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)

The efficacy of benazepril, metoprolol OROS and their combination was evaluated in 29 patients (42 to 74 years of age) with chronic stable angina and documented coronary artery disease in a placebo-controlled, double-blind, crossover trial using serial quantitated exercise testing and ambulatory electrocardiographic (ECG) monitoring. The mean (+/- SEM) exercise time was 8.5 +/- 0.7 min with placebo, 8.3 +/- 0.6 min (95% confidence interval [CI]-1.06 to 0.54) with benazepril, 9.4 +/- 0.5 min (95% CI -0.32 to 2.14) with metoprolol OROS and 9.6 +/- 0.5 min (95% CI -0.25 to 2.47) with the combination of benazepril and metoprolol OROS. The mean exercise time to the development of 1 mm ST segment depression was prolonged from 6.0 +/- 0.6 min with placebo to 6.3 +/- 0.6 min (95% CI -0.93 to 1.45) with benazepril, 7.9 +/- 0.5 min (95% CI 0.83 to 3.0) with metoprolol OROS and 8.1 +/- 0.6 min (95% CI 0.88 to 3.29) with the combination of benazepril and metoprolol OROS. Benazepril did not alter the rest or maximal heart rate, whereas metoprolol OROS alone and in combination significantly lowered the heart rate at rest and during maximal exercise. Systolic blood pressure at rest was nonsignificantly reduced, whereas diastolic blood pressure was lowered significantly by all treatments in comparison with placebo. At maximal exercise, only metoprolol OROS, whether given alone or in combination with benazepril, was able to blunt significantly systolic blood pressure and rate-pressure product.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of benazepril and metoprolol OROS alone and in combination on myocardial ischemia in patients with chronic stable angina. 221 77

In a group of 37 patients with chronic stable angina the authors compared results of bicycle ergometry after a load before and after coronary artery bypass grafting. The group included only patients who had to terminate initial ergometry performed during the last two months before operation on account of stenocardia and signs of myocardial ischaemia on the ECG tracing. On average 20 months after coronary artery bypass grafting ergometry was repeated. Nineteen patients (51%) lacked electrocardiographic signs of myocardial ischaemia, 18 patients (49%) suffered from ischaemia after a load (depression S-T greater than or equal to 2 mm). Of these in 18 patients 8 (44%) no stenocardial attacks were present in another 5 (28%) stenocardia developed only when the depressions were S-T greater than 2 mm. Six patients (33%) had depressions S-T greater than or equal to 3.5 mm at a time when during ergometry they had no complaints and were engaged in similar work loads occasionally also at home. The authors conclude that in the investigated group silent ischaemia after a load was frequent in patients after a coronary artery bypass grafting and frequently it was severe. Patients after coronary artery bypass grafting developed stencardia only after greater S-T depressions than before operation. All patients after coronary artery bypass grafting should be checked by means of loading tests.
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PMID:[Silent stress ischemia in patients after aortocoronary bypass]. 228 17

Forty men with chronic stable angina and no prior myocardial infarction were studied. Exercise tolerance testing was carried out off treatment and after beta blockade. beta Blockers were stopped and the patients were randomised to a control group and a study group of patients who undertook a one year high intensity training programme. The groups were then restudied. Submaximum heart rate was reduced by 13 beats per minute by training and by 23 beats per minute by atenolol. Training increased the maximum heart rate by 10 beats per minute and atenolol reduced it by 29 beats per minute. The double produce ST threshold was increased from 183 to 205 by training but reduced to 143 by atenolol. Maximum ST depression was similarly reduced by both training and atenolol. As a result of the effects on maximum heart rate, training produced a greater improvement in exercise tolerance than atenolol with a treadmill time increased from 741 seconds to 1272 seconds with training compared with 974 seconds with atenolol. Other variables were similarly affected. Thus the antianginal efficacy of exercise training is as good as that achieved by beta blockade and represents an alternative to such treatment.
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PMID:Antianginal efficacy of exercise training: a comparison with beta blockade. 239 Mar 97

To determine the circadian distribution of episodes of myocardial ischemia, studies were performed in 111 patients with chronic stable angina pectoris, positive exercise test results and angiographically proven coronary artery disease. During 24 hours of ambulatory electrocardiographic monitoring, 101 symptomatic and 298 asymptomatic ischemic episodes (ST-segment depression greater than 1 mm, duration greater than 1 minute) were observed. The number of ischemic episodes and the cumulative duration of ischemia showed a circadian variation with the highest values between 8 and 10 A.M. and between 4 and 5 P.M. associated with a similar circadian variation of heart rate. Mean duration of ischemic episodes, maximal amplitude of ST-segment depression during ischemic episodes and increase in heart rate before the onset of ischemic episodes showed no significant circadian variation. Heart rate at the onset of ischemic episodes and maximal heart rate during ischemic episodes were lower between midnight and A.M. than during other times of the day. The morning and afternoon increase in ischemic activity is not paralleled by changes reflecting a decrease in myocardial oxygen supply during these periods (heart rate at onset of ischemia, heart rate increase before onset of ischemia), but is paralleled by a similar circadian variation of heart rate. The circadian variation in ischemic activity is predominantly based on a comparable variation in myocardial oxygen requirements.
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PMID:Circadian distribution of the characteristics of ischemic episodes in patients with stable coronary artery disease. 239 82

