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Persantine (Dipyridamole)

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Generic Persantine is a coumarin anticoagulants. Generic Persantine is indicated as an adjunct to coumarin anticoagulants in the prevention of postoperative thromboembolic complications of cardiac valve replacement. Generic Persantine keeps blood flowing smoothly by preventing blood cells from clumping together (coagulating).

Other names for this medication:

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Argatroban, Plavix, Salagen, Arixtra


Also known as:  Dipyridamole.


Generic Persantine is a coumarin anticoagulants.

Generic Persantine is indicated as an adjunct to coumarin anticoagulants in the prevention of postoperative thromboembolic complications of cardiac valve replacement. Generic Persantine keeps blood flowing smoothly by preventing blood cells from clumping together (coagulating).

Persantine is also known as Dipyridamole.

Generic name of Generic Persantine is Dipyridamole.

Brand name of Generic Persantine is Persantine.


You can take Generic Persantine with or without food.

The recommended Generic Persantine dose is 75-100 mg four times daily.

Try to take this Generic Persantine at the same time each day.

Do not store in the bathroom.

If you want to achieve most effective results do not stop taking Generic Persantine suddenly.


If you overdose Generic Persantine and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Persantine overdosage: warm feeling, flushes, sweating, restlessness, weakness, dizziness.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Persantine are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Generic Persantine if you are allergic to Generic Persantine components.

Be careful with Generic Persantine if you are pregnant, planning to become pregnant, or are breast-feeding.

Be careful with Generic Persantine if you have unstable angina.

Be careful with Generic Persantine if you have had recently sustained myocardial infarction or hypotension.

Be careful with Generic Persantine if you use anticoagulants ("blood thinners"), aspirin, valproic acid.

It can be dangerous to stop Generic Persantine taking suddenly.

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SPECT might represent a useful non-invasive method for assessing coronary vascular function in patients with angina and a normal coronary angiogram.

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Interleukin-8 is a proinflammatory cytokine with chemo-attractive and major activator properties on neutrophils. The very few studies in literature on the IL-8 behaviour in myocardial ischaemia refer only to acute myocardial infarction. This study investigates the IL-8 behaviour in stable angina pectoris after myocardial ischaemia induced by dipyridamole (14 patients) and in unstable angina pectoris, Braunwald's class III (35 patients). In stable exercise angina following dipyridamole-induced myocardial ischaemia, the plasma IL-8 levels did not increase. In unstable angina pectoris increased plasma IL-8 levels were evidenced in 25 of the 35 patients, after an average interval of 20 +/- 1.2 hours from the last spontaneous episode of angina pectoris. The IL-8 behaviour was different in class III B patients as compared to class III A: only 30% of the patients in class III A presented transient increase of IL-8, while 70% of the class III B presented increased IL-8 with a median value of 900 pg/ml within the first 24 hours from the last spontaneous episode of angina pectoris. The increased plasma IL-8 levels within the first 24 hours from the spontaneous episode could represent a marker of primary angina pectoris, Braunwald's class III B.

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The authors reviewed the literature, focusing on the indications and mechanisms of antiplatelet therapy and the perioperative management of patients taking these agents who require exodontia or other dentoalveolar surgery.

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Rehabilitation patients who will undergo noncardiac surgery or strenuous rehabilitation programs often cannot exercise to greater than 85% of predicted maximal heart rate as required for valid treadmill testing. Because many patients have known or suspected coronary artery disease, greatly increasing their risk for a cardiac event, dipyridamole thallium scans are usually performed, despite a cost of approximately $1400, patient radiation exposure, and the need for a gamma camera. Instead, arm-leg cycle stress testing can be continued to an appropriately high heart rate, is done in the physician's office with an electrocardiograph machine and a blood pressure cuff, and costs $250. This study describes nine patients who had both dipyridamole thallium scans and arm-leg cycle ergometry. Four awaited peripheral vascular surgery, one needed bilateral knee replacements, one was an amputee, and three had claudication. Six had documented and three had suspected coronary disease.

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The ability of theophylline and other phosphodiesterase inhibitors to alter contractile responses to cholinergic nerve stimulation was investigated in isolated longitudinal muscle of the guinea pig ileum. Theophylline in low concentrations (10-100 microM), having no or little effect on measured phosphodiesterase activity, antagonized inhibitory effects of exogenous adenosine. In higher concentrations (0.1-10 mM), shown to be effective in inhibiting phosphodiesterase, theophylline as well as a "pure" cAMP phosphodiesterase inhibitor, ZK 62, 711, inhibited contractile responses. Dipyridamole and dilazep, inhibitors of adenosine inactivation, and also selective inhibitors of cAMP and cGMP phosphodiesterase, respectively, were found to enhance effects of exogenous adenosine and to cause a marked leftward shift to adenosine threshold dose. When dipyridamole and dilazep by themselves had inhibitory effects these could be antagonized by theophylline, suggesting an action through increased levels of endogenous adenosine. As a further indication of endogenous adenosine modulating neurotransmission low concentrations of theophylline enhanced responses to transmural stimulation. Endogenous purine concentrations in tissues and bath media were measured by HPLC. Because of tissue and microbial adenosine inactivation direct estimates of extracellular adenosine concentration could not be obtained. However, adenosine levels increased during transmural stimulation, and during inhibition of adenosine inactivation were sufficient, even in the bath medium, to interfere with the cholinergic neurotransmission.

