To extend the duration of high thoracic epidural analgesia (HTEA) treatment compared with the authors' previous studies, to test the hypothesis that the mechanism by which HTEA reduces angina during long-term treatment includes an improvement in myocardial blood flow distribution and a reduction in stress-induced ischemia, and to show that new myocardial infarctions are not masked or missed in patients receiving HTEA.
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Dipyridamole-thallium imaging has been suggested as a method of preoperatively assessing cardiac risk in patients undergoing major surgery. To define more clearly its proper role in preoperative assessment, we prospectively evaluated 111 patients undergoing vascular surgery. In the first set of 61 patients, our data confirmed the value of preoperative dipyridamole-thallium scanning in identifying the patients who suffered postoperative ischemic events. Events occurred in eight of 18 patients with reversible defects on preoperative imaging, compared with no events in 43 patients with no thallium redistribution (confidence interval for the risk difference: 0.624, 0.256). The results also suggested that clinical factors might allow identification of a low-risk subset of patients. To test the hypothesis that patients with no evidence of congestive heart failure, angina, prior myocardial infarction, or diabetes do not require further preoperative testing, we evaluated an additional 50 patients having vascular procedures. None of the 23 without the clinical markers had untoward outcomes, while ten of 27 patients with one or more of these clinical markers suffered postoperative ischemic events (confidence interval for the risk difference: 0.592, 0.148). In the clinical high-risk subset, further risk stratification is achieved with dipyridamole-thallium scanning.
Quantitative coronary angiography of noninfarct arteries was performed on paired cine-angiograms of 149 patients from fibrinolytic trials who had a patent infarct-related artery 3 to 4 weeks following STEMI and who were randomized to either continue the daily combination of 50-mg aspirin and 400-mg dipyridamole or to matching placebo. Follow-up angiography was scheduled at 1 year.
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In high-risk patients with ACS, even in the absence of LAD disease, CFR significantly improves prediction of adverse events when added to standard evaluation. This finding supports a role of CFR in the risk stratification early after ACS and is in context with the concept that CFR reflects global atherosclerotic burden, endothelial dysfunction, and microvascular damage, more than just mirroring focal LAD disease.
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In previous work, we described a group of patients with angina-like chest pain and normal coronary arteries. These patients had impaired coronary vasodilator responses to the stress of rapid atrial pacing and to the administration of dipyridamole, a potent vasodilator of coronary arterioles. This abnormality appears to be localized to the prearteriolar microvascular bed. To determine whether these patients have a more generalized abnormality of vasodilator reserve, we used mercury-in-Silastic strain-gauge plethysmography to compare their hyperemic responses to forearm ischemia with those of normal controls. After 10 minutes of ischemia, peak forearm flow was 39.9 +/- 5.0 ml per minute per deciliter in the controls [corrected] and 31.7 +/- 10.5 in the patients [corrected] (21 percent reduction; 95 percent confidence interval, 4 percent to 37 percent). Flow responses were also significantly reduced after three and five minutes of ischemia. Correspondingly, the vascular resistance after ischemia was also consistently higher in the patients with microvascular angina. The degree of vasodilator impairment in the peripheral circulation correlated well with the degree of vasodilator impairment in the coronary circulation (r = 0.74; P less than 0.004). Thus, patients with microvascular angina appear to have an impairment of vasodilator reserve that affects not only their coronary circulation but also their peripheral arterial bed.
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False thrombocytopenia may result from platelet aggregation, especially in feline ethylenediamine tetra-acetic acid (EDTA) blood specimens. Citrate, theophylline, adenosine and dipyridamole (CTAD) was added to 46 feline EDTA specimens to test its anti-aggregation action. Platelet aggregation was estimated from blood films and a complete blood count was performed with a Sysmex XT-2000iV analyser. Platelet aggregation score was >2 in 11/46 EDTA tubes and only in one EDTA+CTAD specimen. The platelet count was higher in all CTAD-supplemented tubes except one, medians measured by cytometry being 225.5 × 10(9)/l and 249.0 × 10(9)/l in EDTA and EDTA+CTAD, respectively (P = 0.007). Adding CTAD had statistically and analytically significant but moderate effects on other blood variables, the most intense variations being observed for reticulocytes (about 3% higher in EDTA specimens) and reticulocyte indexes. Addition of CTAD to EDTA when sampling feline blood is a useful option to reduce platelet clumping.
