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

Thirteen patients with Prinzmetal's variant angina performed treadmill exercise tests in the early morning and in the afternoon of the same day. The attacks with ST elevation were induced repeatedly in all 13 patients in the early morning, but in only two patients in the afternoon. Propranolol did not suppress the exercise-induced attacks in all 13 patients. Diltiazem suppressed the attacks in all 13 patients and phentolamine in eight of the nine patients. Coronary arteriograms demonstrated that spasm occluding completely or almost completely the large coronary artery supplying the area of myocardium showing ST elevation appeared during the attacks and disappeared along with the attacks after nitroglycerin administration in all four patients in whom the attacks were induced by arm exercise in the catheterization laboratory. We conclude that there is circadian variation of exercise capacity in patients with Prinzmetal's variant angina caused by coronary arterial spasm induced by exercise in the early morning but not in the afternoon.
 ...
PMID:Circadian variation of exercise capacity in patients with Prinzmetal's variant angina: role of exercise-induced coronary arterial spasm. 42 6

To twenty six patients with angina at rest (including 13 patients with Prinzmetal's variant angina), propranolol 40--50 mg, dilitiazem 60--90 mg, dipyridamole 50 mg, atropine sulfate 0.6 mg and phenoxybenzamine 10--20 mg were given at 9:00 p.m. and 2:00 a.m. (except phenoxybenzamine which was given only at 9:00 p.m.) to examine the effect of these drugs on the attack. Propranolol was not only ineffective in suppressing the attack but rather tended to aggravate it in all the cases of Prinzmetal's variant angina. It was effective to some degree in 5 of 13 cases of angina at rest other than Prinzmetal's variant angina. Diltiazem suppressed the attack completely and dramatically in all the cases of angina at rest (including Prinzmetal's variant angina). Dipyridamole was ineffective in all the cases except one in suppressing the attack. Atropine sulfate and phenoxybenzamine suppressed the attack in 13 of 21 cases and in 6 of 12 cases respectively. Coronary arteriography was done before and after the intravenous administration of 10 mg of diltiazem in 8 patients and it was demonstrated that diltiazem dilates large coronary arteries in all these patients. It is concluded that diltiazem, a calcium antagonistic drug, is specifically effective in suppressing the attack of angina at rest by dilating large coronary arteries and that the autonomic nervous system plays a role in the genesis of the attack probably by constricting large coronary arteries by way of alpha adrenergic receptors.
 ...
PMID:Pathogenesis and treatment of angina pectoris at rest as seen from its response to various drugs. 63 93

The effects of epanolol (a new selective beta-adrenoceptor antagonist), diltiazem and placebo were compared in a group of 16 patients with chronic stable angina pectoris. Each patient received each treatment in random order. Diltiazem reduced weekly angina attack rate from 7.2 (95% CI 3.9-10.5) to 3.9 (1.9-5.9) (P less than 0.01), whereas a lesser reduction was observed after epanolol. Both drugs produced a small but significant (P less than 0.05) increase in treadmill exercise time (placebo 474 s (374-574), epanolol 527 s (431-623) and diltiazem 554 s (462-646). However, aerobic work capacity, assessed by peak achieved oxygen consumption, was not different from the placebo value of 21.2 (18.0-24.4) ml.min-1.kg-1, and clearly subnormal when compared to age- and sex-matched controls (33.0 (30.1-35.9) ml.min-1.kg-1). Ventilatory abnormalities and increased lactate levels on active treatment were observed at peak exercise only. We conclude that the cardiodepressant effects of both active drugs limit blood supply to working skeletal muscle, and that chest pain may be replaced by dyspnoea or fatigue as the limiting factors to exercise.
 ...
PMID:Comparative effects of epanolol and diltiazem on exercise performance and respiratory gas exchange in angina pectoris. 135 16

A number of studies have addressed the response to calcium antagonists, used alone or combined with other therapy, in patients with silent myocardial ischemia (SMI). Nifedipine, the first calcium antagonist to be studied, was shown to be superior to pindolol in patients with effort angina. Although both nifedipine and diltiazem significantly reduced episodes of ST depression, compared with placebo, in patients with stable effort angina, the addition of nifedipine to diltiazem removed the beneficial effect of diltiazem in another study. Studies have shown a reduced incidence of ischemic episodes during nicardipine treatment in patients with ambulatory ischemia, predominantly SMI, and rest angina due to coronary artery spasm. Other workers similarly reported that verapamil was superior to both placebo and propranolol in reducing painful and painless ischemia in patients with angina at rest. It has been demonstrated that, compared with placebo, nifedipine reduced ischemic episodes by 50% and also markedly reduced total ischemic time in totally asymptomatic men with coronary artery disease and SMI. It was suggested that the well-documented increase in SMI occurring between 0600 and 1200 h was reduced, but not eliminated, by nifedipine. Diltiazem may also attenuate the circadian variation in SMI. Nifedipine has been shown to be particularly effective in SMI when combined with a beta-blocker. This has been substantiated in a large group of patients; both drugs reduced the number of episodes of SMI when used as monotherapy, and the combination decreased the incidence by 95%. These findings collectively indicate that calcium antagonists are effective in reducing or preventing SMI.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Clinical effects of calcium antagonists in silent ischemia. 136 8

