Gene/Protein Disease Symptom Drug Enzyme Compound
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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The efficacy of a once daily, sustained release formulation of verapamil (Verapamil SR, 360 mg) was evaluated in 19 patients with chronic angina pectoris using a double-blind placebo-controlled crossover protocol. Evaluation by exercise testing, 24 hour electrocardiographic ambulatory monitoring and blood drug level assays was performed at the end of each 2 week phase, 21 to 23 hours after the last dose. After the crossover protocol, all patients were given sustained release verapamil for 4 weeks and the evaluation was repeated. Exercise time (mean +/- SEM) increased from 7.4 +/- 0.6 minutes with placebo to 9.6 +/- 0.8 minutes with verapamil (p less than 0.001) and to 9.5 +/- 0.7 minutes (p less than 0.001) after 4 weeks of therapy. The mean time to 1 mm ST depression also increased significantly, from 4.5 +/- 0.4 and 4.8 +/- 0.5 minutes in bipolar leads CM5 and CC5, respectively, with placebo, to 5.5 +/- 0.6 (p less than 0.05) and 6.2 +/- 0.5 minutes (p less than 0.01) with verapamil. Maximal ST depression and rest and peak heart rates were not altered significantly. The mean rate-pressure product was 208 +/- 9.9 with placebo and decreased to 189 +/- 7.7 (p less than 0.05) with verapamil but rose to 200.6 +/- 10.4 (p = NS) after 4 weeks of therapy. The mean hourly heart rates were lower with the drug than with placebo throughout the 24 hour period but there was no significant bradycardia, arrhythmia or heart block.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sustained release verapamil, a once daily preparation: objective evaluation using exercise testing, ambulatory monitoring and blood levels in patients with stable angina. 310 85

To assess the dosing equivalency and the early and late antianginal efficacy of a gastrointestinal therapeutic system for once-daily, continuous-release nifedipine (N-GITS), 10 patients with stable angina pectoris, who were previously receiving chronic treatment with nifedipine, completed a 12-week trial comparing N-GITS with standard nifedipine. All patients (nine men and one woman; mean age 54 +/- 2 [SEM] years) who were receiving standard nifedipine (mean dose 40 +/- 5 mg/24 hr) for more than 2 weeks (mean 8 +/- 2 months, range 2 to 36 months) were switched to an equivalent once-daily dose (39 +/- 5 mg/24 hr) of N-GITS. Standard nifedipine and N-GITS were compared by symptom-limited exercise treadmill tests with a baseline test (A) performed 3 hours after a standard dose of nifedipine. Exercise tests were also performed after 2 weeks of treatment with N-GITS 3 hours (B) and 24 hours (C) after the drug was given, and after 12 weeks of treatment with N-GITS, 24 hours after dosing (D). Results of exercise tests showed no significant difference in mean exercise time--(A) 422 +/- 25 vs (B) 426 +/- 36 vs (C) 438 +/- 35 vs (D) 487 +/- 37 seconds. Likewise, there was no significant mean difference in peak double product, resting heart rate, peak exercise heart rate, or resting or maximal systolic blood pressure for any of the exercise test points. Furthermore, five patients (50%) reported side effects with standard nifedipine (all vasodilator-flushing, dizziness, or both), which resolved after treatment with N-GITS (p +/- 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative dosing and efficacy of continuous-release nifedipine versus standard nifedipine for angina pectoris: clinical response, exercise performance, and plasma nifedipine levels. 335 8

The pharmacokinetics of diltiazem and its major metabolites, deacetyldiltiazem and N-monodemethyl-diltiazem, were studied after single and chronic oral administration in eight patients aged 45 to 69 years with unstable angina pectoris, treated by diltiazem, 120 mg t.i.d. After a single oral dose the time to peak plasma diltiazem concentration was 3.4 (2.1 to 5.0) hours and the elimination half-life was 6.6 hours (4.4 to 10.8 hours). These were unchanged after repeated oral administration (16 to 19 doses). The mean trough (8 hours after administration) plasma diltiazem level after six consecutive doses was 167 micrograms/L (63 to 286 micrograms/L) and was thereafter stable. With chronic administration the AUC increased by a factor of 2.24 +/- 0.31 (SEM; P less than 0.01). Plasma protein binding of diltiazem in these patients ranged from 83% to 93% whereas deacetyldiltiazem binding ranged from 58% to 75%. Plasma protein binding was independent of drug concentration and duration of treatment. Thus an average dose of 120 mg diltiazem given every 8 hours would appear to be a suitable regimen of treatment in most patients with angina pectoris, although users should be aware that there is a significant interpatient variability in steady-state diltiazem concentrations and that a significant accumulation of diltiazem occurs with chronic therapy.
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PMID:Pharmacokinetics of diltiazem in patients with unstable angina pectoris. 335 90

