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)

A cohort of 99 patients with severe, stable angina pectoris participated in a 26-week double-blind, between-patient trial of a transdermal therapeutic system (TTS) Nitroglycerin-TTS 5 mg/24 h and long-acting nitroglycerin tablets, 10.4 mg daily. The variables registered included daily sublingual nitroglycerin requirement, daily anginal attack rate, exercise test performance with ECG recordings, and a subjective patient evaluation on a visual analogue scale. There were no significant differences in the efficacy of the treatment between the two groups. Nor could we find any difference in the efficacy between the initial single-blind placebo treatment and the active nitroglycerin treatments.
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PMID:Comparison of nitroglycerin-TTS and long-acting nitroglycerin tablets in the treatment of angina pectoris: a double-blind controlled study. 311 67

Clinical efficacy of 5 mg per 24 hours transdermal nitroglycerin was studied in a placebo controlled, randomized, double-blind crossover trial, with three days wash-out period at the beginning, in 40 patients with chronic stable angina pectoris during two periods of 14 days. Assessment was carried out by means of a diary method, by the multistage treadmill exercise test, five hours after dosing, and by 24-hour ambulatory ECG recordings. Nitroglycerin patch demonstrated significant improvement of exercise tolerance comparing to placebo, in exercise time to the onset of angina pectoris and ST-segment depression of greater than or equal to 1.0 mm (+45% and +47%), in maximum walking time (+13%), as well as in diminished severity of maximum angina (-38%), in lower maximal ST-segment depression (-32%) and in faster recovery of ST-depression 3 and 6 minutes after the test (-28% and -44%). Nitroglycerin patch showed 33% less angina attacks, mainly severe and moderate, resulting in 37% less sublingual nitroglycerin consumption. A significant fall in the number of ST-segment depression episodes of 1.5 mm or more (-60%) was shown in the 24-hour ECG. All these changes were confirmed to be significant compared to placebo values, at a level of P less than 0.01, by multivariate analysis. This study revealed a positive effect of low dose nitroglycerin patch on improvement of exercise functional capacity and signs of myocardial ischaemia after 14 days of continuous therapy.
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PMID:A randomized placebo controlled, double-blind, crossover trial of transdermal nitroglycerin in stable angina pectoris. 313 73

Increasingly longer balloon inflation times during coronary angioplasty can create significant left ventricular ischemia, amelioration of which was attempted in this study using nitroglycerin. Hemodynamic variables were assessed during inflation of an angioplasty balloon in the proximal left anterior descending coronary artery of 10 patients. Regional wall motion was assessed by left ventriculography during a separate balloon inflation. Nitroglycerin (200 micrograms) was then administered intravenously, and hemodynamic and ventriculographic assessments during balloon inflations were repeated. Balloon inflation resulted in a marked increase in left ventricular end-diastolic pressure (from 9.2 +/- 2.1 to 19.4 +/- 2.9 mm Hg) and time constant of left ventricular relaxation (from 44.2 +/- 6.2 to 62.3 +/- 11.3 ms) and a decrease in distal coronary artery perfusion pressure (from 54 +/- 9 to 33.1 +/- 4 mm Hg). Time to onset of angina was 29 +/- 3 seconds and time to ST segment depression of 1 mm or greater was 30 +/- 3 seconds. Regional wall motion analysis 30 seconds after onset of balloon inflation revealed marked hypokinesia and akinesia in the anteroapical segments with graduated depression of inferior wall motion, greatest at the apex. After the administration of nitroglycerin, balloon inflation resulted in a smaller increase in end-diastolic pressure (from 5.0 +/- 2.7 to 8.3 +/- 2.6 mm Hg) and time constant (from 47.9 +/- 4.7 to 54.4 +/- 9.2 ms; both p less than 0.01 versus standard balloon inflation). Distal coronary artery pressure remained similar to standard balloon inflation (32 +/- 3 mm Hg) despite lower mean arterial pressure (89 +/- 5 mm Hg, p less than or equal to 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amelioration by nitroglycerin of left ventricular ischemia induced by percutaneous transluminal coronary angioplasty: assessment by hemodynamic variables and left ventriculography. 316 Jul 55

