rate of distal anastomoses was 11% in the aspirin plus dipyridamole group versus 15% in the aspirin group (relative risk 0.76, 95% CI 0.54-1.05) and 13% in the oral anticoagulants group. Clinical events occurred in 20.3% of patients receiving aspirin plus dipyridamole compared with 13.9% of the aspirin group (relative risk 1.46, 95% CI 1.02-2.08) and 16.9% of the oral anticoagulants group. Our data provide no convincing evidence that addition of dipyridamole to 50 mg aspirin per day improves aortocoronary vein-graft patency. Moreover, there is evidence that the combination increases the overall clinical-event rate. Compared with aspirin, oral anticoagulants provided no benefit.

Acenocoumarol↗
PubMed1981

The metabolism of arachidonic acid is changed by dipyridamole in isolated hamster lungs.

14C-Arachidonate (50 nmol) was injected into the pulmonary circulation of isolated perfused lungs of female hamsters and the metabolites were analysed from the nonrecirculating perfusion effluent. Pulmonary infusion of dipyridamole (20 microM) increased the amount of radioactivity in the perfusion effluent of 0-4 min from 12.8 +/- 1.0% to 17.2 +/- 1.5% (2P less than 0.05) of the injected amount. Dipyridamole increased the amounts of PGF2 alpha, PGE2 and two unidentified metabolite groups in the effluent. An increasing trend was seen also in the amount of 6-keto-PGF1 alpha and TxB2. A decreasing trend was, however, seen in the amount of metabolites migrating near to unlabelled 15-keto-PGE2. When 20 nmol of 14C-PGE2 was injected into the pulmonary circulation of isolated hamster lungs, the amount of 15-keto-metabolites of PGE2 in the effluent was decreased and that of unmetabolized PGE2 increased by dipyridamole dose dependently. The rate of efflux of radioactivity from the lungs was increased by dipyridamole. Dipyridamole was in vitro not an inhibitor of 15-hydroxyprostaglandin dehydrogenase in the 100.000 supernatant fraction of homogenized hamster lungs. At 20 microM and 100 microM it even caused a slight in vitro activation of 15-hydroxyprostaglandin dehydrogenase. Thus the decreased pulmonary inactivation of PGE2 by dipyridamole is obviously due to the decreased uptake of PGE2 into the lungs. This could explain partly the detected changes in the pulmonary metabolism of arachidonic acid by dipyridamole.

Animals↗
PubMed1995

Effect of dipyridamole on myocardial perfusion and function using technetium-99m MIBI.

Myocardial perfusion imaging with dipyridamole is an accepted method for diagnosing coronary artery disease. However, the simultaneous effect of dipyridamole on perfusion and function in the detection of coronary artery disease has not been studied extensively. The aim of this study was to investigate this effect using technetium-99m methoxy isobutyl isonitrile (Tc-MIBI) imaging. Twenty-eight patients with proven coronary artery disease participated in a 2-day protocol (rest and then 0.56 mg/kg dipyridamole i.v.) using Tc-MIBI for first-pass radionuclide ventriculography followed by SPECT imaging. Fifteen patients (54%) demonstrated a decrease in left ventricular ejection fraction from rest to dipyridamole and/or wall motion abnormality, while 21 patients (75%) showed abnormal perfusion by dipyridamole MIBI SPECT imaging. Concordance between perfusion and function was 65%. Correlation for one-, two- and three-vessel disease (coronary angiography) to perfusion versus function were: 54% vs. 38%, 80% vs. 60% and 80% vs. 80%, respectively. Left ventricular dysfunction using dipyridamole was noted in patients with multivessel disease, and with multi-reversible perfusion filling defects. We conclude that dipyridamole in combination with Tc-MIBI for assessment of perfusion and function serves as a valuable tool to identify patients with multivessel disease and a high amount of myocardium at risk.

Aged↗
PubMed1983

The effects of aspirin and dipyridamole on the metabolism of arachidonic acid in human platelets.