Vasodilator stress echocardiography can cause myocardial ischaemia in patients with severe aortic valve stenosis and angiographically normal coronary arteries. The aim of the study was to determine the mechanism of ischaemia in this clinical model.
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Stable bicarbonate biorelevant buffers could be established to perform intrinsic dissolution rate determinations for indomethacin and dipyridamole as long a continuous gas sparging of CO2(g) was used. Depending of the pH of the dissolution medium, the intrinsic dissolution rates of both indomethacin and dipyridamole were affected by the bicarbonate concentration. Sparging with CO2(g) to create physiologic buffers has a unique advantage over conventional buffers in that gas sparging serves as a continuous source of bicarbonate buffer species. This advantage was demonstrated by performing dissolution experiments at pH values typically associated with the fed state (pH 5) and applying relatively low CO2(g) pressures, resulting in bicarbonate concentrations less than 0.5 mM. It was demonstrated that CO2(g) sparging at a pH consistent with the fed state created an in-situ bicarbonate buffer at low concentrations, which had a significant impact on the dissolution of a basic drug such as dipyridamole.
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In 41 patients with a history of an acute myocardial infarction, the location of myocardial ischemia was studied by 201Tl emission computed tomography immediately and 3 h after intravenous dipyridamole. Distant ischemia was distinguished from peri-infarctional ischemia by the presence of transient thallium defects in, or slow thallium washout from myocardium not supplied by the infarct-related coronary artery. Ischemia at a distance occurred in 13 patients and was always accompanied by peri-infarctional ischemia. Peri-infarctional ischemia without distant ischemia was observed in 15 patients. The occurrence of distant ischemia was found to be dependent on the severity of stenosis in non-infarct coronary vessels. 12 (86%) of 14 patients with non-infarct stenosis of 75% or greater had distant ischemia, but only 1 (4%) of 27 patients with a stenosis of less than 75% in another vessel. In the presence of distant ischemia, peri-infarctional ischemia was in 11 patients (85%) associated with collaterals supplying the infarct zone, whereas in 13 (87%) of the patients with peri-infarctional ischemia only, incomplete obstruction of the infarct-vessel was observed. It is concluded that, by the distinction between peri-infarctional and distant ischemia, the presence of a significant stenosis in non-infarct vessels can be non-invasively predicted from tomographic thallium scintigraphy with dipyridamole.
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The effects of cepharanthin and dipyridamole depot capsules (RAD) on the fate of Teflon fluorocarbon resin grafts used for replacement of the canine superior vena cava were studied. After short-term observation of 11 implanted grafts, 57 adult mongrel dogs underwent superior vena caval replacement with these Teflon grafts. Cepharanthin (2 mg/kg daily) and RAD (10 mg/kg daily) were administered after surgery to 28 and 14 animals, respectively. Dogs were killed at 12 days to 6 months after graft implantation. Fifteen dogs served as controls. In the cepharanthin-treated group, three grafts exhibited luminal obstruction with severe intimal hyperplasia, but smooth, semitransparent thin neointima was recognized in 25. The endothelial cell lining of the neointima exhibited excellent spread 2 months after implantation. Although one graft was obstructed with hyperproliferative fibrosis in the RAD-treated group, a well-developed neointima with complete coverage of endothelial cells was confirmed in 14 dogs. With regard to the rate of occurrence of luminal obstruction, these data were significantly different from those of the control group, which suggests that intimal hyperplasia can be reduced by treatment with antiplatelet agents.
