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PubMed1990

Transient left ventricular cavitary dilation during dipyridamole-thallium imaging as an indicator of severe coronary artery disease.

Transient left ventricular (LV) cavitary dilation during dipyridamole-thallium imaging was reported in 45 of 510 (9%) consecutive patients referred for dipyridamole-thallium imaging. Clinical and hemodynamic effects observed during dipyridamole infusion were not predictive of transient cavitary dilation on the thallium images. Coronary angiography was performed in 32 of the 45 patients: 75% had either left main, 3-vessel or "high-risk" 2-vessel coronary artery disease. Although 25 of 45 patients (56%) with transient cavitary dilation were either asymptomatic or had only grade 1/4 effort angina, 16 of 25 patients (64%) not referred for coronary revascularization sustained a cardiac event during a mean follow-up of 12 months. Most events were cardiac deaths (75%) and 87% of events occurred within 4 months of the test. Noncardiac surgery was performed in 187 of the 510 patients. The postoperative cardiac event rate was 2% in the 101 patients with normal scans or fixed defects, 19% in 75 patients with reversible perfusion defects and 58% in 12 patients with reversible cavitary dilation (p less than 0.0001). Thus, transient LV dilation during dipyridamole-thallium imaging is a marker of severe underlying coronary artery disease, denotes a poor prognosis and predicts a high risk of postoperative cardiac complications in patients who undergo noncardiac surgery.

Coronary Angiography↗
PubMed1990

Significance of dipyridamole-induced transient dilation of the left ventricle during thallium-201 scintigraphy in suspected coronary artery disease.

The occurrence and significance of transient dilation of the left ventricle during dipyridamole stress-redistribution thallium-201 scintigraphy was studied in 73 patients who underwent both dipyridamole thallium-201 study and coronary angiography. Transient dilation ratio was calculated from planar anterior images by dividing the computer-derived left ventricular area on the initial image by that of the 4-hour image. In 11 patients with normal coronary arteriograms or less than 50% coronary stenosis, the transient dilation ratio was 0.98 +/- 0.046. An abnormal transient dilation ratio was defined as greater than or equal to 1.12, representing greater than or equal to 3 standard deviations above the mean normal value. When the 15 patients with an abnormal ratio were compared with the 58 with a normal ratio, the former group had a significantly higher frequency of 3 critical (greater than or equal to 90%) coronary stenoses (33 vs 5%), higher prevalence of collaterals (67 vs 24%), more extensive myocardial reversible defects by planar (71 vs 10%) or by single-photon emission computed tomography (87.5 vs 35%) imaging and a higher incidence of dipyridamole-induced anginal chest pain (53 vs 22%). No significant difference between the 2 groups was noted with respect to age, gender, prior myocardial infarction, single or double critical coronary stenosis, dipyridamole-induced ischemic electrocardiographic response and increased lung uptake. An abnormal transient dilation ratio of greater than or equal to 1.12 was a specific marker of multivessel (87%) or 3-vessel (85%) critical coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Prevalence and correlates of increased lung/heart ratio of thallium-201 during dipyridamole stress imaging for suspected coronary artery disease.

There is little information concerning the prevalence and clinical correlates of increased pulmonary thallium-201 uptake during dipyridamole thallium-201 stress imaging. Accordingly, the clinical characteristics and quantitative thallium-201 findings were correlated with quantitative lung/heart thallium-201 ratio in 87 patients undergoing dipyridamole thallium-201 stress testing. Nineteen patients (22%) had an elevated ratio (greater than 0.51). These patients were more likely to have had an infarction, to be taking beta blockers, and have a lower rate-pressure product after dipyridamole administration than those with a normal ratio (p less than 0.03). An elevated ratio was associated with a greater likelihood of initial, redistribution and persistent defects, as well as left ventricular cavity dilatation on thallium-201 imaging (p less than 0.05). In addition, the number of myocardial segments demonstrating initial, redistribution and persistent defects was also greater in patients with increased ratios (p less than 0.03). Multivariate analysis demonstrated that the presence of redistribution and left ventricular cavity dilatation were the most significant correlates of lung/heart thallium-201 ratio. It is concluded that the prevalence of increased lung/heart thallium-201 ratio with dipyridamole thallium-201 stress imaging is similar to that seen with exercise stress imaging. As with exercise thallium-201 imaging, increased pulmonary thallium-201 uptake may be a marker of functionally more significant coronary artery disease.

