Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been suggested that a generalized coronary vasomotion disorder is present in variant angina and that evaluation of baseline coronary artery tone may be useful for predicting the occurrence of coronary artery spasm. The vasomotor response of angiographically normal proximal and distal coronary artery segments was studied in 9 patients with atypical chest pain and normal coronary arteriograms (control group), 13 patients with active variant angina and 41 patients with chronic stable angina. Ergonovine (intravenous, 100 to 300 micrograms, or intracoronary, 8 to 20 micrograms, was administered to all 22 patients in the control and variant angina groups and to 11 of the 41 patients with chronic stable angina. All patients also received intracoronary isosorbide dinitrate (1 to 2 mg). Computerized coronary artery diameter measurement of angiographically normal segments was carried out before and after ergonovine and nitrate administration. Mean baseline intraluminal diameter of proximal and distal coronary segments was not significantly different in control patients and those with variant angina (nonspastic segments only) or coronary artery disease (proximal 2.89 +/- 0.15, 2.83 +/- 0.14 and 2.82 +/- 0.09 mm; distal 1.60 +/- 0.08, 1.63 +/- 0.07 and 1.62 +/- 0.06 mm, respectively). After ergonovine, proximal segments constricted by 10 +/- 2%, 15 +/- 3% and 11 +/- 4% and distal segments by 11 +/- 3%, 11 +/- 2% and 14 +/- 3% in control, variant angina and coronary artery disease groups, respectively (p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of epicardial coronary artery tone and reactivity in Prinzmetal's variant angina and chronic stable angina pectoris. 200 3

Twenty-four patients were randomized to a double-blind, triple placebo controlled, latin square protocol to examine the relative efficacy of propranolol or diltiazem given as monotherapy or in combination with isosorbide dinitrate. Treatment phases were preceded and followed by placebo control periods. At the end of each phase, symptom-limited treadmill exercise stress tests were performed, as well as rest and exercise radionuclide ventriculography. Both forms of monotherapy were effective in reducing episodes of angina and nitroglycerin use, and in improving exercise tolerance. Diltiazem monotherapy was associated with slightly higher treadmill times (509.9 +/- 123 s) compared to propranolol (462.7 +/- 131 s, P less than 0.05). The addition of isosorbide dinitrate to either form of monotherapy allowed no further improvement in any of the measured clinical responses. Radionuclide ventriculography showed no significant difference in resting left ventricular function. The addition of isosorbide dinitrate to propranolol showed a reduction in end diastolic volume in keeping with a reduction in preload. In response to exercise, stress-induced left ventricular dysfunction was equal in all groups except for the diltiazem-nitrate combination, which was associated with a higher ejection fraction (56.2 +/- 8.6%) compared to monotherapy (52.6 +/- 10.9%, P less than 0.01). A higher cardiac output could be achieved in the groups treated with diltiazem; this was related to increased heart rate and maintenance of stroke volume. It was concluded that diltiazem is equally effective as propranolol for the treatment of chronic stable angina and, in terms of exercise capacity and cardiac output, superior to beta-blockade. The addition of isosorbide dinitrate appears to impart no overt benefits, but some evidence suggests a reduction in left ventricular decompensation in the face of stress.
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PMID:Clinical response and effects on left ventricular function of isosorbide dinitrate added to propranolol or diltiazem monotherapy in patients with chronic stable angina. 204 86

Following a one-week placebo-controlled washout phase, 24 patients with stable angina pectoris (ST segment depression under ergometric exercise greater than or equal to 0.2 mV) were monitored and randomized to three months treatment with 1 x 10 mg nisoldipine/day or 3 x 60 mg diltiazem/day. Ergometries were performed 2 hours after administration of the first medication, and after 6 weeks and 3 months of treatment. Other parameters were the weekly incidence of angina pectoris attacks, and nitrate consumption, as well as laboratory tests prior to and at the end of treatment. Resting blood pressure and heart rate were only marginally influenced by both medications. The rate-pressure product at maximum ergometric load decreased by about 6% under both nisoldipine and diltiazem. The ST segment depression at maximum work load decreased under nisoldipine by approximately 75% (from 0.27 to 0.07 mV), and under diltiazem by about 55% (from 0.28 to 0.13 mV; p less than or equal to 0.01). In the nisoldipine and diltiazem groups, the number of weekly angina pectoris attacks decreased from an initial 3.4 and 3.3, respectively, to 0.16 and 1.0, respectively, after 6 weeks, and 0.14 and 0.9, respectively, after 3 months' treatment (p less than or equal to 0.01). The weekly consumption of nitrate decreased accordingly. The present data show that, in particular during long-term treatment of angina pectoris, the once-daily dose of 10 mg nisoldipine is superior to diltiazem 3 x 60 mg/day.
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PMID:[Nisoldipine in stable angina pectoris. Efficacy and tolerance in comparison with diltiazem]. 207 Oct 85