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The purpose of the present study was to investigate the oral absorption simulation of free base drugs. In the case of a low solubility free base drug, a portion of drug particles remains incompletely dissolved during the stomach transit and can reach the small intestine. As the pH is neutralized in the small intestine, the solubility of the drug decreases and the concentration gradient around the particles becomes a negative value. The drug particles would then grow because of this negative concentration gradient resulting in a reduction of the dissolved drug concentration. The modified Nernst Brunner equation was used to simulate both particle dissolution and growth (particle growth is the opposite phenomena of particle dissolution). Albendazole, aprepitant, dipyridamole, gefitinib and ketoconazole were used as model drugs (all free solid form (not salts)). The effect of stomach pH on oral absorption was appropriately simulated. Based on the simulation results, it was suggested that the dissolution patterns in the gastrointestinal tract were significantly different depending on the dose-solubility ratio in the stomach.

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The metabolism of endogenous adenosine and 2-deoxy-adenosine was studied in cultures of fetal mouse calvaria. Adenosine deamination was the most important pathway of metabolism. This was blocked by erythro-2-(2-hydroxy-3-nonyl)adenine (1 microM). Albumin in the medium could not account for the deaminase activity. The disappearance of adenosine from the medium was not influenced by two inhibitors of adenosine transport, dipyridamole and dilazep, but was competitively inhibited by 2-deoxy-adenosine. During culture there was a net increase in adenosine and inosine, possibly originating from damaged cells.

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Of the 54 women patients who underwent MPI, 7 underwent exercise stress testing, 26 had stress testing with adenosine, 18 with dipyridamole and 3 with dobutamine. Eighteen patients (53%) had same number of vessels predicted by MPI and coronary angiography (7 patients with triple vessel disease, 7 with 2-vessel disease and 4 with single vessel disease). Five (3 with intermediate and 2 with high risk scans) out of the 54 patients (9.3%) were dead at 2 years. The sensitivity, specificity and positive predictive value of MPI as compared to angiography were 87.2%, 26.7%, 75.6% and 44.4% respectively.

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The study design is a retrospective cohort study, looking at fall trauma among patients aged 60 to 80 years from 2009 to 2013 at a university hospital in the United States. The statistical analysis, conducted with SPSS software with a threshold for statistical significance of P < .05, was stratified by anticoagulation status and then further by type of anticoagulation (aspirin, warfarin, clopidogrel, enoxaparin, and dipyridamole). Outcomes variables include mortality, length of stay (LOS), intensive care unit (ICU) admission, and complications.

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This initial experience suggests that reverse remodeling of the peri-infarct zone with reduction in peri-infarct zone volume may take place in patients with ischemic cardiomyopathy. Quantification of this process may be feasible with DGE-MRI, but further studies are needed to confirm this hypothesis and to further clarify the role of DGE-MRI for the assessment of changes in peri-infarct zone volume in patients with ischemic cardiomyopathy.

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ATP is a gliotransmitter released from astrocytes. Extracellularly, ATP is metabolized by a series of enzymes, including ecto-5'-nucleotidase (eN; also known as CD73) which is encoded by the gene 5NTE and functions to form adenosine (ADO) from adenosine monophosphate (AMP). Under ischemic conditions, ADO levels in brain increase up to 100-fold. We used astrocytes cultured from 5NTE (+/+) or 5NTE (-/-) mice to evaluate the role of eN expressed by astrocytes in the production of ADO and inosine (INO) in response to glucose deprivation (GD) or oxygen-glucose deprivation (OGD). We also used co-cultures of these astrocytes with wild-type neurons to evaluate the role of eN expressed by astrocytes in the production of ADO and INO in response to GD, OGD, or N-methyl-D-aspartate (NMDA) treatment. As expected, astrocytes from 5NTE (+/+) mice produced adenosine from AMP; the eN inhibitor α,β-methylene ADP (AOPCP) decreased ADO formation. In contrast, little ADO was formed by astrocytes from 5NTE (-/-) mice and AOPCP had no significant effect. GD and OGD treatment of 5NTE (+/+) astrocytes and 5NTE (+/+) astrocyte-neuron co-cultures produced extracellular ADO levels that were inhibited by AOPCP. In contrast, these conditions did not evoke ADO production in cultures containing 5NTE (-/-) astrocytes. NMDA treatment produced similar increases in ADO in both 5NTE (+/+) and 5NTE (-/-) astrocyte-neuron co-cultures; dipyridamole (DPR) but not AOPCP inhibited ADO production. These results indicate that eN is prominent in the formation of ADO from astrocytes but in astrocyte-neuron co-cultures, other enzymes or pathways contribute to rising ADO levels in ischemia-like conditions.

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Ongoing antiischemic therapy at the time of testing heavily modulates the prognostic value of pharmacological stress echo. In the presence of concomitant antiischemic therapy, a positive test is more prognostically malignant, and a negative test less prognostically benign.

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Isometric contractions of rabbit renal artery rings were subjected to increasing concentrations of the ionic contrast medium sodium/meglumine diatrizoate (DIA) and the nonionic contrast media iopamidol (IOP) and iodixanol (IOD) and compared with a potassium chloride control. Subsequently increasing concentrations of the nonselective phosphodiesterase inhibitors theophylline and papaverine and the following selective phosphodiesterase inhibitors were applied: vinpocetine, trequinsin, zardaverine, rolipram, and dipyridamole (subtypes I-V) before restimulation of the arterial tissue with contrast medium.

