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Radionuclide ventriculography (RNV) was used to assess the peak filling rate (PFR) in 20 patients with coronary artery disease (CAD). Dipyridamole RNV was used in 5 normal subjects and 10 patients with CAD with the view to evaluating PFR increase. Significant difference in PFR values was established between normal subjects and CAD patients. Decreased value of PFR was found in 78% CAD patients, and 72% of them had normal ejection fraction (EF). During dipyridamole RNV increase of PFR was not significantly different between normals and CAD patients. The peak filling rate is a very sensitive indicator of LV dysfunction in CAD patients, and is useful in early detection of abnormalities in diastolic function in CAD patients.
A different rate and timing of subacute stent thrombosis after percutaneous coronary intervention was reported with various peri-interventional antithrombotic regimens. Next to platelet activation, coagulation triggered by tissue factor (TF) may play a key role in this process. Thirty-one consecutive patients with stable and unstable angina undergoing coronary stenting were randomly assigned to adjunct oral anticoagulation/anti-platelet therapy (coumadin, dipyridamole, aspirin and heparin; n = 16) or adjunct anti-platelet therapy with thienopyridin (ticlopidine, aspirin and heparin; n = 15). Antigen levels of plasma TF, total tissue factor pathway inhibitor (TFPI) and TFPI/ activated factor X (TFPI/FXa) complex were determined before and for up to 6 days after intervention by immunoassay. At baseline, significantly higher levels of plasma TF and TFPI/FXa were found in patients with unstable angina [TF, 161 pg/ml (126-191 pg/ml); TFPI/FXa, 7.8 ng/ml (6.1-9.6 ng/ml)] compared with stable angina [TF, 62 pg/ml (46-82 pg/ml), P < 0.0001; TFPI/FXa, 4.5 ng/ml (3-7.6 ng/ml), P= 0.003]. One hour after intervention, an increase of plasma TF and TFPI/FXa was seen in both treatment groups. In unstable angina patients, plasma levels of TF, TFPI and TFPI/FXa were more efficiently reduced by adjunct ticlopidine therapy compared with adjunct coumadin/dipyridamole. These data suggest reduced release of circulating TF by combined anti-platelet therapy with ticlopidine and aspirin after coronary artery stenting, which may-contribute to the lower incidence of subacute stent thrombosis previously observed.
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This study demonstrates that preserved synchronous ventricular activation with RVOT pacing prevents the long-term deleterious effects of RVA pacing on myocardial perfusion and function in patients implanted with a permanent pacemaker.
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Labelled adenine, noradrenaline (NA), and gamma-aminobutyric acid (GABA) were taken up by the transversely cut hippocampal slice. [3H]NA and [14C]GABA were retained as such, [3H]- (or [14C]-) adenine mainly as adenine nucleotides. There was a spontaneous overflow of all three types of compounds ranging from 0.1 (GABA) to 0.21 (NA) %/min. The rate of [3H]NA overflow increased rapidly during electrical field stimulation. The release rate was well maintained over a 15-min period. The rate of [14C]GABA release also increased rapidly but it was not maintained over a 15-min period even if uptake and/or metabolism was inhibited by nipecotic acid (1 mM) and aminooxyacetic acid (AOAA, 0.1 mM). The bulk of the purines was released after the stimulation period. For all compounds the amounts released were frequency- and calcium-dependent. At a frequency of 3 Hz a 10 V stimulation was sufficient to cause a maximal [3H]NA release and 20 V to cause maximal [14C]GABA release, but 14C-purine release was increased further by increasing the voltage to 40 V. The evoked purine release was inhibited by a nucleoside uptake inhibitor (dipyridamole). On stimulation of [3H]NA-labelled slices the released radioactivity was composed of greater than 95% unchanged NA. The specific activities of NA in the slice and in the superfusate were practically identical. In [3H]adenine-labelled slices the released radioactivity was composed of adenosine, inosine, and hypoxanthine, but the activity in the slice of ATP, ADP, and AMP.(ABSTRACT TRUNCATED AT 250 WORDS)
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The Persantine Aspirin Trial is a double-blind multi-centered cooperative study focusing primarily on the question of whether the administration of the combination of aspirin and dipyridamole (Persantine) will result in a greater reduction of cerebral or retinal infarction or death than the administration of aspirin alone. Fifteen centers in the United States and Canada are participating. More than 750 individuals with a history of recent carotid territory transient ischemic attacks (TIAs) have been admitted over the past four years and randomly allocated to either aspirin (325 mg) plus placebo four times daily or aspirin (325 mg) plus Persantine (75 mg) four times daily. It is anticipated that the study will continue through 1983. Analysis and publication of results are planned for 1984.