The significance of U-wave inversion during coronary arterial spasm was investigated in 188 consecutive ergometric tests performed in 69 patients. All patients had previously undergone coronary arteriography which had clearly shown coronary spasm either at rest or after a single 0.4 mg injection of ergometrine. The ergometrine tests were then performed at the patient's bedside using a standard protocol with injection of incremental doses of ergometrine: 0.05, 0.1, 0.2 and 0.4 mg every 5 minutes with 12-lead ECG recordings every minute. Fifty of the 59 patients with positive tests had classical signs of spasms: ST elevation or depression and/or T wave inversion; the other 9 patients had inversion of the U wave alone (2 cases) or associated with classical ST segment changes in the remaining cases. The 10 other patients had no ECG changes although 2 of them suffered typical anginal pain. Negative U waves were observed in 4 of the 12 patients with spasm of the left anterior descending artery, accompanied by ST elevation in the anterior wall leads. A negative U wave would appear to be a sign of less ischaemia than the classical ECG changes because anginal pain is less common: 4 out of 9 cases in which U wave inversion was a very early change, 8 out of 9 cases in which it was the first or only abnormality. The recognition of a negative U wave increases the sensitivity of the electrocardiogram during resting angina and allows earlier treatment of coronary spasm with nitrate derivatives after an ergometrine test.
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PMID:[Value of negative U waves in coronary artery spasm]. 210 54

The organic nitrates are effective agents in the management of patients with angina pectoris. They are the agents of choice in the treatment of acute episodes of angina pectoris and are useful in angina prophylaxis. While the organic nitrates are extremely effective in angina prophylaxis during acute therapy, there is increasing evidence that with many dosing regimens for oral and transdermal therapy, substantial attenuation of the antianginal effects develops. Thus, during acute therapy the organic nitrates improve exercise tolerance for many hours, but during sustained therapy designed to provide antianginal efficacy throughout the 24-h period there is significant attenuation of the beneficial effects. It has been documented that treatment regimens designed to provide a period of nitrate washout prevent or reverse nitrate tolerance, and such changes in dosing regimens have been shown to provide continued antianginal protection. It is clear that the objective of providing 24-h antianginal protection with the organic nitrates cannot be achieved. With appropriate dosing schedules, however, it is possible to improve exercise tolerance throughout the major portion of the 24-h dosing period.
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PMID:Nitrate tolerance. A problem during continuous nitrate administration. 211 1

Nitrates are highly effective both in terminating acute attacks of angina pectoris and in the prophylaxis of symptomatic and asymptomatic myocardial ischemia. Preload reduction by venodilatation is the prevailing mechanism of nitrates in patients with chronic stable angina and is the unique feature distinguishing them from beta and calcium-channel blockers. Nitrates dilate coronary arteries not only in pre- and poststenotic vessels, but also in eccentric lesions. In patients with endothelial dysfunction, nitrates seem to be the physiological substitute for endothelium-derived relaxing factor. During the past decade, however, there has been substantial evidence of a clinically relevant loss of the anti-ischemic effects ("nitrate tolerance"). Many studies with oral dosing of isosorbide dinitrate or isosorbide-5-mononitrate at least three times daily have proven nitrate tolerance in patients with coronary artery disease and/or congestive heart failure. Complete loss of anti-ischemic effects after repetitive, continuous patch attachments has also been found. As we first showed in 1983, intermittent therapy with once-daily ingestion of high-dose sustained-release isosorbide dinitrate was successful in preventing the development of tolerance. Similarly, tolerance to isosorbide-5-mononitrate also does not develop when it is ingested once daily. It is now generally accepted that a daily low-nitrate interval is required to prevent tolerance development. Although the minimal patch-free interval required to prevent tolerance needs further investigation, a 12-h patch-free interval should prevent tolerance in most patients. The prolonged duration of action of once-daily high-dosage administration of sustained-release formulations, the improved patient compliance with a single daily administration, and the increased likelihood of maximal anti-ischemic effects are important reasons for recommending high single daily doses of isosorbide dinitrate or isosorbide-5-mononitrate.
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PMID:Nitrates: why and how should they be used today? Current status of the clinical usefulness of nitroglycerin, isosorbide dinitrate and isosorbide-5-mononitrate. 211 3

