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)

Continuous therapy with nitrates rapidly produces tolerance along with loss or diminution of circulatory, antianginal, and anti-ischemic effects. Development of tolerance can be avoided by various approaches. In patients with stable angina, intermittent use of nitrates with long nitrate-free intervals, use of transdermal nitroglycerin during the day or oral isosorbide dinitrate or isosorbide-5-mononitrate twice daily in the morning and early afternoon, and intermittent use of nitrates in combination with another class of antianginal agent are appropriate. In patients with unstable angina, continuous therapy with intravenous nitroglycerin is recommended during the acute phase of angina. Despite development of partial tolerance, oral isosorbide dinitrate, 30 to 60 mg four times a day, plus hydralazine may be useful for patients with congestive heart failure who cannot tolerate angiotensin-converting enzyme inhibitors. Concomitant use of sulfhydryl donors or angiotensin-converting enzyme inhibitors, agents that might theoretically prevent nitrate tolerance, is not recommended. Data on these agents are conflicting, and added costs and adverse effects are likely to preclude their use in the future.
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PMID:Nitrate tolerance. How to prevent it or minimize its effect. 156 Nov 69

Nitrates have been used for the last 130 years to treat and control the symptoms of angina pectoris. Within the last 15 years, nitrates also have been shown to limit infarct size and to be beneficial in the treatment of patients with severe intractable heart failure, cardiogenic shock, severe mitral and aortic regurgitation, hypertensive episodes, and portal hypertension. The adequate use of nitrates to treat these disorders requires the ability to document a hemodynamic response and to closely monitor the adverse consequences of this therapy. Nitrates work by directly relaxing smooth muscle in resistance and capacitance vessels, thereby causing generalized dilation. Nitrates reduce preload and, at higher doses, reduce systemic vascular resistance and afterload. This chapter reviews the physiologic mechanisms that underlie nitrate therapy, the appropriate indications for nitrate use, the usefulness of specific agents, and their appropriate nursing implications.
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PMID:Nitrates. 157 38

The hemodynamics influencing effect of Nitromint sublingual tablet and aerosol (EGIS Pharmaceuticals) has been examined in 22 ischaemic heart disease patients during heart catheterisation. The patients were hospitalized and took also the earlier prescribed drugs. On the basis of the results of examinations it may be concluded that Nitromint aerosol has a therapeutic action comparable to other short-acting nitrate preparations such as sublingual nitroglycerin tablet. According to the observations of the patients the drug action develops within a significantly shorter period. Considering the type of side-effects there was no difference between the two drug forms. Primarily, Nitromint tablet caused systemic effects (headache, dizziness, throbbing head) while aerosol caused predominantly local symptoms (burning of the tongue, disagreeable taste). These effects were only temporary and ceased within 10 minutes. According to the above described observations Nitromint aerosol may successfully be used as a new nitroglycerin containing drug form in all forms of angina pectoris: in rest angina, effort angina, as a prophylaxis, in mixed type angina pectoris, as a first-aid in emergency cases in acute left heart failure, preceding the application of infusion.
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PMID:Comparative haemodynamic examination of Nitromint (sublingual tablet and aerosol). 158 77

The magnitude of tolerance to the anti-anginal efficacy of transdermal nitroglycerin and the efficacy and safety of short (4 h) and long (10 h) nitrate-free intervals for its prevention, were investigated in a randomized, double-blind, placebo-controlled crossover trial of 4 week-long treatment regimens: placebo, continuous therapy with a 50 mg patch (10 mg.24 h-1), and 4 h and 10 h nitrate-free periods. Only patients showing greater than 1 min increase in time to 1 mm ST depression after acute patch administration were eligible. Twelve men completed the study. One other anti-anginal medication (a beta-blocker in nine and calcium antagonist in two) was permitted in a constant dose throughout the study. Patients underwent exercise testing on days 1 and 7 of each treatment period, and 24 h ambulatory ECG monitoring on day 6. Compared to placebo, transdermal nitroglycerin on day 1 significantly improved time to 1 mm ST depression by 35%, and time to angina, exercise duration and maximal workload by 21%, 13% and 9% respectively. These improvements were totally lost after 7 days' continuous therapy, but completely maintained by a 10 h nitrate-free period (improvements of 35%, 25%, 16% and 11% respectively) but not by a 4 h nitrate-free period (non-significant improvements of 15%, 2%, 4% and 1% respectively). The differences between 10 and 4 h nitrate-free were significant for each end-point. Neither duration of ambulatory ischaemia, nor the proportion of patients experiencing greater than or equal to 5 min ischaemia during the scheduled nitrate-free interval differed between treatments.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Efficacy, safety and duration of nitrate-free interval to prevent tolerance to transdermal nitroglycerin in effort angina. 161 12