The effect of dipyridamole on proteinuria was studied in 60 children with various renal diseases. A significant decrease in 24-hour urine protein excretion was observed within a few months after treatment in 32 (53%) of the patients with minimal or moderate mesangial proliferation. The effect was reproducible and parallelled by a reduction in plasma levels of beta-thromboglobulin. Renal function in patients significantly improved with the therapeutical effect. The appropriate dosage was 4-10 mg/kg daily and no serious toxicity was seen despite large dosage and even in long-term application. The data suggest that dipyridamole treatment appears safe and has a beneficial effect on proteinuria dependent on its effect on platelets in renal disease.
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With platelet activation, there is modulation of platelet surface molecule expression. In flow cytometric analyses of in vivo platelet activation, results are often confounded by activation induced in vitro by the preparative procedures. It is particularly important therefore to prevent or retard platelet activation as soon as possible after withdrawal of the blood sample. Taking blood into paraformaldehyde, or fixing the cells with paraformaldehyde as soon as possible after withdrawal, has been employed to prevent platelet activation in vitro, but paraformaldehyde-fixed platelets cannot be further used in functional studies. We investigated the efficacy of Diatube-H, a commercially available combination of platelet antagonists (theophylline, adenosine, and dipyridamole), in preventing or retarding platelet activation in vitro, along with its effects on modulation of platelet membrane glycoproteins (GP) and adhesion molecules. In contrast to blood taken into EDTA, blood taken into Diatube-H vacutainer tubes could be stored at room temperature for up to 4 hr prior to paraformaldehyde fixation without significant in vitro platelet activation, as measured by CD62P, CD63 and modulation of GPIb and GPIIbIIIa surface expression. Hence, paraformaldehyde fixation could be deferred for several hours, permitting transport of samples from distant sites. Studies of thrombin-induced platelet activation indicated that platelets taken into Diatube-H remained functional i.e. were able to be activated. Expression of the CD29, CD49b and CD31 adhesion molecules on the platelet surface was unaffected by storage in Diatube-H. The results suggest that Diatube-H may be a useful reagent for flow cytometric studies of platelets when the samples cannot be processed immediately.
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The first patient was a 17-year-old boy with septic arthritis; the second patient was a 12-year-old boy with a liver abscess. Both had hemocultures positive for Staphylococcus aureus. The diagnosis of DIC was defined by clinical signs of septicemia with fever, tachypnea, peripheral vasoconstriction, and low platelet counts (67,000/mm3 and 47,000/mm3, respectively). The second patient also presented with acute ischemia of the fingers and toes. General care was provided in the intensive care unit, and high doses of antibiotics were provided continuously (metronidazole and oxacillin or ceftriaxone). A 5% glucose solution containing dipyridamole (Persantine; Istituto De Angeli/Boheringer Ingelheim, Reggello, Italy) was administered by continuous intravenous infusion (20 mg/24 hours). In addition, regular heparin (Liquemin; Roche, Indianapolis, IN, USA) was administered at a dosage of 250 microg/kg per hour or 25 IU/kg per hour (6 mg/kg per 24 hours). These heparin doses are not able to promote complete blood anticoagulation. Treatment with heparin and dipyridamole was maintained for 10 days in the first patient and for 18 days in the second.
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Although off-pump coronary artery bypass grafting (CABG) has been recognized less invasive than conventional CABG on cardiopulmonary bypass, off-pump CABG may be partly invasive especially to the coronary endothelium. The present study was designed to evaluate the adverse effects of coronary snaring with looped sutures and gas insufflation on the coronary endothelium. The protective efficacies on the coronary endothelium of coronary snaring with elastic sutures or humidified gas insufflation with/without heparin and dipyridamole-added were also tested.
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The influence of blood withdrawal (vacuum or slow aspiration) and anticoagulants (ethylenediaminetetraacetic acid [EDTA]; heparin; citrate; a mixture of citrate, theophylline, adenosine, and dipyridamole [CTAD]; and D-phenylalanyl-L-prolyl-L-arginine chloromethyl ketone [PPACK]) on clotting activity, hematologic data, and rheologic measurements (whole blood and plasma viscosity, red cell filtration in one study) were investigated. No difference was found between the two blood withdrawal techniques on the basis of the affected measurements. EDTA appeared to be the best anticoagulant with regard to blood cell preservation and showed the lowest whole blood viscosity over a wide range of shear rates (0.1 to 87.0 sec-1). PPACK was the most potent inhibitor of clotting activity as monitored by fibrinopeptide A concentration. The results suggest that EDTA is probably a reasonable choice for rheologic studies of whole blood and should be combined with PPACK when plasma properties are studied.
