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)

In order to examine the possible role of coronary artery spasm in the pathogenesis of unstable angina, provocative testing for coronary spasm was performed in 43 patients with unstable angina who had 0- or 1-vessel disease. Coronary spasm was induced in 20 (65%) of 31 patients by hyperventilation testing (ST increases in 18, ST decreases in 2). Anginal attacks with either ST-segment elevation or ST-segment depression in patients without a significant organic stenosis were induced in 23 (55%) of 42 patients during treadmill exercise testing. Coronary artery spasm, showing severe (> or = 90%) vasoconstriction with angina and/or ischemic electrocardiographic ST-segment deviation, was also documented angiographically in 42 (98%) of 43 patients following intracoronary injection of acetylcholine. We conclude that dynamic coronary obstruction plays an important role in the genesis of attacks in patients with unstable angina who had 0- or 1-vessel organic coronary artery disease.
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PMID:Pathogenesis of unstable angina with 0- or 1-vessel disease. Important role of coronary artery spasm. 136 32

In this double blind randomised placebo controlled study, we investigated the antianginal efficacy of oral captopril in 33 patients of angiographically documented coronary artery disease (chronic stable angina). Apart from sublingual nitrates, all other antianginal drugs were withdrawn. Patients were then evaluated both subjectively by questionnaire and objectively by treadmill stress test. No patient had more than mild hypertension and all patients had good left ventricular function. One group of patients received oral captopril while the other group was given placebo. A repeat assessment was done after six weeks and the results compared with baseline. Anginal attacks decreased from 20.11 +/- 1.86 per week on placebo to 9.92 +/- 1.38 (p < 0.01) on captopril as also the number of sublingual nitrates (18.84 +/- 3.01 to 11.14 +/- 2.94, p < 0.01). Assessment by the treadmill stress test showed that in comparison to the pretreatment test, captopril therapy resulted in a significantly increased exercise duration (6.26 +/- 0.21 to 6.98 +/- 0.31 minutes, p < 0.05), total work done (6.76 +/- 0.26 METS to 7.48 +/- 0.29 METS, p < 0.05). In addition there was a significant increase in time to angina (6.16 +/- 0.18 to 6.85 +/- 0.24 min, p < 0.05) and time to 1mm ST depression (5.18 +/- 0.26 to 6.46 +/- 0.30 min, p < 0.01). We conclude that captopril is an effective monotherapy for patients with chronic stable angina and has both antianginal as well as anti-ischemic effects, possibly secondary to direct coronary vasodilation.
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PMID:Use of captopril as an isolated agent for the management of stable angina pectoris--a double blind randomised trial. 142 46

Cardiac imaging with dipyridamole infusion has been proposed as an exercise-independent tool for the diagnosis of coronary artery disease. Dipyridamole acts through the accumulation of adenosine, which reduces sympathetic tone in vasomotor nuclei of the brainstem and inhibits norepinephrine release in noradrenergic neurons but also activates arterial chemoreceptors. The aim of this study was to assess whether dipyridamole administration (up to 0.84 mg/kg over 10 minutes, a dosage commonly employed for diagnostic testing) may modulate sympathetic activity either directly or indirectly through blood pressure reduction or myocardial ischemia, which may be evoked by dipyridamole infusion and represent two recognized sympathetic stimuli. Twenty patients were studied with infusion combined with two-dimensional echocardiography and 12-lead ECG monitoring. Blood pressure was recorded each minute by a cuff sphygmomanometer. In all patients, we obtained venous blood samples for epinephrine (an index of adrenomedullary catecholamine release) and norepinephrine (an index of neuronal activity) both in resting conditions and at peak dipyridamole, ie, at the first minute after termination of dipyridamole infusion in negative cases or in the presence of obvious ischemia in positive cases (ie, as soon as a regional ventricular dyssynergy or an ST segment depression greater than 0.1 mV appeared). Epinephrine and norepinephrine determinations were made by a high performance liquid chromatography (HPLC) method. After dipyridamole, there was a significant rise in norepinephrine, while epinephrine did not change significantly. Dipyridamole-induced percentage variations of norepinephrine from baseline were not significantly correlated with mean blood pressure changes (r = .1, p = ns) and were of a similar extent in patients with (n = 10) and without (n = 10) dipyridamole-induced ischemia (+68 vs +73 percent, p = ns). Dipyridamole administration provokes an activation of sympathetic tone which can be detected even in the absence of myocardial ischemia and is not related to blood pressure changes. The increased catecholamine release appears to be of neuronal rather than adrenomedullary origin.
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PMID:Activation of sympathetic tone during dipyridamole test. 164 30

