Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty-one patients were studied in a randomized double-blind placebo-controlled crossover trial to compare the antianginal actions of nicardipine 30 mg thrice daily and nifedipine 10 mg thrice daily. Efficacy was assessed using objective criteria from computer-assisted multistage graded exercise testing, performed after a two-week placebo run-in period and at the end of each four-week active treatment period. Thirty-seven patients completed both legs of the crossover trial. The mean (+/- standard error of the mean) baseline exercise time to development of angina was 6.7 +/- 0.4 min and this increased to 9.5 +/- 0.6 min on nicardipine (p less than 0.001) and 9.5 +/- 0.5 min on nifedipine (p less than 0.001 vs baseline; NS vs nicardipine). Both drugs significantly prolonged the time to the development of 1mm ST segment depression. The baseline resting heart rate of 83 +/- 2 beats/min increased to 87 +/- 3 beats/min during nicardipine (p less than 0.05) and remained unaltered at 83 +/- 2 beats/min during nifedipine therapy (p = NS vs baseline and p less than 0.02 vs nicardipine). Similarly, both drugs increased significantly the maximal heart rate at peak exercise. One patient was lost to follow-up during the placebo run-in period and four patients (two each on nicardipine and nifedipine) were withdrawn due to adverse effects. Our results indicate that nicardipine is comparable in efficacy to nifedipine and has a similar adverse effect profile and can also be considered a useful therapeutic agent for the treatment of chronic stable angina pectoris.
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PMID:Randomized double-blind placebo-controlled comparison of nicardipine and nifedipine in patients with chronic stable angina pectoris. 351 Aug 23

Thirty patients (28 males and 2 females) aged 46-68 years with established chronic stable angina were studied in a placebo-controlled double-blind crossover trial to examine the efficacy of oral ticlopidine (an antiplatelet agent) 250 mg twice daily. The baseline mean +/- SEM exercise time of 7.5 +/- 0.5 min rose to 8.1 +/- 0.6 min after 2 weeks of placebo run-in, 8.8 +/- 0.7 min after 4 weeks of double-blind placebo, and to 9.2 +/- 0.6 min with ticlopidine therapy; none of these changes achieved statistical significance. Similarly, time to the development of 1 mm ST-segment depression, maximal ST-segment depression, heart rate, and rate-pressure product failed to show any statistically significant changes during ticlopidine therapy. Ambulatory electrocardiographic monitoring showed that the mean number of episodes of ST-segment depression greater than 1 mm remained unaltered during ticlopidine therapy. Four patients (3 during placebo, 1 during ticlopidine) stopped treatment prematurely because of unstable angina and two because of adverse effects. Our data suggest that ticlopidine has no significant effect on objective indices of myocardial ischemia in patients with chronic stable angina, that placebo has no effect on the objective indices of myocardial ischemia derived from exercise testing and ambulatory electrocardiographic monitoring, and that exercise testing and ambulatory electrocardiographic monitoring in patients with chronic stable angina pectoris are reproducible.
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PMID:Are anti-platelet drugs of value in the management of patients with chronic stable angina? A study with ticlopidine. 353 37

Ten patients with chronic stable angina were treated with 4 incremental doses of tiapamil (200 mg, 400 mg, 600 mg and 800 mg) in a double-blind, placebo-controlled study. Treadmill exercise electrocardiograms were performed before and after single oral doses of tiapamil. A dose-dependent increase in exercise duration occurred after tiapamil with significant improvement after tiapamil 600 mg and 800 mg. Mean exercise duration increased from 327 +/- 41 seconds (control) to 399 +/- 49 seconds (P less than 0.01) after tiapamil 600 mg and from 314 +/- 39 seconds (control) to 416 +/- 49 seconds after tiapamil 800 mg, P less than 0.001. There was an associated improvement in mean exercise time to onset of 1 mm ST-segment depression from 240 +/- 41 seconds (control) to 300 +/- 48 seconds in 10 patients after tiapamil 600 mg, (P less than 0.02) and from 206 +/- 35 seconds (control) to 272 +/- 51 seconds in 9 patients after tiapamil 800 mg, P less than 0.01. Two patients were free of angina and 1 patient normalized his ST-segments after tiapamil 800 mg. Dose-dependent side-effects were mild and tolerable. Tiapamil is safe and highly effective in improving exercise tolerance and relieving myocardial ischaemia in patients with chronic stable angina.
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PMID:Efficacy of incremental doses of tiapamil on exercise performance in patients with chronic stable angina pectoris. 353 14