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Two hundred and thirty-six consecutive patients had GMPS at rest and post-stress. The summed stress and rest scores and the summed difference score (SDS) were calculated using a 17-segment model analysis of GMPS. An SDS >3 indicated significant ischaemia. The REF and SEF were automatically generated and the DEF (SEF-REF) was calculated.
To determine the prognostic value of the high-dose (0.84 mg/kg over a 10-minute period) dipyridamole echocardiography test (DET) after a first acute myocardial infarction (AMI) in comparison with clinical, electrocardiographic, echocardiographic, and angiographic variables, follow-up data over an average period of 16 months were obtained in 93 consecutive patients. There were 41 total cardiac events (TCE): one death, two reinfarctions, 13 postinfarction anginas, five percutaneous transluminal coronary angioplasty procedures, and 20 coronary artery bypass graft procedures. TCE without revascularization procedures were considered adverse cardiac events (ACE). The DET result was positive in 28 of 41 patients with TCE and in only 4 of 52 patients without TCE (p < 0.001). The sensitivity, specificity, and accuracy of positive DET in predicting TCE were 68%, 92%, and 82%, respectively. According to Cox's proportional regression model the best predictor of TCE was positivity of DET (p = 0.002, relative risk ratio 4.3), followed by multivessel coronary artery disease (p = 0.018, relative risk ratio 2.9) and patent infarct-related artery (p = 0.042, relative risk ratio 2.9). DET was positive in 12 of 16 patients with ACE and 20 of 77 patients without ACE (p = 0.001). The sensitivity, specificity, and accuracy of DET in predicting ACE were 75%, 74%, and 74%, respectively. According to Cox's proportional regression model significant predictors of ACE were positivity of DET (p = 0.002, relative risk ratio 29.4) and ejection fraction < or = 40% at the time of DET (p = 0.017, relative risk ratio 22.2).(ABSTRACT TRUNCATED AT 250 WORDS)
The assay of residual adenosine deaminase (ADA) activity was used as a sensitive measure of the transport of deoxycoformycin (dCF) into human erythrocytes. Contrary to prior reports from this laboratory, the inactivation of intraerythrocytic ADA by dCF was linear rather than log-linear, with time. Linear inactivation rates were also seen when erythrocytes were preloaded with a 5-fold excess of calf intestinal ADA. The uptake of tritium-labeled dCF molecules and the rate of inactivation of ADA molecules showed an approximate 1:1 stoichiometry. The nucleoside transport inhibitors, 6-[(4-nitrobenzyl)thio]-9-beta-D-ribofuranosylpurine (NBMPR) and dipyridamole, and the permeant, uridine, inhibited dCF transport with Ki values of 35 nM, 45 nM, and 340 microM respectively. The affinity of dCF for the nucleoside transporter was low with a Ki of approximately 10 mM for the inhibition of adenosine influx.
The myocardial uptake kinetics of 14(R,S)-[18F]fluoro-6-thia-heptadecanoic acid (FTHA) were evaluated in humans with PET. The relationship between human myocardial FTHA uptake kinetics and the rate-pressure product (RPP) as an index of myocardial oxygen consumption was investigated in seven normal subjects under fasting conditions.
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The scintigraphic studies showed perfusion defects in 13 patients (87 percent) after dipyridamole and in 15 patients (100 percent) after adenosine. 201Tl uptake and clearance were quantitated in nine myocardial segments and in four extracardiac segments in each patient. 201Tl uptake was not significantly different between adenosine and dipyridamole studies in most cardiac regions. Extracardiac 201Tl uptake was significantly less in the liver and splanchnic regions following adenosine compared with dipyridamole. 201Tl clearance was not significantly different following adenosine and dipyridamole except in the anterolateral region in the anterior view. Hemodynamic changes following administration of intravenous adenosine and oral dipyridamole were not significantly different. Adverse effects were more common with adenosine than with dipyridamole. Adverse effects with adenosine were transient; however, adverse effects with dipyridamole were prolonged and required reversal with aminophylline in 2 patients. No patients required termination of the adenosine infusion or administration of aminophylline.
