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Although the importance of antiplatelet treatment in preventing early bypass occlusion has been clearly recognized, questions regarding the optimal drug regimen remain. To study the efficacy of low-dose aspirin, alone or in combination with dipyridamole, 927 consecutive patients were enrolled in a multicenter, randomized, double-blind, placebo-controlled trial comparing aspirin, 50 mg t.i.d., aspirin, 50 mg t.i.d. plus dipyridamole, 75 mg t.i.d., and placebo. Both aspirin and aspirin plus dipyridamole reduced the occlusion rate of distal anastomoses, but only aspirin plus dipyridamole reduced the number of patients with at least one occluded graft. Logistic regression analysis identified distal vessel diameter, bypassed artery, graft type, and postoperative antiplatelet treatment as independent predictors of graft patency.
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Antiplatelet agents (APA) are used to reduce the risk of major cardiovascular events in various settings. When used for secondary prevention, antiplatelet monotherapy is associated with a relative risk reduction of such ischemic events of 25% compared to a placebo. New strategies are based on dual APA therapy. Aspirin-clopidogrel combination therapy is effective in situations of acute vessel injury such as myocardial infarction, coronary stenting and, possibly, peripheral stenting. GPIIb/IIIa inhibitors and loading doses of clopidogrel also have a place in these acute settings. In contrast, the aspirin-clopidogrel combination has proven disappointing in stable patients with cardiovascular disease, with no beneficial effect and, often, more bleeding events. Combination therapy with aspirin and extended-release dipyridamole may be more beneficial than very low doses of aspirin in ischemic stroke, but its use is limited by adverse effects. Overall, aspirin remains the first-line monotherapy of choice for patients with atherothrombosis, while clopidogrel is a valuable alternative. New antiplatelet strategies are in the pipeline, and clinically relevant laboratory tests of APA response may soon help to tailor treatment.
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The prevalence of severe coronary artery disease in peripheral vascular patients exceeds 50 per cent. It is therefore not surprising that complications of coronary artery disease are the most common causes of mortality following peripheral vascular operations. If the incidence of cardiac complications is to be reduced, it is first necessary to identify patients at risk through screening tests that will reliably detect hemodynamically important coronary occlusive disease. The operative risk can then be reduced by modifying the magnitude of the procedure, taking measures that can enhance the tolerance for a specific operation, or employing a combination of both. Screening methods in current use include risk factor analysis, exercise testing, routine coronary angiography, and dipyridamole thallium-201 scintigraphy. The risk factor approach has the advantage of being widely applicable since it makes use of historical, physical, and electrocardiographic findings that are already familiar to surgeons and anesthesiologists. It is also inexpensive. However, it may overlook the patient who has no symptoms of coronary artery disease, possibly as a result of the sedentary lifestyle imposed by complications of peripheral vascular disease. The electrocardiographically monitored stress test will identify the asymptomatic patient with occult coronary disease and is helpful in predicting operative risk. However, a meaningful test is dependent on the patient's ability to exercise--an activity that is frequently limited by claudication, amputation, or arthritis. Exercise testing also suffers from a lack of sensitivity and specificity when compared with coronary arteriography. Routine preoperative coronary angiography overcomes the exercise limitation of treadmill testing but is not widely applicable as a screening test for reasons of cost and inherent risk. Dipyridamole thallium-201 scanning, on the other hand, is safe and of relatively low cost and does not require exercise. Further, it has a high degree of sensitivity and specificity when compared with coronary arteriography. It appears to be an accurate predictor of postoperative cardiac complications.