The effects of aspirin and dipyridamole on the metabolism of exogenous 14C-arachidonic acid were investigated in intact human platelets in vitro. The formation of thromboxane B2 (TXB2) and 12-hydroxy-5,8,10-heptadecatrienoic acid (HHT) was inhibited dose dependently by aspirin but not by dipyridamole. Neither was the aspirin caused inhibition in TXB2 and HHT formation modified by dipyridamole. At high concentrations aspirin caused a slight increase in the amount of 12-hydroperoxy-5,8,10,14-eicosatetraenoic acid (12-HPETE) and a corresponding decrease in that of 12-hydroxy-5,8,10,14-eicosatetraenoic acid (12-HETE). This was seen also when aspirin was combined with dipyridamole. At high concentrations (100 microM and 1 mM) dipyridamole caused an increased formation of 12-HETE and an unidentified metabolite group. The present study indicates that dipyridamole has no effect on the formation of the cyclo-oxygenase metabolites in human platelets but the lipoxygenase pathway seems to be stimulated by dipyridamole.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1988

Dipyridamole-induced ST segment depression during thallium-201 imaging in patients with coronary artery disease: angiographic and hemodynamic determinants.

To examine the angiographic and hemodynamic determinants of dipyridamole-induced ST segment depression in patients with coronary artery disease, 41 patients with angiographically documented coronary disease who underwent dipyridamole-thallium-201 myocardial scintigraphy were studied. Dipyridamole-induced ST depression occurred in 14 (34%) of the 41 patients. Stepwise multivariate logistic regression was performed to compare the predictive value of angiographic findings (good coronary collateral vessels, jeopardized collateral vessels, multivessel disease), hemodynamic changes (changes in heart rate, systolic pressure, diastolic pressure and rate-pressure product), thallium-201 results (perfusion defect, thallium-201 redistribution) and demographic data (age, gender, medications). Only the presence of good coronary collateral vessels (p less than 0.02) and increases in rate-pressure product after dipyridamole infusion (p less than 0.02) were significant multivariate predictors of dipyridamole-induced ST depression. Good collateral vessels were more common in the group with ST depression (11 [79%] of 14) than they were in the group without ST depression (6 [22%] of 27; p less than 0.001). Rate-pressure product increased 2,835 +/- 1,648 beats/min.mm Hg in the group with ST depression compared with 1,179 +/- 1,417 beats/min.mm Hg in patients without ST depression (p less than 0.005). In conclusion, dipyridamole-induced ST segment depression in patients with coronary artery disease appears to be related to 1) the presence of good coronary collateral vessels, which may act by facilitating "coronary steal", and 2) increases in rate-pressure product, reflecting increased myocardial oxygen demand. These observations may explain the lack of prognostic value of dipyridamole-induced ST segment depression described in previous reports.

Aged↗
PubMed1990

Effects of dipyridamole and aminophylline on hemodynamics, regional myocardial blood flow and thallium-201 washout in the setting of a critical coronary stenosis.

Experiments were performed to characterize the interaction of intravenous dipyridamole and aminophylline on thallium-201 transport kinetics, regional myocardial blood flow and systemic hemodynamics in the presence of a critical coronary artery stenosis. In 12 dogs with a critical left anterior descending coronary artery stenosis, arterial pressure decreased from a mean value (+/- SEM) of 107 +/- 6 to 94 +/- 3 mm Hg (p less than 0.05) and distal left anterior descending artery pressure decreased from 70 +/- 7 to 55 +/- 4 mm Hg (p less than 0.05) after intravenous administration of dipyridamole (0.25 mg/kg body weight). In the left anterior descending perfusion zone, the endocardial/epicardial flow ratio decreased from 0.70 to 0.36 and the intrinsic thallium washout rate was significantly prolonged. Intravenous aminophylline (5 mg/kg) reversed the dipyridamole-induced systemic hypotension and transmural coronary steal and restored the thallium washout rate to baseline values. In six other dogs, aminophylline alone resulted in no alterations in systemic and coronary hemodynamics or regional myocardial blood flow. As expected, dipyridamole-induced vasodilation and coronary steal were prevented by aminophylline pretreatment. These data show that in a canine model of partial coronary stenosis, systemic hypotension, adverse regional flow effects (coronary steal) and prolonged thallium-201 washout consequent to intravenously administered dipyridamole are promptly reversed by intravenous aminophylline administration. Aminophylline alone had no significant hemodynamic and coronary flow effects. This study provides further insight into the altered thallium kinetics occurring as a consequence of dipyridamole-induced vasodilation and suggests that the prompt reversal of symptoms and signs of ischemia with aminophylline in patients receiving intravenous dipyridamole for clinical imaging studies probably reflects the reversal of transmural coronary steal.