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We have investigated the role played by cyclic nucleotide phosphodiesterases (EC 22.214.171.124) in the control of T-lymphocyte response to mitogenic agents by their ability to influence the cellular level of cAMP. The importance of this messenger as a negative regulator in this cell type is well established. Multiple isoenzymes of phosphodiesterase were fractionated from the cytosol of rat thymic lymphocytes by high performance liquid chromatography on an anion exchange column. In addition to the type II, III, IV isoforms that we have already described [Valette et al., Biochem. Biophys. Res. Commun. 169:864-872 (1990)], a phosphodiesterase fraction sharing several of the characteristics of type V, cGMP-binding phosphodiesterase, was detected. Non-isoform-selective inhibitors of phosphodiesterase such as dipyridamole, papaverine, and methyl-isobutylxanthine were able to totally prevent the proliferative response of thymocytes to stimulation by the mitogenic lectin concanavalin A. In contrast, the selective inhibitor of type IV phosphodiesterases rolipram induced a rather moderate inhibition of proliferation, not exceeding 60%; and the selective inhibitors of type III and type V phosphodiesterases, milrinone and M&B 22,948, respectively, displayed only marginal inhibitory effects. The association of the type III and IV phosphodiesterase inhibitors produced synergistic inhibition of proliferation, which could then be almost totally suppressed. These inhibitory effects on cell multiplication were reflected at the level of the cell cAMP content; only rolipram was able to induce a significant (approximately 50%) increase in cAMP, and this increase was potentiated by the presence of milrinone, reaching almost 100%. The type V phosphodiesterase selective inhibitor M&B 22,948 displayed similar properties to those of milrinone, which suggests that it indirectly inhibited the type III, cGMP-inhibitable isoenzyme, by inducing a cGMP rise. This hypothesis was supported by evidence of a significant raising effect of M&B 22,948 on cGMP level, and by the ability of a cGMP-elevating agent, sodium nitroprusside, to mimic the synergistic effects of milrinone associated with rolipram. Furthermore, 8-bromo-cGMP, a potent activator of cGMP-dependent protein kinase, which showed only weak inhibitory effects on thymic type III phosphodiesterase, failed to alter the effects of rolipram on the cell proliferation. These results allow us to delineate a role for types III, IV, and V phosphodiesterase in the control of cAMP level during the proliferative response of thymic lymphocytes. They also suggest that endogenously formed cGMP might participate in the regulation of cAMP level in the cells by means of the inhibition of the type III phosphodiesterase.(ABSTRACT TRUNCATED AT 400 WORDS)
A case of Bjork-Shiley mitral valve dysfunction is presented. The patient has not responded to anticoagulant therapy and had hypotension, dyspnea, chest pain, and a pulse deficit but normal sinus rhythm. Simultaneous echocardiogram, ECG, and arterial pulse tracing were used as noninvasive means of monitoring. Nonsurgical correction of a clinical emergency restored the patient to prior normal baseline cardiovascular function. This case illustrates the possibility of restoring normal prosthetic function by supporting the patient medically while undertaking diagnostic testing and arranging surgical intervention. To our knowledge, this is the first reported case of a malfunctioning Bjork-Shiley mitral valve corrected without surgery.
Two-day 99mTc-MIBI MPS after stress and rest were obtained for 507 patients subdivided according to the type of stress used, sTPD values, and ΔLVEF. Subsequent cardiac events were determined through a standardized questionnaire applied 1, 2, and 6 years after MPS. Independent of the type of stress used, the 6-year event rate with progressive perfusion and functional abnormalities combined was significant for total events, all-cause death, cardiac death, and revascularization but not for myocardial infarct. When ΔLVEF decreased by more than -10%, only those individuals with sTPD of 5% or less had increased 6-year total event rates [5.9% vs 15% for those submitted to treadmill test (P < 0.001) and 8.3% vs 19% when submitted to pharmacological stress (P = 0.001)]. An sTPD greater than 5% was the only variable predictive of total events when multivariate analysis was applied (P < 0.001 for treadmill exercise and P = 0.033 for dipyridamole).
Quantitative MCE is feasible for the diagnosis of CAD with dipyridamole/exercise stress. Dipyridamole prolongs postexercise hyperemia, augmenting the degree of hyperemia at the time of imaging.
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Copper-62 (II)-pyruvaldehyde bis(N(4)-methyl-thiosemicarbazone) (PTSM) has been proposed for cardiac imaging with positron emission tomography (PET). This study evaluated the agreement between Cu-62-PTSM and coronary angiography in the detection of occlusive coronary artery disease. The normalcy rate for Cu-62-PTSM PET in a group of healthy volunteers was also assessed.