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Recent data demonstrate that dipyridamole-thallium (DTHAL) and sestamibi (DMIBI) are not predictive of adverse perioperative cardiac events in moderate-risk patients (one or more Eagle risk factors) undergoing major elective vascular surgery. Less data are available regarding the ability of DTHAL/DMIBI to predict adverse cardiac events on long term follow-up. We sought to determine whether an abnormal DTHAL/DMIBI is predictive of adverse cardiac events on long-term follow-up in moderate-risk patients undergoing major elective vascular surgery. Patients were enrolled prospectively between June 1997 and June 1999 at West Los Angeles VA and Harbor-UCLA Medical Centers. Adverse cardiac events were defined as congestive heart failure (CHF), myocardial infarction (MI), unstable angina (USA), and ventricular arrhythmias. Follow-up was obtained via clinic visits, telephone calls, and chart review. We studied 75 patients (76% male, 24% female) with a mean age of 65 years. Operative procedures were primarily femorodistal (83%) and aortic (16%). DTHAL/DMIBI results were normal in 35 patients (47%), demonstrated reversible ischemia in 26 (35%), and showed a fixed defect alone in 14 (18%). From the follow-up results of this study we conclude that there is no association between a reversible ischemia or an abnormal (fixed or reversible) DTHAL/DMIBI and adverse cardiac events or mortality on long-term follow-up in moderate-risk patients who have undergone major vascular surgery.

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On the VerifyNow, HTPR on aspirin was identified in 4 of 51 patients (8%) on aspirin-dipyridamole combination therapy (≥ 550 aspirin reaction units on the aspirin cartridge). Eleven of 25 (44%) patients had HTPR on clopidogrel (≥ 194 P2Y12 reaction units on the P2Y12 cartridge). On the PFA-100, 21 of 51 patients (41%) on aspirin-dipyridamole combination therapy had HTPR on the collagen-epinephrine (C-EPI) cartridge. Twenty-three of 25 patients (92%) on clopidogrel had HTPR on the collagen-adenosine diphosphate (C-ADP) cartridge. The proportion of patients with antiplatelet HTPR was lower on the VerifyNow than PFA-100 in patients on both regimens (P < .001).

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The inherent ability of ventricular myocardium to increase its force of contraction in response to an increase in contraction frequency is known as the cardiac force-frequency relation (FFR). This relation can be easily obtained in the stress echo lab, where the force is computed as the systolic pressure/end-systolic volume index ratio, and measured for increasing heart rates during stress. Ideally, the noninvasive, imaging independent, objective assessment of FFR would greatly enhance its practical appeal.

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The prevalence of HF in diabetic patients was high and HF predominantly occured in association with myocardial ischemia.

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Dipyridamole (DIP), a coronary vasodilator, presents coactivator activity for a number of antitumor drugs as well as antioxidant activity in membrane systems. DIP and derivatives interact with membrane systems such as micelles, phospholipid monolayers and vesicles. The antioxidant effect of DIP and several derivatives upon iron-induced lipoperoxidation on mitochondria has been reported and a good correlation between the hydrophobicity and their protective effect was found (M.F. Nepomuceno et al., Free Radic. Biol. Med., 23 (1997) 1046-1054). In the present work an effort is made to better understand the role of DIP as inhibitor of Fe2+-induced lipid peroxidation in mitochondria. At low concentration, no significant effect on either state IV or state III respiration was found, discarding a possible direct interaction of DIP or RA-25 with the peripheral benzodiazepine receptor. The association constants for DIP and RA-25 in mitochondria were estimated, being 0.7 (mg/ml)-1 for DIP and 0.2 (mg/ml)-1 for RA-25. Oxygen consumption studies in the presence of FeSO4 showed that the antioxidant effect of DIP or RA-25 did not involved the initial step of Fe2+ oxidation. Our data strongly support the hypothesis that the antioxidant effect of both DIP and RA-25 is related to their partition in the lipid phase of the mitochondrial membrane and not to a specific interaction with membrane proteins. This protection may be due either to a direct inhibition of the propagation steps or a scavenger effect on the radicular species that would trigger the peroxidative process.

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LV mass, dimensions and diastolic function were similar in the study groups. Baseline myocardial blood flow was similar (0.83 +/- 0.21 vs. 0.80 +/- 0.22 ml/g per min, group 1 vs. group 2, respectively, p = NS), and a significant increase in flow was detected after dipyridamole infusion (0.56 mg/kg body weight in 4 min intravenously) in both groups. However, the flow response to dipyridamole was significantly lower in group 1, leading to lower hyperemic flow in group 1 than in group 2 (2.85 +/- 1.20 vs. 3.80 +/- 1.44 ml/g per min, respectively). Consequently, the coronary flow response was lower in hypertensive than in normotensive men (3.46 +/- 1.23 vs. 4.99 +/- 2.5 ml/g per min, group 1 vs. group 2, respectively, p < 0.05).

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Studies including a combination of aspirin/dipyridamole in human subjects were evaluated. Emphasis was placed on randomized, controlled trials.

