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)

Silent myocardial ischaemia is the most frequent consequence of coronary artery disease and occurs in almost 70 per cent to 80 per cent of ischaemic episodes. In some studies, it has some predictive value of cardiovascular events either in stable or unstable angina or after myocardial infarction. In this last case, one year mortality is 30 per cent and 11 per cent respectively with and without silent ischaemia that has been recorded on the 8th day after myocardial infarction. This review has focused on controlled studies in patients with angina and Holter recorded ischaemia. Nitrates are very likely to be active substances on Holter recorded angina but no controlled studies have been performed to really demonstrate it. The efficacy of beta-blocking agents is well established with a 60 per cent reduction in the number of ischaemic events and a 80 per cent reduction in total ischaemic duration. Nifedipine efficacy appears lower than that of beta-blockers with an evaluated mean reduction of 39 per cent for the number of events and of 43 per cent for duration of episodes. Diltiazem induces a 48 per cent reduction of both ischaemic parameters. For drug associations, addition of a calcium antagonist to a beta-blocking agent provides only little benefit. The relationship between anti-ischaemic efficacy and long term prevention of cardiovascular events remains to be established for a given anti-ischaemic therapy.
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PMID:[Myocardial ischemia detected by Holter monitoring: analysis of therapeutical trials realised in stable angina]. 763 Dec 86

Controlled-delivery once-daily diltiazem (qd), 180 mg and 360 mg, was assessed in two multicenter, randomized, double-blind, placebo-controlled trials using a 3 x 3 Latin square design. Both studies compared the controlled-delivery dosage form to the same total daily dose of immediate-release diltiazem administered three times daily (tid) and to placebo. The primary measure of efficacy was the time to termination of the exercise tolerance test (ETT) at 2, 8, and 24 hours after the morning dose. There were no significant differences in time to ETT termination between the qd and tid formulations at any time, except at 24 hours with 180 mg qd versus 60 mg tid. The comparison to placebo showed that diltiazem 180 mg qd, 360 mg qd, and 120 mg tid significantly lengthened the time to ETT termination (p < 0.05) at all time points, while diltiazem 60 mg tid did not differ from placebo at any time point. The qd formulation also increased the time to 1-mm ST-segment depression and reduced the number of angina attacks and the amount of nitroglycerin used when compared to placebo. No new or unusual adverse events were noted. Diltiazem controlled-release capsules administered once daily are safe and effective for the treatment of patients with chronic stable angina.
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PMID:Antianginal efficacy and safety of controlled-delivery diltiazem QD versus an equivalent dose of immediate-release diltiazem TID. 766 99

In a randomized, double-blind, cross-over, multicenter study with a placebo run-in phase, the efficacy and safety of two oral formulations of diltiazem, standard three or four times daily (t.i.d. or q.i.d.) and controlled release twice daily (b.i.d.), were compared in 49 patients with stable angina pectoris. ST-segment depression at maximum exercise 12 h after tablet intake was less frequently observed with diltiazem controlled release than with standard diltiazem (34 of 49, 69% vs. 43 of 49, 88%, p = 0.007). In patients with ST-segment depression after both treatments (n = 33), the average time to 1-mm ST-segment depression was 55.4 +/- 19.9 s longer with diltiazem controlled release than with standard diltiazem [476 +/- 195 vs. 422 +/- 163 s, p = 0.009; 95% confidence interval (CI) 14.8-96 s]. Reduction in mean number of anginal attacks and nitroglycerin (NTG) intake was not significantly different between treatment with standard diltiazem and diltiazem controlled release. The incidence of side effects was low and not different between the two treatments. Both formulations are equally effective in reducing the number of anginal attacks and are well tolerated. Diltiazem controlled release is more effective than standard diltiazem in preventing myocardial ischemia 12 h after tablet intake. Thus, diltiazem controlled release allows twice-daily intake frequency and may therefore be preferable to standard diltiazem in treatment of stable angina pectoris.
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PMID:Comparison of diltiazem standard formulation and diltiazem controlled release in patients with stable angina pectoris: a randomized, double-blind, cross-over, multicenter study. 768 99

The 3-month efficacy and safety of a once-daily controlled formulation of diltiazem (180 to 360 mg/day) were assessed in a study of 54 patients with angina pectoris. This multicenter study was a nonrandomized, placebo run-in, open-label, 3-month trial followed by a 1-week, double-blind, randomized period during which most patients (89%) received placebo. There were only minimal changes in the time to termination (mean change +/- SEM -5.8 +/- 9.6 seconds), time to onset of angina (10.5 +/- 12.2 seconds), and the time to 1 mm ST-segment depression (2.9 +/- 12.5 seconds) from the end of the titration phase to the end of the open-label study. There were, however, statistically significant differences between the end of the 3-month treatment phase and the end of the 1-week randomized placebo phase for those 3 efficacy parameters (-37.3 +/- 11.2, -58.6 +/- 13.6, and -45.6 +/- 16.4 seconds, respectively). Diltiazem significantly decreased the frequency of anginal attacks and nitroglycerin use at the end of the 3-month treatment phase compared with results at the end of the randomized double-blind placebo phase. No new or unusual adverse events were reported during treatment. The present results suggest that there is no loss of efficacy of once-a-day diltiazem when administered for a long period to patients with chronic stable angina pectoris.
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PMID:Three-month efficacy and safety of once-daily diltiazem in chronic stable angina pectoris. 771 May 63