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Effects of beraprost sodium, a chemically stable prostacyclin analogue, on renal dysfunction in an experimental rat model of glomerulonephritis were investigated. Beraprost sodium (30, 100 and 300 microg/kg) was orally given twice daily from the late stage of nephritis in which renal dysfunction was already developed. Beraprost sodium treatment inhibited the increase in urinary protein, serum creatinine and blood urea nitrogen, and the decrease in creatinine clearance. The elevation of serum creatinine was also inhibited by predonisolone (1 mg/kg). However, captopril (25, 50 and 100 mg/kg) and dipyridamole (20 and 60 mg/kg) failed to inhibit the elevation of serum creatinine. In the beraprost sodium-treated nephritic rats, the increase in mRNA levels for monocyte chemoattractant protein-1 (MCP-1) and collagen in the kidney was inhibited. These results suggest that beraprost sodium ameliorates developed renal dysfunction and is possibly an effective agent for the treatment of human glomerulonephritis.
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Various drugs are associated with adverse respiratory disorders (ARDs) ranging in severity from mild, moderate to severe and even fatal. Cardioselective and nonselective beta-blockers, calcium antagonists and dipyridamole can induce asthma. ACE inhibitors are mainly associated with cough. Amiodarone is related to a form of interstitial pneumonitis (IP) which can be fatal, tocainidine and flecainidine to a form of IP, and hydrochlorothiazide to a form of IP and pulmonary oedema. Antiasthmatic drugs can be associated with a paradoxical bronchospasm, while leukotriene antagonists are linked to the development of Churg-Strauss syndrome. Nonsteroidal anti-inflammatory drugs including aspirin (acetylsalicylic acid) may induce asthma. Gold is mainly related to IP, penicillamine to IP, systemic lupus erythematosus, bronchiolitis obliterans, and Goodpasture's syndrome. Acute respiratory reactions to nitrofurantoin include dyspnoea, cough, IP, and pleural effusion while IP and fibrosis are common in chronic reactions. Other antibacterials mainly evoke pneumonitis, pulmonary infiltrates and eosinophilia, and bronchiolitis obliterans. ARDs are similar for most categories of cytotoxic agents, with chronic pneumonitis and fibrosis being the most common. Noncardiogenic pulmonary oedema occurs as the most common respiratory complication in opioid agonist addiction. Psychotropic drugs such as phenothiazides, butyrophenones and tricyclic antidepressants can also induce pulmonary oedema. Oral contraceptives may produce asthma exacerbation, while long term use and/or high doses of postmenopausal hormone replacement therapy increase the risk of asthma. Bromocriptine is mainly associated with pleural effusion, while methysergide is usually associated with pleural effusion and fibrosis. Some anorectic agents have been linked to the development of primary pulmonary hypertension. The possibility of the occurrence of ARDs should be taken into account in each individual patient. Although in most cases the adverse effects are unpredictable, they can be reduced to a minimum or prevented if some drugs are avoided or stopped in time.
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Dipyridamole therapy produces protection against post-resuscitation myocardial injury in rats.
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In 14 patients (10 men and 4 women) with arterial hypertension and 8 normotensive subjects, minimal coronary resistance and vasodilator reserve (dipyridamole: 0.5 mg/kg body wt, gas chromatographic argon method) were determined after the angiographic exclusion of relevant coronary artery disease. Coronary reserve was depressed in hypertensive patients (2.7 +/- 2.3 vs 4.6 +/- 1.3, P < or = .05) due to increased minimal coronary resistance (0.64 +/- 30 vs 0.24 +/- 0.055 mm Hg.min.100 g.mL-1, p < or = 0.002). In right septal biopsies, mean external arteriolar diameter (21.6 +/- 2.3 vs 17.2 +/- 2.5 microns, P < or = .001), mean arteriolar wall area (271 +/- 61 vs 172 +/- 62 microns 2, P < or = .01), percent medial wall area (69.9 +/- 4.0 vs 66.0 +/- 3.2%W, P < or = .05), mean periarteriolar fibrosis area (216 +/- 122 vs 104 +/- 68 microns 2, P < or = .05), and volume density of total interstitial fibrosis (3.6 +/- 1.8 vs 1.9 +/- 0.5Vv% fibrosis, P < or = .05) were increased in hypertensive patients compared with normotensive subjects. Minimal coronary resistance correlated with %W (r = .6, P < or = .003) and Vv% fibrosis (r = .62, P < or = .002). Left ventricular mass index (111 +/- 21 vs 97 +/- 17 g/m2, P = NS) and left ventricular end-diastolic pressure (12 +/- 6 vs 8 +/- 3 mm Hg, P = NS) did not correlate significantly with minimal coronary resistance. In multivariate analysis, both %W and Vv% fibrosis explained half of the variability of minimal coronary resistance (r2 = .5, P < or = .002).