The antianginal efficacy and duration of action of slow-release (SR) diltiazem were evaluated in 12 patients with stable angina. Patients underwent maximal symptom limited bicycle exercise testing and 24-hour Holter monitoring at the end of 1-week placebo run-in phase and after 1-month therapy with either placebo or SR-diltiazem (120 mgs bid) using a placebo controlled, double-blind, randomized cross-over trial. No concomitant antianginal therapy, except sublingual nitroglycerin, was allowed during the trial. Exercise testing was performed 3 and 12 hours after drug administration. Blood samples were obtained for the determination of diltiazem plasma concentrations. After diltiazem administration, peak exercise duration increased significantly in comparison both with placebo and the run-in phase: from 292 +/- 48 to 378 +/- 113 s at 3 hours and from 286 +/- 59 to 366 +/- 109 s 12 hours after drug administration. Similarly, ST depression time increased from 240 +/- 59 to 374 +/- 123 s at 3 hours and from 231 +/- 57 to 332 +/- 123 s 12 hours after diltiazem. No significant changes of heart rate, blood pressure and double product were detected. Diltiazem plasma concentrations averaged, respectively, 175 +/- 86 pg/ml and 109 +/- 43 pg/ml 3 and 12 hours after its administration. No correlation was found between plasma concentrations and antianginal effects of diltiazem. At 24 hours Holter monitoring, SR-diltiazem induced a significant decrease of mean heart rate with a reduction in the number and duration of ischemic episodes.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[The antianginal effects of a new delayed-release formulation of diltiazem in patients with stable angina pectoris: its evaluation by the ergometry test and dynamic electrocardiogram]. 139 48

Plasma bradykinin and prostaglandin metabolism are related to the anginal pain modulating system in patients with ischemic heart disease. We carried out a placebo controlled single blind test of diltiazem (30 mg three times a day) in 15 patients with chronic stable angina. The effect of diltiazem was evaluated by exercise treadmill testing and 48-h ambulatory electrocardiographic monitoring. Plasma bradykinin, thromboxane B2, and 6-keto-prostaglandin F1 alpha levels were determined by radioimmunoassay prior to and during diltiazem therapy. Diltiazem significantly increased the exercise time and reduced episodes of angina. Diltiazem, however, did not appreciably improve either the frequency of silent myocardial ischemic episodes or the total duration of the silent myocardial ischemic episodes. Diltiazem also tended to decrease plasma bradykinin, thromboxane B2, and 6-keto-prostaglandin F1 alpha levels. When ischemic episodes on ambulatory electrocardiographic monitoring are categorized according to heart rate change at the onset of episode (type A, preceded by heart rate increase > or = 5 beats/min; type B, no preceding heart rate increase), diltiazem was only effective on type A ischemic episodes as well as on symptomatic ischemia. Further, bradykinin was significantly decreased by diltiazem only in patients with exercise-induced silent ischemia or no exercise-induced ischemia, while the thromboxane B2/6-keto-prostaglandin F1 alpha ratio was unaffected by the administration of diltiazem. Thus, silent and symptomatic ischemia may be associated with different bradykinin and prostaglandin responses.
 ...
PMID:Effect of diltiazem on silent ischemic episodes, plasma bradykinin and prostaglandin metabolism. 145 74

Among 366 unstable angina pectoris patients at our hospital, myocardial infarction was common (15.7%) in those with attacks of chest pain lasting for at least 20 min. There was also a high incidence (30.3%) when chest pain continued after the start of inpatient treatment. To investigate the etiology of unstable angina, coronary arteriography was performed in both the unstable and stable stages in these patients and the results were compared. The role of coronary spasm and coronary thrombosis in unstable angina was investigated, and the efficacy of continuous infusion of either diltiazem or isosorbide dinitrate as treatment for these patients was compared. Coronary arteriography in the unstable stage showed, no clear differences in the morphology of the stenotic site and the degree of stenosis between the patients with and without infarcts when urokinase or isosorbide dinitrate were injected into the coronary arteries. When drug treatment was effective, the angina was stabilized without any improvement in the degree of stenosis or the morphology of the involved coronary vessel. Thus, it was difficult to predict the response to treatment from coronary arteriography performed in the unstable stage. Diltiazem was more effective than isosorbide dinitrate, and it appears that some action other than coronary dilatation was involved in achieving the remission of unstable angina.
 ...
PMID:The response to drug therapy in unstable angina on the basis of coronary angiography findings. 145 41