Aminophylline↗
PubMed1991

Comparison of coronary vasodilation with intravenous dipyridamole and adenosine.

Although both intravenous dipyridamole and adenosine have been used to produce coronary vasodilation during cardiac imaging, the relative potency of the commonly administered doses of these agents has not been evaluated. Accordingly, the coronary and systemic hemodynamic effects of intravenous adenosine (140 micrograms/kg per min) and intravenous dipyridamole (0.56 mg/kg over 4 min) were compared with a maximally dilating dose of intracoronary papaverine in 15 patients. Coronary blood flow responses were assessed using a Doppler catheter in a nonstenotic coronary artery. The protocol was discontinued in two patients because of transient asymptomatic atrioventricular (AV) block during adenosine infusion. The mean heart rate increased more with adenosine (11 +/- 9 beats/min) and dipyridamole (11 +/- 7 beats/min) than with papaverine (4 +/- 3 beats/min, p less than 0.05 vs. adenosine and papaverine). The mean arterial pressure decreased less with dipyridamole (-10 +/- 3 mm Hg) and papaverine (-9 +/- 4 mm Hg) than with adenosine (-16 +/- 5 mm Hg, p less than 0.01 vs. dipyridamole and papaverine). The peak/rest coronary blood flow velocity ratio was greater with papaverine (3.9 +/- 1.1) than with adenosine (3.4 +/- 1.2, p less than or equal to 0.05 vs. papaverine) or dipyridamole (3.1 +/- 1.2, p less than 0.01 vs. papaverine). A larger decrease in coronary resistance as measured by the coronary vascular resistance index occurred with papaverine (0.25 +/- 0.06) and adenosine (0.26 +/- 0.09) than with dipyridamole (0.31 +/- 0.10, p less than 0.01 vs. papaverine, p less than 0.05 vs. adenosine).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1992

Transesophageal dipyridamole echocardiography for diagnosis of coronary artery disease.

The value of transthoracic dipyridamole echocardiography has been extensively documented. However, in some patients, because of a poor acoustic window, the rest transthoracic examination is not always feasible and the transesophageal approach is more convenient. Therefore, transesophageal echocardiography with high dose dipyridamole (up to 0.84 mg/kg body weight over 10 min) was performed in 32 patients in whom the transthoracic dipyridamole test either was not feasible (n = 29) or yielded ambiguous results (n = 3). The transesophageal echocardiographic test results were considered abnormal when new dipyridamole-induced regional wall motion abnormalities were observed. All 32 patients underwent coronary angiography; significant coronary artery disease was defined as greater than or equal to 70% lumen diameter narrowing in at least one major vessel. All patients also performed a bicycle exercise test 1 day before transesophageal dipyridamole echocardiography. Transesophageal stress studies were completed in all patients, with a maximal imaging time (in tests with a negative result) of 20 min. No side effects or intolerance to drug or transducer was observed. The left ventricle was always visualized in the four-chamber and transgastric short-axis views. High quality two-dimensional echocardiographic images were obtained in all patients both at rest and at peak dipyridamole infusion and were digitally analyzed in a quad-screen format. Coronary angiography showed coronary artery obstruction in 24 patients: 6 had single-, 9 double- and 9 triple-vessel disease. The transesophageal dipyridamole test showed a specificity of 100% and an overall sensitivity of 92%. The sensitivity of this test for single-, double- and triple-vessel disease was 67%, 100% and 100%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Angiography↗
PubMed1988

Reversibility by dipyridamole of thallium-201 myocardial scan defects in patients with sarcoidosis.