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From a mutagenized population of wild-type mouse (S49) T-lymphoma cells, a clone, 80-5D2, was isolated in a single step by virtue of its ability to survive in 80 nM 5-fluorouridine. Unlike previously isolated nucleoside transport-deficient cell lines (A. Cohen, B. Ullman, and D. W. Martin, Jr., J. Biol. Chem. 254:112-116, 1979), 80-5D2 cells were only slightly less sensitive to growth inhibition by a variety of cytotoxic nucleosides and were capable of proliferating in hypoxanthine-amethopterin-thymidine-containing medium. The molecular basis for the phenotype of 80-5D2 cells was incomplete deficiency in the ability of the mutant cells to translocate nucleosides across the plasma membrane. Interestingly, mutant cells were more capable than wild-type cells of transporting the nucleobase hypoxanthine. Residual transport of adenosine into 80-5D2 cells was just as sensitive to inhibition by nucleosides and more sensitive to inhibition by hypoxanthine than that in wild-type cells, indicating that the phenomena of ligand binding and translocation can be uncoupled genetically. The 80-5D2 cells lacked cell surface binding sites for the potent inhibitor of nucleoside transport p-nitrobenzylthioinosine (NBMPR) and, consequently, were largely resistant to the physiological effects of NBMPR. However, the altered transporter retained its sensitivity to dipyridamole, another inhibitor of nucleoside transport. The biochemical phenotype of the 80-5D2 cell line supports the hypothesis that the determinants that comprise the nucleoside carrier site, the hypoxanthine carrier site, the NBMPR binding site, and the dipyridamole binding site of the nucleoside transport function of mouse S49 cells are genetically distinguishable.

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Pharmacologic stress testing is an accepted alternative in those patients unable to perform exercise stress testing. The most prevalent form of pharmacologic stress testing remains thallium imaging during vasodilator stress with either dipyridamole or adenosine infusions. More recently, dobutamine stress echocardiography has emerged as a promising new technique for the evaluation of patients with known or suspected coronary disease. The rationale for the use of dobutamine infusion as a stress agent lies in its ability to simulate physical exercise through its beta-receptor agonist activity. This causes a supply-demand mismatch which in turn, creates regional myocardial dysfunction which can be detected by two-dimensional echocardiography. A major advantage in the use of echocardiography over other adjunctive imaging techniques is its ability to detect all forms of anatomic heart disease which may be associated with chest pain or may mimic ischemic chest pain. Our current dobutamine protocol involves stepwise infusion of dobutamine beginning at 5 micrograms/kg/min and increasing to 10, 20, and a peak of 30 micrograms/kg/min in three minute stages. Images are recorded in standard parasternal long axis and short axis, four chamber and two chamber views, digitized and displayed for comparison in a quad screen format. A 16 segment model is used for scoring wall motion abnormalities. Ischemia is considered present when a wall motion abnormality develops in an area with normal or only hypokinetic resting wall motion. The overall accuracy is between 85 and 90% for the detection of patients with coronary disease. In over 600 studies at our institution, no major side effects or complications have occurred.(ABSTRACT TRUNCATED AT 250 WORDS)

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A reaction scale was used to assess noncardiac adverse reactions exhibited by nuclear medicine outpatients receiving intravenous dipyridamole for pharmacological stress testing.

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A case of atypical proliferative glomerulonephritis (PGN) without mesangial immunoglobulin (Ig) A deposition (so-called non-IgA PGN) showing exacerbation of heavy proteinuria under long-term observation is reported. Examinations of first renal biopsy specimens revealed membranoproliferative glomerulonephritis (MPGN)-like findings. Urinary protein excretion completely disappeared after treatment with prednisolone (PSL) and an antiplatelet drug, i.e., dipyridamole. Negative reaction for urinary protein continued for more than 10 years. Fourteen and a half years after the first biopsy, the patient had heavy proteinuria again. Results of the second renal biopsy showed marked proliferation of glomerular mesangial cells. Under electron microscopy, lobulation and double contours of the glomerular capillary walls were also observed segmentally. Depositions of IgG, IgM, IgA, and C3 were observed mainly in the glomerular capillary walls, but not in the mesangial areas; however, these findings were not compatible with IgA nephropathy or MPGN. No hypocomplementemia was observed during the clinical course. The patient was treated with 30 mg of PSL and 75 mg of dipyridamole daily and showed a good response to such treatment. It appears that this patient had a rare case of atypical non-IgA PGN.

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Stroke is a common disorder and a leading cause of disability and death. Ischaemia is a more common cause than haemorrhage and radiological imaging is required to accurately differentiate these. Some specific risk factors for stroke are non-modifiable--these include age, gender, racial and hereditary factors. Certain risk factors for ischaemic stroke can be identified and modification of these can be used for secondary prevention--examples include hypertension, heart diseases, atrial fibrillation, diabetes mellitus, dyslipidaemia, smoking, excessive alcohol consumption and carotid stenosis. Carotid endarterectomy is valuable in selected patients. In ischaemic stroke and transient ischaemic attack antithrombotic therapy is an option used in secondary prevention. In atrial fibrillation, warfarin should be used where possible in secondary prevention. When warfarin is contraindicated aspirin should be used. In other patients, an antiplatelet regime is appropriate--aspirin is commonly used and is the least expensive regime. Other antiplatelet agents such as dipyridamole, ticlopidine and clopidogrel may have a place. Younger patients with ischaemic stroke may have a thrombophilia state and should be appropriately investigated.

