Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A randomized, double-blind, crossover study tested the antiischemic and antianginal efficacy of felodipine, extended-release 5-10 mg, versus amlodipine, 5-10 mg once daily. Fifty-two patients with documented exercise-induced angina pectoris and myocardial ischemia during 24-h electrocardiographic monitoring were included in the study. Forty-seven patients completed the 8-week treatment period, whereas five patients withdrew from the study. The mean number of ischemic episodes/24 h was reduced from 19.9 at baseline to 2.3 during amlodipine and to 2.4 during felodipine; the total duration of ischemic episodes decreased from 69.8 min/24 h to 15.2 min and 15.5 min during amlodipine and felodipine, respectively (for both variables, p = 0.83 and p = 0.53 between treatments, and for both treatments, p < 0.001 compared with baseline). Eighteen (38%) patients receiving amlodipine and 19 (40%) patients receiving felodipine showed no ST-segment depression during treatment. Maximal ST-depression was reduced from an average of 2.1 mm to 1.1 and 1.2 mm on amlodipine and felodipine, respectively (p = 0.68 between treatments and p < 0.001 compared with baseline). Mean heart rate remained unchanged compared with baseline. Anginal attacks were reduced from 16.4/week at baseline to 4.7/week with amlodipine and to 4.3/week with felodipine (p = 0.26 between treatments, and p < 0.001 vs. baseline). Accordingly, nitrate consumption was reduced from 14.7 capsules per week to 4.0 and 3.8 with amlodipine and felodipine, respectively (p = 0.40 between treatments, and p < 0.001 compared with baseline). Adverse reactions were infrequent and distributed similarly between the two treatments. It is concluded that both drugs effectively reduced ischemic episodes and anginal attacks and were well tolerated in patients with stable angina pectoris. There was no evidence that the two regimens were different in their antiischemic and antianginal properties.
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PMID:Felodipine and amlodipine in stable angina pectoris: results of a randomized double-blind crossover trial. 915 63

This study was designed to compare once-daily administration of 5-10 mg amlodipine with two daily doses of 40 mg sustained-release isosorbide dinitrate in 59 patients with stable angina using a randomized, double-blind, crossover study design. Anginal episodes, nitroglycerin consumption, and possible adverse events were recorded in a diary. A maximal symptom-limited bicycle exercise test and 48-hour ambulatory ECG monitoring were performed at baseline and at the end of each 5-week period of therapy. Exercise time, time to angina, time to ST depression, and maximal ST depression were measured during exercise. During ambulatory monitoring, the number of ischemic episodes and the duration per hour of ST depression were assessed. Amlodipine significantly reduced anginal episodes (P < 0.001) when compared with isosorbide dinitrate. Furthermore, amlodipine prolonged time to ST depression (P < 0.001) and time to angina (P < 0.05) when compared with isosorbide dinitrate. The number and duration of ischemic episodes during ambulatory monitoring were significantly reduced with amlodipine when compared with baseline values (P < 0.05), whereas no differences were found between isosorbide dinitrate and baseline. Adverse events were reported more frequently with isosorbide dinitrate than with amlodipine (P < 0.02). Amlodipine appears to be more effective and tolerable than sustained-release isosorbide dinitrate as monotherapy for chronic stable angina.
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PMID:Effects of amlodipine and isosorbide dinitrate on exercise-induced and ambulatory ischemia in patients with chronic stable angina pectoris. 949

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

We investigated whether adenosine neuromodulation is involved in a benzodiazepine (midazolam)-induced depression of excitatory synaptic transmissions in the CA1 and dentate gyrus (DG) regions in rat hippocampal slices. Field excitatory postsynaptic potentials (fEPSPs), evoked by electrical stimulation of the CA1-Schaffer collateral or the DG-perforant path, were recorded with extracellular microelectrodes from CA1-stratum radiatum or DG-stratum moleculare in oxygenated ACSF. The initial slope of the fEPSPs was analyzed for assessing the drug effects. Midazolam (1 microM) transiently depressed CA1- and DG-fEPSPs. The fEPSPs were depressed to approximately 75% of the control values, and then gradually recovered. The depression was not affected by bicuculline, a GABAA receptor antagonist, although it was completely antagonized by aminophylline, an adenosine receptor antagonist. Dipyridamole (5 microM), an adenosine uptake inhibitor, depressed the fEPSPs in a similar manner to midazolam. An adenosine deaminase inhibitor, EHNA, also transiently depressed the fEPSPs, but in a different manner. Exogenous adenosine persistently depressed the fEPSPs. The effects of the drugs were not significantly different in the CA1 and DG regions. The results suggest that midazolam (1 microM) depresses excitatory synaptic transmissions through the adenosine neuromodulatory system by inhibiting adenosine uptake in the CA1 and DG regions of the hippocampus.
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PMID:Involvement of the adenosine neuromodulatory system in the benzodiazepine-induced depression of excitatory synaptic transmissions in rat hippocampal neurons in vitro. 1009 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