PURPOSE: In order to clarify the significance of anginal pain and myocardial thallium-201 scan defects in cardiac sarcoidosis, the pharmacologic effect of dipyridamole on myocardial perfusion was assessed by planar thallium-201 myocardial scintigraphy in patients with sarcoidosis. PATIENTS AND METHODS: Thallium-201 myocardial scintigraphy was performed at rest and after 0.56 mg/kg intravenous dipyridamole during four minutes in 16 patients with sarcoidosis. The myocardial scan (45-degree and 70-degree left anterior oblique, and anterior views) was divided into 15 segments. Results were evaluated by the number of segmental defects and with a global perfusion score (from 0 to 60) by a semi-quantitative index depending on the size and severity of myocardial thallium-201 defects. RESULTS: Thirteen of the 16 patients showed partial or total reversion of their thallium-201 defects on redistribution scanning either at rest or after dipyridamole. The mean (+/- SD) number of myocardial perfusion defects that were present in all the patients decreased from 5.31 +/- 1.78 at rest to 3.25 +/- 2.52 after redistribution (p less than 0.001) and to 2.19 +/- 2.10 after dipyridamole (p less than 0.001). The mean global perfusion score increased from 53.2 +/- 3.0 at rest to 56.2 +/- 2.9 after redistribution (p less than 0.001) and to 57.2 +/- 2.7 after dipyridamole (p less than 0.001). A significant correlation (r = 0.82, p less than 0.001) was found between the increase of global perfusion score on redistribution and after dipyridamole. CONCLUSION: The reversibility of myocardial scan defects is a common finding in sarcoidosis. It makes unlikely the role of scar fibrosis or extensive confluent granulomas as a mechanism for such defects. The effect of dipyridamole suggests the presence of reversible disorders lying at the coronary microvascular level.

Adult↗
PubMed2002

Dobutamine versus dipyridamole for inducing reversible perfusion defects in chronic multivessel coronary artery stenosis.

OBJECTIVES: We hypothesized that, although the effects of dipyridamole and dobutamine on myocardial blood volume (MBV) and mean microbubble velocity (VEL) are different, the magnitude of perfusion deficit during both forms of stress is the same because both drugs unmask abnormal myocardial blood flow (MBF) reserve. BACKGROUND: Both dipyridamole and dobutamine are used clinically as pharmacologic stress agents to induce reversible perfusion defects in patients with chronic coronary artery disease (CAD), but the basis for doing so for dobutamine is not clear. METHODS: Eleven chronically instrumented closed-chest dogs with multivessel coronary stenosis were studied. Hemodynamics, radiolabeled microsphere-derived MBF, and myocardial contrast echocardiography (MCE)-derived myocardial perfusion were measured at rest, after dipyridamole infusion (0.56 mg x kg(-1)), and at peak dobutamine dose (either 30 or 40 microg x kg(-1) x min(-1)). Abnormal beds were defined as those demonstrating an MBF reserve <3 with dipyridamole. RESULTS: In the presence of either drug, MBV increased more in the normal bed than in the abnormal bed, but the increase was higher in both beds with dobutamine than with dipyridamole. The slope of the relationship between MBF reserve and MBV reserve was greater during dobutamine than dipyridamole (p < 0.05). The converse was true for VEL reserve (p < 0.05). Consequently, the relationship between the ratios of either variable, or the product of the two, between the abnormal bed and normal bed was similar for both drugs. CONCLUSIONS: Although the effects of dipyridamole and dobutamine on MBV and VEL are different, both are equally effective in detecting physiologically relevant coronary stenoses on MCE. Both can therefore be used interchangeably with myocardial perfusion imaging for the detection of CAD.

Animals↗
PubMed1986

Thallium-201 myocardial imaging during pharmacologic coronary vasodilation: comparison of oral and intravenous administration of dipyridamole.