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Dipyridamole thallium scintigraphy (TI-DP) and dipyridamole two-dimensional echocardiography (Echo-DP) were performed on 38 patients (pts), 11 +/- 4 days after acute myocardial infarction. Our study intends to assess whether or not imaging methods are useful both in identifying residual jeopardized myocardium and in selecting pts for coronary angiography. No serious side effects were induced during the DP test. In 11 pts angina was not induced, worsening of wall motion abnormalities was not detected on Echo-DP; no reversible defects were found on TI-DP. The remaining 27 pts who showed transient defects on TI-DP underwent coronary angiography. All pts had either multivessel coronary disease or severe single-vessel disease and myocardial revascularisation was performed in all of them. Of these 27 patients, only 5 suffered angina and showed ST-T depression; only in 15 dyskinetic wall motion development was detected on Echo-DP. Finally we can conclude: the DP-test can be safely performed in the early post-infarction period; both the reported imaging methods enable the identification of jeopardized myocardium even if with different ranges of sensitivity; pts negative to both TI-DP and Echo-DP can be safely followed without coronary angiography; pts with transient defects on TI-DP can be reasonably referred to coronary angiography.

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We recruited 120 diabetic patients with no history of myocardial infarction or angina, a normal 12-lead electrocardiogram (ECG), and two or more additional risk factors. SMI assessment was carried out by means of an ECG stress test, a thallium-201 myocardial scintigraphy with dipyridamole, and 48-h ECG monitoring. CAN was searched for by standardized tests evaluating heart rate variations. Accurate follow-up information for 3-7 years (mean 4.5) was obtained in 107 patients.

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This is one of the few studies to investigate patients using a dipyridamole stress test early after primary PCI. We conclude that it is safe to perform myocardial perfusion imaging under dipyridamole administration, just a few days after primary PCI. Additionally, a high incidence (17%) of myocardial perfusion defects was seen in this group of patients. According to our investigational protocol, a second myocardial perfusion imaging examination is scheduled for six months later, in order to clarify how many of these patients suffer from restenosis, or whether the finding was merely due to early endothelial dysfunction.

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Among high vascular risk patients, acetylsalicylic acid (ASA) reduces the relative risk of serious vascular events by about one fifth. However, because ASA fails to prevent four fifths of serious vascular events, more effective, yet equally safe and affordable, antiplatelet regimens are desired. Compared with ASA, clopidogrel alone reduces the odds of serious vascular events by about 10%, and the combination of dipyridamole and ASA reduces the odds of serious vascular events by about 6%. Combining ASA with an orally administered platelet glycoprotein (GP) IIb/IIIa blocker is not effective, and indeed more hazardous than ASA alone. Among patients with non-ST-segment acute coronary syndromes (ACS), the addition of an intravenously administered GP IIb/IIIa receptor antagonist to ASA reduces the risk of vascular events by about 10% compared with ASA, and the addition of clopidogrel to ASA reduces the risk of vascular events by 20% compared with ASA alone. Among patients undergoing percutaneous coronary intervention (PCI), both the addition of an intravenously administered GP IIb/IIIa receptor antagonist to ASA, and the addition of clopidogrel to ASA reduce the risk of vascular events by 30% compared with ASA alone. The greater efficacy of the combinations of ASA with clopidogrel, and ASA with an intravenously administered GP IIb/IIIa receptor antagonist, in patients with ACS and those undergoing PCI has fostered several ongoing and planned trials of these regimens in the acute and long-term management of patients with ischaemic brain syndromes. The combination of ASA and clopidogrel is being compared with ASA alone within 12 h of onset of symptoms of TIA in two trials (FASTER, ATARI), and the use of an intravenously administered GP IIb/IIIa receptor antagonist is being compared with placebo within 6 h of onset of acute ischaemic stroke in two trials (AbESST, AbESST-2). Six trials are assessing the combination of clopidogrel and ASA in the long-term management of patients with ischaemic brain syndromes due to atherothrombosis (MATCH, CHARISMA, ARCH, CARESS, SPS3) or atrial fibrillation (ACTIVE). The MATCH trial of clopidogrel and ASA versus clopidogrel alone in patients with recent TIA or ischaemic stroke is the first which is likely to report its results - in mid 2004. The combination of dipyridamole and ASA is being compared with ASA in the ESPRIT trial and with the combination of clopidogrel and ASA in the planned PRoFESS trial. These ongoing and planned clinical trials of antiplatelet therapy promise to further define the role of combination antiplatelet therapy in the acute and long-term management of patients with ischaemic brain syndromes.

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We sought to elucidate the flow-function relation in chronic postischemic dysfunction during vasodilator stress.

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persantine dosing chart 2015-03-09

Our patients were mostly young male buy persantine workers and from the industrial sector. Our success rate of 87% was similar to the current literature. The overall complication rate from minor wound infection was 35% and total finger loss was 13%. Medicinal leeches had minimal satisfactory results. Chemical leeching was more effective.

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Twenty patients received the HMII and 13 patients received other devices. Eight (40%) HMII recipients suffered at least one episode of GI bleeding while buy persantine no GI bleeding occurred in recipients of other devices (p = 0.012). Of 17 total bleeding episodes, no definitive source could be identified in 11 instances (65%).

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For patients who presented with arterial vascular disease, there was no evidence that dipyridamole, in the presence or absence of another antiplatelet drug reduced the risk of vascular death, though it may reduce the risk of further vascular events. However, this benefit was found in only one single large trial and only in patients presenting after cerebral ischaemia. There was no evidence that dipyridamole alone was more efficacious than aspirin. Further trials comparing the effects of the buy persantine combination of dipyridamole with aspirin versus aspirin alone are justified.

