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

The role of medical treatment of patients who had resting nocturnal angina as well as exertional angina was investigate. The effects of atenolol 100 mg a day, nifedipine 20 mg three times a day, and isosorbide mononitrate 40 mg twice a day were investigated in a double blind, triple dummy randomised study. Nine patients with coronary artery disease, early positive exercise tests, and transient daytime and nocturnal ambulatory ST segment changes were initially assessed off all antianginal medication. They were then treated with each drug for three five day periods. Angina diaries were reviewed and maximal treadmill exercise tests and 48 hour ambulatory ST segment monitoring were performed at the end of each treatment period. Resting and exercise heart rate and blood pressure were significantly lower on atenolol than on either isosorbide mononitrate or nifedipine. The duration of exercise to 1 mm ST segment depression was significantly greater on atenolol than on isosorbide mononitrate. Only one patient had an improvement in exercise tolerance on nifedipine that was greater than the improvement on atenolol; this patient had single vessel disease. The total number and duration of episodes of ST segment change during ambulatory monitoring were significantly lower with atenolol than on either isosorbide mononitrate or nifedipine. Nocturnal ST segment changes were abolished in six patients on atenolol, in six patients on nifedipine, and in five patients on isosorbide mononitrate. When nocturnal ST segment changes occurred, their frequency was reduced with all three drugs. Pain was abolished in four patients on atenolol and pain relief was significantly better on atenolol than on isosorbide mononitrate. There was no significant difference in pain relief between isosorbide mononitrate and nifedipine. Thus beta receptor blockade with atenolol was the most effective means of reducing myocardial ischaemia both during exercise and at rest at night without causing deterioration in any patient. Nocturnal myocardial ischaemia in patients with severe coronary artery disease can be effectively treated with beta receptor antagonists and vasodilators.
 ...
PMID:Medical treatment of patients with severe exertional and rest angina: double blind comparison of beta blocker, calcium antagonist, and nitrate. 330 67

The newer dihydropyridine calcium antagonists are structurally related to nifedipine, but may provide greater vascular selectivity and wider clinical utility. Five new dihydropyridines-nisoldipine, nicardipine, nimodipine, felodipine and nitrendipine-are reviewed with regard to their preclinical pharmacology, haemodynamic effects and clinical indications. Nisoldipine is a potent arterial vasodilator with minimal electrophysiological and negative inotropic effects. Although data are still preliminary, the drug has shown some efficacy in both exertional angina and essential hypertension. The dosing interval is not yet clearly established, but may be twice daily. Utility in congestive heart failure awaits confirmation, but preliminary studies are promising. Nicardipine is an especially potent peripheral, cerebral and coronary arterial vasodilator that causes 10-fold less myocardial depression in animals than nifedipine, and may provide important cardioprotective effects during ischaemia. Human haemodynamic studies have confirmed nicardipine's lack of negative inotropism, its ability to reduce coronary and peripheral vascular resistance, and its lack of effect on cardiac conduction. Several controlled trials have documented its efficacy in exertional angina, vasospastic angina, and essential hypertension. Nicardipine's potential as an antiatherosclerotic agent is currently under investigation. Nimodipine is undergoing a unique clinical development programme aimed at cerebrovascular disorders. In almost all species, nimodipine selectively increases cerebral blood flow and reverses cerebral artery spasm without altering cerebral oxidative metabolism or systemic blood pressure. In humans, a large, double-blind, placebo-controlled trial in subarachnoid haemorrhage showed that nimodipine significantly reduced the severity of neurological deficits associated with delayed cerebral vasospasm. Several uncontrolled trials with larger numbers of patients support these results. Nimodipine has also proved useful in reducing cerebral artery spasm during intracranial surgery, and in the prophylactic treatment of migraine headaches. A preliminary study of nimodipine in acute stroke showed promising results in limiting neurological disability. Felodipine is a very potent systemic arterial vasodilator with negligible myocardial depressant activity. It is also a renal artery vasodilator. Unlike the other new dihydropyridines, felodipine prolongs the A-H interval on electrophysiological testing, but only to about 50% of that observed with verapamil. Felodipine is undergoing clinical trials in essential hypertension.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:'Second generation' dihydropyridine calcium antagonists. Greater vascular selectivity and some unique applications. 331 91