To assess the left ventricular function of patients who suffer from post-infarction angina and left ventricular failure in the coronary care unit, 79 consecutive survivors (mean age 48 years) of a first acute myocardial infarction were prospectively studied and followed-up for a mean 18- (10-34) month period. Forty-seven had an uncomplicated infarction, 17 suffered from post-infarction angina and 15 had left ventricular failure. The left ventricular function of these patients prior to discharge from hospital was assessed by cross-sectional echocardiography and radionuclide angiography. Analysis of left ventricular wall motion was performed in all patients using a 11-segment model of the left ventricular. The ejection fraction was determined by echocardiography in 47 patients and by radionuclide angiography in 50. The mean echocardiographic wall motion score of post-infarction angina patients (4.8 +/- 0.8) (+/- SEM) was lower than that of patients with left ventricular failure (9.5 +/- 0.5) (P less than 0.001), but was not different from patients suffering uncomplicated infarctions (4.6 +/- 0.3). The mean echocardiographic ejection fraction was also similar in post-infarction angina (45.3 +/- 4.0; n = 16) and patients with uncomplicated infarction (51.9 +/- 2.7; n = 17), but was lowest in the group of patients with left ventricular failure (35.1 +/- 3.3; n = 14). Similarly, the radionuclide ejection fraction of patients with post-infarction angina (41.4 +/- 3.4; n = 17) and patients with uncomplicated infarction (45.6 +/- 2.7; n = 19) did not differ, but was lower in patients with left ventricular failure (25.9 +/- 2.8; n = 14). The echocardiographic ejection fraction correlated with that obtained by radionuclide angiography in all 46 patients (r = 0.71, P less than 0.001). The wall motion score correlated with the radionuclide ejection fraction in all 50 patients (r = -0.73, P less than 0.001) and with the echocardiographic ejection fraction in 47 patients (r = -0.55, P less than 0.001). During follow-up, 3 (18%) patients suffering post-infarction angina and 2 (13%) with left ventricular failure died. New infarction was seen in 2 (12%) and 1 (7%) patients in these groups, respectively. We conclude that the left ventricular function of patients who suffer from post-infarction angina in the coronary care unit is good, but is impaired in those with even transient left ventricular failure. Echocardiographic assessment of cardiac function prior to hospital discharge was highly successful and may be performed in all such patients.
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PMID:Left ventricular function of survivors of a first complicated acute myocardial infarction. A prehospital discharge cross-sectional echocardiographic study. 337 75

We studied 40 patients with preoperative ejection fraction (EF) of 0.35 or less who underwent aortocoronary bypass. An average of 3.1 saphenous vein grafts per patient were inserted and revascularization was considered complete in 33 (82%) of the subjects in the group. Mean follow-up period was 29 months (range 12-65 months). Early mortality was 5% (2 patients) and there were 7 late deaths (3 cardiac and 4 non-cardiac). The 5-year cardiac actuarial survival rate was 74 +/- 13% (+/- SEM). Angina has improved in 29 (94%) of the 31 long-term survivors with 23 (74%) being totally asymptomatic. Twenty-two of the long-term survivors performed an exercise test at the end of their follow-up period. These tests revealed that bypass surgery in such patients results in significantly enhanced myocardial oxygen consumption with concomitant increase in effort level and duration. The exercise ability is probably directly related to the degree of revascularization.
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PMID:Exercise performance in patients with impaired left ventricular function following aorto coronary bypass. 349 94

Between February 1978 and October 1982, 40 patients with preoperative ejection fraction (EF) of 0.35 or less underwent aortocoronary bypass. An average of 3.1 saphenous vein grafts per patient were inserted and revascularization was considered complete in 33 (82%) of the subjects in the group. Mean follow-up period was 29 months (range 12-65 months). Early mortality was 5% (2 patients) and there were seven late deaths (3 cardiac and 4 non-cardiac). The five-year cardiac actuarial survival rate was 74% +/- 13% (+/- SEM). Angina has improved in 29 (94%) of the 31 long-term survivors with 23 (74%) being totally asymptomatic. Twenty-two of the long-term survivors performed an exercise test at the end of their follow-up period. These tests revealed that bypass surgery in such patients results in significantly enhanced myocardial oxygen consumption with concomitant increase in effort level and duration. The exercise ability is probably directly related to the degree of revascularization.
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PMID:Improved functional results following myocardial revascularization in patients with left ventricular dysfunction. 349 95

To determine whether endogenous opioids play a role in modulating the appreciation of chest pain in angina pectoris, the specific opioid antagonist, Naloxone, was used. The hypothesis was that the appearance time of ischemic myocardial pain should decrease after Naloxone if centrally mediated pain perception is significantly influenced by the endorphin system in angina pectoris. A randomized double blind clinical trial was conducted in 5 men with effort-induced angina pectoris associated with ST segment changes. Three multi-stage exercise tests, using the Bruce protocol were performed on the same day and time, on three successive weeks. Chest pain was reported 4.3 +/- 0.3 (SEM) minutes after starting exercise on the first or baseline test. On subsequent tests patients received either Naloxone 2 mg IV or a similar volume of saline placebo. Angina pectoris occurred significantly (p. less than 0.05) earlier (1.6 +/- 0.2 minutes) after Naloxone compared to placebo. There were no significant differences in myocardial ischemia indicated by ST segment changes and no significant differences in resting or exercise blood pressure and heart rate between Naloxone and placebo. Thus, these data focus attention on a neglected area of myocardial ischemic pain and suggest that endogenous opioids play a significant role in the recognition of the pain of effort-related angina pectoris.
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PMID:Effect of naloxone on exercise-induced angina pectoris: a randomized double blind crossover trial. 351 46