Adult↗
PubMed1990

Effects of atrial pacing and dipyridamole administration on coronary hemodynamics of collateralized myocardial regions in stable angina pectoris.

Great cardiac vein blood flow by thermodilution and great cardiac vein oxygen saturation were measured in 14 patients with stable exertional angina and an angiographic pattern of complete occlusion of the proximal left anterior descending artery retrogradely filled by collateral vessels supplying still viable myocardium. Measurements were obtained under control conditions, at peak atrial pacing and after dipyridamole administration (0.56 mg/kg intravenously over 4 minutes). Both stress tests induced ischemic electrocardiographic changes in all patients, but dipyridamole administration resulted in greater ST-segment depression in 11 patients (1.6 +/- 0.5 vs 2.4 +/- 1.6 mm, p less than 0.05) and transient ST-segment elevation in 3 patients. Dipyridamole provoked ischemia at a lower value of rate-pressure product (145.3 +/- 30.6 vs 202.9 +/- 36.6 beats/min . mm Hg . 10(-2), p less than 0.0005) and anterior region myocardial oxygen consumption (9.32 +/- 4.76 vs 11.39 +/- 3.91 ml/min, p less than 0.05), despite a greater increase in great cardiac vein flow (139.4 +/- 45 vs 93 +/- 27.4 ml/min, p less than 0.0025) and a greater decrease in the calculated index of anterior region coronary resistance (0.87 +/- 0.27 vs 1.46 +/- 0.43 mm Hg/ml/min, p less than 0.0005). Moreover, great cardiac vein oxygen saturation increased more significantly during dipyridamole-induced ischemia than at peak pacing (63 +/- 12 vs 35 +/- 8%, p less than 0.0005).(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1991

Noninvasive identification of significant narrowing of the left main coronary artery by dipyridamole thallium scintigraphy.

To evaluate the usefulness of dipyridamole thallium scintigraphy with low-level exercise for the identification of left main (LM) coronary artery disease (CAD), 466 consecutive patients with CAD were studied. Thirty-eight patients (8%) had LM stenosis (diameter narrowing greater than or equal to 50%). The LM scintigraphic pattern was present in 9 of 38 patients with LMCAD and 38 of 428 CAD patients without LMCAD (24 vs 9%; p less than 0.005). This pattern was present in 6 of 9 patients with LMCAD without right CAD and in only 3 of 29 patients with LM and right CAD (67 vs 10%; p = 0.0005). Patients with LMCAD had a higher incidence of premature cessation of low-level exercise (53 vs 21%; p less than 0.0001), chest pain (68 vs 48%; p less than 0.02), blood pressure decrease of greater than or equal to 20 mm Hg (44 vs 16%; p less than 0.002) and greater ST depression (0.17 +/- 0.13 vs 0.06 +/- 0.10 mV; p less than 0.001) during dipyridamole loading than patients without LMCAD. Stepwise discriminant analysis revealed that the LM scintigraphic pattern and markers of ischemia during dipyridamole loading best identified (p less than 0.0001) patients with LMCAD without right CAD (sensitivity 67%, specificity 91%), but this predictability is no better than the LM scintigraphic pattern alone. The combination of clinical markers of ischemia during dipyridamole loading and scintigraphic findings of diffuse slow washout, extensive fixed defects and the LM pattern best identified (p less than 0.0001) patients with LM and right CAD (sensitivity 72%, specificity 80%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Dose and test for dipyridamole infusion and cardiac imaging early after uncomplicated acute myocardial infarction.

