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PubMed1984

Radionuclide imaging after coronary vasodilation: myocardial scintigraphy with thallium-201 and radionuclide angiography after administration of dipyridamole.

Tl-201 imaging was performed in 194 patients who had undergone coronary angiography which had demonstrated coronary artery disease in 149 and normal coronary vessels in 45.91 patients had had previous myocardial infarction. Sensitivity for dipyridamole stress imaging was 92% for all 149 patients. 79% for the patients without previous infarction. Specificity was 81%. In a subgroup of 40 patients (32 patients with reversible Tl-201 defects and 8 normals), an additional dipyridamole wall motion study was performed in order to evaluate the correlation of Tl-201 perfusion abnormalities and ventricular function after dipyridamole. Only 19% of the patients had a dipyridamole-induced drop of global left ventricular ejection fraction, 31% showed dipyridamole-induced wall motion abnormalities; the predictability of specific vessel involvement by regional wall motion and regional ejection fraction assessment was 26% as compared with 70% for thallium imaging. Tl-201 perfusion defects after dipyridamole administration can also occur independent of ischaemia-induced changes in global and regional ventricular function. Coronary vasodilation with dipyridamole using Tl-201 imaging is a reliable alternative method in patients with coronary artery disease with an accuracy comparable to exercise studies with the advantage of not necessarily needing ischaemia as an endpoint of the test.

Cineangiography↗

PubMed1995

Significance of dipyridamole loading in ultrafast x-ray computed tomography for detection of myocardial ischemia. A study in patients with Kawasaki disease.

BACKGROUND AND RATIONALE: To examine the significance of dipyridamole loading as a stress in ultrafast computed tomography (CT) to improve the detection of left ventricular myocardial ischemia. METHODS: Thirty-eight patients with coronary arterial involvement of Kawasaki disease and 18 control subjects received cardiac ultrafast CT with intravenous long-bolus iodinated contrast injection; dipyridamole was loaded in 40 examinations. Early (first-pass) and late (4 minutes) M/Ls (ratio of postcontrast incremental increases in the left ventricular myocardial [M] and luminal [L] CT number) were analyzed. RESULTS: Dipyridamole induced a prominent increase in early M/L of the normal myocardium in control subjects (no loading: 26.8%, dipyridamole: 39.2%; P < 0.001) with small influence on late M/Ls. In ischemic or infarcted myocardium in Kawasaki disease, dipyridamole early M/Ls (20.4%, 16.0%) and late M/Ls showed no difference from corresponding values without loading. Using early M/L with dipyridamole, sensitivity and specificity for detection of ischemic abnormalities were 89% and 100%, respectively. CONCLUSIONS: Dipyridamole-loaded first-pass contrast ultrafast CT was proven to have excellent detectability for myocardial ischemia comparable with stress thallium scintigraphy.

Adolescent↗

PubMedDate not supplied

Effect of dipyridamole on sympathetic nerve function: role of adenosine and presynaptic purinergic receptors.

The effect of dipyridamole on cardiac sympathetic neurotransmission was studied in pentobarbital-anesthetized dogs. Additional studies were performed to determine the involvement of adenosine and presynaptic purinergic receptors in the action of dipyridamole. Dipyridamole (2 mg/kg) produced significant impairment of the cardioacceleration observed during the stimulation of cardioaccelerator nerve, whereas the positive chronotropic effect of intravenous norepinephrine was not affected. This inhibitory effect of the compound could be antagonized by prior treatment of the animals with theophylline. Doses of adenosine (0.1 and 0.2 mg/kg/min) that did not have any effect on cardiac sympathetic nerve function in control animals caused significant impairment of the positive chronotropic effect of cardiac nerve stimulation in animals treated with a smaller dose of dipyridamole (0.5 mg/kg), which could also be antagonized by theophylline. The smaller dose of dipyridamole did not affect responses to cardiac nerve stimulation. Dipyridamole did not modify the effect of 2-chloroadenosine, an adenosine analog reported to be resistant to uptake and deamination, on sympathetic nerve function. A larger dose of 2-chloroadenosine, however, did produce inhibition of the positive chronotropic effect of cardiac nerve stimulation which could be antagonized by theophylline. These results demonstrate that dipyridamole can cause inhibition of sympathetic neurotransmission to the myocardium, and they further suggest that this action of the compound is mediated by endogenous adenosine acting on presynaptic purinergic receptors.