It is now widely accepted that percutaneous transluminal coronary angioplasty (PTCA) is an effective nonsurgical technique for achieving coronary revascularization. Exercise electrocardiography remains the standard procedure for functional evaluation before, early, and late after angioplasty because of its availability, safety, and limited cost. The drawback of exercise testing is its low specificity and the fact that the attainment of diagnostically useful data requires a level of exercise that substantially increases myocardial oxygen demand. Exercise thallium imaging has been shown to be highly predictive of restenosis and adverse events after angioplasty, but it is possible that myocardial perfusion may not return to normal immediately after successful revascularization. Stress echocardiography has many practical advantages over scanning tests, as result of its lower cost, shorter imaging time, and the absence of radiation exposure. Dipyridamole echocardiography testing (DET) is an exercise-independent method of evaluating patients who have to undergo coronary angioplasty. Before PTCA, DET allows the clinician to localize the site and extent of myocardial ischemia anatomically. Early after a successful procedure, DET identifies a group at high risk for the late recurrence of symptoms. Late after PTCA, DET is more accurate than exercise electrocardiography in detecting restenosis or disease progression. In asymptomatic patients with exercise-induced ST depression, DET has the same good diagnostic accuracy as thallium scintigraphy. For these reasons, as well as because of its noninvasive nature and availability, DET should be considered an attractive option for the evaluation of patients after anatomically successful angioplasty.
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PMID:Strategy of diagnostic imaging before and after PTCA. 1015 Apr 76

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

Dipyridamole nuclear myocardial perfusion test is a safe and effective alternative to exercise nuclear perfusion testing for detecting myocardial ischemia. It is the procedure of choice in selected patients who are unable to exercise adequately. Intravenous dipyridamole causes coronary vasodilation with resultant maldistribution and heterogeneity of coronary flow in the presence of significant coronary artery disease. True ischemia, causing symptoms or ST-segment depression, is uncommon, in part because there is no increase in myocardial oxygen demand. A patient in whom myocardial ischemia developed, manifested by ST-segment elevation, during dipyridamole stress testing is described. Scintigraphic images illustrated a myocardial perfusion defect, which was consistent with coronary angiographic findings. This case report addresses the importance of dipyridamole-induced ST-segment elevation, its correlation with angiographic findings, and the need for continued hemodynamic and electrocardiographic monitoring in patients following dipyridamole infusion.
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PMID:Dipyridamole-induced ST-segment elevation indicative of transmural myocardial ischemia--a case report. 1151 95

Increased dispersion of the QT interval has been observed during pacing or exercise stress testing in patients with coronary artery disease (CAD). It has not been established whether this phenomenon is a consequence of ischemia. Therefore, we sought to evaluate whether dipyridamole-induced myocardial ischemia, as directly detected by echocardiographic monitoring of regional contractile function, would affect QT dispersion. Twenty-four patients with nonsignificant and 34 patients with significant CAD but no previous myocardial infarction underwent dipyridamole stress echocardiography while not taking medications. QT dispersion was measured on a 12-lead electrocardiogram at baseline and at various times after dipyridamole infusion. Dipyridamole infusion did not influence QT dispersion in patients without CAD. QT dispersion was similarly unaffected in patients with CAD in whom dipyridamole did not induce wall motion abnormalities. In contrast, in patients with positive dipyridamole stress test findings, QT dispersion increased from 60 +/- 17 ms at baseline to 94 +/- 25 ms during peak infusion (p <0.0001), with a time course mirroring that of development of contractile abnormalities. QT dispersion returned to 63 +/- 25 ms upon relief of ischemia by administration of aminophylline. The increase in QT dispersion was significantly related to the extent of contractile dysfunction induced by dipyridamole. Although ST-segment depression occurred in only 40% of patients with positive dipyridamole stress test findings, 88% of such patients had an increase in QT dispersion. Analysis of the receiver-operating characteristic curve showed that a QT dispersion increase of > or =20 ms identified positive findings for dipyridamole stress echocardiography with 68% sensitivity and 91% specificity. Thus, QT dispersion is acutely affected by myocardial ischemia induced by the administration of dipyridamole. Measurement of QT dispersion may improve detection of stress-induced ischemia on surface electrocardiograms.
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PMID:Effects of acute myocardial ischemia on QT dispersion by dipyridamole stress echocardiography. 1258 49


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