To evaluate the relation of the dose of intravenous dipyridamole on results of thallium and echocardiographic testing, the results of standard- (0.56 mg/kg/4 minutes) versus high- (0.84 mg/kg/10 minutes) dose dipyridamole were obtained 9 +/- 3 days after uncomplicated acute myocardial infarction in 57 patients. New wall motion abnormalities were compared with redistribution of thallium imaging and results of discharge coronary angiography. The sensitivity of thallium in predicting the presence of multivessel coronary artery disease was significantly (p < 0.01) higher (85%) than echocardiography (53%) and was unaffected by the dose. However the sensitivity of echocardiography was better with the higher dose (53 vs 14%). Minor adverse effects occurred in 34 patients (59%) after receiving the high dose and only in 4 patients (7%) after the standard dose (p < 0.001). Thus, thallium-201 scintigraphy during standard-dose dipyridamole infusion is more effective than high-dose dipyridamole echocardiographic testing in safely identifying patients who could benefit from early invasive evaluation and therapy.

Angina Pectoris↗
PubMed1993

Exercise thallium scintigraphy versus high-dose dipyridamole echocardiography testing for detection of asymptomatic restenosis in patients with positive exercise tests after coronary angioplasty.

The usefulness of high-dose (< or = 0.84 mg/kg over 10 minutes) dipyridamole echocardiography testing was compared with that of exercise thallium-201 scintigraphy in detecting restenosis (> 70% lumen reduction) in 50 asymptomatic patients with ST-segment depression during maximal exercise testing 3 months after successful coronary angioplasty. Dipyridamole echocardiography testing and exercise thallium scintigraphy showed a similar sensitivity (75 vs 83%; p = NS) and specificity (90 vs 84%; p = NS) for the detection of restenoses, which occurred in 12 patients. It is concluded that dipyridamole echocardiography testing is as accurate as exercise thallium testing for the noninvasive detection of severe restenosis in patients with exercise-induced asymptomatic ST-segment depression after successful angioplasty. Furthermore, the site, extent and severity of the thallium perfusion defects during exercise are correlated to those of the dyssynergy during dipyridamole echocardiography.

Angioplasty, Balloon, Coronary↗
PubMed1994

Preoperative clinical assessment and dipyridamole thallium-201 scintigraphy for prediction and prevention of cardiac events in patients having major noncardiovascular surgery and known or suspected coronary artery disease.

The aim of this study was to assess the relative prognostic use of clinical risk stratification and intravenous dipyridamole thallium-201 scintigraphy in patients with an intermediate to high prevalence of coronary artery disease (CAD) who have undergone major noncardiovascular surgery, and to assess the effects of medical therapy or coronary revascularization based on the result of this clinical scintigraphic screening on perioperative cardiac morbidity and mortality. Patients (n = 161) with an intermediate to high likelihood of CAD had clinical assessment and intravenous dipyridamole planar thallium-201 testing which was analyzed semiquantitatively. Cardiac events were cardiac death (n = 9), nonfatal myocardial infarction (n = 6), acute pulmonary edema (n = 6), and unstable angina (n = 4). Multiple (> or = 2) clinical risk variables predicted any cardiac event (p = 0.04). Presence of multiple (> or = 2) abnormal thallium-201 segments was the only independent predictor of cardiac death or nonfatal myocardial infarction (p < 0.001), and was the most powerful multivariate predictor of any cardiac event (p < 0.002). Patients with an abnormal dipyridamole thallium-201 scan had a higher risk of perioperative cardiac death, myocardial infarction (18% vs 2%; p < 0.001), or any perioperative cardiac event (27% vs 6%; p < 0.001) when compared with those with a normal scan. Preoperative changes in anti-ischemic therapy or coronary revascularization in 36 of 72 patients with abnormal dipyridamole thallium-201 studies reduced perioperative death or myocardial infarction from 31% to 6% (p < 0.01), and all cardiac events from 47% to 8% (p < 0.001) compared with those in patients without intervention.(ABSTRACT TRUNCATED AT 250 WORDS)

Chi-Square Distribution↗
PubMed1994

Dipyridamole stress echocardiography in patients with severe left main coronary artery narrowing. Echo Persantine International Cooperative (EPIC) Study Group--Subproject "Left Main Detection".