A transdermal nitroglycerin (TNG) patch (10 mg.24 h-1), using a daily overnight 8-h free interval, was assessed by means of a multicentre trial in 96 elderly patients with stable angina (age greater than or equal to 65 years). The main entry requirement was a reproducible exercise-induced ST depression (greater than or equal to 1 mm) appearing at a load of 60 to 90 W, during an incremental bicycle ergometer test (10 W.min-1). During the study only one other antianginal drug and sublingual TNG tablets were allowed. The protocol consisted of a run-in period (mean 10 days), followed by a double-blind, randomized, parallel, placebo-controlled 28-day phase and a single-blind active treatment phase of the same duration. The exercise test parameters, the number of spontaneous anginal attacks and any unwanted effects were evaluated at the end of every study phase. In the double-blind phase, no ergometric values changed with placebo while transdermal TNG significantly improved total workload and double product by 36.4% and 7.7% at the maximal workload respectively and by 49.8% and 13.5% at the time to onset of 1 mm ST depression respectively and reduced ST depression (-58.8%) at the equivalent baseline workload. Anginal attacks decreased by 61.5% and 30.8% with TNG patch and placebo respectively. A similar trend was seen at the end of the single-blind active treatment period in patients who had received placebo in the double-blind phase. Nine patients failed to complete the study; six for unwanted effects (four in the active group and two in the placebo group) and three for other reasons.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Discontinuous transdermal nitroglycerin as treatment for stable angina in the elderly: a double-blind multicentre study. The Transdermal TNG Trial Group of Istituto Nazionale Ricovero e Cura Anziani (I.N.R.C.A.). 178 32

To examine the incidence of arrhythmias in dipyridamole infusion and the relation between dipyridamole-induced arrhythmias and ST-segment depression, dipyridamole electrocardiography tests were performed on 100 patients with coronary artery disease. Dipyridamole was infused at a rate of 0.568 mg/kg for 4 min, and 87-lead body surface mapping was performed to determine ischemic ST-segment depression. Positive ischemic response was defined as greater than or equal to 0.10 mV horizontal or downsloping ST-segment depression below the baseline, lasting 80 msec after the J point. Arrhythmias were observed by continuous electrocardiographic monitoring using a CM-5 lead electrocardiography. With respect to ventricular premature contractions (VPC), a group of patients with previous myocardial infarction (MI group) had a significantly higher incidence than a group of patients without previous myocardial infarction (non-MI group) before (16.7% vs. 1.7%, p less than 0.01) and after (38.1% vs. 3.4%, p less than 0.005) the dipyridamole infusion. The incidence of supraventricular premature contractions (SVPC), however, was not significantly different between the MI and non-MI groups. A group of patients with positive ischemic response had a significantly higher incidence of SVPC after the dipyridamole infusion than a group of patients with negative ischemic response (p less than 0.005). However, there was no significant difference in the incidence of VPC between the negative and positive ischemic response groups. These results suggest that dipyridamole-induced VPC is not always associated with ischemic ST-segment depression, but dipyridamole-induced SVPC is associated with dipyridamole-induced ischemic ST-segment depression in patients with coronary artery disease.
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PMID:Relation between the incidence of arrhythmias and ischemic ST-segment depression during dipyridamole electrocardiography test in patients with coronary artery disease. 181 Oct 84