The acute antianginal effects of 5 mg and 20 mg nisoldipine were compared with 20 mg nifedipine and placebo. Maximal treadmill exercise testing was performed before and 3 hours after drug administration in 10 patients with chronic stable angina. Resting heart rate and systolic blood pressure were unchanged following low-dose nisoldipine, but 20 mg nisoldipine and 20 mg nifedipine increased heart rate and decreased systolic arterial pressure (p less than 0.05). Time (in seconds) to the onset of 0.1 mV ST segment depression was significantly prolonged after 5 mg nisoldipine (+60 +/- 53; p less than 0.05) and 20 mg nisoldipine (+100 +/- 78; p less than 0.01) but not after 20 mg nifedipine (+48 +/- 131; p = NS). Total exercise duration increased significantly following 5 mg and 20 mg nisoldipine (p less than 0.01 and p less than 0.001, respectively) but only slightly following nifedipine (p = NS). The maximal rate-pressure product was increased to a similar degree following doses of both nisoldipine and nifedipine (p less than 0.05). Nisoldipine is an effective antianginal agent which performs well in comparison to nifedipine.
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PMID:Comparative antianginal effects of nisoldipine and nifedipine in patients with chronic stable angina. 354 54

To examine the effects of chronic oral therapy with verapamil, 120 mg three times a day, and nifedipine, 20 mg four times daily, on left ventricular ejection fraction and regional wall motion at rest and exercise, 10 patients with chronic stable angina pectoris underwent serial rest and exercise radionuclide angiography. Pre drug control study revealed a resting left ventricular ejection fraction (LVEF) of 0.62 +/- 0.08, falling to 0.54 +/- 0.12 at peak exercise (p less than 0.05). Wall motion score deteriorated from a resting value of 13.8 +/- 2.3 to 10.6 +/- 1.8 (p less than 0.01) with exercise. Patients were subsequently randomized to verapamil or nifedipine for 4 weeks each in an open-labeled crossover design. Rest and exercise radionuclide angiography were repeated at the end of each 4-week period. Neither verapamil nor nifedipine had a significant effect on resting LVEF (verapamil LVEF = 0.61 +/- 0.10, nifedipine LVEF = 0.64 +/- 0.02). Likewise, they had no significant effect on resting wall motion score (verapamil = 14.2 +/- 2.2, nifedipine = 14.4 +/- 1.6). Both verapamil and nifedipine significantly increased LVEF at peak exercise (verapamil = 0.63 +/- 0.09, nifedipine = 0.65 +/- 0.08, p less than 0.05 vs pre drug control) and improved peak exercise wall motion score (verapamil = 13 +/- 1.9, nifedipine = 13.8 +/- 1.6, p less than 0.05 vs pre drug control). Both drugs significantly reduced maximal ST depression at peak exercise and prolonged exercise duration. Episodes of angina and nitroglycerin use were also significantly reduced. In summary, verapamil and nifedipine improved left ventricular performance at exercise in patients with angina pectoris.
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PMID:Improved left ventricular performance during exercise with verapamil or nifedipine in patients with chronic stable angina. 354 95

Ambulatory electrocardiographic (ECG) monitoring of ischemia in patients with coronary artery disease (CAD) provides a new technique for the assessment of ischemic activity and the evaluation of therapies outside of the hospital. Numerous studies have demonstrated that the majority of patients with CAD have episodes of symptomatic and asymptomatic ST segment depression during routine daily activities. Rubidium-82 positron-emission tomographic studies have provided evidence for decreased myocardial perfusion during these episodes of ST segment depression. The prognostic importance of asymptomatic ischemia has been shown in patients with unstable angina to be a marker for early unfavorable cardiac events. Preliminary results suggest a poorer outcome for those patients with chronic stable angina who show episodes of ischemia as well. Ambulatory monitoring studies suggest that total ischemic activity may be underestimated by conventional testing. Whether all ischemic activity detected by ambulatory monitoring requires treatment awaits further study.
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PMID:Characteristics and significance of ischemia detected by ambulatory electrocardiographic monitoring. 355 18

Transient ST segment changes are thought to be an indicator of intermittent myocardial ischemia in patients with chronic stable angina pectoris, and ambulatory ECG monitoring is a potentially useful means of quantifying these changes. In order to evaluate their repeatability, the automated analytical system developed in our department was carefully validated. Ambulatory ST segment monitoring was then performed on two occasions, 6 weeks apart, in 16 patients with established chronic stable angina pectoris of at least 1 year's duration. Both periods of monitoring were undertaken after administration of placebo for 2 weeks, and two bipolar ECG leads (CM5 and CC5) were monitored on both occasions. The total number (mean +/- SEM) of episodes of ST segment depression greater than 1 mm and of 3 minutes' duration or more in 24 hours was 4.9 +/- 1.0 and 5.1 +/- 1.0 on the first and second recordings (p = NS), and the total duration of ST segment depression in 24 hours was 83.6 +/- 27.7 minutes and 78.9 +/- 20.8 minutes, (p = NS) respectively. The maximal depth of ST segment depression observed during 24 hours was 3.5 +/- 0.3 mm and 3.4 +/- 0.2 mm, respectively, in lead CM5 (p = NS), with similar findings from lead CC5. These results demonstrate that ambulatory ST segment depression observed during uncontrolled normal daily activity in patients with established chronic stable angina pectoris is reproducible. This technique could provide a valuable method for assessment of antianginal drugs and patterns of ST segment changes during normal daily activities, provided that manual checks to ensure artifact exclusion are used to supplement the automated analysis.
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PMID:Reproducibility and validity of ambulatory ST segment monitoring in patients with chronic stable angina pectoris. 357 1