We studied the effects of alpha 1-adrenoceptor blockade with indoramin on exercise tolerance in 15 patients with chronic stable angina using a double-blind crossover protocol. Thirteen patients had been receiving beta-adrenoceptor blocking drugs and nitrates. The therapy of these patients was continued unchanged throughout the study. Indoramin, in a dose of 25 mg three times daily, prolonged exercise duration by 17% (p less than 0.01) and increased oxygen consumption during exercise by 21% (p less than 0.01), while the maximal double product was unchanged. This increase in exercise capacity was associated with significant attenuation in ST segment depression during exercise. To investigate the mechanism of this antianginal effect, we studied the effects of indoramin (0.2 mg/kg i.v.) on coronary and systemic haemodynamics in a further 11 male patients with chronic stable angina who were receiving beta-adrenoceptor blocking drugs. Measurements were obtained during sinus rhythm and during atrial pacing from 100 beats/min, incremented by 20 beats/min at intervals of 3 min until the onset of angina. Indoramin had no effect on resting heart rate (64 +/- 2 vs. 67 +/- 2 beats/min), but did prolong pacing time to angina (7.4 +/- 0.7 vs. 5.4 +/- 0.5 min; p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antianginal and haemodynamic effects of alpha 1-adrenoceptor blockade. 242 88

To examine the antianginal and antihypertensive efficacy of nitrendipine, a new calcium channel blocking agent, 25 patients with chronic stable angina pectoris (NYHA I-III) and systemic hypertension underwent cardiac catheterization and treadmill exercise tests. Acute hemodynamic results were obtained before and 2 h after oral administration of 20 mg nitrendipine. They showed a significant decrease in aortic pressure (162.1 +/- 27.4/80.0 +/- 12.1 vs. 134.9 +/- 23.5/74.2 +/- 13.1 mm Hg), pulmonary arterial pressure (25.4 +/- 5.4/11.3 +/- 3.7 vs. 21.9 +/- 5.4/9.9 +/- 3.7 mm Hg), and pulmonary wedge pressure (10.0 +/- 4.4 vs. 6.6 +/- 3.8 mm Hg). Cardiac index (+31%) and stroke volume (+33%) increased markedly, whereas heart rate remained unchanged (66.9 +/- 11.4 vs. 66.8 +/- 10.8 beats/min). Chronic hemodynamic results and exercise tolerance tests were obtained before and 8 weeks after oral nitrendipine therapy. A significant decrease in arterial blood pressure was observed (167 +/- 22/86 +/- 10 vs. 126 +/- 32/76 +/- 19 mm Hg). Exercise tolerance improved concerning test duration (+22%) and total exercise capacity (+37%). Maximal ST-segment depression decreased by 30% (0.2 +/- 0.03 vs. 0.14 +/- 0.02 mV) and subsequently the anginal frequency was reduced from 7.8 +/- 2.1 to 3.8 +/- 1.7 attacks/week (-50%). The maximal rate-pressure product during exercise remained unchanged. Plasma levels of cholesterol, triglycerides, and LDL- and HDL-cholesterol did not show any significant alterations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute and chronic effects of nitrendipine on hemodynamics and myocardial ischemia in patients with combined angina pectoris and hypertension. 246 68

Fifty-four patients with chronic stable angina were studied to determine and compare weekly variability of indexes for the detection of myocardial ischemia. All patients underwent three single-blind placebo periods, each lasting 1 week. An exercise treadmill test, 24 h ambulatory electrocardiographic (Holter) monitoring (analyzed blindly) and an accurate diary of anginal attacks and nitroglycerin use were obtained at the end of each placebo period. An unbalanced, completely random component of variance analysis was used to calculate a component for within subject variability and a component for among subject variability. The coefficient of variation and percent variation (within subjects) of onset of chest pain during exercise were 19% and 30%, respectively; the corresponding values were 28% and 33% for onset of 1 mm ST depression, 15% and 15% for exercise duration, 44% and 27% for number of ischemic episodes/24 h, 56% and 43% for anginal frequency and 55% and 27% for nitroglycerin consumption, respectively. With use of this statistical method and variation within subjects, the change in the value of each variable necessary to exceed those attributable to spontaneous variation was determined. The trade-off between repeated measurements and number of subjects, the sample size estimated for planning studies and the minimal sample size for using various designs were also determined. Although the data indicate that all indexes for myocardial ischemia, both during exercise and during daily activity, vary considerably, but the exercise variables have less variability and are more reproducible.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Variability of indexes for myocardial ischemia: a comparison of exercise treadmill test, ambulatory electrocardiographic monitoring and symptoms of myocardial ischemia. 249 43