Adenosine↗

PubMedDate not supplied

Dipyridamole and aspirin in relation to platelet aggregation and vessel wall prostaglandin generation.

Modification of platelet function and vessel wall prostaglandin synthesis by pharmacologic intervention has attracted considerable attention. We report our observations on the effects of aspirin and dipyridamole alone and their combination on platelet aggregation and vessel wall prostacyclin (PGI2) generation. Although dipyridamole alone had no effects on platelet aggregation, it potentiated the platelet aggregation inhibitory effects of aspirin in vitro in a dose-related fashion. Dipyridamole also enhanced the platelet aggregation inhibitory effect of synthetic PGI2 in vitro. Potentiation of aspirin- and PGI2-induced platelet aggregation inhibition was observed in therapeutic range (5-10 micrograms/ml). In an isolated umbilical vein model dipyridamole stimulated release of PGI2 at much higher concentration (50-100 microgram/ml). Treatment of umbilical vein with aspirin (180 micrograms/ml) for 10 min blocked the spontaneous release of PGI2. In aspirin-treated umbilical vein segments dipyridamole treatment did not cause PGI2 release as in the untreated segments. These experiments suggest that although dipyridamole enhances both aspirin- and PGI2-induced platelet aggregation inhibition in clinically achieved concentrations, much higher levels are necessary for PGI2 release from intact human vessels. Furthermore, aspirin treatment of human vessels may prevent release of PGI2 in response to dipyridamole by blocking cyclooxygenase enzyme.

6-Ketoprostaglandin F1 alpha↗

PubMed1993

Thallium myocardial perfusion tomography using intravenous dipyridamole combined with maximal dynamic exercise.

Exercise thallium imaging is effective and provides information on exercise tolerance and symptoms, but is less sensitive if exercise is submaximal. When dipyridamole alone is used for such patients, the exercise parameters are lost and high background uptake results. This study examines dipyridamole combined with maximal exercise, to capitalize on the strengths of both techniques. Thallium tomography was performed in 122 patients with dipyridamole (group 1), exercise (group 2), or dipyridamole with maximum exercise (group 3). In patients with coronary artery disease, thallium tomography was abnormal in 92, 93 and 95% (P = ns), with reversible ischaemia in 82, 81 and 84% (P = ns) in the three groups, respectively. Among patients in groups 2 and 3 who exercised submaximally, detection of individual arterial stenoses was improved in group 3 (P < 0.05) and larger defects were found (2.4 versus 4.2 segments, P < 0.01). In group 3, no serious complications occurred and fewer vasodilatory side effects were seen than in group 1 (P < 0.01). The heart to splanchnic count ratio in groups 2 and 3 (1.61 versus 1.65, P = ns) was significantly greater than in group 1 (1.28, P < 0.0001). Compared with exercise alone, additional dipyridamole improved diagnostic accuracy in patients with limited exercise potential. Compared with dipyridamole alone, additional exercise provided useful exercise information, reduced vasodilatory side effects and improved scan quality. Combined dipyridamole and exercise stress is safe, and could be used routinely, but a larger study is required to establish if there is an overall diagnostic improvement.

Adult↗

PubMed2000

Intracoronary administration of dipyridamole prior to percutaneous transluminal coronary angioplasty provides a protective effect exceeding that of ischemic preconditioning.