From a population of 2,698 patients (579 evaluated early after an uncomplicated acute myocardial infarction) who underwent dipyridamole echocardiography testing (DET) and subsequent coronary angiography, left main (LM) stenosis > or = 50% was present in 73 (61 men and 12 women, mean age 62 +/- 8 years). These 73 patients were compared with a control group comprising 100 consecutive coronary patients without LM disease. Both groups were similar regarding mean age, sex, incidence of previous myocardial infarction, left ventricular function at rest, and severity of coronary artery disease by the number of diseased vessels excluding the LM. The proportion of patients receiving antianginal therapy during DET was higher in the LM than in the non-LM group (32 vs 14%; p < 0.01). No major complication (severe hypotension, sustained arrhythmia, myocardial infarction or death) occurred during DET. Of 73 patients with LM disease, 68 had positive DET (sensitivity 93%), dipyridamole time was 7.1 +/- 3.8 minutes, and the rest-peak stress variation in dipyridamole wall motion score index (1 = normal to 4 = dyskinesia, in an 11-segment model) was 0.37 +/- 0.23; 14 patients (19%) were resistant to aminophylline and needed nitrates to resolve ischemia. In the non-LM group, DET was positive in 72% (p < 0.001 vs LM), with a longer dipyridamole time (9.6 +/- 5.2 minutes; p < 0.001 vs LM), lower rest-peak stress wall motion score index variation (0.29 +/- 0.25; p < 0.05 vs LM), and less frequent antidote resistance (1%; p < 0.001 vs LM).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

Prognostic value of dipyridamole echocardiography early after uncomplicated myocardial infarction: a large-scale, multicenter trial. The EPIC Study Group.

PURPOSE: To determine the prognostic capability of the dipyridamole echocardiography test (DET) early after an acute myocardial infarction. PATIENTS AND METHODS: On the basis of 11 different echocardiographic laboratories, all with established experience in stress echocardiography and fulfilling quality-control requirements for stress echocardiographic readings, 925 patients were evaluated after a mean of 10 days from an acute myocardial infarction and followed up for a mean of 14 months. RESULTS: During the follow-up, there were 34 deaths and 37 nonfatal myocardial infarctions; 104 patients developed class III or IV angina and 149 had coronary revascularization procedures (bypass or angioplasty). Considering all spontaneous events (angina, reinfarction, and death), the most important univariate predictor was the presence of an inducible wall motion abnormality after dipyridamole administration (chi 2 = 45.8). With a Cox analysis, echocardiographic positivity, age, and male gender were found to have an independent and additive value. Considering survival (and, therefore, death as the only event), age was the most meaningful parameter, followed by the wall motion score index during dipyridamole administration (chi 2 = 12.1). Among other parameters, the resting wall motion score index was a significant predictor of death. In a multivariate analysis, the prognostic contributions of age (relative risk estimate = 1.08) and wall motion score index during dipyridamole administration (relative risk estimate = 4.1) were independent and additive. In particular, considering death only, the event rate was 2% in patients with negative DET results, 4% in patients with positive high-dose DET results, and 7% in patients with positive low-dose DET results. CONCLUSIONS: DET is feasible and safe early after uncomplicated myocardial infarction and allows effective risk stratification on the basis of the presence, severity, extent, and timing of the induced dyssynergy.

Adult↗
PubMed1988

Potentiation of quinazoline antifolate (CB3717) toxicity by dipyridamole in human lung carcinoma, A549, cells.

A potent quinazoline antifolate inhibitor of thymidylate synthase, CB3717, inhibits the growth of A549 human lung carcinoma cells: ID50 2.74 +/- 0.53 microM. The toxic effects of thymidylate synthase inhibition may be prevented by salvage of exogenous thymidine. The nucleoside transport inhibitor, dipyridamole, at the non-toxic concentration of 1 microM, inhibited [3H]thymidine uptake/incorporation by more than 95% and significantly reduced the ID50 of CB3717 to 0.98 +/- 0.28 microM. Elimination of salvageable thymidine by the use of dialysed serum also enhanced CB3717 toxicity. Since dipyridamole was equally effective in the presence or absence of dialysed serum and was more effective than dialysed serum alone, inhibition of nucleoside efflux may be an important aspect of its potentiation. Efflux of [5-3H]deoxyuridine was inhibited by 89% and [3H]thymidine efflux by 61% in the presence of 1 microM dipyridamole. Inhibition of thymidylate synthase increases the deoxyuridine nucleotide/thymidine nucleotide pool ratio. Dipyridamole could exacerbate the nucleotide pool imbalance caused by CB3717, thereby potentiating its toxicity.