The effects of different types of exercise on ischemic threshold were studied in 33 patients with chronic stable angina, documented coronary artery disease, and reproducible positive exercise test results. On average, ST segment depression developed at a significantly higher heart rate and rate-pressure product when the standard modified Bruce protocol was preceded by a warm-up period (113 +/- 13 vs 119 +/- 15 beats/min and 18,813 +/- 3682 vs 20,357 +/- 4227 beats/min X mm Hg, respectively; p less than 0.05 and less than 0.01). No significant changes were observed when the exercise was started abruptly. Analysis of results in individual patients showed that changes in rate-pressure product at 1 mm ST segment depression greater than or equal to 2000 beats/min X mm Hg developed with different types of exercise in 11 patients (group I), whereas in 22 patients little or no change occurred (group II). All patients also underwent exercise testing before and after 0.5 mg of sublingual nitroglycerin; improvement induced by nitroglycerin was significantly greater in group I than in group II (22 +/- 8 vs 8 +/- 9 beats/min and 4896 +/- 1998 vs 1064 +/- 2145 beats/min X mm Hg; p less than 0.01). Furthermore, isometric handgrip exercise carried out during angiography resulted in significant reduction of luminal diameter at the site of the stenosis of group I (1.22 +/- 0.39 vs 0.99 +/- 0.35 mm; p less than 0.01) but not in group II (1.12 +/- 0.22 vs 1.16 +/- 0.3 mm, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ischemic threshold varies in response to different types of exercise in patients with chronic stable angina. 250 3

The anti-anginal effect of sustained release diltiazem, isosorbide-5-mononitrate (IS-5-MN) and their combination has been evaluated in 25 patients in 4 blinded treatment periods of 2 weeks each. The number of anginal attacks during each treatment period was reduced from a mean of 23 during placebo to 15 during diltiazem and 15 during combination therapy, but it was not significantly changed after IS-5-MN-20. A similar pattern was seen for nitroglycerin consumption and number of angina-free days. Maximal exercise capacity was also significantly improved following diltiazem and the drug combination, and it was not changed after IS-5-MN. ST segment depression was less pronounced after diltiazem and the combination compared to IS-5-MN. There was no difference in exercise capacity or ST segment change between diltiazem and the combination. The PR interval was slightly prolonged after diltiazem, but this was of no clinical importance. Adverse effects of diltiazem treatment were rare. Headache was common following IS-5-MN (13 patients) and the combination (11 patients). Thus, sustained-release diltiazem was of value in the treatment of chronic stable angina pectoris, whereas IS-5-MN was not effective, either as a single therapy or in combination with diltiazem. The reason for the inefficacy of IS-5-MN is not known, but the development of tolerance and an inadequate dose are possible explanations.
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PMID:Effects of diltiazem and isosorbide-5-mononitrate, alone and in combination, on patients with stable angina pectoris. 250 59

1. The effects of adding slow release nifedipine in doses of 20 mg and 40 mg twice daily to atenolol therapy (50 mg twice daily) were assessed in 18 patients with chronic stable angina. 2. The addition of the lower dose of nifedipine to atenolol did not significantly alter the weekly consumption of glyceryl trinitrate or the mean number of anginal attacks as assessed by diary cards. However, 2 h after dosing there was a significant prolongation during stress testing in the time to onset of both 1 mm ST depression on the ECG (by 28%) and to angina (by 37%) compared with atenolol alone, but no benefit was apparent by 12 h after dosing. 3. At a dose of 40 mg twice daily, nifedipine significantly reduced glyceryl trinitrate consumption by 25% and the number of anginal attacks by 36%. The times to onset of ST depression and angina were increased by 37% and 55% respectively at 2 h and by 24% and 26% respectively 12 h after dosing. 4. Analysis of the frequency distribution of anginal attacks showed decreasing efficacy with time after administration of nifedipine. The overall results also suggest a relationship between efficacy and the plasma nifedipine concentration, with a mean 20% improvement in time to development of angina occurring at a nifedipine plasma concentration of approximately 30-40 ng ml-1. 5. In conclusion, the reduction of effort-related angina by nifedipine is related to its plasma concentration and the effective duration of action of the 20 mg slow release formulation is less than 12 h.
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PMID:Slow release nifedipine plus atenolol in chronic stable angina pectoris. 251 11


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