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1. The in vitro effect of the vasodilators papaverine, dipyridamole, nifedipine, prenylamine and glyceryl di-, tri- and tetranitrate on the oxygen saturation curve of human hemoglobin (Hb) was evaluated. The Hb dissociation curve was measured spectrophotometrically both for freshly obtained heparinized blood and for purified Hb A after incubation with the drugs. 2. For both purified Hb and whole blood samples, incubation with papaverine, dipyridamole and nifedipine modified P50 (PO2 for half saturation of the Hb/oxygen sites) at pH 7.4: 30.9 mmHg for 0.72 mM papaverine vs 23.9 mmHg for control; 23.9 mmHg for 1.43 mM dipyridamole vs 20.8 mmHg for control; 1.09 mmHg for 2.73 mM nifedipine vs 1.14 mmHg for control stripped Hb. The effects of the three vasodilators on Hb were correlated with pH, methemoglobin formation, temperature and incubation time. 3. P50 values were determined for Hb of the blood of angina patients treated with one of the vasodilators, and blood 2,3-diphosphoglycerate (2,3-DPG) levels were also measured. In contrast to the in vitro data, neither P50 nor 2,3-DPG levels were significantly modified in the blood of patients treated with one of the vasodilators. 4. These in vitro studies demonstrated that the vasodilators papaverine and dipyridamole decrease, and nifedipine increases buy persantine the oxygen affinity of Hb in red blood cells or as a purified hemoglobin.

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Nearly 4 of 10 patients receiving warfarin management care were receiving warfarin and antiplatelet combination therapy. The findings suggest that this practice is widespread, especially among patients with established cardiovascular disease, and involves a substantially higher number of patients than previously reported. The clinical outcomes associated with this practice require further buy persantine investigation.

persantine 10 mg 2015-06-06

Isolated myenteric ganglion networks were prepared from guinea pig ileum and were used in a perifusion protocol to examine the effects of interstitial adenosine on evoked release of substance P-like immunoreactivity (SPLI). The release of SPLI evoked by elevated extracellular K+ concentration was increased in the presence of tetrodotoxin (TTX), indicating tonic inhibition of SPLI release and revealing net inhibitory interganglionic transmission. Perifusion in the presence of the adenosine A1 receptor-selective antagonist 1,3-dipropyl-8-cyclopentylxanthine enhanced evoked SPLI release, which buy persantine was further enhanced in the additional presence of TTX, indicating that adenosine contributes some, but not all, of the overall inhibitory tone within the networks. In addition to neural release of adenosine per se, an additional source was investigated. Perifusion in the presence of alpha, beta-methylene-ADP plus guanosine 5'-monophosphate, which inhibits ecto-adenosinetriphosphatase (ATPase) activity, enhanced SPLI release, indicating that hydrolysis of released ATP contributes to the total interstitial nucleoside concentration and thereby to the overall inhibitory tone. It is concluded that endogenous adenosine, some of which arises from ATP metabolism, is an important contributor to the overall inhibitory tone present in myenteric ganglion networks.

persantine oral dose 2015-03-05

ATL-193 and ATL-146e are highly potent and selective Ado A(2A) receptor agonists with excellent potential for use as vasodilators buy persantine for myocardial perfusion imaging. An important advantage of ATL-146e is the ability to administer it by bolus injection.

persantine dose 2015-09-03

Dual bolus dipyridamole stress perfusion CMR exams were performed in 67 patients with clinical indications for assessment of myocardial ischemia. Stress perfusion images alone were analyzed with a fully quantitative perfusion (QP) method and 3 semiquantitative methods including contrast enhancement ratio, upslope index, and upslope integral. Comprehensive exams (cine imaging, stress buy persantine /rest perfusion, late gadolinium enhancement) were analyzed qualitatively with 2 methods including the Duke algorithm and standard clinical interpretation. A 70% or greater stenosis by quantitative coronary angiography was considered abnormal.

persantine dosage 2017-09-20

While treatment with heparin for women considered to be at particularly high risk of adverse pregnancy complications secondary to placental insufficiency was associated with a statistically significant reduction in risk of perinatal mortality, preterm birth before 34 and 37 weeks' buy persantine gestation, and infant birthweight below the 10th centile for gestational age when compared with no treatment for women considered at increased risk of placental dysfunction, to date, important information about serious adverse infant and long-term childhood outcomes is unavailable.

persantine cost 2015-09-16

We report a 7-month-old girl with malignant atrophic papulosis (Degos' disease). She also showed spontaneous aggregation buy persantine of platelets. A good clinical response was obtained by treatment with aspirin and dipyridamole.

persantine dose calculation 2015-10-14

A therapeutic trial of prostacyclin (PGI), was done in a patient with thrombotic thrombocytopenic purpura resistant to treatment with antiplatelet drugs and plasmapheresis. Despite marked thrombocytopenia and continued treatment with aspirin, sulfinpyrazone, and dipyridamole, the urinary excretion of 2,3-dinor-thromboxane B2, a major thromboxane urinary metabolite, was within the normal range (90.3 to 368 pg/mg creatinine) at 96 pg/mg creatinine. Because of its potent antiaggregatory properties and the possibility of a defect in endogenous PGI2 production in thrombotic thrombocytopenic purpura, synthetic PGI2 (4 to 10 ng/kg-1 . min-1) was infused intravenously, first for 72 hours and then continuously for 18 days. Prostacyclin markedly reduced the excretion of 2,3-dinor-thromboxane B2, and the platelet count rose steadily to reach 100 000/mm3 by the eighth day of the second infusion. The patient remains in clinical remission, on no therapy, 7 months later. A controlled evaluation of PGI2 in thrombotic thrombocytopenic purpura is warranted. Apparent therapeutic failure in previous cases may have resulted buy persantine from inadequate prolongation of PGI2 infusion.