Dipyridamole-echocardiography (echo) testing, exercise stress testing and coronary arteriography were performed in 141 patients with effort chest pain. Patients were separated into 5 groups according to the dose of dipyridamole needed to induce ischemia (0.56 mg/kg over 4 minutes vs 0.84 mg/kg over 10 minutes) and to the time of onset of the asynergy with the small dose (within vs beyond 3 minutes after the end of dipyridamole administration): group 1--early positive response to a small dose (33 patients); group 2--late positive response to a small dose (29 patients); group 3--negative response to a small dose, positive response to a large dose (17 patients); group 4a--negative response to both large and small doses, with significant coronary artery disease (CAD) (32 patients); and group 4b--negative response to small and large doses, without CAD (30 patients). All patients in groups 1, 2 and 3 had significant CAD. The rate-pressure product on exercise stress testing was measured at 0.10 mV of ST-segment shift in patients with a positive response and at peak exercise in patients with a negative response. Rate-pressure product significantly separated group 1 and group 2 from each other (157 +/- 46 and 229 +/- 33 mm Hg X beats/min X 1/100, respectively, mean +/- standard deviation) and from group 3, group 4a and group 4b (284 +/- 40, 290 +/- 51, and 298 +/- 45 mm Hg X beats/min X 1/100); values in the 3 latter groups overlapped.2+ Thus, the dipyridamole-echo test can stratify groups of patients with different levels of ischemia threshold on effort.
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Antiplatelet agents, in this review largely low dose aspirin, have small-moderate benefits when used for prevention of pre-eclampsia. Further information is required to assess which women are most likely to benefit, when treatment should be started, and at what dose.
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As part of a multicentre WHO MONICA-Project the present drug consumption by Warsaw population was assessed (evaluated by DDD). In Warsaw population 2646 inhabitants aged 35-64 years were examined. Ischaemic heart disease was diagnosed in 30% screened persons. Only 39% of subjects were involved in taking cardiovascular drugs. In ischaemic heart disease the drugs used most frequently were pentaerythritol tetranitrate and dipyridamole. The influence of several psychosocial factors on the fact of undertaking of pharmacological therapy was analysed using multivariant logistic function method. Significant relationships were found for age, health self-care self-estimation of health status and fact of medical consultation. Persons with high values of MLF (fifth quintile) underwent drug treatment six time more often, then persons with low values of MLF (first quintile).
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Blood and plasma from 109 patients with atherosclerosis and 70 healthy volunteers were tested to study the rate of prostacyclin (PGI2) hydrolysis. It has been reported that patients with atherosclerosis have the enhanced velocity of PGI2 degradation. The increase in the velocity was more marked in blood than in plasma. The significant negative correlation between antiaggregation effects of pentoxifylline, nifedipine, and dipyridamole and the velocity of PGI2 degradation in the patients was found. These data suggest that the increase of PGI2 biosynthesis by the drugs studied can enhance their antiaggregation effect if processes of PGI2 degradation in blood are not accelerated.
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PET with 13N-ammonia permits the noninvasive quantification of myocardial blood flow (MBF) in humans. The present study was done to assess the reproducibility of quantitative blood flow measurements at rest and during pharmacologically induced hyperemia in healthy individuals.
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A total of 44 patients (39 men) underwent same-day Tc-99m sestamibi stress/rest MPI. High-speed SPECT images were performed within 30 min after conventional SPECT. Stress and rest acquisition times were 16 and 12 min for conventional imaging and 4 and 2 min for high-speed SPECT, respectively. Myocardial counts/min (cpm) were calculated for both conventional SPECT and high-speed SPECT. Images were visually analyzed, and the summed stress score (SSS) and summed rest score (SRS) were calculated. Image quality and diagnostic confidence were qualitatively assessed.
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Analyses of the stroke data after vorapaxar yielded from thrombin-receptor antagonist vorapaxar in acute coronary syndromes (TRACER) and TRA2P clinical trials, and affiliated Food and Drug Administration (FDA) reviews.
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Simultaneous biplane RNA accurately detects wall motion abnormalities frequently missed by single-plane RAO imaging.