Diltiazem is a calcium antagonist widely used in the treatment of angina and hypertension. The contributions of metabolites of diltiazem to the vasorelaxant effects of diltiazem were investigated. The synthesis and spectroscopic characterization of eight major cis-diltiazem metabolites are described. Three of the compounds--N, O-didemethylated metabolite (21), O-demethylated metabolite (22), and diltiazem N-oxide (27)--have been recently reported and have not previously been synthesized. The identities of all eight synthetic metabolites have been verified with samples obtained from human urine using combined LC-MS/MS. The Ca2+ antagonistic activities of diltiazem and its metabolites (except 27) were studied on hamster aorta preparations depolarized with KCl. The order of potencies (IC50 +/- SE, microM) is as follows: diltiazem (0.98 +/- 0.47) greater than 17 (2.46 +/- 0.38) greater than or equal to 23 (3.27 +/- 1.02) greater than 26 (20.2 +/- 10.5) greater than 22 (40.4 +/- 15.4) greater than or equal to 25 (45.5 +/- 18.1) greater than 21 (112.2 +/- 33.2) greater than or equal to 24 (126.7 +/- 24.2). Structure-activity relationships are also discussed.
 ...
PMID:Synthesis, characterization, and Ca2+ antagonistic activity of diltiazem metabolites. 150 10

Calcium antagonists are effective cardioprotective agents in experimental models of myocardial infarction. However, clinical trials in acute myocardial infarction and in postinfarction secondary prevention led to conflicting results related to the small size of the majority of the trials and possible differences among individual agents with distinct ancillary properties. Furthermore, one has to consider separately the trials in patients with Q-wave infarction and in others with non-Q-wave infarction. Q-wave patients do not seem to benefit from therapy with calcium antagonists. However, the efficacy of early administration of verapamil or diltiazem cannot be ruled out as the available data are not conclusive, mainly because of the small size of the trials and the delay in administering the drugs. We have shown encouraging results with diltiazem, which, compared to placebo, decreased the infarct size measured with serial thallium SPECT defect scores, and increased left ventricular ejection fraction in acute Q-wave infarctions. Non-Q-wave infarction is another area where evidence of positive beneficial effects of diltiazem is strong, as shown by a recent trial conducted by Gibson et al. Diltiazem reduced the early reinfarction rate and postinfarction angina and 1-year cardiac mortality and nonfatal reinfarction rate. Consistent with these findings are results from subgroup analysis of the multicenter diltiazem postinfarction trial. Prophylactic use of diltiazem may be useful and should be considered in patients with non-Q-wave infarction along with aspirin, as no other treatment is yet available for this condition, at least for the time being and until the thrombolysis TIMI phase III trial is terminated.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Calcium antagonists in myocardial infarction. 170 9

In 15 randomized, double-blind studies with blood pressure measured at the end of the dosing interval, diltiazem sustained-release or conventional tablets were found to be equal in efficacy to hydrochlorothiazide, beta-blockers, angiotensin-converting enzyme inhibitors, and other calcium-channel antagonists. The total number of patients with adverse effects and those who drop out due to adverse effects are similar for diltiazem and the other drugs. Combination therapy with diltiazem and captopril showed additive effects, and combination of diltiazem with hydrochlorothiazide or atenolol showed additional, but perhaps less than additive, effects. Six studies in older and younger patients have shown no overall effect of age on the antihypertensive effect of diltiazem. Two studies showed no difference in mean antihypertensive response between black and non-black patients. In contrast to diuretics and beta-blockers, diltiazem does not have adverse metabolic effects on electrolytes, carbohydrate metabolism, and lipid metabolism. Diltiazem is an excellent antianginal agent. It has been shown in one study to decrease proteinuria as effectively as lisinopril, and it may have renal protective effects. The antihypertensive efficacy of diltiazem as monotherapy is equal to that of all other antihypertensive classes, and it is tolerated as well or better than most other antihypertensive drugs. Diltiazem is particularly indicated in patients with hypertension and concurrent angina pectoris, diabetes, hyperlipidemias, and, perhaps, chronic renal disease.
 ...
PMID:Diltiazem: its place in the antihypertensive armamentarium. 172 39


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