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A patient was admitted to the hospital with acute chest pain. After acute myocardial infarction was ruled out, he underwent a stress thallium 201 scintigraphy using oral dipyridamole and developed persistent angina with ST-segment elevation. This complication has not been reported previously. It is recommended that appropriate intervention be available if severe ischemia develops following administration of dipyridamole for diagnostic imaging.
Stress-echocardiography (SE) has been proven to be a valuable method for the diagnosis of coronary artery disease. For patients who cannot exercise, pharmacological stress-echocardiography represents an alternative method for the induction of cardiovascular stress. Few studies exist concerning the value of dipyridamole-SE for the detection of restenosis in patients after primary successful PTCA. It has been demonstrated that the addition of atropine can significantly increase the diagnostic potential of dipyridamole-SE, especially in patients with 1- or 2-vessel disease. The purpose of our study was to investigate the diagnostic value of high-dose dipyridamole-SE plus atropine (DASE) for the detection of restenosis after primary successful PTCA. We investigated 65 patients 3-6 months after PTCA before a control angiography was performed. Restenosis was defined as > 70% lumen narrowing, determined by quantitative coronary angiography. In 20/27 patients with restenosis, the DASE was pathological (sensitivity 74%); in 34/38 patients without restenosis the DASE was normal or showed no induced WMA (specificity 89%). Patients with tight restenosis (> 90%) were always correctly detected by DASE. Concerning the different vessels, restenosis of the LAD was correctly predicted by DASE in 11/12 patients, restenosis of the LCX in 6/9 patients and restenosis of the RCA in 8/11 patients. From the results of our study we conclude that DASE is a reliable diagnostic method for the non-invasive evaluation of patients after PTCA. DASE can identify patients with relevant restenosis after PTCA and help to select those patients who will probably benefit from further coronary interventions, for repeat angiography.
During recent years, platelets have been increasingly implicate in the pathogenesis of coronary artery disease and its complications. This is based on new knowledge of platelet physiology as well as on clinical observations. Experimentally, it can be demonstrated that platelet vessel wall interaction is important in atherogenesis. In animal, platelet aggregates in the arterial circulation may cause ischemic myocardial lesions. In patients who died suddenly platelet thrombi can often be found in the microcirculation at autopsy. Compounds released during platelet aggregation may cause a spasm of the coronary arteries. Hyperactive platelets can be demonstrated in patients with CAD as well as in patients with the known risk factors of CAD. In some clinical trials, platelet function inhibitors reduced death from cardiac causes. Here we review the theoretical and experimental basis of the "platelet hypothesis" of CAD and its complications as well as the rationale for treating patients with CAD with "'antiplatelet" drugs.
In patients, no significant difference was observed among the 3 methods of measurement-Doppler CFR, 1.73 +/- 0.57; regularized factor analysis MPR, 1.71 +/- 0.68; FDG MPR, 1.83 +/- 0.49-using a Friedman 2-way ANOVA by ranks. MPR measured with the regularized factor images correlated significantly with CFR (y = 1.17x - 0.30; r = 0.97). In the global population, the regularized factor analysis MPR and FDG MPR correlated strongly (y = 0.99x; r = 0.93). Interoperator repeatability on regularized factor images was 0.126 mL/min/g for rest MBF, 0.38 mL/min/g for stress MBF, and 0.34 for MPR (19% of mean MPR).
Regional myocardial perfusion by SPECT, performed with (99m)Tc tetrafosmin, scored qualitatively and also quantitated as per cent maximum activity.
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A random-order, double-blind crossover study compared the effects of placebo, dipyridamole and dipyridamole plus aspirin on smoking-induced changes in endothelium and platelets. Each of 12 male habitual smokers with coronary artery disease was given dipyridamole (75 mg) and aspirin (324 mg), dipyridamole (75 mg) and placebo for aspirin, or a placebo for each drug 3 times daily for 1 week before each of three 20-minute periods (separated by 2 weeks) of smoking 2 cigarettes after a 12-hour period of abstinence. During each period of smoking there were increases in the mean values of the plasma concentrations of beta-thromboglobulin, platelet factor 4 and nicotine, the endothelial cell count and the blood level of carboxyhemoglobin. In addition, the mean platelet aggregate ratio decreased during each period. After administration of placebos for both dipyridamole and aspirin, the respective mean values +/- standard deviations before and after smoking were 28 +/- 8 and 30 +/- 7 ng/ml (beta-thromboglobulin), 7.4 +/- 1.0 and 8.2 +/- 1.4 ng/ml (platelet factor 4), 3.7 +/- 0.6 and 15.7 +/- 3.5 ng/ml (nicotine), 4.2 +/- 1.4 and 5.4 +/- 1.7/counting chamber (endothelial cell count), 5.0 +/- 2.2 and 6.6 +/- 2.2% (carboxyhemoglobin) and 0.80 +/- 0.07 and 0.68 +/- 0.10 (platelet aggregate ratio). Each of the differences between the means before and after smoking was statistically significant (p less than or equal to 0.02). Neither dipyridamole alone nor in combination with aspiring significantly affected the mean smoking-induced change in any of these variables.(ABSTRACT TRUNCATED AT 250 WORDS)
This was a retrospective, longitudinal pharmacoepidemiologic review. Adult patients receiving warfarin managed by a clinical pharmacy service who had documented antiplatelet (aspirin, clopidogrel, and/or dipyridamole) use (combination therapy cohort) or non-use (monotherapy cohort) were identified as of September 30, 2005. Utilizing integrated, electronic medical records, anticoagulation-related adverse events (death, hemorrhage, thrombosis) and coronary events were identified during a six-month follow-up (October 2005 through March 2006). Proportions of events were compared between cohorts. Independent associations between the cohorts and the outcomes were assessed with adjustment for potential confounding factors.