This study was designed to analyze the effects of carbocromene and dipyridamole on the haemodynamic and electrocardiographic side-effects resulting from imipramine infusion in anaesthetised rats and dogs. Imipramine was infused at 1 mg/kg/min until cardiac failure and vascular collapse terminated the experiment at 21 +/- 2.3 min in rats and at 29.5 +/- 2.1 min in dogs. This was characterized by hypotension, bradycardia, intraventricular conduction delay, cardiac tachyarrhythmia and A-V block. Carbocromene (4 mg/kg i.v., followed by 80 micrograms/kg/min) protected the animals against heart failure. This was associated with delayed hypotension and negative inotropy, and lower incidence of heart block. Survival time increased to 37 +/- 1.5 min (P less than 0.05), and 54.2 +/- 2.6 min (P less than 0.02) in rats and dogs, respectively. Dipyridamole (0.5 mg/kg i.v., followed by 80 micrograms/kg/min) failed to decrease imipramine toxicity as judged by the haemodynamic and electrocardiographic parameters and did not alter survival time of imipramine controls. These results suggest that carbocromene is an effective treatment for imipramine-induced cardiovascular collapse and cardiac arrhythmias, the beneficial effects being largely due to metabolic and membrane stabilizing effects. Carbocromene has both therapeutic and prophylactic value and appears to be superior to dipyridamole therapy.
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A total of 415 hypertensive patients underwent rest and stress (exercise in 278 and dipyridamole in 137) gated 99mTc-sestamibi SPECT and prospective follow-up for the composite endpoint of death and acute coronary syndrome. Patients undergoing revascularization were censored. The individual effect of clinical and stress imaging data on outcome was evaluated by Cox regression analysis. Model validation was performed using bootstrap methods adjusted by the degree of optimism in estimates. Survival analysis was performed using the product-limit Kaplan-Meier method.
Dilazep (i.p.), a coronary vasodilator and an uptake inhibitor of adenosine, dose dependently potentiated acute ethanol-induced motor incoordination in mice. In view of peripheral cardiovascular depressive effects of dilazep, the effect of i.c.v. dilazep (25, 50 and 75 micrograms), and its metabolites, 1,4-bis(3-hydroxypropyl)perhydro-1,4-diazepine (BHPD) (15, 31 and 62 micrograms) and 1-[3-(3,4,5-trimethoxybenzoyloxy)propyl]perhydro-1,4-diazepine (TBPD) (62 and 125 micrograms) on ethanol-induced motor incoordination was studied. Dose-related potentiation of ethanol-induced motor incoordination was noted with dilazep and its metabolites. Whereas dilazep (i.p.) produced no apparent central nervous system (CNS) effects, by i.c.v. route, it caused CNS excitation including tonic-clonic seizures. Adenosine uptake inhibition, Ca2+ entry blockade or direct activation of adenosine receptors was ruled out as the possible mechanism of seizures because dipyridamole, verapamil or N6-(2-phenylisopropyl)-adenosine (R-PIA) administered i.c.v., while potentiating ethanol (i.p.)-induced motor incoordination did not produce seizures. The CNS excitation was minimal with BHPD and none with TBPD. Theophylline pretreatment partially blocked potentiation of ethanol-induced motor incoordination by dilazep and BHPD and not by TBPD. The data suggest dilazep-induced potentiation of ethanol-induced motor incoordination is partially due to central adenosine receptor mechanism and partly due to other yet unknown mechanism(s) and further supported our earlier reports about adenosine involvement in the CNS effects of ethanol. The data also suggest that dilazep (i.c.v.)-induced seizures are due to mechanism(s) other than adenosine uptake inhibition, Ca2+ entry blockade or direct adenosine receptor activation.
The primary outcome is stroke recurrence and its severity ('ordinal recurrence' based on modified Rankin Scale) at 90 days, with masked assessment centrally by telephone. Secondary outcomes include vascular events, functional measures (disability, mood, cognition, quality of life), and safety (bleeding, death, serious adverse events).
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Eighteen patients with ischaemic peripheral vascular disease were treated for a 5-week period with either 20 mg aspirin daily, 75 mg dipyridamole three times daily or a combination of these two treatments. Before and after 4 weeks' treatment autologous platelet labelling with 111In was carried out and sites of active vascular platelet uptake monitored, and platelet half-life measured. Neither aspirin nor dipyridamole alone had any effect on platelet uptake or on platelet half-life. The combination of aspirin and dipyridamole resulted in a significant decrease in platelet uptake and a nonsignificant trend towards prolongation of platelet half-life. These findings suggest that this combined therapy may be of benefit in the treatment of atherosclerosis in man.