The sensitivity of nuclear myocardial perfusion imaging in detecting coronary artery disease is high. However, false-negative results may be encountered if all the myocardial territories were uniformly affected. Ischemic stunning after dipyridamole-stress on gated SPECT may be an indicator of severe and extensive coronary artery disease, and can help the interpretation of borderline perfusion images and the elimination of false-negatives secondary to relatively balanced lesions in three-vessel disease.
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Recently developed unstable angina clinical practice guidelines have recommended risk stratification with dipyridamole thallium-201 myocardial imaging in patients at "intermediate" pretest clinical risk who cannot exercise maximally. The prognostic value of predischarge dipyridamole technetium 99m sestamibi (MIBI) tomography has not been assessed in this clinical setting. To this end, 128 medically treated patients with unstable angina at intermediate pretest clinical risk underwent follow-up for 16 +/- 11 (mean +/- SD) months after predischarge intravenous dipyridamole MIBI tomography. An abnormal MIBI scan result was present in 99 patients (77%), of whom 47 had one or more reversible and 76 had one or more fixed perfusion defects. Cardiac events occurred in 68 (53%) patients after dipyridamole testing: recurrent unstable angina (n = 36), nonfatal acute myocardial infarction (n = 6), or death (n = 26). A cardiac event occurred in 10% of patients with normal MIBI tomography results compared with 69% of those with abnormal results (p < 0.01). Event rates associated with specific perfusion defects were similar (reversible = 68%; fixed = 71%) and were greater than rates in patients without defects (both p < 0.05). Clinical variables associated with increased risk of cardiac events by univariate analysis included a history of congestive heart failure, prior myocardial infarction, and diabetes mellitus (all p < 0.05). Independent multivariable predictors (Cox proportional hazards model) of any cardiac event were an abnormal result of MIBI scan (relative risk [RR] = 4.3, 95% confidence interval [CI] 1.5 to 12.0) and a reversible (RR = 1.8, 95% CI 1.1 to 2.9) or a fixed perfusion defect (RR = 2.9, 95% CI 1.6 to 5.4).(ABSTRACT TRUNCATED AT 250 WORDS)
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Pure qualitative assessment of 3 T MRI had acceptable performance in detecting severe CAD. There is no overall benefit of incorporating semi-quantitative data; however a higher sensitivity can be obtained by adding MPRI, especially in the detection of LCx lesions.
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A frequent clinical problem is to document the elusive entity of electrocardiographically silent myocardial ischemia. Since echocardiography offers a practical tool to detect reversible mechanical changes due to ischemia, 32 patients with angina on effort, and coronary artery disease, and 15 patients with angina at rest were studied. In all 47 patients electrocardiographic changes during effort or rest pain were inconclusive. Combined 12 lead electrocardiographic and 2-Dimensional echocardiographic monitoring were performed: during ergonovine testing in the 15 patients with angina at rest; during dipyridamole testing in the 32 patients with effort angina and a non diagnostic stress test. Interpretable echocardiograms were obtained in all the patients studied. Positivity of both the Ergonovine-Echocardiographic test and the Dipyridamole-Echocardiographic test was based upon the detection of regional transient asynergy. Of the 15 patients who had chest pain at rest in the absence of diagnostic electrocardiographic changes, Ergonovine-Echocardiographic test was positive in 6 (40%). Of the 32 patients who had chest pain in absence of diagnostic electrocardiographic changes during exercise stress testing, the Dipyridamole-Echocardiographic test was positive in 18 (56%). Echocardiographic monitoring in combination with provocative testing (ergonovine and dipyridamole) may be a practical, non invasive, inexpensive tool which is feasible in all patients with good basal echocardiograms and is able to unmask electrocardiographically silent myocardial ischemia by providing objective mechanical evidence of the ischemic event.