Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anginal patients who remain symptomatic despite optimally dosed beta blockade may also be given dihydropyridine calcium antagonists. This treatment regimen was examined in a double-blind parallel, randomized, controlled study in 147 patients with angina and positive bicycle exercise tests despite optimal beta blockade with atenolol (heart rate at rest <60 beats/min). Patients were randomized to atenolol and/or placebo (control), and atenolol and/or amlodipine. The main outcome measurement was exercise tolerance after 8 weeks compared with baseline. After 8 weeks, no significant differences in time to 0.1-mV ST-segment depression, time to chest pain, and time to end of exercise were observed. The number of patients with chest pain during exercise decreased significantly in the amlodipine group (p = 0.04 vs controls). The subgroup of patients with an early (<6 minutes) onset of chest pain at baseline showed a significant increase in time to chest pain after amlodipine (p = 0.0001 vs controls). In the amlodipine group, ST depression and rate-pressure product at submaximum comparable workload decreased to 0.4 mm (0.56) (p = 0.03 vs controls) and 1.223 (2.652) beats/ min x mm Hg (p = 0.01 vs controls). The number of patients in each group with adverse events was not different. The addition of amlodipine to the treatment of patients with myocardial ischemia, despite optimal beta blockade, is well tolerated and may lead to improvement in symptomatic anginal patients, who have a rapid onset of exercise-induced ischemia.
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PMID:Value of the addition of amlodipine to atenolol in patients with angina pectoris despite adequate beta blockade. 959 92

The clinical significance of silent myocardial ischemia (SMI) in the elderly was assessed in 91 patients with Q wave infarction who showed ischemic ST depression during treadmill stress testing, as well as reversible defect (RD) during dipyridamole thallium imaging. They were divided into two groups (47 patients with silent ST depression and 44 patients with painful ST depression) and compared for scintigraphic and coronary arteriographic features, and prognosis. There was no significant difference in age, gender and site of infarction between the two groups. The prevalence of single and double vessel coronary stenosis was higher in patients with SMI (66%) than in those with painful ischemia (p < 0.05). The results of treadmill stress testing showed a longer exercise duration (4.7 +/- 1.7 vs. 4.1 +/- 1.8 min) and higher maximal heart rate (138 +/- 15/vs. 126 +/- 20/min) in patients with SMI than in those with painful ischemia (p < 0.01). Dipyridamole thallium imaging revealed a larger infact (18.8 +/- 9.1 vs. 14.6 +/- 10.2 segments) in patients with SMI than in those with painful ischemia (p < 0.05). The prevalence of RD in the area of infarction was also higher in patients with SMI (74%) than in those with painful ischemia (45%) (p < 0.05). Although a higher proportion of the patients with painful ischemia (42%) underwent CABG or PTCA as their initial therapy, compared with those with SMI (25%) (ns), there was no difference in the cardiac event rate between the two groups who were initially treated medically. Dipyridamole thallium imaging is useful in the assessment of SMI in elderly patients with Q wave myocardial infarction. Those with SMI may have a larger infarct and a higher prevalence of ischemia localized within the infarction than those with painful ischemia.
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PMID:[Assessment of exercise-induced silent myocardial ischemia by dipyridamole thallium imaging. (2). Its significance in Q wave myocardial infarction]. 959 82