The feasibility, safety and usefulness of dipyridamole echocardiography (two-dimensional echocardiography and 12 lead electrocardiographic monitoring during dipyridamole infusion, up to 0.84 mg/kg over 10 min) were evaluated in 94 asymptomatic patients 8 to 10 days after uncomplicated acute myocardial infarction. The results were compared with those of symptom-limited treadmill exercise testing and correlated with coronary angiography. Two mechanical patterns of positivity of dipyridamole echocardiography could be identified: 1) a new wall motion abnormality confined to the infarct zone or to the adjacent segments (24 patients), and 2) transient remote asynergy (33 patients). The success rate in recording adequate images during dipyridamole infusion was 100%. Interobserver agreement concerning diagnosis occurred in 89 (93%) of 94 patients. Dipyridamole echocardiography was well tolerated; no complication was observed during or after the test. Seventy-three patients underwent coronary angiography within 6 weeks after acute myocardial infarction. Transient remote asynergy on echocardiography was present in 27 of 40 patients with multivessel disease and in none of 33 patients without multivessel disease. Results of treadmill exercise testing were positive in 28 patients with multivessel disease and 8 patients without multivessel disease. Thus, the sensitivity of dipyridamole-induced transient remote asynergy was 68% compared with 52% for treadmill testing (p less than 0.05); specificity was 100% and 72%, respectively (p less than 0.005). The overall accuracy of dipyridamole echocardiography (81%) was higher than that of dipyridamole stress electrocardiography (63%) or exercise electrocardiography (60%) (p less than 0.02). It is concluded that dipyridamole echocardiography is a useful, feasible and inexpensive nonexercise-dependent test for detecting the extent of coronary artery disease early after acute myocardial infarction.
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Patients with essential arterial hypertension demonstrate abnormal vasodilator capacity either during increased cardiac metabolic demand or during pharmacological vasodilation. Structural and functional damage to the coronary microcirculation has been proposed as one of the major causes of impaired coronary reserve in this disease. To assess the role of microvascular impairment in regional myocardial blood flow (MBF), 27 patients with essential hypertension were evaluated by dynamic positron emission tomography (PET) at rest, during atrial pacing and after dipyridamole infusion and compared with 13 healthy subjects. All patients had normal coronary arteries, 17 had moderate to severe hypertension and 10 had mild hypertension. Baseline mean MBF of 0.97 +/- 0.25 ml/min/g was significantly increased to 1.60 +/- 0.38 during atrial pacing and 2.35 +/- 0.95 after dipyridamole infusion (p < 0.01); however, mean flow during atrial pacing and after dipyridamole infusion was significantly lower than in healthy subjects (2.15 +/- 0.73 and 3.71 +/- 0.86 ml/min/g, p < 0.05 and p < 0.01, respectively). The MBF response to atrial pacing and dipyridamole infusion was similarly depressed in patients with mild and severe hypertension. The study was repeated after 6 months of antihypertensive treatment with the calcium antagonist verapamil or the angiotensin converting enzyme (ACE) inhibitor enalapril in a subgroup of 20 patients as part of a randomised, single-blind clinical trial. This study is still in progress; the initial 16 patients treated with verapamil or enalapril showed an obvious improvement in MBF values during atrial pacing and after dipyridamole infusion after 6 months of therapy (mean MBF: 2.10 +/- 0.64 and 2.99 +/- 1.63 ml/min/g, respectively, p < 0.05 vs pretreatment values). In conclusion, obvious impairment of MBF during atrial pacing and after dipyridamole infusion was observed in hypertensive patients with normal coronary arteries and this appeared unrelated to the severity of hypertension. Therapy with verapamil or enalapril improved coronary reserve and MBF response to an increase in myocardial oxygen demand.
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The results of our study demonstrate that the transient dilation index does not differ when patients undergo exercise stress test on a treadmill or pharmacological stress by dipyridamole.
