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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dynamic coronary stenoses may be the cause of a variable angina threshold and rest angina in patients with chronic stable angina. It has been suggested that eccentric but not concentric coronary artery stenoses have the potential for dynamic changes of caliber in response to vasoactive stimuli. The vasomotor response of eccentric (asymmetric narrowing) and concentric (symmetric narrowing) coronary stenoses to ergonovine (20 micrograms intracoronary or 300 micrograms intravenous) and isosorbide dinitrate (1 mg intracoronary) was studied in 51 patients with chronic stable angina. Diameter of reference segments (angiographically normal segments proximal to the stenoses) and that of eccentric (n = 30) and concentric (n = 35) coronary stenoses that ranged from 50% to 90% luminal diameter reduction were measured by computerized quantitative angiography before and after ergonovine and isosorbide dinitrate. Ergonovine reduced stenosis diameter (by greater than or equal to 10%) in 80% of eccentric stenoses and 42% of concentric stenoses (p less than 0.05). Mean (+/- SEM) diameter reduction with ergonovine was 19 +/- 3% and 9.5 +/- 2% for eccentric and concentric stenoses, respectively (p less than 0.05). Isosorbide dinitrate increased coronary diameter (by greater than or equal to 10%) in 70% of eccentric and 43% of concentric stenoses (p less than 0.05). Mean diameter of eccentric stenoses increased from 1.15 +/- 0.05 to 1.35 +/- 0.06 mm after nitrate (18.6 +/- 2.5%), whereas diameter of concentric stenoses increased from 1.05 +/- 0.05 to 1.14 +/- 0.05 mm (10 +/- 2.5%) (p less than 0.05). Average dilation of reference segments with administration of isosorbide dinitrate and constriction with ergonovine were not significantly different in patients with concentric and eccentric stenoses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reactivity of eccentric and concentric coronary stenoses in patients with chronic stable angina. 199 79

The vasomotor response of proximal and distal angiographically normal coronary artery segments was studied in 12 patients with syndrome X, 17 age- and gender-matched patients with chronic stable angina and 10 control subjects with atypical chest pain and a normal coronary arteriogram. Ergonovine (300 micrograms by intravenous injection) and isosorbide dinitrate (1 mg by intracoronary injection) were administered to all patients. Computerized coronary artery diameter measurement (angiographically normal segments only) was carried out before and after the administration of ergonovine and nitrate. Baseline intraluminal diameters (mean +/- SEM) of proximal and distal coronary segments were not significantly different in control subjects and patients with syndrome X or coronary artery disease (proximal 2.88 +/- 0.19, 3.01 +/- 0.13 and 2.86 +/- 0.13 mm; distal 1.57 +/- 0.09, 1.70 +/- 0.10 and 1.61 +/- 0.06 mm, respectively). With ergonovine, proximal segments constricted by 10 +/- 2%, 7 +/- 2% and 11 +/- 3% and distal segments by 12 +/- 3%, 14 +/- 3% and 14 +/- 2% in control subjects and patients with syndrome X or coronary artery disease, respectively (p = NS). With isosorbide dinitrate, proximal coronary segments dilated by 11 +/- 2%, 10 +/- 2% and 8 +/- 2% (p = NS) and distal segments by 15 +/- 2%, 11 +/- 3% and 13 +/- 2% (p = NS) in control subjects and patients with syndrome X or coronary artery disease, respectively. Within groups, constriction in response to ergonovine and dilation in response to nitrate were not significantly different in proximal and distal segments.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Epicardial coronary artery tone and reactivity in patients with normal coronary arteriograms and reduced coronary flow reserve (syndrome X) 205 Sep 41

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

Although beta blockers are effective for the treatment of angina pectoris, chronic adverse effects produced by these agents--including lethargy, fatigue, and male impotence--can adversely affect patient acceptance and treatment compliance. To assess the clinical effects of switching from anti-anginal treatment with beta blocker only (phase I) to half-dose beta blocker plus the calcium blocker nifedipine (phase II) or nifedipine alone (phase III), 18 patients with chronic stable angina pectoris and side effects to beta blockers were evaluated in a 12-week, open-label trial. Three patients did not complete the study, one secondary to new unstable angina and two secondary to nifedipine side effects. Of the 15 patients completing the trial (13 men and two women; mean age, 54 +/- 5 [SEM] years), all sequentially participated in the one-month phases. Weekly angina frequency assessed from patient diaries was significantly less for treatment with nifedipine only (phase III) as compared with beta blocker (phase I) (1.7 +/- 1 versus 3.9 +/- 1 episodes per week), while phase II was not significantly different. Exercise test time was maintained throughout all phases (phase I, 457 +/- 39; phase II, 458 +/- 40; and phase III, 498 +/- 48 seconds, p not significant). All 15 patients in phase I (100 percent) had side effects to beta blockers, but these side effects were lessened in 12 patients (80 percent) in phase II and 13 patients (86 percent) in phase III, with total alleviation of symptoms in two patients (13 percent) in phase II, and eight patients (53 percent) in phase III. Thus, in patients with side effects to beta blockers, switching to nifedipine is associated with a significant reduction in beta blocker adverse symptoms and equal anti-anginal efficacy.
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PMID:Alternative medical treatment for patients with angina pectoris and adverse reactions to beta blockers. Usefulness of nifedipine. 287 34

