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108 in-patients (mean age 50+/-11 years) with cardiac chest pain underwent dipyridamole stress-Echo with ECG-analysis, wall motion analysis by 2-dimentional imaging (2D) and coronary flow reserve (CFR) evaluation in both LAD and PDA by pulse-wave Doppler. The 2D test was considered positive when more or equal 2 segments demonstrated wall motion abnormalities. CFR was calculated as ratio of hyperemic to basal peak diastolic blood flow velocity. CFR <2.0 was considered reduced. Coronary angiography was performed within one week after stress-Echo.
Adenosine formation and release were studied in 48-h-old cultured ciliary ganglia and confluent peripheral and CNS glial cultures from embryonic chicks. Metabolic poisoning induced by 30 mM 2-deoxyglucose and 2 micrograms/ml oligomycin reduced ATP concentration by 90%. An increase in adenosine accounted for 15-40% of the fall in ATP. Dilazep (3 X 10(-6) M), a nucleoside transport inhibitor, decreased both incorporation of adenosine (an index of nucleoside transport) and release of adenosine by 80-90%. Dilazep trapped the newly formed adenosine intracellularly. A concentration of alpha, beta-methylene ADP that inhibited ecto-5'-nucleotidase by 80-90% did not alter the concentration of adenosine or AMP in neurons, glia, or medium. The results demonstrate that adenosine is formed intracellularly and exported out of the cell via the nucleoside transporter. The participation of ecto-5'-nucleotidase was excluded.
Aspirin, sulfinpyrazone and the combination of aspirin/dipyridamole, which inhibit some aspects of platelet function, have been evaluated in large-scale clinical trials in secondary prevention of myocardial infarction. The Persantine-Aspirin Reinfarction Study using dipyridamole, and Anturane Reinfarction Trial and Anturan Reinfarction Italian Study with sulphinpyrazone did not yield conclusive results. There have been five trials in which aspirin has been compared with a placebo. When the results were pooled, the outcome was consistent with a reduction during aspirin treatment of 5-10% in mortality and 20% in coronary event-rate. Whether this small benefit to an individual patient is worthwhile, and whether the effect of aspirin is influenced by coexistent beta-blocker treatment, is not clear.
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This study suggests that an episode of myocardial ischemia is able to change in a dramatic manner the frequency-contained within of the QRS complex, in spite of an unchanged ST segment in the conventional exercise ECG. We suggest that the HFS could be a good method for identifying myocardial ischemia. Its advantages could be important, particularly when the conventional exercise ECG is non informative.
The most accurate and logistic method of identifying injured but viable myocardium remains a diagnostic challenge.
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To compare the ticlopidine and dipyridamole effects on platelets count and aggregation in patients with stable coronary artery disease.
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Abnormal small coronary artery function may cause limited coronary flow responses to stress, resulting in anginal symptoms and ischemia in some patients with chest pain despite angiographically normal coronary arteries. To assess the exercise hemodynamic correlates of coronary flow abnormalities measured in the cardiac catheterization laboratory, 105 patients with microvascular angina (defined as an increase in coronary vascular resistance during pacing stress after ergonovine administration in the absence of significant epicardial constriction and associated with provocation of the patient's typical chest pain) and 27 patients without any coronary flow abnormality (normal) were analyzed. Of the 105 patients with microvascular angina, 75 had normal electrocardiographic responses to treadmill exercise testing, 22 had ischemic responses, and eight had bundle branch block during exercise. All 27 normal patients had normal electrocardiographic responses to exercise. Patients with ischemic electrocardiographic responses (0 +/- 7%, p less than 0.01), and those with bundle branch block (-2 +/- 6%, p less than 0.01) had abnormal left ventricular ejection fraction responses to exercise compared with the normal group, who demonstrated an 8 +/- 6% increase in left ventricular ejection fraction by radionuclide angiography during exercise, and microvascular angina patients with a normal electrocardiographic response to exercise, who demonstrated a 5 +/- 7% increase in ejection fraction. Although the microvascular response to ergonovine was no different among the three microvascular angina exercise groups, the administration of dipyridamole caused less coronary vasodilation in those patients with apparently ischemic or bundle branch block responses to exercise compared with those with normal electrocardiograms during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