Regardless of the factor assumed responsible for precipitation of myocardial ischemia - varying from coronary occlusion in acute myocardial infarction to increased oxygen demand in exertional angina pectoris and reduced myocardial oxygen supply due to plaque rupture or changes in vasomotor tone in unstable angina - its incurrence may or may not be associated with pain. In the vast majority of cases, silent myocardial ischemia is observed in patients with established symptomatic coronary artery disease. Interindividual comparisons have not enabled reliable differentiation between those with painful and those with silent ischemia based on the anatomic extent of coronary artery disease, left ventricular function or previous myocardial infarction. Similarly, functional parameters such as exercise capacity, exercise duration, time to onset of ST-segment depression during exercise as well as heart rate and blood pressure both at rest and during exercise have failed to reveal differences between the symptomatic and the asymptomatic patients. Intraindividual differences have also been noted, but not consistently corroborated, and postulated as responsible for the fact that ischemia in a given patient alternates in its presence with and without pain. Since most patients with silent ischemia either have, or at some time in the past have experienced, painful ischemia, the integrity of the appropriate nervous system function can be assumed to be intact and neurocardiologic factors seem most likely to account for apparent discrepancies in pain perception. Prior to precipitation of pain, myocardial ischemia must elicit an adequate stimulus. According to some investigators, the adequate stimulus is that associated with a duration of the ischemic episode of at least three minutes and with increase in left ventricular filling pressure of more than 7 mm Hg. This threshold, consequently, represents a prerequisite but not invariably sufficient criteria for the occurrence of pain. The next step in the sequence of pain is generation of an action potential, that is, transduction by means of chemical or mechanical stimuli. During this process, a latency of 20 to 40 seconds is incurred such that the appearance of pain usually has its onset after derangement of relaxation and contraction, increased filling pressure and the observation of ECG changes. Through conduction, the information is forwarded to the central nervous system after coding of the details with regard to intensity. The intensity, in turn, is determined by the number of receptors (free nerve endings) in the field activated by the ischemic event.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:[Pathophysiology of painful and silent myocardial ischemia]. 332 3

To investigate the antianginal efficacy, duration of action and tolerability of 2 doses of the new calcium antagonist felodipine, 15 patients (14 men and 1 woman, mean age 62 years) with stable exertional angina pectoris and angiographically demonstrated coronary artery disease were randomly given felodipine, 5 and 10 mg, and placebo on 3 different days. A bicycle ergometer exercise test was performed 3 and 10 hours after dosing. In comparison with placebo, felodipine 5 and 10 mg significantly increased resting heart rate and decreased resting systolic and diastolic blood pressure 3 hours after administration (p less than 0.001). Ten hours after administration, only supine systolic blood pressure was still significantly lower (p less than 0.001). Anginal (time to mild chest pain) and ischemic (time to 1 mm ST depression) thresholds, as well as duration of exercise and total work at peak exercise, were higher in comparison with placebo at 3 and 10 hours (p less than 0.001). In comparison with the lower dose, 10 mg felodipine induced a decrease in supine (p less than 0.05) and sitting (p less than 0.01) systolic blood pressure at rest and an increase in total work to anginal threshold (p less than 0.01), as well as in total work and duration of exercise at peak exercise (p less than 0.05). These results suggest that a single administration of felodipine, 5 and 10 mg, may improve exercise capacity over a 10-hour period in patients with stable exercise-induced angina due to atherosclerotic heart disease.
 ...
PMID:Acute effects of felodipine in exertional angina pectoris. 335 31

The effectiveness and duration of the anti-anginal action of two sustained-release preparations, molsidomine (8 mg) and isosorbide dinitrate (20 mg), were assessed by means of serial exercise tests in 12 patients with angina of effort. The tests, which were limited by the symptoms, were carried out on three consecutive days using the Bruce protocol. Each patient was tested four times each day: the first test was performed before treatment and the others were carried out 1, 4 and 8 h after administration of the drug or placebo. One hour after administration of molsidomine, the appearance of signs of ischaemia in the ECG were considerably delayed and they were reduced in magnitude. Furthermore, the length of time during which the patients were free of angina increased. After 4 h both drugs significantly delayed the onset of angina and depression of the ST segment by 1 mm. The conclusion is that at the doses used both drugs prolong the length of time in which there is no angina, but that they have no significant effect at 8 h.
 ...
PMID:An assessment of single doses of 8 mg sustained-release molsidomine using serial exercise tests. 338 79

The aim of this study was to explore the capability of isosorbide dinitrate (ISDN) infusion to quench the 'hot phase' of unstable angina, a real cardiological emergency. Fifteen patients consecutively admitted to CCU because of angina at rest, with at least 4 ischaemic attacks per day, resistant to the usual therapy with oral and/or topical nitrates and calcium-antagonists, were included in the study. During ischaemia the electrocardiogram showed ST-segment elevation in 7 patients, ST-segment depression in 4, an alternation of ST-segment elevation and depression in 3 and pseudonormalization of a basally negative T wave in 1 patient. History of exertional angina with variable degrees of effort was reported in 6 patients and 9 had an old myocardial infarction. Coronary arteriography performed in 10 patients showed a significant stenosis of 1, 2 and 3 vessels in 5, 2 and 3 patients, respectively. ISDN infusion was started at 1.0 mg h-1, and was increased stepwise when persistence of ischaemic episodes had to be faced. The mean dosage infused was 3.5 mg h-1 (range 1.00-12). The mean duration of intravenous therapy was 8.3 days (range 2-25). Eleven of the 15 patients (73%) showed an effective decrease in the number of ischaemic episodes during ISDN infusion, as assessed by regression and variance analysis. After discharge (mean follow-up 59 months, range 2-96), 7 patients were free from ischaemic attacks, 3 underwent coronary by-pass surgery, 2 complained of some attacks and 3 died (2 because of sudden death three years after this study). In conclusion, ISDN infusion--individually tailored for dosage and duration--can be effective in 'cooling down' the storm of ischaemic episodes in unstable angina. An effective intravenous therapy with nitrates can represent, in some patients, a temporal remedy on the way to elective coronary bypass surgery and/or towards elective PTCA. Furthermore, in a sizeable number of patients with unstable angina, this approach can attain a complete abolishment of the ischaemic attacks.
 ...
PMID:Cooling down unstable angina with high dosage of isosorbide dinitrate (ISDN) continuously infused. 340 12