In recent years, concern has been expressed over attenuation of therapeutic effect in patients receiving continuous nitroglycerin therapy for the treatment of angina. Studies have shown that exercise tolerance time does not improve with continuous nitroglycerin regimens, although the frequency of anginal attacks may decrease. Intermittent therapy, which incorporates a nitrate-free interval, improves both exercise time and clinical angina. The optimal duration of the nitrate-free interval has yet to be determined. Future research is likely to focus more on supply-side factors in angina. Of the available antianginal drugs, nitrates have been shown to be highly effective coronary vasodilators, particularly in areas of stenosis.
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PMID:Angina: evolution of the role of nitrates. 211 46

The 24-hour application of transdermal nitrate patches has been associated with rapid development of therapeutic tolerance. Recent reports suggest maintenance of clinical benefit by introducing a daily patch-free period. This study investigates, by means of serial treadmill testing, the efficacy of a new transdermal delivery system when used with an eight hour patch-free period in 16 subjects with chronic stable angina. Concomitant antianginal therapy was permitted. After demonstration of exercise test reproducibility and nitrate responsiveness, subjects entered a double-blind randomised placebo-controlled crossover trial comprising one week of active nitroglycerin patches (10mg/24hrs) and one week of an identical placebo patch. Exercise tests were conducted four hours after patch application on the last day of each of the treatment arms. Daily angina frequency and nitroglycerin consumption were also monitored. There was significant improvement in total exercise duration (16.5%), time to onset of angina (26%), time to 1mm ST depression (22%), and peak heart rate blood pressure product with active patch application. Angina frequency was reduced during the week of active therapy. These results demonstrate the additional efficacy of intermittent transdermal nitroglycerin in a group of subjects with continuing angina despite therapy with beta-blockers and calcium antagonists.
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PMID:Clinical benefit of transdermal glyceryl trinitrate when used with an eight hour patch-free period. 212 27

Sixty one patients with exercise-induced angina were examined. The development of sustac forte tolerance was found to be related to lower levels of phosphatidylserine and phosphatidylethanolamine in erythrocyte membranes. The changes in the phospholipid composition of cell membranes were demonstrated to be largely caused by the effects of prolonged nitrates themselves. Essential given to patients with exercise-induced angina who were tolerant to the nitrates elevated the levels of phosphatidylserine and phosphatidylethanolamine in the erythrocyte membranes, which was accompanied in most cases by higher exercise tolerance as evidenced by a repeated bicycle ergometric test when the same dose of sustac forte was used. This allows the authors to recommend to use essential to abolish prolonged nitrate tolerance.
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PMID:[Significance of changes in phospholipid condition of cell membranes in the development of tolerance to long-acting nitrates in patients with exercise-induced angina pectoris]. 212 63

Nitroglycerin (glyceryl trinitrate) has been used for many years via the sublingual route for treating acute anginal attacks. In recent years transdermal delivery of nitroglycerin has gained popularity for prophylaxis against angina. However, nitrate tolerance appears to be a therapeutic problem with all long-acting nitrates regardless of delivery mechanism, and it occurs in most patients with stable angina treated with continuous 24-hour application of nitroglycerin patches. Since continuous 24-hour plasma concentrations of nitroglycerin do not appear to be desirable, alternative approaches to therapy are needed. A simple method to minimise tolerance with transdermal nitroglycerin patches is to remove the patch at bedtime and reapply a new patch in the morning. Such intermittent therapy allows a patch-free period during the night, when most patients experience few angina attacks, but optimises nitrate sensitivity during the daytime. However, the place of intermittent nitroglycerin patch therapy in the treatment of stable angina needs clarification with further study, particularly comparisons with other long-acting forms of nitrates. There are insufficient data to recommend the use of transdermal nitroglycerin patches in the treatment of patients with unstable angina or congestive heart failure. In conclusion, transdermal nitroglycerin patches offer a convenient and cosmetically acceptable dosage form which has potential use in stable angina if administered as an intermittent regimen providing a patch-free period each night.
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PMID:Transdermal nitroglycerin (glyceryl trinitrate). A review of its pharmacology and therapeutic use. 212 41


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