persantine drug 2015-06-26

No significant difference was observed between resting blood flow at baseline or follow-up (15.8% +/- 15.8%; p = ns). Baseline and follow-up resting blood flow were linearly correlated (r = 0.63, p < 0.005). Normalization of resting blood flow to the rate pressure product improved the reproducibility significantly (15.8% +/- 15.8% versus 10.1% +/- 10.5%, p < 0.05). Baseline and follow-up hyperemic myocardial blood flow did not differ (11.8% +/- 9.4%; p = ns) and buy persantine were linearly correlated (r = 0.69, p < 0.0005).

persantine drug interactions 2017-04-03

The aim of this study was to compare resting coronary flow velocity, determinants of myocardial oxygen demand, and coronary vasodilator capacity in subjects with physiological, exercise-induced, and hypertensive left ventricular hypertrophy. Sixteen healthy sedentary men, 16 endurance athletes, and 16 hypertensive subjects (mean+/-SEM for left ventricular mass index: 94.9+/-5.5, 184.6+/-8.4, 154.4+/-9.5 g/m(2), respectively) were studied by transesophageal and transthoracic Doppler echocardiography. Coronary flow velocity in left anterior descending artery and cross-sectional area of left main artery were assessed at rest and during dipyridamole-induced vasodilation buy persantine . Myocardial oxygen demand was estimated through rate-pressure product, left ventricular wall stress, and inotropic function. Coronary flow reserve and minimum coronary resistance were comparable to those of sedentary men in athletes (mean+/-SEM: 3. 23+/-0.16 versus 3.60+/-0.18 and 0.96+/-0.06 versus 1.04+/-0.04 mm Hg. s. cm(-1)), while in hypertensive subjects they were decreased and increased, respectively (mean+/-SEM: 2.31+/-0.08 and 1.21+/-0.10 mm Hg. s. cm(-1); P:<0.05 for both). Resting flow velocity was directly related to rate-pressure product in sedentary men and athletes and also to wall stress in athletes, while these correlations were absent in hypertensives. Dilation of left main artery after dipyridamole was significantly higher in athletes than in sedentary men and hypertensive subjects (mean+/-SEM for area change: 32.9+/-3.7% versus 12.8+/-2.5% and 6.4+/-3.3%; P:<0.05 and 0.01). These data indicate that vasodilator capacity of coronary microcirculation is not impaired in athletes with physiological hypertrophy, in contrast to hypertensive patients. The relationship between resting flow velocity and determinants of oxygen demand is preserved in physiological hypertrophy but missing in hypertensive hypertrophy. Furthermore, the vasodilator capacity of coronary macrocirculation is also enhanced in exercise-trained subjects.

persantine drug classification 2015-04-28

Patients with IDC have anatomically normal coronary arteries, and it has been assumed that myocardial buy persantine ischemia does not occur.

persantine tablets 2016-08-07

The effects of dipyridamole, a coronary and peripheral vasodilator drug, on cardiac performance were investigated in nine patients with severe chronic heart failure. Dipyridamole (30 to 80 mg IV) increased cardiac index (1.63 to 2.65 l/min/m2) and decreased systemic vascular resistance (2097 to 1124 dyn/sec/cm-5). Left ventricular filling pressure decreased (23.7 to 20.7 mm Hg) without significant changes in mean right atrial pressure or heart rate. These effects were similar to the hemodynamic responses after 100 mg hydralazine in the same patients, but they were of shorter duration (less than 90 min). In contrast Levaquin Normal Dosage , oral dipyridamole induced only modest responses in three of eight patients despite large single doses of the drug (150 to 300 mg). Dipyridamole is a rapid-acting short-lived vasodilator, which exerts predominantly arterial vasodilator actions similar to those of hydralazine. Due to inconsistent response after oral doses, however, the therapeutic application of dipyridamole in long-term management of chronic heart failure appears to be limited.

persantine overdose 2016-10-24

BCS is a rare form of portal hypertension in children. The authors describe two cases of BCS with differing presentations. Case 1: Previously healthy four-yr-old girl. BCS was diagnosed during the course of an episode of acute gastroenteritis with dehydration. Despite conservative therapy for two months, the condition was progressive resulting in liver failure leading ultimately to LT. Molecular studies showed that she was heterozygous for the Factor (F) V Leiden. At follow-up, six yr post-LT (two yr without anticoagulation therapy), no thromboembolic/bleeding events were apparent. Case 2: Three-yr-old boy with IgA deficiency and liver disease. Following a febrile episode, he developed fulminant liver failure requiring urgent LT from a living donor (father). Molecular studies disclosed MTHFR C677T homozygosity and FV Leiden heterozygosity. The father was homozygous for the MTHFR mutation. Three months post-LT, persistent graft dysfunction was associated with stenosis of the IVC, which improved upon stent placement. He received dipyridamole and aspirin for five yr, after which time dipyridamole Duphaston Generic Philippines was discontinued. Evidence is sparse on the follow-up of BCS cases with liver transplant. The authors discuss their findings, particularly the need for long-term anticoagulation.

persantine generic 2017-05-07

We assessed coronary flow reserve (CFR) by sestamibi imaging in patients Depakote Drug Interactions with type 2 diabetes without coronary artery disease and normal coronary vessels.