The purpose of this study was to investigate platelet effects on postischemic heart function in conjunction with adenosine effects on intracoronary platelet adhesion. Homologous platelets were infused into the coronaries of isolated guinea pig hearts, either during low-flow ischemia or during reperfusion, and external heart work (EHW) and intracoronary platelet adhesion were determined. In most experiments, thrombin was added to the perfusate. The influence of endogenous adenosine was studied by use of the uptake blocker dipyridamole and the unspecific adenosine-receptor blocker theophylline, the A1-receptor blocker 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), and the A2-receptor blocker 3,7-dimethyl-1-propargylxanthine (DMPX). The importance of nitric oxide and prostaglandin I2 (PGI2) was tested by using nitro-L-arginine (NOLAG) and indomethacin, respectively. When platelets were applied with thrombin during low-flow ischemia, EHW recovered to only 63 +/- 4% of the preischemic value, as compared with 89 +/- 3% without platelets (p < 0.05). Despite thrombin, platelets incurred no significant functional loss when applied in the first minute of reperfusion (but again in the fifth minute); however, when theophylline was also present, recovery of EHW amounted to only 42 +/- 12%. Intracoronary adhesion of platelets was negligible without thrombin, and highest during low-flow ischemia with thrombin (35 +/- 3% of the applied number). No adhesion occurred during the first minute of reperfusion, whereas in the fifth minute, adhesion was again 20.8 +/- 4%. Dipyridamole increased adenosine release and attenuated adhesion at this time. Theophylline increased adhesion in the first minute of reperfusion (33 +/- 6.4%), whereas NOLAG and indomethacin proved to be ineffective. DPCPX and DMPX each increased platelet retention during the first minute of reperfusion, their effects being additive. Intracoronary adhesion of platelets induced by thrombin in isolated hearts can reduce postischemic recovery of heart function. During reperfusion, but not during low-flow, endogenous adenosine can prevent platelet adhesion and loss of myocardial function, an action mediated both by A1- and A2-receptor-dependent mechanisms.
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PMID:Adenosine endogenously released during early reperfusion mitigates postischemic myocardial dysfunction by inhibiting platelet adhesion. 967 36

Dipyridamole single-photon emission computed tomography (SPECT) has a high negative predictive value for perioperative cardiac events, but events are infrequent in patients with a positive test. In contrast, dipyridamole echocardiography is more selective for detection of multivessel disease and thus may have a greater specificity for cardiac events. We therefore compared the ability of dipyridamole SPECT and echocardiography to predict perioperative and long-term cardiac events in 133 patients referred for vascular surgery. The group was also evaluated based on clinical features and ejection fraction. Four patients had surgery cancelled because of high risk and were excluded from further analysis. Among the 129 remaining patients, 21 had coronary revascularization (n=12) or an early cardiac end point (n=9). The sensitivity of SPECT for the prediction of early events (90%) was not significantly different from that of echocardiography (66%, p=NS). The specificity of SPECT (68%) was less than that of echocardiography (88%, p <0.001%), as was the accuracy (72% vs 84%, p=0.02). These findings were replicated after exclusion of patients with treatment end points. During long-term follow-up, 12 patients experienced > or = 1 event: 6 died from cardiac causes, 4 underwent revascularization, and 3 had myocardial infarction. Thus, the specificity of SPECT and echocardiography for late events were 58% and 80%, respectively (p <0.001). The 3-year survival of patients without ischemia during echocardiography or at SPECT was not different (93% vs 94%, p=NS).
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PMID:Comparison of dipyridamole stress echocardiography and perfusion scintigraphy for cardiac risk stratification in vascular surgery patients. 987 49

For patients with recent myocardial infarction, the main determinants of prognosis are: extent of transmural necrosis, state of the infarct-related artery and the presence and extent of myocardium at risk. The basic principle underlying the use of stress echocardiography states that myocardial ischaemia produces abnormalities of regional wall motion which are by themselves early, sensitive and specific markers of decreased perfusion. Dobutamine infusion allows for evaluation of myocardial contractile reserve by increasing inotropism. In low doses it gives us information on regional viability. In high doses, wall motion under increased oxygen demand, it becomes dependent on the ability of the coronary arteries to increase blood flow. Dipyridamole induces coronary vasodilation. In low doses it produces an increase in the blood flow. In high doses the steal effect deviates blood from the regions dependent on stenosed arteries. Ischaemia and regional wall motion abnormalities ensue. A negative stress echocardiogram, either under dobutamine or dipyridamole, has an excellent negative predictive value while a positive stress echocardiogram is predictive of an increased rate of events in the follow-up.
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PMID:[Stress echocardiography in myocardial infarct]. 995 Oct 56