Atrial natriuretic factor (ANF) release is modulated by several haemodynamic factors, including ventricular and atrial wall stretch. Dipyridamole infusion, which is commonly used as a pharmacological stressor in patients with coronary artery disease, can acutely increase ventricular and atrial pressure via myocardial ischaemia. The aim of this study was to assess whether dipyridamole infusion (up to 0.84 mg kg-1 over 10') can affect ANF release in man. Nineteen patients (13 men, 6 women) with a history of chest pain were studied. Their drug regimen was interrupted and instead they were administered a dipyridamole infusion, combined with two-dimensional echocardiography and 12-lead ECG monitoring. Plasma ANF was measured by RIA while the patients rested, and after dipyridamole infusion. Eight patients had no evidence of myocardial ischaemia, as measured by electrocardiographic and/or echocardiographic criteria, during dipyridamole infusion: among them, ANF values were similar while they were at rest and at peak dipyridamole administration (23.9 +/- 9.5 vs 23.4 +/- 6.9 pg ml-1, P = ns). Eleven patients had dipyridamole-induced transient ischaemia (regional ventricular dyssynergy and/or ST segment depression): among them, ANF values rose significantly at peak dipyridamole administration (31.8 +/- 13.8 vs 65.5 +/- 36.4, P less than 0.01). We conclude that dipyridamole infusion does not increase ANF release in man in the absence of ischaemia. The induction of myocardial ischaemia acutely increases ANF release, probably through a rise in ventricular and atrial wall stress.
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PMID:Dipyridamole-induced myocardial ischaemia increases ANF release in man. 183 May 52

Doppler assessment of left ventricular filling and ejection during dipyridamole stress may supplement wall motion analysis for detection of myocardial ischemia and coronary artery disease (CAD). Thirty-four patients taking no cardioactive therapy were studied using intravenous dipyridamole (0.6 mg/kg) during 2-dimensional and pulsed Doppler echocardiography. Twelve patients had normal coronary arteries (group 1) and the remainder, who had significant CAD, were divided into groups 2 (n = 11) and 3 (n = 11). Only subjects in group 2 developed myocardial ischemia manifest as reversible regional asynergy and ST-segment depression. Heart rate increased (16 +/- 9 beats/min, p less than 0.01) and mean blood pressure decreased (-5 +/- 8 mm Hg, p = not significant) uniformly across groups. Exaggerated hyperkinesia of normally contracting wall segments was the common response to dipyridamole infusion in patients with CAD. The respective mean percent changes in peak early diastolic velocity, peak atrial velocity, their ratio and ejection peak velocity, and mean acceleration for groups 1 (20, 42, -13, 20 and 23%), 2 (22, 32, -2, 10 and 14%) and 3 (23, 33, -6, 16 and 18%) were similar. Comparisons between normal patients and those with CAD and between groups 2 and 3 revealed no significant differences in the effect of dipyridamole on any variable. However, a decrease in both peak velocity and mean acceleration of left ventricular ejection was seen in 3 of 4 group 2 patients who developed severe ischemia. Dipyridamole-Doppler echocardiography is insensitive for detection of CAD and appears unable to identify myocardial ischemia unless this is severe. Hemodynamic changes and compensatory wall motion induced by dipyridamole may explain these findings.
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PMID:Evaluation of dipyridamole-Doppler echocardiography for detection of myocardial ischemia and coronary artery disease. 187 75

Dipyridamole echocardiography testing is a highly feasible, inexpensive, and safe diagnostic tool, with excellent specificity and good sensitivity--especially in patients with multivessel disease and/or resting dyssynergy--for the diagnosis of coronary artery disease. The test does not offer an "all or none" binary result but rather a complex stratification of the ischemic response along the coordinates of time and space, accurately identifying the degree of physiological impairment of coronary reserve, the severity and extent of coronary disease, the geographic location of the area at risk, and the prognostic outlook. It offers highly competitive diagnostic information versus more sophisticated, time-consuming, and costly radionuclide techniques; in comparison with other stress echocardiography techniques, it is more feasible than exercise and less invasive and better tolerated than pacing. The electrocardiogram usefully integrates the information provided by the mechanical marker of ischemia during dipyridamole testing. The finding of echocardiographically silent ST segment depression represents a clue to the identification of angiographically normal coronary arteries. On the basis of this evidence, dipyridamole testing with two-dimensional echocardiography and 12-lead electrocardiography can be considered a reasonable choice for the exercise-independent diagnosis of coronary artery disease.
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PMID:Dipyridamole echocardiography. A new diagnostic window on coronary artery disease. 202 42