The involvement of different subtypes of voltage-sensitive (Ca2+ channels in the initiation of field stimulation-induced endogenous adenosine triphosphate (ATP) and [3H]acetylcholine ([3H]ACh) release was investigated in the superfused rat habenula slices. ATP, measured by the luciferin-luciferase assay, and [3H]ACH were released simultaneously from the tissue in response to low frequency electrical stimulation (2 Hz, 2.5 msec, 360 shocks). The N-type Ca(2+)-channel blocker omega-conotoxin GVIA (omega-CgTX, 0.01-1 microM) reduced the stimulation-evoked release of ATP and [3H]ACh in a dose-dependent manner. Similarly, the P-type Ca2+ channel antagonist omega-agatoxin IVA (omega-Aga IVA) (0.05 microM) and the inorganic Ca(2+)-channel blocker Ca2+ (0.2 mM) inhibited the outflow of both transmitters, while Ni2+ (0.1 mM) was without significant effect. A high correlation was observed between the percent inhibition of ATP release and percent inhibition of ACh release caused by the different Ca2+ antagonists. Long-term perfusion (i.e., 90 min) with Ca(2+)-free solution inhibited the evoked-release of ATP and [3H]ACh. In contrast, perfusion of slices with the same media for a shorter time (i.e., 20 min) did not reduce the release of [3H]ACh and ATP but even increased the evoked-release of ATP about fourfold. The breakdown of extracellular ATP was not blocked under low [Ca2+]0 condition, measured by the creatine phosphokinase assay and HPLC-UV technique. Application of extra- or intracellular Ca2+ chelators, and dipyridamole (2 microM), the nucleoside transporter inhibitor, did not reduce the excess release of ATP after short-term perfusion with Ca(2+)-free media. Tetrodotoxin (TTX, 1 microM), while inhibiting the majority of ATP release under normal conditions, was also unable to reduce release under low [Ca2+]0 conditions. In summary, we showed that both N- and P-type Ca2+ channels are involved in the initiation of electrical stimulation-evoked release of ATP and [3H]ACh in the rat habenula under normal extracellular calcium concentration. Under low [CA2+]0 conditions an additional release of ATP occurs, which is not associated with action potential propagation.
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One hundred forty-one subjects with type 2 diabetes mellitus without known cardiac disease and asymptomatic, aged >45 to <76 years, were randomized into the screening arm for CAD (71 patients) or to the control arm (70 patients). The screening consisted in performing an exercise electrocardiogram test and dipyridamole stress echocardiography; if 1 test was abnormal, coronary angiography is done. Screening was positive in 15 subjects (21.4%). At coronary angiography, which was performed in 14 of 15 patients, stenoses > or =50% of vessel diameter were present in 9 patients, of these 4 underwent coronary artery bypass grafting and 4 underwent percutaneous transluminal coronary angioplasty. Stenoses <50% of vessel diameter were present in 5 patients.
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Perfusion imaging showed a reversible perfusion decrease in the hypertrophic septum. Cine-gated imaging of the septum showed dyskinesia and a severe abnormality of systolic thickening during the poststress period, whereas it showed nearly complete recovery at rest. Quantified regional perfusion and function indices also showed this perfusion decrease and myocardial dysfunction after dipyridamole stress.
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To assess the feasibility, safety and usefulness of gradient-echo magnetic resonance imaging (MRI) combined with pharmacologic stress testing for the detection of coronary artery disease, 23 patients without previous myocardial infarction but with significant stenosis (greater than 70% diameter stenosis) of greater than or equal to 1 major coronary artery were selected for dipyridamole-MRI stress testing. Each patient underwent MRI at rest, and high-dose dipyridamole-MRI (0.75 mg/kg over 10 minutes) of corresponding basal and midventricular short-axis tomograms. Additionally, these patients performed symptom-limited exercise stress tests. All short-axis tomograms were evaluated on a standardized segmental basis by grading each segment as normal, hypokinetic, akinetic or dyskinetic. Dipyridamole-MRI was considered pathologic if segmental wall motion deteriorated by greater than or equal to 1 grade after dipyridamole. For comparison with coronary angiography, segmental wall motion gradings were related to the respective coronary artery territories in the short-axis plane. Pathologic dipyridamole-MRI was obtained in 18 of 23 (78%) patients. For 1- and 2-vessel diseases, sensitivity was 69 and 90%, respectively. Exercise stress tests were pathologic in 14 of 23 (66%) patients. For 1- and 2-vessel diseases, sensitivity of exercise stress test was 58% (7 of 12 patients) and 77% (7 of 9), respectively. Sensitivity/specificity of dipyridamole-MRI for the localization of the stenosed coronary artery was 78/100% for left anterior descending, 73/100% for left circumflex, and 88/87% for right coronary artery stenoses. It is concluded that dipyridamole-MRI is a feasible nonexercise-dependent test for detection and localization of functionally significant coronary artery disease.