BACKGROUND: Ischemic preconditioning renders hearts more resistant to the deleterious consequences of ischemia. Adenosine is an important mediator in the induction and maintenance of ischemic preconditioning. Percutaneous transluminal coronary angioplasty (PTCA) allows the investigation of the consequences of ischemia in humans. The severity of myocardial ischemia decreases with subsequent balloon inflations during the course of PTCA. OBJECTIVE: To compare the effect of intracoronary administration of dipyridamole with the effect of consecutive balloon inflations. METHODS: We investigated 30 patients undergoing PTCA of the left anterior descending coronary artery in the setting of stable angina pectoris. Patients were randomly allocated to be administered either 0.5 mg/kg body weight dipyridamole intracoronarily or an equal amount of saline. Patients administered saline served as a control group. All patients were subjected to three consecutive balloon inflations. Severity of myocardial ischemia was assessed in terms of severity of chest pain, electrocardiographic signs of ischemia, and duration of balloon inflation tolerated. RESULTS: Patients administered dipyridamole intracoronarily tolerated significantly longer durations of balloon inflation than did patients in the control group. Severity of anginal pain and extent of electrocardiographic signs of ischemia were significantly lower after intracoronary administration of dipyridamole. The reductions in anginal pain and ST-segment shift caused by intracoronary administration of dipyridamole during the first balloon inflation were even more pronounced than the protection that was afforded by the third balloon inflation for patients in the control group. CONCLUSIONS: Intracoronary administration of dipyridamole prior to PTCA is associated with a significant gain in tolerance of ischemia. The protection afforded by intracoronary administration of dipyridamole is even more pronounced than the effect of ischemic preconditioning.

Angioplasty, Balloon, Coronary↗

PubMed1988

Enhancing effect of dipyridamole inhalation on adenosine-induced bronchospasm in asthmatic patients.

The study was performed on 13 asthmatic patients to determine whether inhaled dipyridamole would act directly by inducing bronchoconstriction or indirectly by potentiating the adenosine-induced bronchoconstriction. The study was performed in 3 consecutive days. On the first day adenosine challenge was performed and the PD20 value calculated. On the other days the adenosine challenge was done 5 min after randomized inhalations of dipyridamole or a control solution. The mean percent change in FEV1 after dipyridamole (delta % = 2.0) and control solution (delta % = 1.0) was not significant. Inhaled adenosine caused bronchoconstriction with a geometric mean PD20 of 1.09 mg. After control solution inhalation, a mean PD20 value of 1.31 mg was observed. Dipyridamole inhalation increased adenosine hyperresponsiveness and in all subjects shifted the dose-response curves of adenosine challenge to the left with a mean PD20 value of 0.40 mg. This enhancing effect of dipyridamole was significant when compared with the baseline value (P less than 0.01) and control solution (P less than 0.01). The study demonstrated that dipyridamole inhalation increased airway responsiveness to adenosine in all subjects. This effect is due to indirect activity of dipyridamole on airways without changes in baseline airway caliber.

Adenosine↗

PubMed2004

Modification of transmitter release from periarterial nerve terminals by dipyridamole in canine isolated splenic artery.

1. The aim of the present study was to determine the modulatory effects of dipyridamole on purinergic and adrenergic transmission in the canine isolated, perfused splenic artery. 2. Periarterial nerve electrical stimulation readily induced a double-peaked vasoconstriction consisting of an initial transient, predominantly P2X receptor-mediated constriction followed by a prolonged, mainly alpha1-adrenoceptor-mediated response. 3. Exposure of tissues to dipyridamole (0.1-1 micro mol/L) dose-dependently inhibited both the first and second peaks of the vasoconstrictor response at a low frequency of stimulation (1 Hz), whereas at an intermediate frequency of stimulation (4 Hz), the first peak of the response was depressed without any significant effect being observed on the second peak of constriction. 4. At a higher dose (1 micro mol/L) dipyridamole potentiated vasoconstrictor responses to noradrenaline (0.03-1 nmol). At any doses used, dipyridamole had no effect on the vasoconstrictor responses to ATP (0.03-1 micro mol). 5. Tyramine (0.01-0.3 micro mol) induced vasoconstriction in a dose-dependent manner. The dose-response curves for tyramine were shifted to the right following treatment with dipyridamole (0.1-1 micro mol/L). 6. The present results indicate that dipyridamole may inhibit purinergic and adrenergic transmission presynaptically, whereas postsynaptically dipyridamole may potentiate the adrenergic vascular constriction by inhibition of transmitter uptake.