The aim of this study was to evaluate the effects of verapamil administration on dipyridamole-induced transient wall-motion abnormalities as detected by two-dimensional echocardiographic monitoring in patients with coronary artery disease. Twenty-eight patients (16 men and 12 women; mean age, 60+/-7 years) with angiographic evidence of significant coronary artery disease, positive dipyridamole echocardiography test results at basal condition on two consecutive days, were prospectively studied. Patients were randomized to verapamil (360 mg/day) or placebo treatments, given in three divided doses daily for 7 days; at the end of this time, each patient crossed over to the alternate regimen. Dipyridamole echocardiographic testing was repeated at the end of each treatment period. Our data demonstrate that verapamil significantly reduces the dipyridamole-induced wall-motion score index, a quantitative marker of acute myocardial ischemia (1.7+/-0.4 vs. 1.3+/-0.2; p<0.001). Hemodynamic data show that the drug reduces heart rate and rate-pressure product at basal condition (heart rate from 75+/-8 to 67+/-9 beats/min; p<0.001; rate-pressure product from 99+/-13 to 86+/-13 U x 10(-2); p<0.001) and at peak dipyridamole infusion (heart rate from 96+/-8 to 89+/-6 beats/min; p<0.001; rate pressure product from 127+/-21 to 118+/-13 U x 10(-2); p<0.05) with respect to placebo treatment. We conclude that verapamil is able to reduce dipyridamole-induced ischemia, as detected by two-dimensional echocardiographic monitoring, in patients with coronary artery disease by reducing, at least partially, myocardial oxygen consumption. Moreover, its beneficial action could be related to the effects of the drug on coronary collateral circulation and on sympathetic modulation.
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PMID:Verapamil reduces dipyridamole-induced myocardial ischemia in patients with coronary artery disease. 1006 72

Intravenous dipyridamole is a potent coronary vasodilator that has been extensively investigated over the past several years in the noninvasive assessment of patients with suspected coronary artery disease when exercise cannot be performed or is suboptimal. As an alternative to exercise studies, dipyridamole has been used in combination with different cardiac imaging techniques such as echocardiography, thallium scintigraphy, and radionuclide ventriculography. Extensive experience has been obtained with dipyridamole thallium-201 imaging for coronary artery disease screening, risk stratification, and prognosis after an acute coronary event. However, experience with the use of dipyridamole in combination with two-dimensional echocardiography has been limited. Dipyridamole increases coronary blood flow in nondiseased coronary vessels relative to coronary vessels with significant luminal narrowings. These provide the basis for detecting regional differences in flow by using different cardiac imaging techniques. Two-dimensional echocardiography would show regional wall-motion abnormalities in response to those regional differences in coronary blood flow. In this article, the most commonly used protocols, safety, and practicability of dipyridamole echocardiography are reviewed. As an alternative to exercise, dipyridamole echocardiography shares all the indications of a standard exercise test. Clinical applications of dipyridamole echocardiography include coronary artery disease screening, suspected coronary artery spasm, postmyocardial infarction risk stratification, evaluation of percutaneous transluminal coronary angioplasty results, and prognosis following an acute coronary event. Compared to conventional (ECG) exercise testing, dipyridamole echocardiography appears to be equally sensitive but more specific. Compared to atrial pacing, dipyridamole provokes ischemia at a lower rate pressure product and results in a greater ST segment depression suggesting that dipyridamole induces more profound myocardial ischemia than atrial pacing. Dipyridamole thallium and exercise thallium have shown to be equally sensitive and specific in the assessment of coronary artery disease. High dose dipyridamole echocardiography appeared to be equally sensitive and more specific. Experimental studies have demonstrated that dobutamine appears to be a more powerful pharmacological agent in inducing wall-motion abnormalities. Dipyridamole echocardiography as compared to stress echocardiography offers the advantage of obtaining better quality postintervention images. With regard to sensitivity and for coronary artery disease diagnosis, both techniques appear to render similar results. Although further studies are needed, the available data indicates that cardiac ultrasound imaging prior to and following the intravenous administration of dipyridamole may be an attractive alternative to thallium perfusion imaging in the clinical setting, particularly when radionuclide capabilities are not present.
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PMID:Dipyridamole echocardiography. 1014 77