Although the diagnostic utility of thallium-201 myocardial imaging after dipyridamole infusion is well established, the intravenous form of the drug is not yet commercially available in North America. Fifty patients referred for coronary angiography were prospectively studied. Within a 2 week period, each patient underwent cardiac catheterization and thallium-201 myocardial imaging after both oral and intravenous dipyridamole administration. For the oral protocol, patients were randomly assigned to treatment with either 200 or 400 mg of dipyridamole in tablet form. Coronary artery stenoses of 70% or greater were considered significant. For the 25 patients who received a 200 mg oral dose of dipyridamole, the scintigraphic study showed perfusion defects in 65% of patients with significant coronary artery disease after the oral dose and in 85% of patients after the intravenous dose. For the 25 patients who received a 400 mg oral dose, the sensitivity of the scintigram was 84% after the oral dose and 79% after the intravenous dose. Except for headache and nausea, side effects were less severe and less frequent with oral (either 200 or 400 mg) than with intravenous dipyridamole. Because of the delayed and variable absorption of dipyridamole tablets, the oral studies required a longer period of medical supervision (45 to 60 minutes), and aminophylline was empirically administered after completion of the first set of thallium-201 images. It is concluded from this study that thallium-201 myocardial imaging after coronary vasodilation with a 400 mg oral dose of dipyridamole is a safe, widely available and reliable alternative for the evaluation of coronary artery disease in patients unable to achieve an adequate exercise level on stress testing.

Administration, Oral↗
PubMed1986

High dose dipyridamole echocardiography test in effort angina pectoris.

The dipyridamole echocardiography test (intravenous dipyridamole with two-dimensional echocardiographic monitoring) was performed in 93 patients with effort chest pain and in 10 control subjects. The test was considered positive when regional asynergy appeared after dipyridamole administration. When negative at the low dose (0.56 mg/kg body weight in 4 minutes), the test was repeated on a different day with a higher dose (0.84 mg/kg in 10 minutes). All 93 patients underwent coronary arteriography; 72 of them had significant (greater than 70% luminal reduction) coronary artery disease. Thirty-eight of the 93 patients had a positive low dose dipyridamole echocardiography test; 15 other patients with a negative low dose test had a positive high dose test. All 53 patients with a positive test had significant coronary artery disease; 12 of them had a negative exercise stress test. In relation to the presence of coronary artery disease, the dipyridamole echocardiography test had an overall specificity higher than that of the exercise stress test (100 versus 71%) and a similar overall sensitivity (74 versus 69%). The dipyridamole echocardiography test is feasible in all patients with a good baseline echocardiogram. It detects the site of apparent ischemia more precisely than does an exercise stress test, and can unmask electrocardiographically silent ischemia. If performed in patients with a negative low dose dipyridamole echocardiography test, the high dose test adds sensitivity (probably by achieving maximal dilation in patients in whom the low dose is only partially effective), without any loss in specificity and with no apparent increase in risk.

Adult↗
PubMed1996

Pharmacologic myocardial protection during percutaneous transluminal coronary angioplasty by intracoronary application of dipyridamole: impact on hemodynamic function and left ventricular performance.

OBJECTIVES: The aim of this study was to investigate whether intracoronary infusion of dipyridamole represents a suitable tool for preventing deterioration of left ventricular performance and hemodynamic function during percutaneous transluminal coronary angioplasty (PTCA). BACKGROUND: Coronary angioplasty represents a suitable model for establishing myocardial ischemia in humans. Balloon inflation is usually accompanied by significant deterioration in left ventricular systolic and diastolic properties. A brief episode of ischemia followed by reperfusion, termed preconditioning, has been identified as a mechanism for rendering the myocardium more resistant to ischemia. Adenosine is considered an important mediator of preconditioning. Dipyridamole is an important drug that interferes with myocardial adenosine metabolism by inhibiting its cellular reuptake. METHODS: In 20 patients undergoing elective coronary angioplasty of a major vessel, assessment of angiographic left ventricular performance and hemodynamic variables was performed before, during and after PTCA. Patients were randomly allocated to pretreatment with intracoronary infusion of dipyridamole before percutaneous transluminal coronary angioplasty (10 patients) or conventional pretreatment without dipyridamole (10 patients). RESULTS: Dipyridamole pretreatment resulted in significant preservation of systolic and diastolic left ventricular performance during percutaneous transluminal coronary angioplasty, as documented by an unaffected global ejection fraction (vs. a deterioration of 29.2% with conventional pretreatment, p < 0.01) and an increment in diastolic stiffness of only 12.7% (vs. an increment of 57.3% with conventional pretreatment, p < 0.01). Apart from one instance of coronary steal phenomenon, no significant side effects of dipyridamole infusion could be detected. CONCLUSIONS: It is concluded that intracoronary application of dipyridamole may result in the induction of myocardial preconditioning by improving systolic and diastolic ventricular performance during percutaneous transluminal coronary angioplasty, thereby potentially reducing the risk of the angioplasty procedure.