Diltiazem is a calcium antagonist used in angina pectoris and hypertension. There is little information concerning the slow-release (SR) formulation in the literature. The pharmacokinetics of diltiazem SR (120 mg) have been assessed over a 36h period in healthy volunteers after single- (SD) and multiple-dose (MD) administrations. Cmax, AUC0-36, and AUC0-infinity were significantly increased at steady state compared to the extrapolated SD values, suggesting accumulation of the drug. Renal and cardiovascular parameters have also been assessed at intervals of 3-6h during baseline (B) and following single and multiple doses of diltiazem SR. Diuresis over a 24 h period was increased, but not significantly, by the administration of diltiazem SR i.e. 1782 ml (MD) and 1915 ml (SD), versus 1626 ml (B). Natriuresis and creatinine clearance were slightly decreased by diltiazem SR, compared to B values; this might be due to the relatively short period over which steady state was maintained (five days) and the effects of norepinephrine and angiotensine II on renal vasculature and the pharmacokinetics of diltiazem SR. No increase in the systolic blood pressure occurred after the administration of diltiazem SR; diastolic blood pressure and PR interval were decreased and increased respectively by diltiazem SR. These results do not appear to be clinically significant. Finally, no relation was found between the pharmacokinetics and pharmacodynamics of diltiazem. This may be attributed to the absence of clinically significant effects in healthy volunteers, the presence of active metabolites, the pharmacokinetics of the SR formulation and/or the accumulation of the drug at steady state.
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PMID:Pharmacokinetics and pharmacodynamics of a slow-release formulation of diltiazem after the administration of a single and repeated doses to healthy volunteers. 788 Sep 83

Diltiazem CR tablets 120 mg b.i.d. for 1 week were compared with plain tablets 60 mg q.i.d. in 13 healthy male volunteers in a study of pharmacokinetic variables. Their antianginal efficacy was also compared in 23 patients with stable angina pectoris who were already on metoprolol. Both studies were of randomised, cross over design, and the clinical study was double blind. The pharmacokinetic variables of the two formulations were very similar except for the longer tmax of 4.4 h for diltiazem CR in comparison to 2.9 h for the plain tablets. The mean relative bioavailability of diltiazem CR in comparison with plain tablets was 1.14. The clinical study showed that after four weeks on diltiazem CR 120 mg b.i.d. or diltiazem plain tablets 60 mg q.i.d. in addition to metoprolol, there were significant decreases in weekly anginal attacks from 11 to 5 attacks/week, the number of nitroglycerin tablets consumed from 6 to 3 tablets/week, and an increase in the maximum workload from 116 to 126 and 123 W for diltiazem CR and plain diltiazem tablets, respectively, as compared to placebo. Five of the patients were angina free during diltiazem treatment. No difference in anti-anginal efficacy between the two preparations was seen. It was concluded that CR 120 mg b.i.d. appears bioequivalent to plain diltiazem tablets 60 mg q.i.d.
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PMID:Conventional and controlled release diltiazem. Bioavailability in healthy volunteers and anti-anginal effects in combination with metoprolol in stable angina pectoris. 798 29

Non-Q wave myocardial infarction is associated with a high recurrence rate of ischaemic events (angina and infarction). The artery responsible for the infarction is usually patent but stenosed and seems to be the cause of these complications. This prospective multicenter series of 66 patients treated by Heparin, Aspirin, Diltiazem and undergoing coronary angiography during the hospital period studied the artery responsible for the infarction and the value of coronary angiography in this setting. Several conclusions were drawn from the results: the precise diagnosis of the artery responsible for the infarct may be difficult (14%); the left circumflex artery or one of its branches is often implicated (47%); non-Q wave infarction is a various and heterogeneous group, including: infarctions located on small branch arteries, "warning" ischaemic episodes in the left anterior descending artery territory. definitive infarction of the left circumflex artery territory; nevertheless, this group is an intermediate state between Q wave infarction and unstable angina (low occlusion rate 26% and angiographic lesional appearances similar to those of unstable angina); early coronary angiography (48-72 h) seems to be useful to improve prevention of ischaemic recurrences by adequate revascularisation.
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PMID:[Role of coronary angiography in infarction without Q wave. Results of a prospective angiographic study]. 802 68