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Nitrate tolerance remains a problem despite an enormous number of studies on this phenomenon. The aim of the present study was to compare the efficacy of nitroglycerin transdermal patches intermittently or continuously administered to patients with myocardial ischemia evaluated by the echocardiography dipyridamole stress test. We prospectively studied 34 coronary patients with stable myocardial ischemia. A double-blind, randomized, crossover study technique was used. After a run-in period (1 week) they underwent a dipyridamole stress test to evaluate nitrate responsiveness and then were randomized to 1 week of transdermal nitroglycerine 20 mg/24 h (two patches of 10 mg/24) administered either intermittently or continuously for 1 week. During the following week all patients were given placebo. In the final week, therapy was crossed over the alternate regimen. No significant changes in heart rate, systolic and diastolic blood pressure and rate-pressure product were observed at basal conditions and at peak of dipyridamole infusion among patients after placebo run-in period, after acute, 1 week of intermittent and 1 week of continuous nitroglycerine administration. At peak of dipyridamole infusion after acute administration of nitrate we observed a significant decrease in wall motion score index with respect to placebo. This pattern was similar during intermittent, but not continuous, patch therapy (p < 0.001). Our results suggest that transdermal nitroglycerin patches are an effective anti-ischemic medication, in reducing transient myocardial ischemia induced by dipyridamole. This anti-ischemic effect is lost when an overnight nitrate free dose interval is not used. Moreover the dipyridamole echocardiographic stress test, besides evaluating myocardial ischemia-induced wall motion abnormalities, is adequate to assess both the efficacy and the tolerance of transdermal nitrate therapy.
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In this study, 1001 patients with documented coronary artery disease by coronary arteriography showing any visible coronary artery narrowing underwent rest-dipyridamole PET perfusion imaging. Quantitative severity of dipyridamole-induced, circumscribed, segmental PET perfusion defects was objectively measured by automated software as the minimum quadrant average relative activity indicating localized flow limiting stenoses. Quantitative severity of the graded, longitudinal, base-to-apex myocardial perfusion gradient indicating fluid dynamic effects of diffuse coronary artery narrowing was objectively measured by automated software as the spatial slope of relative activity along the cardiac longitudinal axis.
These results suggest that dipyridamole, a potent coronary vasodilator, produces maldistribution of coronary blood flow in our dog models, whereas sevoflurane does not do this in animal or human studies.
To investigate the value of the echocardiographic observation of the left ventricular hypertrophy (LVH) in diagnosing myocardial microvascular damage in patients with essential hypertension (EH).
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The precore mutation rate was 10/12. The therapeutic effect of the immune therapy on the precore mutation patients (5/7) was better than that on the HBsAg(+), HBeAg(+) patients (2/11), P less than 0.05.
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Caffeine binds to the A2 receptors and inhibits adenosine's action of vasodilation or dipyridamole-induced vasodilation. Patients scheduled for (201)Tl myocardial perfusion using pharmacologic stress with dipyridamole or adenosine are advised to abstain from caffeine for 24 h before the test. This article reports on the residual serum caffeine levels of 36 patients after 24-h caffeine abstention and the clinical implications on dipyridamole (201)Tl myocardial perfusion imaging.
Aqueous and vitreous samples were obtained from bovine eyes after death and from live porcine eyes with the subject under general anesthesia. Samples from live eyes were immediately incubated in the sampling syringe with pentoxifylline, erythro-9-(2-hydroxy-3-nonyl) adenine, and dipyridamole to prevent synthesis or degradation of adenosine during the collection procedure, filtered, and flash-frozen in liquid nitrogen. All samples were then filtered and purified on phenylboronate agarose columns and incubated with chloroacetaldehyde to convert the adenosine present in the sample to the fluorescent derivative 1,N6-ethenoadenosine. The 1,N6-ethenoadenosine was separated by high-pressure liquid chromatography and then measured by fluorometry.
We investigated the postoperative prognostic value of preoperative myocardial SPECT for predicting clinical outcomes, including event-free survival and functional improvement.