The antianginal effects of sustained-released oral nitroglycerin were evaluated in patients with chronic stable angina using a double-blind randomized protocol. Nineteen patients were inducted into the trial and 17 of these completed the study. Two doses of oral nitroglycerin were used; 2.6 mg and 6.5 mg given three times daily for a period of 2 weeks, the patients crossing over to the alternative dose at the end of each period. Evaluation of effect was carried out 2 hours after the morning dose using graded treadmill exercise testing with on-line computer analysis of the electrocardiogram (EKG) (CASE, Marquette Electronics, Inc.). Various exercise parameters were measured and the results compared to placebo values and between the two dosages. The aim was to demonstrate an antianginal effect and to look for a dose-response relationship and for attenuation of effect if any on continued administration. The mean +/- SEM exercise time on placebo was 6.7 +/- 0.6 min, increasing to 8.6 +/- 8 min (p less than 0.02) with 2.6 mg tds dosage and 8.4 +/- 0.7 min (p less than 0.01) with 6.5 mg tds of oral nitroglycerin. None of the other exercise-derived indices were altered significantly by oral nitroglycerin. Two patients were withdrawn because of severe headaches and both were receiving the higher dose. The data did not demonstrate any dose-response relationship but confirmed the anti-anginal efficacy of sustained action oral nitroglycerin. This efficacy did not show any significant attenuation of effect on continued administration, indicating a possible lack of development of tolerance.
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PMID:Oral nitroglycerin in angina pectoris--evaluation of effect by computerized exercise testing using two different doses. 315 16

Ambulatory electrocardiographic (ECG) monitoring of patients with chronic stable angina has demonstrated frequent and prolonged episodes of ischemic ST segment depression, but its clinical use requires an understanding of the components and extent of variability. Therefore, variations in the frequency and duration of episodes of ST segment depression were evaluated with ambulatory ECG recording at daily, weekly, and monthly intervals in 42 patients with chronic stable angina and known coronary artery disease. Data were analyzed with a nested analysis of variance design that yields estimates of variance components. From the estimates of variance components, power calculations and minimum significant percent reductions in frequency and duration of ischemia were derived. During 4,656 hours of ambulatory ECG monitoring, 1,262 episodes of ischemic ST segment depression were detected. The frequency of episodes was 6.3 +/- 0.45/24 hr (mean +/- SEM), and the duration of episodes was 18.3 +/- 2.8/24 hr. Because of variability over time, the ability to detect significant changes was dependent upon the number of subjects, length of monitoring period, and intervals between monitoring periods. In a clinical trial, for example, a sample size of 25 patients monitored for 48 hours with 1 week between control and test conditions would require a 65% reduction in frequency, whereas a sample size of 50 patients monitored under similar conditions would require a 46% reduction in frequency, to attribute the change with 90% power to a therapeutic intervention rather than to a spontaneous variation. When monitoring a single patient for 48 hours with 1 week or 1 month between control and repeat monitoring sessions, episodes of ischemic ST depression must be eliminated to detect significant therapeutic changes in ischemic activity at the 95% confidence level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Variability of transient myocardial ischemia in ambulatory patients with coronary artery disease. 338 11

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

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

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

Identification of a characteristic morphology of a coronary stenosis likely to result in myocardial infarction would facilitate the prospective evaluation of infarct prevention strategies and identification of high-risk patients. We postulated that coronary lesions associated with recent myocardial infarction or unstable angina would have an angiographic morphology suggesting disruption of an atherosclerotic plaque and would appear morphologically different from lesions associated with chronic stable angina. To test this hypothesis, quantitative coronary angiography (Brown-Dodge method) was performed in 15 patients 4 to 30 days after myocardial infarction, in 10 patients with the abrupt onset of unstable angina and single-vessel coronary disease, and in 15 patients with chronic stable angina without prior myocardial infarction. Serial arterial diameters (20 to 40) within each lesion were determined and the degree of luminal irregularity was quantitated by calculation of an "ulceration" index. The majority of all lesions analyzed resulted in severe luminal stenosis (mean 78% area stenosis, all groups). Despite small differences in mean lesion severity among groups, overlap in the degree of luminal compromise prevented precise classification of lesions associated with myocardial infarction or unstable angina based on percent stenosis or minimum luminal cross-sectional area. The mean ulceration index of lesions in patients with unstable angina and in the infarct-related vessel in those with acute myocardial infarction was 0.62 +/- 0.05 (+/- SEM) and 0.61 +/- 0.03, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quantitative angiographic morphology of coronary stenoses leading to myocardial infarction or unstable angina. 394 63


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