Nitroglycerin and the long-acting nitrates are beneficial in stable and unstable angina pectoris and acute myocardial infarction and as adjunctive therapy in congestive heart failure. Nitroglycerin compounds relax vascular smooth muscle, producing venous, arterial, and arteriolar dilatation. These actions are modulated by stimulation of intracellular cyclic guanosine monophosphate. Nitrate efficacy in ischemic heart disease is due to peripheral venous and arterial vasodilatation that results in decreased myocardial oxygen consumption. Nitrates also dilate coronary arteries and collaterals, reverse coronary vasoconstriction, and enlarge some coronary atherosclerotic lesions. Nitrates improve exercise performance in stable angina pectoris. Intravenous nitroglycerin should be used in the initial treatment of unstable angina. Nitrates may be beneficial in myocardial infarction for control of ischemic pain, acute hypertension, and left ventricular failure. In subjects with congestive heart failure, nitrates reduce symptoms and improve exercise tolerance. Nitrate tolerance is a problem with continuous nitrate therapy. Tolerance is most likely to occur with frequent dosing or the use of long-acting nitrates, particularly transdermal nitroglycerin disks, and can be prevented or reversed with intermittent-dosing regimens.
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PMID:A reappraisal of nitrate therapy. 327 14

We have previously reported that cimetidine, a histamine H2-receptor blocker, augments the histamine-induced coronary vasoconstriction at the site of spastic segments in the atherosclerotic coronary arteries of swine. To elucidate whether cimetidine has a coronary vasoconstrictive effect in humans, 14 patients with vasospastic angina (group 1) and 14 controls with atypical chest pain (group 2) were examined angiographically. Nitroglycerin-effective spontaneous angina with electrocardiographic ST-T changes and ergonovine-induced coronary artery spasm were confirmed in group 1, but not in group 2. Cimetidine was administered intravenously in a dose of 200 mg. Cimetidine induced coronary artery spasm in 4 patients in group 1 but none in group 2(29% vs. 0%, p less than 0.01). The extent of coronary vasoconstriction induced by cimetidine was greater at the site of spastic coronary segments than that at the site of non-spastic segments in group 1 or all segments in group 2 [14% vs. 4%, (p less than 0.01) or 14% vs. 2%, (p less than 0.01)] as well as the extent of ergonovine-induced coronary vasoconstriction [46% vs. 14%, (p less than 0.01) or 46% vs. 14%, (p less than 0.01)] and nitroglycerin-induced coronary vasodilatation [58% vs. 25%, (p less than 0.01) or 58% vs. 17%, (p less than 0.01)]. As it was suggested that cimetidine has potential vasoconstrictive effects in patients with coronary artery spasm, it should be administered with caution in patients with the vasospastic angina pectoris.
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PMID:Cimetidine induces coronary artery spasm in patients with vasospastic angina. 359 1

The paper presents an overview of the recent diagnostic and therapeutic feasibilities in acute coronary heart disease. In unstable angina the leading symptoms are new onset or increasing anginal pain or resting pain as well as ST-T-changes in the ecg without a rise in enzymes. Coronary arteriography shows double or triple vessel disease (70%), a left main stenosis (10 to 15%) or normal coronary arteries (10 to 15%). The treatment of unstable angina in the CCU consists of Nitroglycerin-infusion together with calcium channel blockers and/or betablockers. With this regimen, 80% of patients may be stabilized within 24 to 48 hours. Thereafter coronary arteriography is performed to settle the further therapeutic regimen (PTCA, CABG, medical therapy). Acute myocardial infarction is characterized by persisting (more than 30 min) pain, ST-T-changes in the ecg with or without development of Q-waves indicating irreversible myocardial damage. Angiographically, usually a subtotal or total occlusion of the corresponding artery is found. Aims of therapy in acute myocardial infarction is-besides treatment of complications like arrhythmias and left ventricular failure-reperfusion of the myocardium with reopening of the occluded vessels by intracoronary or systemic thrombolysis. Recently, also clot-specific streptokinase derivates and plasminogen activators are used with fewer bleeding complications. After recanalization of the vessel a persisting stenosis should be relieved either by PTCA or CABG to avoid reocclusion. However, these active forms of treatment can only be performed, if the patient reaches the hospital within 4 to 6 hours after the onset of ischemia.
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PMID:[Acute coronary heart disease. Current status of diagnostic and therapeutic possibilities in the intensive care station]. 372 2