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The numbers of and outcome of the stress tests and the cardiac outcome of the patients who underwent cardiac testing and surgery were recorded.
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Key words including inappropriate, Beers, medication, prescribing, elderly, geriatric, and criteria were used to search MEDLINE records from January 1992 to June 1999.
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Right ventricular apical pacing (RVAP) with a left bundle branch block on the electrocardiogram may result in regional wall motion abnormalities and decreased left ventricular function (LVF). Furthermore, perfusion defects in dipyridamole technetium-99m-methoxisobutylisonitrile ((99m)Tc-MIBI) myocardial perfusion imaging may occur despite a normal coronary angiogram. In a 68 years old patient, RVAP resulted in regional wall motion abnormalities, markedly decreased LVF and perfusion defects in dipyridamole (99m)Tc-MIBI myocardial perfusion imaging by single photon emission tomography (SPET). Coronary angiography excluded coronary heart disease. Reprogramming of the pacemaker resulted in physiologic activation of the ventricles. Echocardiography showed a normal LV systolic function. Repeated myocardial perfusion imaging was unremarkable. In conclusion, our case confirms thatRVAP may lead to scintigraphic perfusion defects and wall motion abnormalities despite a normal coronary angiogram and this differentiate between ischemia-induced perfusion defects.
The combined effect of methotrexate (MTX) with dipyridamole, an inhibitor of nucleoside transport, was studied in ascitic Sarcoma 180 cells. It was determined that 10 microM MTX inhibits by greater than 90% deoxy[3H]uridine incorporation into DNA and that this MTX concentration inhibits DNA synthesis as revealed by deoxy[3H]cytidine but not [3H]thymidine incorporation into DNA. Exogenous thymidine (greater than or equal to 1 microM) in the cell culture medium enhances DNA synthesis in nontreated cells and fully restores it in MTX-treated cells, whereas hypoxanthine has no appreciable effect on DNA synthesis. Dipyridamole inhibits deoxy[3H]cytidine and [3H]thymidine uptake by these cells (IC50 = 0.2 and 3 microM, respectively) and blocks the increase in TTP pool produced by 1 microM thymidine in MTX-treated cells (23.1 +/- 4.7 pmol per 1 X 10(6) cells vs. 80.4 +/- 18.9 pmol per 1 X 10(6) cells). Dipyridamole at 10 microM enhances [3H]MTX accumulation by Sarcoma 180 cells and diminishes the efflux of the drug in previously loaded cells. It is suggested that the combination of inhibitors of the de novo pathway for pyrimidine biosynthesis, such as MTX, with inhibitors of the salvage pathway, such as dipyridamole, may increase the cytotoxic activity of MTX alone.
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Dipyridamole increases the toxicity of methotrexate in a concentration-dependent manner. We hypothesized that concurrent intraperitoneal administration of both drugs would result in high peritoneal concentrations with much lower plasma concentrations, permitting a selective increase in the activity of methotrexate against intraperitoneal tumors without enhancing systemic toxicity. Initially, 2.16 mg/m2/d methotrexate and 12 mg/m2/d dipyridamole were delivered together as a constant intraperitoneal infusion for 48 hours. With escalation of chemotherapy, eventually 4.32 mg/m2/d methotrexate was administered for 168 hours. Forty-seven courses were administered to 18 patients. The mean peritoneal to plasma concentration ratios of methotrexate and non-protein bound dipyridamole were 71.6 +/- 34.8 and over 2,300, respectively. Chemical peritonitis was the dose-limiting toxicity. Three patients had some evidence of a response (two with decreasing tumor markers, and the third with a reduction in ascites). We conclude that the drug concentrations are in an appropriate range for selective intraperitoneal biochemical modulation of methotrexate, and that it is feasible to expose tumors confined to the peritoneal cavity to these drugs for long periods of time.