Adenosine Triphosphate↗

PubMed2006

Dipyridamole may induce migraine in patients with migraine without aura.

Dipyridamole inhibits phosphodiesterase 5 (PDE5) and adenosine re-uptake. The most prominent side-effect is headache. We examined the migraine-generating effects of dipyridamole as well as the cerebral blood velocity response in a single-blind study, including 10 patients with migraine without aura and 10 healthy subjects. Dipyridamole 0.142 mg/kg per min was administered intravenously. Headache intensity was scored on a verbal rating scale along with pain characteristics and accompanying symptoms. Blood velocity in the middle cerebral artery (V(mca)), blood pressure and heart rate were recorded repeatedly. Headache was induced in all migraine patients and in eight of 10 healthy subjects (P = 0.47) with no significant difference in headache intensity (P = 0.53). However, five patients but only one healthy subject experienced the symptoms of migraine without aura, according to ICHD-2 criteria, within 12 h (P = 0.14). Four patients reported photophobia after dipyridamole compared with no healthy subjects (P = 0.087). V(mca) decreased (P < 0.001) during and after dipyridamole infusion with no difference between groups (P = 0.15) coinciding with initiation, but not cessation of immediate headache. Thus, dipyridamole induces symptoms of migraine and an initial decrease in V(mca) in migraine patients, but not significantly more than in healthy subjects. This relatively low frequency of migraine induction, compared with nitric oxide donors and sildenafil, is probably due to the less specific action of dipyridamole on the cGMP signalling pathway as well as a possible bidirectional effect of adenosine on migraine induction.

Administration, Oral↗

PubMed1993

Pertussis toxin sensitive effects of dipyridamole on rat atrial rate.

1. In the spontaneously beating rat isolated atria the effects of dipyridamole (0.01, 0.1, 1 and 10 microM) and of adenosine (10 microM) on the chronotropic responses to exogenous noradrenaline (NA) were compared. 2. Dipyridamole (0.01 microM) reduced the chronotropic responses to NA throughout the entire concentration-response curve. A decrease in the maximal response to the agonist was also observed. 3. Neither the spontaneous outflow of [3H]-NA nor its metabolic distribution were altered by dipyridamole (0.01 microM). 4. As observed with dipyridamole, the concentration-response curve to NA was shifted to the right by 10 microM adenosine. 8-Phenyltheophylline (8-PT), 10 microM prevented the decrease in the chronotropic response to NA produced by both 10 microM adenosine and 0.01 microM dipyridamole. 5. The preincubation of rat atria with 1 micrograms ml-1 pertussis toxin prevented the diminution in the chronotropic responses to NA produced by 0.01 microM dipyridamole. 6. The present results suggest that the decrease caused by dipyridamole in rat atrial chronotropic responses involves the participation of adenosine, probably through the interaction with type A1 adenosine receptors.

Adenosine↗

PubMed2006

Mechanism of dipyridamole's action in inhibition of venous and arterial smooth muscle cell proliferation.