Dipyridamole-echocardiography test response can be expressed not only in a black or white (positive vs negative) code but also, in positive tests, by a gray scale integrating the severity and extent of the dyssynergy as well as the ischemia-free stress time. The recognition of the dyssynergy is important to establish the diagnosis; however, the evaluation of the degree of the induced ischemia, stratified according to spatiotemporal coordinates, is even more important because it accurately predicts the coronary anatomical and functional situation, as well as the prognosis of the individual patient. Furthermore, the "shades of gray" in a positive response have proved useful in assessing the beneficial effects of several interventions: coronary angioplasty; coronary artery bypass surgery; thrombolysis; and medical antianginal therapy. Due to its excellent reproducibility, dipyridamole-echocardiography can play a pivotal role for simple, safe, fast, accurate, and objective assessment of therapeutic interventions, either mechanical or pharmacological, based upon the presence, timing, severity, and extent of dipyridamole-induced dyssynergy.
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PMID:Dipyridamole-echocardiography: clinical usefulness following interventions. 1014 86

Factors that influence frequency and location of stress-induced electrocardiographic (ECG) ST depression and the development of chest pain are incompletely understood. We studied 331 patients with ischemic myocardial nuclear defects in response to routine clinical treadmill testing with simultaneous ECG recording. Nuclear defects were analyzed for location and extent of myocardium involved. Exercise-induced ischemic ST changes were demonstrated in 59% of patients (196 of 331). Subjects with stress-induced ECG changes and/or chest pain had more extensive nuclear perfusion defects. Diabetic patients were significantly less likely to experience chest pain (24%) versus nondiabetics (41%) during testing (p = 0.04). Larger perfusion defects were associated with greater magnitude, lead distribution, and incidence of ECG changes. The number of ECG lead zones (anterior, lateral, and inferior) responding positively were related to both magnitude of ST depression and severity of ischemia, but not to location of ischemic defects. Regardless of location of ischemia, ST depression occurred with similar frequency. Thus, exercise-induced ECG ST depression remains a valuable indicator of the severity of myocardial ischemia. Greater ST depression involving multiple leads usually signified extensive myocardial ischemia, but provided no information regarding its location. Anginal-type chest pain induced by exercise testing also denoted more extensive ischemia.
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PMID:Relation between the electrocardiographic stress test and degree and location of myocardial ischemia. 1042 25

Sustained protection against ischemia-reperfusion injury is not available for patients at risk for myocardial infarction who may require emergent reperfusion therapy. Whereas ischemic preconditioning and adenosinergic agents reduce myocardial injury, they are only effective when given immediately before ischemia or reperfusion. We recently found chronic ethanol exposure, an adenosine uptake inhibitor, produced sustained cardioprotection against ischemia-reperfusion injury. We now ask whether chronic dipyridamole therapy, a clinically usable nucleoside transport inhibitor, induces similar cardioprotection. Perfused hearts from guinea pigs, given dipyridamole (4 mg. kg(-1). day(-1)) in their water for 2-6 wk (n = 10 for each group), underwent ischemia-reperfusion. Injury was assessed by recovery of left ventricular developed (LVDP) and end-diastolic (LVEDP) pressures and creatine kinase release. During reperfusion, hearts from dipyridamole-treated animals (6 wk) had 74% higher LVDP, 28% lower LVEDP, and 61% lower creatine kinase release versus controls. Adenosine A(1)-receptor antagonism (8-cyclopentyl-1, 3-dipropylxanthine; 200 nM) abolished the protection of dipyridamole but A(2) antagonism (3,7-dimethyl-1-propargylxanthine; 10 mM) did not. Dipyridamole therapy produces sustained protection against ischemia-reperfusion injury in guinea pigs. This cardioprotection requires adenosine A(1) receptor signaling at the time of ischemia.
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PMID:Chronic dipyridamole therapy produces sustained protection against cardiac ischemia-reperfusion injury. 1056 65


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