In 50 patients with chronic stable angina and in 10 asymptomatic young male volunteers, the behavior of S-wave amplitude was studied during episodes of ischemic ST-segment depression, both induced by exercise testing and occurring during ambulatory electrocardiographic monitoring. With exercise, all patients showed diagnostic ST-segment depression (0.16 +/- 0.05 mV) which, in 49, was associated with an increase in S-wave amplitude. No consistent changes in R-wave amplitude were observed. S-wave amplitude also increased in all control subjects during exercise, but the sum of R and S wave remained constant, while it increased in 42 patients. In the 10 study patients undergoing Holter monitoring we identified 170 episodes of ischemic ST-segment depression, of which 169 were associated with increased S-wave amplitude. Isolated increases in S-wave amplitude without ST-segment changes occurred in 3 of 4 normal subjects. Dipyridamole echocardiography revealed regional wall motion abnormalities in 12 of 21 patients; the changes were invariably associated with increased S-wave amplitude but not necessarily with diagnostic ST-segment depression. An increase in S-wave amplitude is almost invariably associated with subendocardial ischemia, sometimes in the absence of ST-segment changes; this sign could represent a sensitive (although less specific) additional marker of myocardial ischemia.
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PMID:Increase in S-wave amplitude during ischemic ST-segment depression in stable angina pectoris. 359 82

To examine the effect of diltiazem 60 mg thrice daily and propranolol 80 mg thrice daily on myocardial ischaemia during unrestricted daily life, we have studied 14 patients with established effort-induced chronic stable angina pectoris in a double-blind crossover study. Ambulatory electrocardiographic monitoring was performed using frequency modulated (FM) tape recorder after 2 weeks of placebo therapy and at the end of each 4 week treatment period for a minimum of 24 h. The mean (+/- SEM) number of episodes of ST-segment depression greater than 1 mm during placebo treatment were 97 +/- 28, and these fell to 54 +/- 27 during diltiazem treatment (p less than 0.05) and to 12 +/- 6 during propranolol treatment (p less than 0.02). The maximal depth of ST-segment depression in 24 h, which indicates the severity of the episode, was 3.3 +/- 0.4 mm during placebo, 2.5 +/- 0.2 mm during diltiazem (p less than 0.05), and 1.6 +/- 0.5 mm during propranolol (p less than 0.01). Both diltiazem and propranolol treatment produced significant reduction in the total area of ST-segment depression observed during 24 h. A uniform reduction in the mean heart rate during the 24 h was observed during propranolol therapy and not during diltiazem therapy. Both diltiazem and propranolol treatment improved indices of myocardial ischaemia during daily normal unrestricted life, as measured by ambulatory ST-segment monitoring in patients with established chronic stable angina pectoris. Their differing effects on heart rate suggest that they act by different mechanisms.
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PMID:Effect of diltiazem and propranolol on myocardial ischaemia during unrestricted daily life in patients with effort-induced chronic stable angina pectoris. 362 94

Circadian periodicity was examined in 68 patients with chronic stable angina and in 9 patients with Prinzmetal angina. The frequency and duration of transient ischemic episodes were determined from analysis of 1 or more 24-hour Holter recordings by the compact analog technique. Ninety percent of the episodes in both syndromes were silent; 80% of the episodes of Prinzmetal angina were associated with ST-segment elevation and all episodes of chronic stable angina had ST-segment depression. Ischemic episodes were shorter (3 +/- 2 vs 18 +/- 23 minutes, p less than 0.0005) but more frequent (21 +/- 18 vs 6 +/- 4 per 24 hours, p less than 0.0001) in patients with Prinzmetal angina than in those with chronic stable angina. In patients with chronic stable angina, both silent and painful episodes had a peak occurrence in the morning and early afternoon hours (between 8 AM and 3 PM); the fewest episodes were between 1 AM and 5 AM. This distribution was not random by chi-square test (p less than 0.001). Cosinor analysis of ischemic episodes periodicity showed the acrophase at 1 PM, which was not different from that (3 PM) of the circadian rhythmicity for heart rate. In case of Prinzmetal angina, the acrophase of heart rate changes was at 5 PM, but a clear periodicity in the distribution of the ischemic episodes was not found. These differences in the circadian periodicity may reflect differences in the mechanism of ischemia in chronic stable angina and in Prinzmetal angina and are likely to be of therapeutic significance.
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PMID:Circadian variation in occurrence of transient overt and silent myocardial ischemia in chronic stable angina and comparison with Prinzmetal angina in men. 363 Sep 31


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