persantine medication classification 2015-01-30

3,4-Diaminopyridine (3,4-DAP), which is known to decrease K conductance, produced spontaneous repetitive phasic contractions of a regular (28/60) and an irregular (15/60) cycle or tonic contraction (16/60) following a latent period of 5-100 min in isolated porcine coronary arteries. Effects of pinacidil, a newly-synthesized vasodilator, were investigated using the preparation in which 3,4-DAP produced phasic contractions of the regular cycle in comparison with those of various vasodilators. Pinacidil produced dose-dependent prolongation of the cycle and reduced the peak tension and the tension at the relaxation phase, a mode of action that closely resembles that of nicorandil, suggesting the increase in K conductance and hyperpolarization. Nifedipine (10(-8) M) and dilazep (10(-4) M) markedly reduced the Lopid Pill peak tension, while adenosine, dipyridamole and nitroglycerin did not produce such effects. The latter three drugs produced a prolongation of the cycle and reduced the tension of the relaxation phase. These data suggest that reduction of K conductance and activation of the voltage-dependent Ca channel may play an important role in initiation of the spontaneous repetitive phasic contraction in porcine coronary artery.

persantine 25mg tabs 2017-04-07

Sixty-four patients, enrolled in three centers in the U.S., underwent one-day dipyridamole/rest tetrofosmin SPECT. Coronary angiography, performed in 59 patients within 2 mo of the SPECT study, revealed normal coronary arteries or insignificant coronary stenosis in 11 patients and significant (> or = 50% luminal diameter stenosis) coronary Zocor Simvastatin Reviews stenoses in 48 patients.

persantine 25 mg 2016-12-10

All randomised trials comparing antiplatelet agents with either placebo or no antiplatelet agent during pregnancy. Quasi random study designs were excluded. Participants were pregnant women considered to be at risk of developing pre-eclampsia, and those with pre- Kemadrin 5 Mg eclampsia before delivery. Women treated postpartum were excluded. Interventions were any comparisons of an antiplatelet agent (such as low dose aspirin or dipyridamole) with either placebo or no antiplatelet agent.

persantine generic names 2016-11-01

The apparent K (m Trileptal Patient Reviews ) of [(18)F]FLT was comparable to the value reported with purified recombinant TK-1. The uptake of [(18)F]FLT by SW480 cells is inhibited by nitrobenzylthioinosine or dipyridamole indicating that uptake is mediated predominantly by the equilibrative nucleoside transporters in these tumor cells.

persantine medication 2017-12-19

Consecutive patients (n = 2064) who underwent symptom-limited exercise and dipyridamole stress with gated single-photon emission computed tomography (SPECT) imaging, without early revascularization, were studied. Subsequent cardiac death or nonfatal myocardial infarction was related to exercise and gated SPECT variables. Cox proportional hazards regression modeling was performed to identify predictors of adverse outcome. Annualized event rates in patients with normal Protonix 120 Mg and abnormal images were 0.96% and 2.71%, respectively (P < .001). With abnormal imaging, annualized event rates were 0.86% and 3.13% in patients with average to high and fair or poor functional capacity, respectively (P = .019). Abnormal imaging, a severely reduced post-stress ejection fraction, transient ischemic dilation, and fair or poor functional capacity emerged as predictors of adverse outcome. Accordingly, patients were stratified into low-risk, intermediate-risk, and high-risk cohorts with annualized event rates of 0.94%, 2.24%, and 8.19%, respectively (P < .001 in any two-way comparison).

persantine generic name 2015-10-02

Myocardial contrast echocardiography (MCE) is a promising diagnostic tool for detecting microvascular integrity. The aim of the study was to investigate the comparative specificity and sensitivity of intravenous MCE, technetium-99m Sestamibi single-photon emission computed tomography (SPECT) and dipyridamole-dobutamine (DIDO) stress echocardiography for predicting Glucovance Maximum Dosage functional recovery after coronary revascularization in patients with acute myocardial infarction (AMI).

persantine dosage chart 2017-04-20

No severe AE was noted. Overall mild AE incidence was 37.0% (833/2,250 patients). Initial low-dose (25 mg) aminophylline relieved symptoms in 98.8% of patients with mild AEs (823/833 patients). An extra 25 mg aminophylline sufficed to reverse all such AEs. Mean body mass index (BMI) differed significantly between patients with and without any AE [25.6 vs 25.1 (P = .009)]. There was no significant difference between two subgroups in mean age, male gender prevalence, body height and weight, dipyridamole dose/BMI, or prevalence of significant perfusion defect(s) on MPI. Multivariable logistic regression demonstrated BMI remained the independent predictor of dipyridamole-related Feldene Gel Harga AE occurrence (odds ratio 1.028, 95% confidence interval 1.007-1.049, P = .01).

persantine drugs 2015-09-07

This prospective study was conducted in 115 women to directly compare the sensitivity and specificity of thallium-201 (Tl-201), technetium-99m (Tc-99m) sestamibi perfusion and Tc-99m sestamibi electrocardiographic (ECG)-gated single-photon emission computed tomographic (SPECT) studies for detection of coronary artery disease (CAD).

persantine and alcohol 2015-09-19

The left ventricular mass and left ventricular mass index were significantly higher in Group 1 than in Groups 2 and 3. The coronary flow reserve and the posthyperemic mean diastolic flow velocities were significantly lower, while the resting mean diastolic flow velocities were significantly higher in Groups 1 and 3 than in Group 2.