Variable threshold during exertion is a common feature in patients with chronic exertional angina. Changes in coronary vasomotor tone, when occurring at sites of critical narrowings, are a plausible explanation for variability of symptoms in these patients. However, the evidence supporting this hypothesis is still uncertain. Accordingly, we performed four computer assisted, multistage bicycle ergometer tests, without drugs, in 30 patients with chronic exertional angina, exercise induced ST depression, and a history of variable anginal threshold during exertion. Significant coronary artery disease was documented in each case by coronary arteriography. Patients were tested at the same time of day within a two week period. Comparison was made between each single test and the average of the remaining three. Time to 0.1 mV ST depression showed significant (+/- 20%) changes in 27 (90%) patients. Variability was shown in two out of four tests in 25 patients (83%), in three tests in 10 (33%), and in four tests in 2 (7%). Rate pressure product at 0.1 mV ST depression was concurrently changed (+/- 20%) in 20 patients (67%). Variability in two, three and four tests was observed in 7 (22%), 2 (7%) and 2 (7%) patients, respectively. Changes in time to 0.1 mV ST depression paralleled those in rate-pressure product at the onset of ischemia in 6 patients (22%) (dynamic ischemic threshold). Rate pressure product at 0.1 mV ST depression was unchanged despite variations in time to 0.1 mV ST depression in 10 patients (37%) (fixed ischemic threshold). The remaining 11 patients (41%) showed variable exercise tolerance associated with fixed (13 tests) and dynamic (13 tests) ischemic threshold.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Angina of effort with a variable threshold: a unique entity due to different mechanisms?]. 341 Feb 8

The safety and efficacy of a sustained-release preparation of diltiazem (diltiazem-SR), with dose levels of 240 and 360 mg/day, were assessed in 18 patients with stable angina of effort. A double-blind, placebo-controlled, randomized, crossover protocol was used. Diltiazem-SR, when given twice daily, reduced the frequency of weekly anginal attacks from 9.3 +/- 10.4 with placebo to 3.7 +/- 4.7 with 240 mg/day and to 3.1 +/- 4.7 with 360 mg/day (both p less than 0.01 compared with placebo). Treadmill time was increased from 410 +/- 180 seconds during the placebo phase to 519 +/- 177 seconds during the 240-mg/day dose and to 506 +/- 182 seconds during the 360-mg/day dose of diltiazem-SR (both p less than 0.01 compared with placebo). The time to the onset of angina and ischemic ST-segment depression were similarly prolonged by both doses of diltiazem-SR. The beneficial effects of diltiazem-SR appeared partly due to a reduction in the heart rate during submaximal exercise. Diltiazem-SR is effective and safe for the treatment of angina of effort when given twice daily.
 ...
PMID:Efficacy and safety of sustained-release diltiazem in stable angina pectoris. 351 May 25

The effects of placebo were studied in 150 patients (135 men, 15 women) aged 42 to 75 years with stable exertional angina pectoris, using multistage graded exercise testing. Treadmill exercise, using on-line computer analysis of the electrocardiogram, was performed after a basal period, during which time the patients had no treatment for 2 weeks, and after 2 weeks of placebo therapy. Mean exercise time during no treatment was 6.0 +/- 0.2 minutes and during placebo was 6.1 +/- 0.2 minutes (difference not significant). Similarly, time to development of 1 mm of ST-segment depression of 4.0 +/- 0.2 minutes without treatment was 4.1 +/- 0.2 minutes after 2 weeks of placebo therapy (difference not significant). Placebo failed to show any effect on rest or maximal heart rate or on maximal ST-segment depression. It also failed to increase exercise tolerance or to improve other objective indexes of effort-induced myocardial ischemia in both single-and double-blind protocols in patients with stable exertional angina pectoris. Therefore, placebo control of antianginal drug trials that use exercise testing for evaluation of effect is unnecessary and can be omitted.
 ...
PMID:Does placebo improve indexes of effort-induced myocardial ischemia? An objective study in 150 patients with chronic stable angina pectoris. 351 95

Five hundred and seventy coronary patients of both sexes, showing occasional attacks of angina of effort, were subjected to 24-hour ECG monitoring sessions at 1 week intervals during 1 month. Ischemic episodes were detected in 139 (24%) patients. A total of 362 ischemic episodes were already detected at the first ECG monitoring session, the majority of those (97%) being painless. Magnitude and duration of ST depression were similar in the absence of pain and during anginal attacks. Repeated sessions demonstrated considerable spontaneous variability in the frequency of ischemic episodes.
 ...
PMID:[Transitory changes in the ST interval of ischemic heart disease patients with stenocardia during 24-hour ECG monitoring]. 359 29


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>