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We tested the practicability of dipyridamole myocardial nitrogen-13 ammonia positron emission tomography (dipyridamole (13)NH(3 )PET) for the perioperative risk assessment of coronary artery disease (CAD) in a cohort of patients with severe chronic obstructive pulmonary disease (COPD) undergoing lung volume reduction surgery (LVRS). Twenty consecutive LVRS candidates, 13 men and 7 women (mean age 57+/-2 years), without symptoms of CAD were prospectively studied by dipyridamole (13)NH(3 )PET. Side-effects and overall tolerance were assessed by a questionnaire and visual analogue scale. Repeated pulmonary function tests were performed before and 4, 12, 16 and 30 minutes after dipyridamole injection. All dipyridamole (13)NH(3 )PET studies were negative for CAD. Seventeen patients underwent LVRS without cardiac complications; three patients did not undergo LVRS for other reasons. Nine patients suffered intolerable dyspnoea requiring i.v. aminophylline. Mean FEV(1) decreased significantly after dipyridamole infusion: in nine patients the reduction in FEV(1)exceeded 15% from baseline. We found that dipyridamole is not well tolerated and causes significant bronchoconstriction in patients with severe COPD. Although all dipyridamole-induced side effects can be promptly reversed by aminophylline, dipyridamole cannot be recommended as a pharmacological stress in this setting.
MPR and MVR in MS and SS territories were significantly lower than those of NS territories (p < 0.05 for all). Logistic regression analysis identified MPR∙MVR as the best predictor of ≥50% coronary lesion than MPR or MVR alone.
Feasibility of digital exercise echocardiography was 84%; 8 of 88 remaining patients had a nondiagnostic exercise echocardiographic test (inadequate exercise or imaging). In 80 patients with feasible and diagnostic digital exercise echocardiography, sensitivity, specificity and accuracy were, respectively, 89%, 91% and 90%. Eighty of the 104 patients underwent transesophageal atrial pacing and dipyridamole echocardiography. Feasibility of the alternative stress procedures was 77% for transesophageal atrial pacing and 96% for dipyridamole. In 60 patients successfully undergoing both alternative stress procedures, sensitivity and specificity were 83% and 76% for atrial pacing and 43% and 92% for dipyridamole echocardiography, respectively. In the group of 24 patients with nondiagnostic exercise echocardiography and consequent indication to alternative stress procedures, accuracy of transesophageal atrial pacing was higher than that of dipyridamole echocardiography (73% vs. 45%, p = 0.06).
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The aim of this study was to compare the diagnostic value of exercise stress testing, Thallium 201 myocardial scintigraphy or after administration of dipyridamole and left ventricular angioscintigraphy performed either during a static (handgrip) or dynamic exercise (bicycle ergometry) for the positive diagnosis of stenosing coronary artery disease. The exercise angioscintigraphy was performed at equilibrium with 99m Tc red blood cell labelling. The global ejection fraction and that of seven radial segments of the left ventricle were measured, the data being recorded within a period of 2 minutes. The handgrip consisted in compressing a dynamometric ball at 1/3 maximal force for 3 minutes, with both hands; the ergometric exercise was increased by 30 Watt 2 minute increments until a positive ECG or 85% of the theoretical maximal heart rate for age was obtained. Normal subjects (n = 29) increased their global (+ 8%) and regional ejection fractions in each of the seven segments (p less than 0.05) during ergometric exercise: there was no significant change of global (-3% NS) or segmental ejection fractions during the handgrip exercise. In the coronary group (at least one greater than 70% stenosis) (n = 61) the fall in global ejection fraction was the same (-14%) with both forms of exercise; a similar fall in the segmental ejection fraction in the territory distal to the stenosis was observed with the handgrip (-22%) and bicycle ergometry (-28% NS). Dynamic exercise testing seemed superior to handgrip exercise. Therefore, the finding of an abnormal global ejection fraction on exercise (i.e. either a global ejection fraction less than the lower limit of normal on exercise, or lower than the global ejection fraction at rest), or of an abnormal regional ejection fraction (i.e. either a regional ejection fraction less than the lower limit of normal over at least 3 segments, or a regional ejection fraction on exercise lower than the regional ejection fraction at rest over at least 3 segments) detected coronary artery disease with a sensitivity of 94% and a specificity of 72%. Dynamic exercise angiography seemed to be more sensitive than maximal ECG stress testing (94% compared to 64%) more rapidly positive (p less than 0.05), as sensitive (94% compared to 83% NS) than Thallium myocardial scintigraphy, but less specific (72% compared to 90%, p less than 0.05), and as unspecific as ECG stress testing.(ABSTRACT TRUNCATED AT 400 WORDS)