Dipyridamole is a potential pharmacological agent to prevent vascular stenosis because of its antiproliferative properties. The mechanisms by which dipyridamole inhibits the growth of vascular smooth muscle cells, especially venous smooth muscle cells, are unclear. In the present study, dipyridamole transiently but significantly increased cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) levels in human venous and arterial smooth muscle cells in a time- and dose-dependent manner. Peak concentrations of both cyclic nucleotides were achieved at 15-30 min. and correlated with inhibition of proliferation in both cell types. The antiproliferative effects of dipyridamole observed at 48 hr were similar whether drug exposure was only 15 min. or sustained for 48 hr. Specific competitive inhibitors of protein kinases A and G attenuated the antiproliferative effects of subsaturating concentrations of dipyridamole, with the effects of protein kinase inhibition being particularly pronounced in venous smooth muscle cells. Flow cytometry analysis showed that dipyridamole caused an enrichment of cells in G(0)/G(1) and a corresponding reduction of cells in S phase. These data indicate that a transient increase in cGMP and cAMP is sufficient to induce downstream kinase activation and subsequent cell cycle arrest, and that protein kinase G may be more important than protein kinase A in mediating the growth inhibitory effect of dipyridamole in venous protein kinase.

Aorta↗

PubMed2004

Dipyridamole alters cardiac substrate preference by inducing translocation of FAT/CD36, but not that of GLUT4.

In cardiac myocytes, uptake rates of glucose and long-chain fatty acids (FA) are regulated by translocation of GLUT4 and FA translocase (FAT)/CD36, respectively, from intracellular stores to the sarcolemma. Insulin and contractions are two major physiological stimuli able to induce translocation of both transporters and therefore enhance the uptake of both substrates. Interestingly, the cardiovascular drug dipyridamole was able to enhance FA uptake but had no effect on glucose uptake. The selective stimulatory effect of dipyridamole on FA uptake was unrelated to its effects on phosphodiesterase inhibition and on nucleoside transport inhibition. However, dipyridamole-stimulated FA uptake was abolished in the presence of sulfo-N-succinimidylpalmitate, which indicated that FAT/CD36 is involved in the uptake process. Furthermore, the effect was additive to that of insulin but not to that of the AMP-elevating agent oligomycin, indicating that dipyridamole stimulates FAT/CD36-mediated FA uptake by activating the AMP-activated protein kinase (AMPK) signaling pathway. Dipyridamole, however, neither influenced the intracellular AMP content nor induced activation of AMPK. Finally, dipyridamole was able to induce FAT/CD36 translocation from intracellular storage sites to the sarcolemma but had no effect on the subcellular distribution of GLUT4. It is concluded that beyond AMP-activated protein kinase the contraction-induced and AMPK-mediated signal branches off into separate mobilization of GLUT4 and of FAT/CD36, and that dipyridamole activates a yet unidentified target in the FAT/CD36 mobilizing branch.

AMP-Activated Protein Kinases↗

PubMed2000

Intracoronary dipyridamole reduces the incidence of abrupt vessel closure following PTCA: a prospective randomised trial.

OBJECTIVES: To investigate the effect of intracoronary dipyridamole on the incidence of abrupt vessel closure, myocardial infarction, necessity for bypass grafting, and death following percutaneous transluminal coronary angioplasty (PTCA). PATIENTS: Patients were randomly allocated to receive either conventional pretreatment (heparin 15 000 IU and aspirin 500 mg intravenously) or additional intracoronary dipyridamole (0.5 mg/kg bodyweight). Dipyridamole was administered in 550 PTCA procedures (455 interventions in men, mean (SD) age 59.2 (8.4) years; 74 acute coronary syndromes), while conventional pretreatment was administered in 544 interventions (444 interventions in men 58.3 (7.9) years old; 81 acute coronary syndromes). In 53 interventions bail out stenting was performed for threatened abrupt vessel closure. RESULTS: Intracoronary dipyridamole significantly reduced the incidence of abrupt vessel closure (odds ratio 0.42. 95% confidence interval (CI) 0.22 to 0.79). While abrupt vessel closure occurred in 6.1% of interventions following conventional pretreatment, dipyridamole reduced the incidence to 2.5%. Restricting the analysis to balloon angioplasty, this reduction was observed in patients with stable angina (odds ratio 0.49, 95% CI 0.23 to 0.96) as well as in those with acute coronary syndromes (odds ratio 0.29, 95% CI 0.09 to 0.87). Reduction of secondary end points in the dipyridamole treated patients failed to reach significance in the PTCA group. CONCLUSIONS: Intracoronary dipyridamole before PTCA reduces the incidence of abrupt vessel closure following PTCA for stable angina and acute coronary syndromes.