To avoid the development of nitrate tolerance secondary to relatively constant elevated plasma nitrate concentrations, intermittent nitrate dosing has been advocated. However, a nitrate-free interval may induce a rebound increase in myocardial ischaemia, and thus increase anginal symptoms during the latter portion of the dosing interval. This was suggested by the results of recent studies in which nitroglycerin patches were administered intermittently with a 12 h nitrate-free interval. The present investigation was carried out to determine whether a controlled-release formulation of 60 mg isosorbide-5-mononitrate (5-ISMN) would produce such a rebound phenomenon. Seventy-nine patients, who had participated in four crossover, placebo-controlled studies in which the treatment arms lasted for between 1 and 2 weeks, were reviewed. These studies had assessed the efficacy of this nitrate preparation by exercise testing and each had included exercise testing at the end of each treatment phase, 24 h after the last medication had been administered. There were no differences noted in the time to onset of angina, the time to onset of 1 mm ST segment depression or the total exercise duration between the two treatment phases, indicating an absence of rebound phenomena at the end of the dosing interval. The reason for the absence of a detectable pre-dose rebound is unclear, but the plasma concentration profile of 5-ISMN produced by the presently used preparation, resulting in a nitrate-low instead of nitrate-free interval, may have contributed.
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PMID:Absence of pre-dose rebound phenomena with once daily 5-ISMN in a controlled-release formulation. 162 73

"Trough" plasma concentrations of isosorbide-5-mononitrate (IS-5-MN), an active metabolite of isosorbide dinitrate, of less than 95 ng/ml are considered necessary to prevent development of tolerance to isosorbide dinitrate and IS-5-MN. In a double-blind, crossover, placebo-controlled study, the effects of IS-5-MN during twice daily eccentric therapy were evaluated in 18 patients with reproducible exercise-induced angina who were nitrate responders. In a random order, patients received either placebo or IS-5-MN (20 mg) at 8 a.m. and 2 p.m. for 1 week each. Average trough plasma IS-5-MN concentrations before the 8 a.m. and 2 p.m. doses were 67 and 226 ng/ml, respectively, and increased to 382 and 488 ng/ml 2 hours after the 8 a.m. and 2 p.m. doses, respectively. Despite a more than threefold higher trough plasma IS-5-MN concentration before the 2 p.m. dose than before the 8 a.m. dose, the increase in exercise duration 2 hours after the doses was similar (1.21 minutes [21%] after 8 a.m. dose, and 1.08 minutes [19%] after 2 p.m. dose). These increases in exercise duration after IS-5-MN were significantly (p less than 0.01) greater than those observed after placebo (0.17 minutes [3%] after 8 a.m. dose, and -0.05 minute [-0.5%] after 2 p.m. dose). Reduction in standing systolic blood pressure at 2 hours after the doses was also nearly identical after the 8 a.m. and 2 p.m. doses of IS-5-MN (21 [15%] and 19 [14%] mm Hg, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of 8:00 a.m. and 2:00 p.m. doses of isosorbide-5-mononitrate during twice-daily therapy in stable angina pectoris. 163 90

1. Nitrates have a place in the prophylactic treatment of patients with angina pectoris. Their efficacy is not in doubt. 2. However, there may be some practical problems associated with their use, such as unreliable absorption, short duration of action, treatment-induced headache, development of nitrate tolerance and a suggested rebound phenomenon observed during intermittent dosing. Furthermore, patient convenience with treatment schedule and patient compliance have to be considered during prophylactic treatment. The present article discusses how many of these problems may be solved by selection of formulation as well as nitrate compound. 3. The development of controlled-release formulations producing sufficiently high nitrate plasma concentration during part of the day followed by nitrate-poor rather than nitrate-free interval, have the potential to prevent both nitrate tolerance and rebound phenomenon, and produce a sufficiently long duration of action with a convenient once daily regimen.
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PMID:Prophylactic nitrate therapy in angina pectoris--is there an optimal treatment regimen? 163 74