Adenosine or its synthetic analogues were topically applied to the intestinal jejunum while steady-state blood flow was calculated in submucosal arterioles using video microscopy. Blood flow increased (220 or 130% of control) with the serosal application of 10(-6) M N-ethyl carboxamido adenosine (NECA, A2-selective agonist) or 2-chloro adenosine (2CA, nonselective agonist) but not with cyclohexyl adenosine (CHA, A1-selective agonist). The nonselective competitive antagonist, 8-phenyl theophylline, attenuated the response evoked by NECA. The mucosal application of 10(-6) M CHA caused blood flow decreases (81% of control), but neither NECA nor 2CA evoked a response. These observations suggest a mucosal diffusion barrier, so the concentrations of the analogues were raised one hundredfold. Serosal 10(-4) M CHA or NECA caused blood flow increases, but the effects were negligible with mucosal application, suggesting that the mucosa was indeed impermeable to these compounds. The responses evoked by 10(-4) M 2CA were similar on the serosa or mucosa (200-220% of control), submaximal (maximum = 400% of control at 10(-3) M), and not antagonized by 8-phenyl theophylline or by the cellular uptake inhibitor, nitrobenzyl-6-thio guanosine. In context with earlier studies, greater than 10(-6) M 2CA probably evokes vasodilation that is not entirely mediated by extracellular receptors. Serosal adenosine (10(-4) M) caused submaximal blood flow increases (200% of control) that were not potentiated by nitrobenzyl-6-thio guanosine or another transport inhibitor, dipyridamole.(ABSTRACT TRUNCATED AT 250 WORDS)
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Pharmacological stress echo is feasible even very early after acute myocardial infarction via a useful approach based on low-dose dobutamine to assess myocardial viability, and high-dose dipyridamole to assess ischemia. For risk stratification purposes, stress-induced myocardial ischemia outperforms resting function and myocardial viability, and it is independent of angiographic data. Revascularization procedures do not seem to be effective when only viability is present.
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Twenty-four patients (17 males, 7 females; mean age 57+/-11 years) with IDC were consecutively enrolled. After obtaining clinical and hemodynamic stabilization, transthoracic echocardiography was performed including CFR measurement and carvedilol therapy was initiated with 3.125 mg twice daily and titrated to a target dose of 25 mg twice daily. Twenty-three patients reached the target dose in a mean of 11+/-3 weeks. The mean duration of carvedilol therapy was 19+/-3 weeks, after which echocardiography was repeated and findings were recorded at baseline and after dipyridamole infusion. Clinical and echocardiographic findings were compared with those of 23 age- and sex-matched patients (13 males, 10 females; mean age 55+/-4 years) with atypical chest pain.
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The relative performance of alternative stressors for stress echocardiography for the diagnosis of coronary artery disease (CAD) is not well established.
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Twenty-one patients with angiographic evidence of significant coronary artery disease, and positive dipyridamole echocardiographic test results at basal condition and after 7 days of placebo treatment were prospectively studied to see whether beta blockade modifies the effects of dipyridamole echocardiographic testing on regional myocardial contractility. Patients were randomized to propranolol (120 mg/day) or placebo treatment in 3 divided doses for 7 days, after which each patient crossed over to the alternate regimen. Dipyridamole-echocardiographic testing was repeated at the end of each treatment. Propranolol abolished new mechanical signs of transient dipyridamole-induced ischemia (new wall motion abnormalities or an increase in degree of basal asynergies, or both) in 13 of 21 patients. The remaining 8 patients had positive results on dipyridamole echocardiographic testing after the propranolol treatment period. At basal conditions both heart rate and rate-pressure product were significantly reduced with propranolol; there was also a significant decrease in these parameters at peak dipyridamole infusion. At peak dipyridamole infusion heart rate and rate-pressure product were significantly lower in patients with negative than in those with positive echocardiographic test results after propranolol. Our data show that administration of beta blockade significantly reduces the development of transient dipyridamole-induced myocardial asynergies, the earliest markers of acute myocardial ischemia, detected with 2-dimensional echocardiography.
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Thirty eight patients (34 males, 4 females, mean age 59 +/- 2 years), with a history of coronary artery bypass grafting for a total of 42 mammary artery grafts, were studied by means of color Doppler echocardiography at baseline and after vasodilation with dipyridamole infusion (0.56 mg/kg i.v. over 4 min). The evaluated echocardiographic parameters included: systolic (SPV) and diastolic peak velocities (DPV), systolic (SVI) and diastolic velocity-time integrals (DVI), and the DPV/SPV and DVI/SVI ratios. We also calculated the dipyridamole infusion to baseline ratio of the diastolic peak velocities (DPVdip/DPVbaseline), the index of internal mammary artery graft blood flow reserve and the percent DPV increment as an index of graft stenosis.