The evaluation of myocardial perfusion and tissue characteristics gives useful information regarding the indication for surgery. In the present study, two-phase contrast enhanced electron beam computed tomography (EBT) was used to quantitatively examine myocardial perfusion and the tissue characteristics of the left ventricular (LV) myocardium in congenital aortic stenosis (AS). The AS group comprised 15 patients and the control group had 14 non-AS patients. Myocardial ischemia and tissue characteristics were evaluated by the ratio of the incremental CT number of the myocardium (M) and the lumen (L) of the LV (M/L) in, the early phase with and without dipyridamole (Dp) loading and in the late phase after enhancement (respectively). In a comparison between the AS group and the controls, mean early M/Ls were significantly lower in the AS group than in the controls (20+/-5% vs 37+/-10%, p<0.01) and mean late M/Ls in the AS group were also significantly lower (47+/-11% vs 62+/-13%, p<0.01). In the AS patients, early M/Ls in the subendocardial and apical regions were especially lower than those of other segments, but the late M/Ls in these segments were inversely higher than those of other segments. These results suggest 2 things: (1) the existence of latent LV myocardial ischemia in AS patients, which is probably because of a hypertrophied LV wall, in turn caused by afterload, and (2) the presence of more myocardial ischemia and interstitial fibrosis in the subendocardial and apical regions of the AS heart. Using Dp loading for the AS patients increased the clarity of the contrast images. Contrast-enhanced EBT is useful for evaluating myocardial characteristics and perfusion in AS, and gives new insight into the LV wall characteristics in AS, as well as an indication for surgical correction of congenital AS.
Vascular injury during aortocoronary vein bypass graft surgery and arterial angioplasty initiates platelet thrombus deposition and mandates antithrombotic therapy, starting before the procedures to maximize protection against occlusion. This has been shown in studies in animals and in patients undergoing aortocoronary vein bypass graft operation where dipyridamole therapy was started before the operation, heparin was given intraoperatively and combined dipyridamole and aspirin therapy was started 7 hours after operation and markedly reduced vein graft occlusion in patients with grafts at both high and low risk for occlusion without increasing bleeding. Other alternative regimens, particularly preoperative dipyridamole followed postoperatively with aspirin alone, offer a promising future. Therapy should be continued for at least 1 year and perhaps indefinitely. Control of coronary risk factors appears important for long-term therapy to try to retard the atherosclerotic and occlusive process that leads to approximately 50% vein graft attrition by 10 years after operation. The possible role of cod liver oil and internal mammary artery bypass is discussed. Arterial angioplasty appears to cause deep arterial injury that activates both platelets and the coagulation system. These potentiate each other to form macroscopic mural thrombus within 1 hour in more than 90% of arteries that manifested deep arterial injury in pigs. Acute platelet thrombus deposition was retarded but not eliminated by only certain platelet-inhibitor agents. Implications for ongoing trials, current empiric therapy and future therapy are discussed.
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A consistent FFR was obtained in all patients. Both the sensor built and the echo built FFR identifiy pts with normal or abnormal contractile reserve. The best cut-off value of the sensor built FFR was 15.5 g * 10-3 (Sensitivity = 0.85, Specificity = 0.77). Sensor built FFR slope and shape mirror pressure/volume relation during stress. This approach is extendable to daily physiological exercise and could be potentially attractive in home monitoring systems.
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Mean FFR and DST were 0.76 +/- 0.14 and 74 +/- 15%. SPECT showed no significant correlation with both FFR and DST with Kendall's coefficiency of 0.28 (p = 0.05) and 0.13 (p = 0.35). The sensitivity and specificity of SPECT to detect functionally and morphologically significant residual stenosis were 92%, 31% and 83%, 29%.