Aged↗
PubMed1998

Correlation between hemodynamic changes and tomographic sestamibi imaging during dipyridamole-induced coronary hyperemia.

OBJECTIVES: The purposes of this study were to examine the effects of dipyridamole infusion on hemodynamic variables and to compare these changes with myocardial perfusion. BACKGROUND: Dipyridamole stress testing with myocardial perfusion imaging is widely used in the assessment of patients with known or suspected coronary artery disease (CAD). Few studies, however, have correlated the hemodynamic effects of dipyridamole using invasive monitoring with perfusion patterns in patients with chest pain syndromes. METHODS: Hemodynamic measurements were made in the cardiac catheterization laboratory with a Swan-Ganz thermodilution catheter before, during and after infusion of dipyridamole (142 microg/kg body weight per min for 4 min). Technetium-99m sestamibi was injected 3 min after the completion of the infusion. RESULTS: There were 20 patients with and 6 without CAD, as demonstrated by angiography. Compared with baseline values, dipyridamole resulted in an increase in pulmonary capillary wedge pressure (54 +/- 78% vs. 32 +/- 26%, p = NS), cardiac index (36 +/- 21% vs. 40 +/- 18%, p = NS) and stroke volume index (16 +/- 18% vs. 40 +/- 18%, p = NS) and a decrease in systemic vascular resistance (22 +/- 13% vs. 24 +/- 11%, p = NS), aortic pressure (2 +/- 9% vs. 0 +/- 6%, p = NS) and pulmonary vascular resistance (19 +/- 25% vs. 11 +/- 32%, p = NS) in patients with and without CAD. The peak effect of dipyridamole on heart rate, systemic vascular resistance and pulmonary capillary wedge pressure was evident at 3 min after infusion in 70% of patients. Aminophylline, given to 20 patients, improved hemodynamic variables within 2 min. The single-photon emission computed tomographic sestamibi images were normal in the 6 patients without and abnormal in the 18 patients with CAD. CONCLUSIONS: Dipyridamole-induced coronary hyperemia produces mild hemodynamic changes in patients with and without CAD; these changes are at or near peak effect at 3 min after infusion and are rapidly reversed by aminophylline.

Adult↗
PubMed2002

Dipyridamole prevents the coconut oil-induced hypercholesterolemia. A study on lipid plasma and lipoprotein composition.

For a better understanding of the hypolipidemic function of dipyridamole, we have studied the comparative effects of diet supplementation with 10% coconut oil with and without dipyridamole on the lipid plasma and lipoprotein composition in chicks. This study was performed under postprandial and food-deprivation (12h) conditions. Coconut oil induced a clear hypercholesterolemia under both feeding conditions. Simultaneous administration of dipyridamole maintained total and esterified cholesterol at levels similar to those observed in control animals sacrificed under postprandial conditions. Under these conditions, our results also show that dipyridamole significantly reduced cholesterol levels in all the chick plasma lipoproteins that were increased by coconut oil administration. Nevertheless, it should be emphasised that the levels of total cholesterol found in intermediate- and very-low-density lipoproteins were lower than in control. All chemical components of these fractions were significantly decreased by dipyridamole. The effects were not significant in chicks deprived of food. In conclusion, our results show that the hypercholesterolemia induced by coconut oil was prevented by dipyridamole. To our knowledge, this is one of the first reports on the antihypercholesterolemic effects of dipyridamole.

Animals↗
PubMed2003

Additive effects of dipyridamole and Trolox in protecting human red cells during photodynamic treatment.