Adult↗

PubMed1992

Interstitial adenosine with dipyridamole: effect of adenosine receptor blockade and adenosine deaminase.

Dipyridamole is proposed to increase coronary blood flow (CBF) by inhibition of adenosine uptake into cells, resulting in an increase in interstitial fluid (ISF) adenosine and an adenosine-mediated vasodilation. The purpose of this study was to determine the changes in CBF and ISF adenosine, inosine, and hypoxanthine during dipyridamole infusion in the absence or presence of adenosine receptor blockade or adenosine deaminase. To sample cardiac ISF, cardiac microdialysis probes were implanted in the left ventricular myocardium of chloralose-urethan-anesthetized dogs and perfused with Krebs-Henseleit buffer. The metabolite concentration in the effluent dialysate was used as an index of intramyocardial ISF metabolite concentration. In response to dipyridamole, CBF and dialysate adenosine concentration increased 4.4-fold and 2.2-fold, respectively, whereas dialysate inosine was unchanged and dialysate hypoxanthine decreased 50%. Adenosine receptor blockade, achieved by intracoronary 8-(p-sulfophenyl)theophylline infusion, attenuated the increase in CBF induced by dipyridamole without changing dialysate adenosine concentration. Adenosine deaminase fully attenuated the dipyridamole-induced increases in CBF and dialysate adenosine. These results demonstrate that dipyridamole increases ISF adenosine in the dog and suggest that adenosine is the sole mediator of dipyridamole-induced coronary vasodilation.

Adenosine↗

PubMed1994

Role of endogenous adenosine in hypoxic ventilatory response in humans: a study with dipyridamole.

To examine the role of endogenous adenosine in hypoxic ventilatory response, we measured, in nine normal young adults, ventilatory responses to isocapnic progressive hypoxia and subsequent sustained hypoxia [arterial O2 saturation (SaO2); 80%, 20 min] with and without pretreatment with dipyridamole in a double-blind crossover fashion. Dipyridamole, an adenosine uptake blocker, was expected to enhance the effect of endogenous adenosine. Pretreatment with dipyridamole (0.5 mg/kg) significantly augmented the slope of the ventilatory response to isocapnic progressive hypoxia from 0.35 +/- 0.13 (SE) to 0.70 +/- 0.25 l.min-1.%fall of SaO2(-1) (P < 0.01), although there were no significant changes in resting ventilation. On the other hand, minute ventilation, when expressed as a percentage of peak ventilation, declined to 68.4 +/- 4.3% with dipyridamole at the 9-11th min of sustained hypoxia, which was significantly lower than the 90.2 +/- 8.3% with a placebo (P < 0.05), and finally reached 56.1 +/- 7.2% with dipyridamole and 78.7 +/- 9.2% with the placebo (P < 0.1) at the 18-20th min of sustained hypoxia. In an attempt to more specifically examine the role of adenosine, aminophylline (5 mg/kg), an adenosine receptor antagonist, was injected before pretreatment with dipyridamole in four subjects. Aminophylline infusion abolished or at least attenuated the effect of dipyridamole in all four subjects. These data suggest that endogenous adenosine has a modulatory role in hypoxic ventilatory response in adult humans.

Adenosine↗

PubMedDate not supplied

Risk stratification prior to vascular surgery: does the location of a dipyridamole thallium scintigram defect provide prognostic information?