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BIBW22BS was 20- to 100-fold more potent than dipyridamole in the reversal of resistance in the Pgp-positive sublines. Reversal of resistance was obtained in a dose-dependent manner and was complete at concentrations of 0.5-2.5 microM. At non-toxic, equimolar concentrations of 1.0 microM BIBW22BS showed higher modulating potency than the calcium-channel blockers. BIBW22BS did not affect resistance in the non-Pgp sublines. BRO/mdr1.1 s.c. xenografts have stable multidrug-resistance characteristics upon serial transplantation. BIBW22BS, vincristine, or doxorubicin as single agents were not effective in vivo, while the addition of BIBW22BS could significantly reduce the tumor growth expressed as the T/C% of vincristine from 109% to 48% and that of doxorubicin from 55% to 32%. However, reversal of vincristine resistance in BRO/mdr1.1 xenografts was not complete when compared to the efficacy of vincristine in BRO xenografts.
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Myocardial blood flow (MBF) at rest and during dipyridamole-induced hyperemia was quantified in 10 transplant patients (group A) during an acute, biopsy-proven rejection episode and again after successful immunosuppressive treatment and in 6 transplant patients (group B) without prior rejection episode. In group A patients, MBF during rejection averaged 1.7 +/- 0.3 mL.min-1.g-1 at rest and 2.5 +/- 0.9 mL.min-1.g-1 during hyperemia; after recovery, MBF at rest had declined to 1.2 +/- 0.3 mL.-1.g-1 (P < .001) but had increased to 3.9 +/- 1.1 mL.-1.g-1 (P < .001) during hyperemia. Flows after recovery from rejection were similar to those in the group B patients (0.9 +/- 0.2 and 3.9 +/- 0.7 mL.min-1.g-1). Flow reserve in the group A patients was only 1.5 +/- 0.5 during rejection but improved to 3.4 +/- 0.9 at recovery (P < .001) and thus remained lower than in the control patients (4.5 +/- 0.7, P < .05). Minimal coronary resistance during dipyridamole vasodilation was elevated during rejection (40 +/- 11 mm Hg.mL-1.min-1.g-1); after recovery, it no longer differed from that in the group B patients (26 +/- 11 versus 22 +/- 4 mm Hg.mL-1.min-1.g-1). MBF during rejection was increased relative to cardiac work, as demonstrated by significantly higher ratios of blood flow to rate-pressure product than those at recovery and in the control patients.
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To map precise myocardial perfusion anatomy, we correlated detailed coronary arteriographic anatomy for every coronary artery and all secondary branches in the heart that had flow-limiting stenosis with corresponding specific, circumscribed, myocardial perfusion defects by positron emission tomography. Eight hundred ninety-five patients with abnormal coronary arteriograms showing any visible coronary artery narrowing of greater than 10% diameter stenosis underwent positron emission tomography perfusion imaging at rest and after dipyridamole stress; the data obtained were processed automatically into 3-dimensional topographic displays of relative radionuclide uptake in anterior, septal, left lateral, and inferior quadrant views, without attenuation artifacts, depth-dependent resolution, or spatial distortion of polar displays. The selection criterion for detailed anatomic analysis was the presence of a discrete, localized, moderate to severe, dipyridamole-induced perfusion defect, defined by automated algorithms as 1 quadrant view outside 2 SDs of healthy control subjects with which a specific stenotic coronary artery and/or its secondary branches could be correlated unequivocally on the coronary arteriogram for mapping precise perfusion anatomy, not for determining sensitivity or specificity. Because the anatomy of myocardial perfusion is inherently not statistical data, the results are presented as a summary atlas and series of individual cases that illustrate myocardial perfusion anatomy. Because the patterns of myocardial perfusion anatomy were derived from a large number of subjects, the atlas provides generalized information, not previously published, that correlates detailed arteriographic anatomy with perfusion anatomy including secondary diagonal, marginal, and posterior descending branches of the coronary arteries.