Ninety patients with old myocardial infarction were studied to evaluate the efficacy of intravenous dipyridamole 201Tl imaging for the detection of myocardial ischaemia in post-infarction patients, and to compare the prevalence of ischaemia in 63 patients with post-infarction angina (group I) and 27 patients without angina (group II). Thirty-four of the patients in group I and 15 of the patients in group II received coronary arteriography (CAG) for comparison; these were labelled groups IA and IIA, respectively. On 201Tl imaging, the incidence of scar with ischaemia in the infarct zone and scar with ischaemia at a distance were 72% and 42% in all patients, 89% and 52% in group I vs 33% and 19% in group II (P < 0.001 and P < 0.01, respectively). On CAG testing, the rates of infarct-related recanalization vessel and multi-vessel disease were 76% and 68% in group IA vs 40% and 40% in group IIA (P < 0.05 and P > 0.05, respectively). Thus, dipyridamole 201Tl imaging is a useful modality and post-infarction angina a proper indicator in the detection of myocardial ischaemia in post-infarction patients
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The ability to continuously monitor the delicate balance between blood flow and oxygen consumption would be a great asset in the study of myocardial ischemia. The present study was performed, in anesthetized dogs, to validate the use of encased polargraphic oxygen electrodes in the study of myocardial ischemia. Polargraphic oxygen electrodes were placed in the area to be rendered ischemic at fixed tissue depths of 3 mm (epicardium) and 9 mm (endocardium). Endocardial and epicardial oxygen tensions as well as the ratio of endocardial to epicardial oxygen tension and left circumflex coronary flow were monitored. Ischemia was induced by decreasing left circumflex coronary flow by 50%. Upon completion of a 20-min poststenotic period, endocardial pO2, endocardial/epicardial ratio, and coronary flow were significantly decreased (59 +/- 7, 52 +/- 7, and 55 +/- 4%, respectively) whereas epicardial pO2 was slightly decreased. Nitroglycerin (10 micrograms/kg, i.v.) markedly increased endocardial pO2 and endocardial/epicardial ratio above poststenotic control (13 +/- 5 mmHg and 64 +/- 10%, respectively) whereas epicardial pO2 was not significantly decreased. The increases in endocardial pO2 occurred at a point where coronary flow and mean arterial pressure were not significantly changed. Conversely, dipyridamole (125 micrograms/kg, i.v.) significantly increased coronary flow (26 +/- 2 ml/min/100 g) although it did not appreciably alter endocardial or epicardial pO2. It is concluded that encased polargraphic oxygen electrodes provide a quantitative method for determination of oxygen tension in the ischemic myocardium.
A review of the literature disclosed 106 pregnancies (preg.) in 57 women with essential thrombocythemia (ET). The success rate (baby alive) was 57% (60 live births/106 preg.), the rate of miscarriage 43% (46 miscarriages/106 preg.). The most frequent complication was spontaneous abortion during the first trimester in 36% (38 abortions/106 preg.). Other complications such as intrauterine death and stillbirth after the 28th week, which occurred in 5% (7/106), premature delivery in 8% (8/106), pre-eclampsia in 4% (4/106), and fetal growth retardation in 4% (4/106) were rarer events. Placental infarction due to thrombosis seems to be the most consistent pathological event as far as the fetus is concerned. Maternal hemorrhage occurred in 4% (3 minor and 1 major bleeding) and only 2 minor maternal thrombotic episodes have been observed. Interestingly, a decline in platelet count has been observed in 14 women and was associated with a successful preg, in 13/14 cases (93%). Aspirin (ASS) was the most frequently used drug in 47 of 93 recorded cases (51%). In 16 evaluable women treated with ASS the live birth rate was higher (12/16 preg., 75%) than for 21 untreated women (9/21 preg., 43%). In 5 cases interferon alpha (IFN) has been used successfully. In summary, 57% of women with ET had a live birth, maternal complications happened in 6%. Promising treatment modalities might be ASS and IFN. However, no definitive answer can be given on the ideal management for women with ET during pregnancy. A European register should be set up.
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Pharmacologic stress testing with 0.56 mg/kg of intravenous dipyridamole is frequently used to noninvasively detect coronary artery disease (CAD). However, high-dose dipyridamole (0.80 mg/kg) or the combination of standard-dose dipyridamole (0.56 mg/kg) with the isometric handgrip maneuver might evoke a greater coronary hyperemic response.