Carcinoma↗
PubMed1994

Differential effects of the pyrimido-pyrimidine derivatives, dipyridamole and mopidamol, on platelet and vascular cyclooxygenase activity.

The chronic administration of 10 mg/kg/day of dipyridamole to rats produced 33.7% inhibition of platelet aggregation induced with ADP and a 93% increase in 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in vascular samples, versus saline-treated rats. Mopidamol, 8.3 mg/kg/day, caused 50.6% inhibition of ADP-induced platelet aggregation, 37.6% inhibition of aggregation induced with arachidonic acid, a 47.6% decrease in serum levels of thromboxane B2 and a 23.7% increase in the vascular production of 6-keto-PGF1 alpha, versus saline-treated rats. Dipyridamole showed a higher in vitro anti-aggregating effect in whole blood (IC50 6.6 microM) than in platelet-rich plasma (PRP) (IC50 210 microM), when ADP was used as inducer, and had no effect in the presence of arachidonic acid. Mopidamol exerted a similar effect in whole blood (IC50 3.7-20 microM, depending on the inducer) and PRP (IC50 11-17.3 microM), and showed a dose-dependent inhibition of platelet aggregation and thromboxane B2 synthesis induced with arachidonic acid (IC50 16.8-22.3 microM). Mopidamol also inhibited enzymatically induced lipid peroxidation) (IC50 89 +/- 5.9 mumol/L) and had no effect on free radical-induced lipid peroxidation. The dose-dependent increase in 6-keto-PGF1 alpha in vascular samples after incubation with dipyridamole showed a negative linear correlation with inhibition of lipid peroxidation (r2 = 0.77). It is concluded that the phosphodiesterase inhibitors, dipyridamole and mopidamol, interfere in a different manner with platelet function. It seems that mopidamol may also exert a selective effect on platelet thromboxane synthesis.

Animals↗
PubMedDate not supplied

Lack of efficacy of the adenosine reuptake inhibitor dipyridamole in the treatment of anxiety disorders.

We administered dipyridamole, an adenosine reuptake inhibitor, to 12 outpatients with DSM-III-R anxiety disorders (2 patients with generalized anxiety disorder, 10 patients with panic disorder). Dipyridamole was administered at a flexible dose in a single-blinded fashion following a placebo washout phase and elimination of placebo responders. The mean duration of active treatment with dipyridamole was 46 days (range 21-88 days); the mean peak dose of dipyridamole was 202 +/- 55 mg/day (range 100-300 mg/day). Symptom ratings were completed at regular intervals by the patient and by a research nurse unaware of the treatment condition. Clinically significant improvement in anxiety symptoms was not demonstrated. The implications of these findings for an adenosinergic dysfunction model of panic disorder are discussed.

Adenosine↗
PubMed1988

Dynamic cerebral and systemic circulatory effects of adenosine, theophylline and dipyridamole.

The effects of intravenous adenosine, dipyridamole and theophylline on local cerebral blood flow were studied in conscious rabbits. Long-term quantitative blood flow measurements were performed in 5 cerebral structures together with tissue pO2 and pCO2 measurements by a mass spectrometry technique. In an additional study, the time course of the cerebrovascular changes was determined by thermal clearance. It was found that: firstly, adenosine failed to modify local blood flow except in the caudate nucleus; secondly, dipyridamole increased cerebral blood flow in all 5 structures under study, and lastly, theophylline decreased cerebral blood flow in the same 5 structures. The increase in caudate blood flow induced by adenosine was instantaneous and lasted only for the duration of the infusion, whereas the cerebrovascular changes induced by dipyridamole and theophylline were gradual and persisted after their administration. Theophylline blocked the systemic and cerebrovascular changes caused by adenosine alone and by dipyridamole alone. In anesthetized rabbits, the intracarotid infusion of adenosine showed that the caudate reaction only occurred in the ipsilateral hemisphere. Taken together, our findings suggest that the transport system for adenosine in cerebral vessels is not only species-dependent but also structure-dependent. Furthermore, perivascular adenosine helps to maintain resting cerebrovascular tone and finally, cerebral adenosine may be involved in the control of cerebral blood flow via specific adenosine receptors.