Dipyridamole thallium-201 scintigraphy (DP-Tl) and coronary angiography were studied on 74 patients with suspected coronary artery disease. We compared the clinical features, hemodynamic responses, angiographic results and scintigraphic findings of patients who had chest pain during DP-Tl testing ('chest pain' group) with those of patients who did not have chest pain ('no pain' group). Thirty eight (51%) of the 74 patients developed chest pain. Heart rate and rate pressure product during DP infusion of 'chest pain' group were greater than those of the 'no pain' group (p less than 0.05). Ischemic ST depression was more frequently observed among 'chest pain' patients (p less than 0.01). There were no differences in angiographic severity of coronary artery disease between 'chest pain' and 'no pain' group. Also, we could find no differences in extent and severity scores of perfusion defects and washout abnormalities between the two groups. However, when patients with myocardial infarction were excluded, the 'chest pain' group had significantly greater extent and severity scores of washout abnormalities than the 'no pain' group (extent score: 38 +/- 8 vs 18 +/- 5, p less than 0.05, severity score: 55 +/- 15 vs 18 +/- 7, p less than 0.01). Our study indicated that in patients without myocardial infarction, patients with 'chest pain' had more severe ischemia than 'no pain' patients. But in patients with myocardial infarction, myocardial ischemia not accompanied by chest pain might be as severe as that with chest pain. The presence or absence of myocardial infarction might have great influence on results regarding the relation of chest pain to myocardial ischemia.
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PMID:The relationship between chest pain during thallium-201 scintigraphy with dipyridamole and myocardial ischemia. 206 96

Episodes of transient myocardial ischemia during ambulatory activities are common in patients with stable coronary artery disease and who are often asymptomatic. Selection of therapy for episodes of asymptomatic ischemia is limited by a lack of direct comparative studies. To determine the most effective monotherapy for patients with stable angina and a high frequency of asymptomatic ischemic episodes, propranolol-LA (mean daily dose, 293 mg), diltiazem-SR (mean daily dose, 350 mg), nifedipine (mean daily dose, 79 mg) were each compared with placebo, each for 2 weeks, in a randomized, double-blinded, crossover trial. Entry criteria were a positive exercise treadmill test during placebo therapy characterized by 1.0 mm or more ST segment depression and angina pectoris, and six or more episodes of transient ST segment depression of 1.0 mm or more on a 48-hour ambulatory electrocardiogram. One hundred ninety-four patients were screened, 63 were eligible and received randomized therapy, of which 56 patients completed at least two of the four treatment periods and were included in an intent-to-treat analysis. Fifty patients completed all four treatment phases and were included in the protocol-completed analysis. Anti-ischemia efficacy was assessed by 48-hour ambulatory electrocardiographic monitoring, exercise treadmill tests, and anginal diaries. Ninety-four percent of all episodes of ambulatory ischemia were asymptomatic. Compared with placebo, only propranolol was associated with a marked reduction in all manifestations of asymptomatic ischemia during ambulatory electrocardiographic monitoring (2.3 versus 1.0 episodes/24 hr; mean duration of ischemia per 24 hours, 43.6 versus 5.7 minutes; both p less than 0.0001). Diltiazem's reduction of the frequency of episodes compared with placebo (2.3 versus 1.9 episodes/24 hr) was associated with a trend (p = 0.08) in the protocol-completed analysis and with a significant reduction in the intent-to-treat analysis (p = 0.03). Nifedipine had no significant effect on any measured variable of ambulatory ischemia. The dosages of medication used may have been excessive for some patients, and a more beneficial effect may have been evident at a lower dose. In contrast to the marked effects of the active agents on ambulatory asymptomatic ischemia, the effects on exercise performance and angina pectoris were slight. The active agents modestly improved treadmill exercise duration time until 1 mm ST segment depression (3%), and only propranolol and diltiazem had significant effects. Only diltiazem significantly prolonged the total exercise time. Anginal frequency was significantly decreased by both propranolol and diltiazem.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Comparison of propranolol, diltiazem, and nifedipine in the treatment of ambulatory ischemia in patients with stable angina. Differential effects on ambulatory ischemia, exercise performance, and anginal symptoms. The ASIS Study Group. 224 50


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