Nitroglycerin plaster (in 5 cm2, 10 cm2 or 20 cm2 sizes) was applied to 12 patients with coronary heart disease, angina and exercise-induced ischemic reactions in the course of a simple-blind trial with intra-individual crossover in a randomized sequence over one week each. A 15 cm2 plaster served as a placebo. In the placebo phase the mean number of angina attacks was 9.3 per week. It decreased to 6.2 with the 10 cm2 plaster (P less than 0.05), to 2.6 per week with the 20 cm2 plaster (P less than 0.001). The ischemia reaction in the exercise ECG (sum of ST segment depressions), recorded on day 7 of the treatment phase, was improved three hours after plaster application, dependent on the size of the plaster: placebo 6.0 +/- 1.2 mm; 5 cm2 plaster 5.1 +/- 1.0 mm; 10 cm2 4.6 +/- 1.0 mm (P less than 0.05); 20 cm2 3.4 +/- 0.9 mm (P less than 0.001). The angina-free period during ergometry showed dose-dependent improvement 3 and 24 hours after application. Arterial blood pressure was decreased only after 20 cm2 plaster by 8% after three hours, as compared with the placebo (P less than 0.05). There was no effect on heart rate, at rest or on exercise, after any plaster. The results indicate that significant decrease in ischemia reaction occurred with a plaster of 10 cm2 or larger. A 24-hour effect was demonstrable only with respect to the duration of symptom-free exercise.
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PMID:[Anti-anginal effect of transdermally applied nitroglycerin as dependent on the size of the plaster]. 391

The effect of nitroglycerin ointment (30 mg) and isosorbide dinitrate ointment (100 mg) versus placebo on exercise capacity has been investigated in 12 patients. All had angina pectoris and coronary artery disease documented by coronary angiography. Nitroglycerin and isosorbide dinitrate ointment produced a significant increase in exercise capacity, without any significant difference in the beneficial effect of the two. Stress-induced changes of the ST-segment in the electrocardiogram decreased by 65% after nitroglycerin ointment and by 41% after isosorbide dinitrate ointment, compared to placebo. These results indicate that nitroglycerin and isosorbide dinitrate ointment reduce stress-induced myocardial ischemia at similar work loads.
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PMID:[Transcutaneous application of nitroglycerin and isosorbide dinitrate versus placebo: effect in myocardial ischemia]. 392 52

Nitroglycerin has maintained its position in the treatment of angina pectoris for more than a century. Efficacy of oral nitrates has been established and compares well with that of other anti-anginal drugs. New delivery systems are being developed for sustained systemic nitrate action. Beneficial action of nitrates in congestive heart failure and their crucial role in unstable angina and acute myocardial infarction has further widened their therapeutic use. A plausible hypothesis of the mechanism of nitrate-induced vasodilation has been presented, involving production of nitrosothiols and activation of guanylate cyclase in the vascular smooth muscle. Recent developments suggest that the rate degradation of nitrates and formation of nitrosothiols in the vascular smooth muscle are linked, offering an explanation to the relatively rapidly developing, but partial vascular tolerance during high-dose nitrate therapy.
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PMID:Efficacy of different forms of nitrates in angina pectoris. 392 83

The hypothesis was tested that selected patients with coronary artery disease whose rate of angina attacks do not respond to low doses of isosorbide dinitrate (ISDN) (40 mg/day) may respond to high doses (480 mg/day), tolerate them, and maintain their responsiveness over the long term. Twenty-four patients with grade 3 stable angina pectoris were given a placebo for 4 weeks and then had their ISDN dosages titrated up to 120 mg four times a day during another 6 weeks in a single-blind fashion. The 20 patients who responded to (and tolerated) a high dose of ISDN were maintained at that dose for an average of 1 year. The weekly rate of angina attacks fell by 74%, from 6.05 during placebo to 1.6 (p less than 0.01) during long-term ISDN treatment. Nitroglycerin consumption fell similarly. Patient assessment of activity level, well-being, and angina threshold improved in the majority of patients. The within-patient trend of their weekly rate of angina episodes was stable in 13 patients, downward in six, and upward in only one patient. Exercise performance evaluated by a submaximal graded multistage treadmill test showed a small but nonsignificant improvement of 1.8%. It is concluded that (1) some patients who do not respond to the antianginal action of low-dose ISDN may respond to a high dose and tolerate it, (2) this responsiveness and tolerability may last for over a year, and (3) ISDN may be clinically useful in patients with coronary disease even when exercise performance is not significantly improved.
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PMID:High-dose isosorbide dinitrate in management of angina pectoris. 392 47


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