Adenosine↗
PubMed1983

Discrimination by dipyridamole of two types of responses to adenosine and ATP of the carbachol-induced contraction of guinea-pig trachea.

Two types of effect of purines on the carbachol-induced contraction of the guinea-pig trachea in the presence or absence of glucose were evaluated using dipyridamole, and adenosine uptake inhibitor. ATP exerted a greater relaxant effect on the carbachol (10(-6) M)-induced contraction than did adenosine in concentrations ranging from 10(-4) to 10(-3) M. These effects of purines were enhanced by pretreatment with dipyridamole (10(-5) M) but were virtually unaffected by the purine receptor antagonists theophylline (10(-5) M) and quinidine (10(-5) M). The contraction evoked by carbachol was gradually reduced and was almost abolished 4-5 h after exposure to the glucose-free solution. This reduction was almost eliminated by readmitting glucose, and was restored to a certain degree by introducing ATP or adenosine. ATP was less effective than adenosine. This effect of purines but not that of glucose, was markedly diminished by pretreatment with dipyridamole (3 X 10(-6) M to 10(-5) M). The restoration of the carbachol-induced contraction following introduction of purines or glucose was completely antagonized by atropine (10(-6) M). These results suggest that the extracellular effects of adenosine and ATP on the carbachol-induced contraction in normal solution are potentiated by dipyridamole, whereas the possible intracellular effects of these purines in the glucose-free solution are inhibited by this adenosine uptake inhibitor.

Adenosine↗
PubMed1991

Dipyridamole potentiates the anti-aggregating and vasodilator activity of nitric oxide.

The interaction between dipyridamole and nitric oxide (NO) was studied using isolated rabbit platelets and segments of the rabbit aorta. Dipyridamole potentiated the anti-aggregating activity of authentic NO when platelet aggregation was induced by the thromboxane A2 mimetic U-46619 or adenosine diphosphate (ADP). This potentiation was also seen when washed rabbit platelets were exposed to aortic effluent containing endothelium-derived NO. In the thoracic aorta dipyridamole hardly influenced the endothelium-dependent relaxations induced by acetylcholine. However, dipyridamole clearly enhanced the dilatation caused by exogenous NO from four different sources, including endothelial cells.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1986

Adenosine transporters in chromaffin cells. Quantification by dipyridamol monoacetate.

Chromaffin cells from bovine adrenal medulla are a useful model to approach adenosine transport and metabolism in neural cells. Dipyridamol has been shown to be an adenosine transport inhibitor with high affinity. To quantify the adenosine transporters a labelled dipyridamol analogue, [14C]dipyridamol acetate, was synthesized. This compound had a Ki = 5.3 +/- 0.43 nM according to the Dixon method, and 4.58 +/- 0.46 nM when the receptor number molarity was taken into account showing, like dipyridamol, a non-competitive mechanism. The high-affinity receptors present in chromaffin cells showed a Kd = 6.8 +/- 0.8 nM and the receptor number was 630 000 +/- 40 000 per cell.

Adenosine↗
PubMed1988

Chloride mediated inhibition of the phosphate and the sulfate transport by dipyridamole in human erythrocyte ghosts.

The inhibition of the unidirectional phosphate and sulfate flux in human erythrocyte ghosts by dipyridamole has been investigated. The inhibition of the phosphate and the sulfate flux is mediated by chloride. At zero chloride, dipyridamole was found to be completely ineffective. At 10 mM chloride, dipyridamole acts as a noncompetitive inhibitor of the phosphate and the sulfate flux and elicits an up to 95% inhibition of the phosphate and the sulfate transport. The results of our studies provide strong evidence for a cooperative binding of chloride and of dipyridamole to the non-protonated form of the band 3 membrane domain.

Biological Transport↗