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During continuous exposure, cells were more responsive to doxorubicin (DOX) in the presence of dipyridamole (DPM). Translocation of nucleolar phosphoprotein B23 and inhibition of cell growth occurred with a lower dose of DOX and in a shorter incubation time in the presence of DPM. DPM did not change translocation induced by actinomycin D (Act-D). Short exposure of HeLa cells to Act-D induced "reversible" translocation of protein B23 as well as "reversible" inhibition of cell growth. DPM included in the cell culture after removal of Act-D inhibited the recovery of cell growth as well as the corresponding relocalization of protein B23 from the nucleoplasm to nucleoli. DPM administered in the fresh medium after 30 min exposure to DOX had little effect on the potentiation of the induced translocation of protein B23 and inhibition of cell growth. Our results indicated that "B23 translocation" is closely associated with states of cell growth. The potentiation of the inhibition of cell growth by DPM is associated with the extent of enhanced protein B23 translocation. "B23 translocation" may therefore be a simple and rapid method for assessing the inhibition of cell growth and for determining the efficacy of combination cancer chemotherapy.
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Dipyridamole stress testing may be used in the diagnosis of coronary artery disease and risk assessment of patients who are unable to exercise. Although dipyridamole perfusion imaging has a good safety record, serious side-effects may rarely occur. We present a case in which dipyridamole induced high-grade atrioventricular (AV) block that responded promptly to intravenous aminophylline but not to atropine.
The presence of allele 'a' may be a risk factor for microvascular endothelial dysfunction and higher TFCs in SCF patients.
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Thirty patients with valvular disease confirmed by echocardiography underwent 99mTc-MIBI myocardial perfusion imaging using multiSPECT 1h after stress test (exercise, dipyridamole or dobutamine test) and were performed coronary angiography within 1 month before valvular operation.
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Acetylcholine (ACh) is a major excitatory neurotransmitter in the myenteric plexus, and it regulates its own release acting via muscarinic autoreceptors. Adenosine released from stimulated myenteric neurons modulates ACh release preferentially via facilitatory A(2A) receptors. In this study, we investigated how muscarinic and adenosine receptors interplay to regulate ACh from the longitudinal muscle-myenteric plexus of the rat ileum. Blockade of the muscarinic M(2) receptor with 11-[[2-1[(diethylamino) methyl-1-piperidinyl]- acetyl]]-5,11-dihydro-6H-pyrido [2,3-b][1,4] benzodiazepine-6-one (AF-DX 116), 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP) and atropine facilitated [3H]ACh release evoked by short stimulation trains (5 Hz, 200 pulses). Prolonging stimulus train length (>750 pulses) shifted muscarinic autoinhibition towards facilitatory M(3) receptors activation, as predicted by blockade with J104129 (a selective M(3) antagonist), 4-DAMP and atropine, whereas the selective M(2) antagonist, AF-DX 116, was without of effect. Blockade of A(2A) receptors with ZM 241385, inhibition of adenosine transport with dipyridamole, and inhibition of ecto-5'-nucleotidase with concanavalin A, all attenuated release inhibition caused by 4-DAMP. J104129 and 4-DAMP, but not AF-DX 116, decreased ( approximately 60%) evoked adenosine outflow (5 Hz, 3000 pulses). Oxotremorine (300 micromol L(-1)) facilitated the release of [3H]ACh (34 +/- 4%, n = 5) and adenosine (57 +/- 3%, n = 6) from stimulated myenteric neurons. 4-DAMP, dipyridamole and concanavalin A prevented oxotremorine-induced facilitation. ZM 241385 blocked oxotremorine facilitation of [3H]ACh release, but kept adenosine outflow unchanged. Thus, ACh modulates its own release from myenteric neurons by activating inhibitory M(2) and facilitatory M(3) autoreceptors. While the M(2) inhibition is prevalent during brief stimulation periods, muscarinic M(3) facilitation is highlighted during sustained nerve activity as it depends on extracellular adenosine accumulation leading to activation of facilitatory A(2A) receptors.
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Forty-eight patients were randomized to adenosine or dipyridamole cardiac stress (82)RB-PET. Respiratory rates and depths were measured by a respiratory gating system in addition to registering actual respiratory rates. Patients undergoing adenosine stress showed a decrease in measured respiratory rate from initial to later scan phase measurements [12.4 (±5.7) vs 5.6 (±4.7) min(-1), P < .001] and tended to have a lower frequency of successful respiratory gating compared to dipyridamole (47% vs 71%, P = .12). As a result, imaging quality was superior in the dipyridamole group compared to adenosine.