BACKGROUND AND OBJECTIVES: Photodynamic treatment (PDT) of red blood cell (RBC) suspensions has been reported to result in virus inactivation, but also in deterioration of cell quality. Recently, we have demonstrated the potential usefulness of the reactive oxygen species scavenger dipyridamole in selectively protecting RBCs against the harmful side-effects of PDT. Unfortunately, dipyridamole-conferred protection against long-term photohaemolysis was incomplete. In the present study, dipyridamole was applied in combination with Trolox (a hydrophilic vitamin E analogue) in order to augment RBC protection. MATERIALS AND METHODS: Leucodepleted RBC suspensions (30% haematocrit) were treated with 1,9-dimethylmethylene blue (DMMB) and red light, and the effect of inclusion of dipyridamole and Trolox was assessed on potassium leakage as well as on short-term and long-term photohaemolysis. Possible interference of the scavenger cocktail with virus inactivation was examined using extracellular pseudorabies virus (PRV). RESULTS: Treatment of RBC with DMMB and red light resulted in enhanced potassium leakage and both short- and long-term haemolysis. Dipyridamole and Trolox showed additive protective effects against induction of potassium leakage and photohaemolysis, suggesting different protection mechanisms for the two scavengers. Combined inclusion of dipyridamole and Trolox did not interfere with efficacy of PRV inactivation. CONCLUSIONS: Combined inclusion of dipyridamole and Trolox results in substantially improved selectivity of photodynamic treatment of RBC suspensions.

Antioxidants↗
PubMed2001

Effects of dipyridamole on coronary collateralization and myocardial perfusion in patients with ischaemic cardiomyopathy.

AIMS: There is evidence that oral dipyridamole, a nucleoside uptake blocker that increases myocardial adenosine levels, lessens myocardial ischaemia by inducing coronary collateral growth in animal models of ischaemic heart disease. However, whether dipyridamole can exert a similar effect in humans with coronary artery disease is controversial. METHODS AND RESULTS: We studied 30 male patients (mean age 55+/-9 years) with coronary artery disease and left ventricular systolic dysfunction (ejection fraction >40%). Patients were randomized into three matched groups. Group A patients (n=10) received dipyridamole alone at a dose of 75 mg t.i.d. orally for 8 weeks. Group B patients (n=10) underwent exercise training at 60% of peak .VO(2)three times a week for 8 weeks, and received dipyridamole. Group C patients (n=10) had neither exercise testing nor dipyridamole. On study entry and after 8 weeks all patients underwent an exercise test with gas exchange analysis, dobutamine stress echocardiography, 201-thallium planar myocardial scintigraphy, and coronary angiography. Peak .VO(2)increased significantly only in trained patients. Thallium uptake of the collateral-dependent myocardium, coronary collateral score and wall thickening score increased significantly only in groups receiving dipyridamole, the greatest improvement being in group B patients. Plasma adenosine levels were also the highest in group B (P<0.001 vs A and C). Correlations were found between changes in adenosine levels and increases of both thallium uptake (r=-0.70;P=0.001) and collateralization (r=0.72;P=0.001). CONCLUSION: Exercise training potentiates the effects of dipyridamole on coronary collateralization and myocardial perfusion in humans with ischaemic cardiomyopathy.

Adenosine↗
PubMed1984

Activation of platelets by autogenous vein grafts is not prevented by acetylsalicylic acid and dipyridamole.

We have shown previously that experimental autogenous vein grafts activate platelets for up to four months following operation. In the present study, animals were treated with middle dose ASA (10 mg X kg-1 X 24 h-1) plus dipyridamole (8 mg X kg-1 X 24 h-1) and followed for 8 months. Despite this treatment, platelets were activated by the vein graft for up to four months after operation but not after this time. Similarly, treatment with low dose ASA (0.5 mg X kg-1 X 24 h-1) plus dipyridamole (8 mg X kg-1 X 25 h-1), high dose ASA (40 mg X kg-1 X 24 h-1) plus dipyridamole (8 mg X kg-1 X 24 h-1), or dipyridamole alone (8 mg X kg-1 X 24 h-1), did not prevent the vein graft-induced activation of platelets. Full inhibition of platelet arachidonic acid metabolism was demonstrated in the high dose ASA plus dipyridamole group. These results suggest that the interaction between the vessel wall and platelet is not inhibited by ASA plus dipyridamole. Platelets have first to be activated before causing intimal hyperplasia. Since aspirin and dipyridamole did not prevent activation of platelets by the graft, this drug combination is unlikely to prevent the development of intimal hyperplasia in the graft wall.

Adenosine Diphosphate↗