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The most common side effects under each stress were ventricular premature beats in 34.1% (dobutamine echocardiography), ventricular premature beats in 14.4%(exercise), and headache in 24.3% (dipyridamole). Serious side effects occurred in one patient(0.05%). The case of acute myocardial infarction was caused by dipyridamole echocardiography, and the patient needed emergency coronary angioplasty. Seven patients needed other drug therapy for nonsustained ventricular tachycardia(one), paroxysmal supraventricular tachycardia(two), sinus bradycardia(three), and bronchial asthma(one). There was no incidence of death, shock, or ventricular fibrillation, sustained ventricular tachycardia or other conditions requiring inpatient observation during stress echocardiography.
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The study involved 20 patients (2 men and 18 women with a mean ± SD age of 52.96 ± 12.51 years) with diffuse SSc who had no signs or symptoms of cardiovascular disease (CVD) and 20 age- and sex-matched controls. All subjects underwent a dipyridamole echocardiographic stress test that included a determination of CFR and an evaluation of CIMT, arterial stiffness, and plasma ADMA levels.
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Phosphorylation of vasodilator-stimulated phosphoprotein (VASP), an established marker of NO/cGMP effects in human platelets, was quantified by phosphorylation-specific antibodies and Western blots. Serotonin secretion and thromboxane synthase activity were determined by fluorometric quantification of derivatized serotonin and synthase products, respectively.
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Exercise testing in the magnetic resonance (MR) scanner is difficult because of space restriction and movement artefact, which limit its use in the investigation of patients with suspected coronary artery disease. Pharmacological stress, however, can be used as a substitute for exercise. Therefore, a patient with angina underwent MR ventricular wall motion studies before and after intravenous dipyridamole. Reversible abnormal regional contraction of the myocardium was demonstrated and correlated with a reversible perfusion defect on subsequent thallium myocardial perfusion imaging and a blocked artery at coronary angiography. A clinically useful investigative procedure may be developed.
Statins protect against ischemia-reperfusion injury and limit myocardial infarct size (IS). This effect is dependent on increased generation of adenosine by ecto-5' nucleotidase and downstream activation of cyclooxygenase-2 (COX2). Dipyridamole (DIP) augments the IS-limiting effects of statins by blocking the cellular reuptake of adenosine; whereas aspirin (ASA) attenuates the effect by inhibiting COX2. We studied the effect of acute administration of DIP, ASA and their combination on the IS-limiting effect of simvastatin (SIM).
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Vascular access grafts implanted in dialysis patients are prone to failure in the long-term because of stenosis and occlusion caused by neointimal hyperplasia. Local delivery of antiproliferative drugs may be effective to prevent this consequence while minimizing the systemic side effects they cause. We developed a combination of poly(lactide-co-glycolide) (PLGA) microspheres with ReGel, an injectable copolymer, as a sustained-release system for perivascular delivery of an antiproliferative drug, dipyridamole. Dipyridamole-incorporated PLGA microspheres with various molecular weights (MWs) of PLGA were prepared by oil-in-water emulsion method. Encapsulation efficiency and surface morphology of microspheres were characterized. In vitro release kinetics of dipyridamole from ReGel or from microspheres/ReGel was experimentally determined. Without microspheres, 40% of the dipyridamole was released from ReGel as an initial burst in the first 3 days followed by continuous release in the subsequent 2 weeks. The use of PLGA microspheres decreased the initial burst and extended dipyridamole release from 23 to 35 days with increasing MW of PLGA. The highest MW PLGA showed a lag time of 17 days before consistent drug release occurred. Mixing microspheres and ReGel with two different MW PLGA achieved a continuous release for 35 days with little initial burst. In vivo release of dipyridamole from microspheres/ReGel exhibited a comparable release pattern to that seen in vitro. This injectable platform is a promising technique for sustained perivascular delivery of antiproliferative drugs.
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To evaluate septal perfusion and contractility in patients with left bundle branch block (LBBB).
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A 64-year-old man was admitted to our hospital with chief complaint of chest discomfort. He received coronary artery bypass grafting utilizing the in situ left internal thoracic artery 10 years ago. Coronary and left subclavian artery angiogram revealed coronary subclavian steal syndrome and 90% stenosis in the proximal left subclavin artery. Ultrasonography of neck vessels demonstrated 75% stenosis in the bifurcation of left carotid artery. We performed axilloaxillary artery bypass grafting to avoid brain ischemia. Myocardial thallium scintigraphy on dipyridamole testing after axilloaxillary artery bypass grafting could not detect myocardial ischemia. Axilloaxillary artery bypass grafting was effective for coronary subclavian steal syndrome.