BACKGROUND: While the value of myocardial scintigraphy using dipyridamole thallium is accepted for risk assessment prior to vascular surgery, it is unknown whether the location of the thallium abnormalities provides prognostic information. METHODS: Records from 435 consecutive patients scheduled for vascular surgery were reviewed and patients with dipyridamole thallium abnormalities involving the anterior distribution (ANTERIOR n = 62), or inferior or inferolateral distribution (INFERIOR n = 105) were assessed for cardiac complications of surgery (death, myocardial infarction, unstable angina or ischemic congestive heart failure). RESULTS: Patients with a normal dipyridamole thallium scintigraphy had few surgical cardiac complications: 2/86 (2%). Patients with an ANTERIOR dipyridamole thallium defect had a 12% incidence of surgical cardiac complications (7/57) without any cardiac deaths, while patients with an INFERIOR dipyridamole thallium defect had a similar incidence of surgical cardiac complications, 18% (18/100; p = 0.65 vs. ANTERIOR) including 4 cardiac deaths. CONCLUSIONS: Significant inferior or inferolateral dipyridamole thallium scintigraphy abnormalities are not associated with a lower risk of cardiac complications following vascular surgery than anterior abnormalities. Rather, any clearly abnormal dipyridamole thallium study is a marker for increased risk of perioperative events and may warrant further evaluation and treatment.

Aged↗

PubMed1987

Effect of the antiplatelet agents ticlopidine and dipyridamole on nephrotoxic serum nephritis in rats.

The effect of the antiplatelet agents, ticlopidine and dipyridamole, on nephrotoxic serum nephritis (NTN) was evaluated in rats. An accelerated form of NTN was induced with preimmunization of rabbit IgG 7 days before injection of rabbit antirat nephrotoxic serum. Twelve animals received a peroral dose of 20 mg of ticlopidine daily, and 12 animals received a peroral dose of 10 mg of dipyridamole twice daily for 7 days. It was shown that both ticlopidine and dipyridamole were able to significantly reduce urinary protein excretion. There was, however, no significant difference in glomerular changes between treated animals and nontreated controls. Ticlopidine and dipyridamole were found to suppress the development of proteinuria in accelerated NTN. Although the antiaggregative action of dipyridamole was relatively weak in vivo, dipyridamole was found to be rather effective on protein excretion in the present study. These results support the significant role of platelets in the development of proteinuria in glomerulonephritis, and it is suggested that dipyridamole may have an antiproteinuric effect other than inhibition of platelet aggregation.

Animals↗

PubMed1999

Perioperative prognostic value of dipyridamole echocardiography in vascular surgery: A large-scale multicenter study in 509 patients. EPIC (Echo Persantine International Cooperative) Study Group.

BACKGROUND: Patients undergoing major vascular surgery are at a relatively high risk of cardiac events, and pharmacological stress echocardiography is increasingly used for perioperative risk stratification. The aim of the current study was to evaluate the value of dipyridamole echocardiography test (up to 0.84 mg/kg over 10 minutes) in predicting cardiac events in a large-scale, multicenter, prospective, observational study design. METHODS AND RESULTS: Five hundred nine patients (mean age 66+/-10 years) were studied before vascular surgery by dipyridamole stress echocardiography in 11 different centers. All patients underwent preoperative clinical risk assessment according to the American Heart Association guidelines. No major complications occurred during dipyridamole stress echocardiography. Technically adequate images were obtained in all patients; however, in 4 patients only the low dipyridamole dose (0.56 mg/kg over 4 minutes) was given for limiting side effects. Eighty-eight (17.3%) had a positive test. Perioperative events occurred in 31 (6.1%) patients: 6 deaths, 11 myocardial infarctions, and 14 episodes of unstable angina. Sensitivity and specificity of dipyridamole stress echocardiography for predicting spontaneous cardiac events were 81% and 87%, respectively, with a positive predictive value of 28% and negative predictive value of 99%. By multivariate analysis, the difference between wall motion score index at rest and peak stress (Deltawall motion score index), test positivity, and ST-segment depression during dipyridamole infusion were independent predictors of any perioperative cardiac event. CONCLUSIONS: Dipyridamole stress echocardiography is safe and well tolerated in patients undergoing major vascular surgery and provides an effective preoperative screening test for the risk stratification of these patients, mainly because of the extremely high negative predictive value, which is a potent predictor of complication-free procedure.

Aged↗