Unstable angina is a term which encompasses several clinical syndromes (crescendo angina, angina de novo, resting angina, postinfarction angina), intermediary between stable angina and myocardial infarction. The results of coronary angioscopy have allowed differentiation of accelerated effort angina which seems related to ulceration of an atheromatous plaque from resting angina, more commonly associated with intraluminal thrombosis. The diagnosis of unstable angina is clinical and justifies immediate hospital admission to a coronary care unit because of the risk of myocardial infarction and/or sudden death. Medical management comprises triple anti-ischemic therapy (nitrate derivatives, betablockers, calcium antagonists), anticoagulants and platelet antiagregants. Randomised therapeutic trials versus placebo have shown that this treatment decreases the incidence of refractory angina and myocardial infarction. Several studies are under way to assess the role of thrombolytic therapy in unstable angina. When unstable angina is refractory to maximal medical therapy, emergency coronary angiography should be performed. However the outcome is usually favourable and coronary angiography can be performed several days after the acute event. The coronary lesion responsible for unstable angina is often "complex", an eccentric, irregular, severe stenosis or appearances of thrombosis. Whenever possible, depending on the coronary lesion, myocardial revascularisation by coronary angioplasty or aorto-coronary bypass should be proposed. Surgical treatment has been shown to be more effective (symptomatic relief, improved survival) than medical therapy in patients with triple vessel disease. However, the results of studies comparing medical or surgical treatment with coronary angioplasty are not yet available.
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PMID:[Unstable angina: from physiopathology to therapeutics]. 167 84

The purpose of this study was to compare the efficacy of three standard antianginal agents, nitrate, Ca antagonist, and beta blocker on myocardial ischemia in patients with effort angina (EA) using ambulatory electrocardiographic monitoring (AEM). Forty-three patients, mean age 57 +/- 11 years, with positive exercise tests were studied. AEM was performed for 24-hours, initially with the patients off all antianginal medication and then after 1-2 weeks treatment with each agent. Antianginal drugs used were long-acting isosorbide dinitrate 40-80 mg/day for nitrate (17 patients), diltiazem 90-180 mg/day for Ca antagonist (13 patients), and propranolol 30-60 mg/day or metoprolol 60-120 mg/day for beta blocker (13 patients). The following results were obtained: 1) The severity of ischemia (total magnitude and duration of ST depression) was improved with each three agent. 2) Although the number of total ischemic episodes was reduced significantly with each three agent, the number of asymptomatic episodes was reduced significantly only with beta blocker. 3) Circadian variation of ischemic episodes displayed a pattern with a peak frequency in daytime. In addition, nitrate and Ca antagonist did not reduce ischemic episodes in daytime (especially asymptomatic episodes), while beta blocker reduced both symptomatic and asymptomatic episodes in daytime resulting in change in the pattern of circadian variation of ischemia. Thus, it was concluded that beta blocker was the most effective means of reducing myocardial ischemia, including silent ischemia, in patients with EA.
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PMID:[Comparative effect of anti-anginal drugs on myocardial ischemia in patient with effort angina: evaluation by ambulatory electrocardiographic monitoring]. 168 Jul 82

Many patients with angina pectoris whose symptoms are not completely controlled by beta-blockers are treated with several types of drugs, but it is not clear whether addition of a calcium-channel antagonist and/or a nitrate confers any advantage over beta-blockade alone. 18 patients receiving atenolol for stable angina pectoris completed a double-blind, randomised, crossover trial of atenolol treatment plus placebo, isosorbide mononitrate, nifedipine, and mononitrate and nifedipine (triple therapy). The patients were assessed subjectively and by treadmill exercise testing and 24 h ambulatory electrocardiographic recordings at the end of each 4-week treatment period. There were no significant differences among the treatment periods in angina attack rates, glyceryl trinitrate consumption, exercise duration to onset of angina or 1 mm ST depression, or duration of symptomless ischaemia. Total exercise duration was longer on atenolol plus mononitrate than on atenolol alone (mean difference 46 [95% confidence interval 18-88] s; p = 0.005), atenolol plus nifedipine (36 [2-71] s; p = 0.04), or triple therapy (28 [6-61] s; not significant). In 12 patients the exercise time was shorter on triple therapy than on atenolol plus mononitrate alone. Although "maximum" antianginal treatment with two or three drugs is commonly accepted, this approach confers no substantial advantage over optimum beta-blockade as monotherapy. If a second drug is needed, there is a slight advantage in favour of isosorbide mononitrate, but if this is not effective, treatment should be changed rather than added. Many patients with angina pectoris seem to be pharmacologically overtreated.
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PMID:Efficacy of nifedipine and isosorbide mononitrate in combination with atenolol in stable angina. 168 63


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