Three cases of diabetic myocardiopathy having history of diabetes, angina and left ventricular dysfunction of various degrees and confirmed by coronary angiography and endomyocardial biopsy were reported. Electrocardiography showed significant ST-T changes simulating coronary insufficiency but without definite localization. As to the treatment, nitrate preparations, inotropic agents such as strophanthin K, digoxin etc. were used to relieve the symptoms; insulin was also administered to control the blood glucose level. Diltiazem, a calcium blocker, is also of help in alleviating the symptoms. It is shown in the present study and in the literatures as well that diabetic myocardiopathy is a disease showing intramural microvascular endothelial proliferation and swelling as well as subendothelial accumulation of acid glycogen deposition cells. The transportation of intracellular calcium ions and the cellular metabolism are thus affected, so there are extensive ischemia, focal necrosis and fibrosis in the myocardium with resulting cardiac dysfunction. The authors are, therefore, of the opinion that diabetic myocardiopathy is a specific and separate clinical entity.
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PMID:[Diabetic myocardiopathy]. 804 81

The efficacy of a new sustained-release formulation of diltiazem was examined in a placebo-controlled, double-blind trial in patients with stable angina. Doses of 60 mg BID, 90 mg BID, 180 mg BID and 240 mg BID were compared with placebo in 208 patients at 3 hours and 12 hours after dosing. Diltiazem, in doses of 90 mg BID and 180 mg BID, was statistically superior to placebo with respect to increasing total exercise time. Treadmill exercise time at 3 hours postdose increased with placebo from 356.1 +/- 118.7 sec to 375.7 +/- 119.8 sec (NS); with 90 mg BID, 382.7 +/- 111.8 sec to 445.4 +/- 117.5 sec (P < 0.005); and with 180 mg BID, 386.8 +/- 145.9 sec to 467.2 +/- 166.2 sec (P < 0.0001). At 12 hours postdose, treadmill exercise time with placebo increased from 357.6 +/- 128.3 sec to 383.8 +/- 128.7 sec (NS); with 90 mg BID, 395.2 +/- 119.4 sec to 449.7 +/- 123.1 sec (P = 0.053); with 180 mg BID, 395.3 +/- 141.4 sec to 476.6 +/- 165.6 sec (P < 0.0001). Time to onset of angina was also increased by the 180-mg-BID dose both at 3 hours postdose (257.3 +/- 126.8 sec to 354.3 +/- 158.7 sec; P < 0.0001) and at 12 hours postdose (274.7 +/- 131.2 sec to 377.4 +/- 186.2 sec; P < 0.0001). Sustained-release diltiazem is effective and safe in treating patients with chronic stable angina.
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PMID:A double-blind, placebo-controlled trial of sustained-release diltiazem in patients with angina. Sustained-Release Diltiazem Study Group. 811 4

Today calcium antagonists (Ca-antagonists) are widely used agents in the management of various diseases of the circulatory system. More than 20 years ago the Ca-antagonists of the so-called 1st generation (Verapamil, Diltiazem, Nifedipine) were introduced for treatment of angina pectoris and later of essential hypertension. In the last decade an increasing number of agents structurally related to dihydropyridines were developed for the treatment of hypertension and/or coronary heart disease or cerebral disorders; the main target was to reduce side effects and to guarantee once or at least twice daily administration. Therefore the Ca-antagonists of the so-called 2nd generation (e.g. Amlodipine, Felodipine, Isradipine, Nitrendipine, Nicardipine, Nimodipine, Nisoldipine) tend to longer elimination-half-lives; Amlodipin is an exception with an elimination-half-life of 30 hours on the average. Apart from elimination rates, however, the biopharmaceutical and pharmacokinetic characteristics of all Ca-antagonists are similar: they are highly cleared drugs and are relatively highly protein bound. As they are subject to significant hepatic first-pass-metabolism old age and hepatic disease will increase their plasma-concentrations. Renal impairment affects little their pharmacokinetics since the fraction eliminated unchanged by the kidneys is small. For most agents, plasma-concentration-response relationships have been described. With exception of nicardipine a linear pharmacokinetic in all Ca-antagonists was demonstrated. Drugs and food affecting hepatic blood flow and drug metabolising capacity have predictable interaction potential. With regard to the acute pharmacodynamic effects the Ca-antagonists show similar qualitative effects, though there are quantitative differences. Orally administered dihydropyridine-derivatives induce acute hypotensive effects, whereas the other compounds show clinically relevant hypotensive effects only when administered chronically per os or less pronounced when given as intravenous infusion.
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PMID:[Principles of the pharmacokinetics and pharmacodynamics of calcium antagonists]. 813 31


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