Fifteen patients with coronary artery spasm completed a double-blind placebo-controlled trial comparing diltiazem and nifedipine. Increasingly, higher daily doses (diltiazem, 90 to 360 mg; nifedipine, 30 to 120 mg) were administered to achieve optimal clinical effects. Daily diaries and ambulatory electrocardiographic recordings were used to assess efficacy and side effects. Both drugs significantly decreased angina frequency compared with that in the preceding placebo period (diltiazem 1.4 +/- 0.4 [mean +/- SEM] to 0.4 +/- 0.2 episodes per day; nifedipine 1.4 +/- 0.3 to 0.4 +/- 0.1 episodes per day; both p less than 0.05). Ambulatory electrocardiographic recordings showed fewer ST shifts than were expected during all treatment periods (0.02/h recorded during placebo, none during diltiazem and 0.02/h during nifedipine therapy). Although some patients responded better to one drug than the other, neither drug resulted in a clearly superior clinical response. Diltiazem was discontinued in one patient because of urticaria, but the total number of side effects was higher with nifedipine (12 of 15 patients) than with diltiazem (5 of 15, p less than 0.01). Nine patients remained symptomatic on single drug treatment and entered open label treatment with the combination of diltiazem and nifedipine. Three patients did not tolerate the combination because of important side effects; the other six also had side effects, but these were relatively minor. Four patients received no more benefit from the combination than from a single agent; the condition of two patients improved. Both diltiazem and nifedipine provide effective antianginal therapy for coronary spasm, but diltiazem has fewer side effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of diltiazem and nifedipine alone and in combination in patients with coronary artery spasm. 354 92

The antiischaemic properties of intravenous diltiazem in recommended therapeutic doses are disputed. In 17 patients with coronary artery disease the systemic and coronary haemodynamic effects of diltiazem were assessed during a high-dose infusion (0.4 mg kg-1 per 5 min, followed by 0.4 mg kg-1 per 10 min). In addition, its potential antiischaemic properties were investigated during identical pacing stress tests, 30 minutes before (P1) and immediately after diltiazem administration (P2). Diltiazem reduced left ventricular systolic pressure from 133 +/- 5 to 116 +/- 5 mmHg (P less than 0.005, means +/- SEM), persisting until after P2. It decreased systemic and coronary resistance by 32% (P less than 0.001) and 29% (P less than 0.005), respectively, with a sustained increase in cardiac output from 5.9 +/- 0.4 to 7.3 +/- 0.6 l min-1 (P less than 0.01), but a brief 20% rise in coronary flow (P less than 0.05), after the bolus infusion only. Heart rate, contractility, left ventricular filling pressure and myocardial O2 consumption remained unchanged. Despite high plasma levels (673 +/- 81 micrograms l-1) diltiazem was well tolerated. During identical maximal pacing rates diltiazem considerably reduced myocardial O2 demand (double product: 16.3 +/- 0.8 (P2) vs 21.1 +/- 1.1 (P1), P less than 0.005), due to an 18% decrease in left ventricular systolic pressure, resulting in diminished coronary flow and myocardial O2 consumption during P2 (14% and 15%, respectively, P less than 0.05 vs P1). Diltiazem also significantly reduced pacing-induced ischaemia, indicated by normalization of myocardial lactate extraction (1 +/- 8% (P2) vs -41 +/- 12% (P1), P less than 0.05), and left ventricular filling pressure (13 +/- 2 (P2) vs 27 +/- 3 mmHg (P1), P less than 0.01), less ST-segment depression (0.12 +/- 0.01 (P2) vs 0.24 +/- 0.02 mV (P1), P less than 0.01) and improved contractility (Vmax 59 +/- 5 (P2) vs 48 +/- 3 s-1 (P1), P less than 0.05). Angina was absent or less in 15 patients during pacing after diltiazem. Thus, diltiazem, in high dosages, induces continuing systemic but short lasting coronary vasodilation, improves pump function without negative chronotropic and inotropic effects and has pronounced antiischaemic properties, predominantly due to diminished myocardial O2 demand.
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PMID:Acute antiischaemic properties of high dosages of intravenous diltiazem in humans in relation to its coronary and systemic haemodynamic effects. 366 56

The correlation of angina attacks with ST segment changes detected during ambulatory Holter monitoring was evaluated in patients with unstable angina. Forty hospitalized patients had one to three 24-hour Holter recordings each. Twenty-three patients had a cardiac catheterization, confirming significant coronary artery disease. The Holter recordings, scanned blindly by computer, were evaluated for ST segment shifts (defined as +/- 1.5 mm from baseline, lasting 60 seconds or longer). Angina attacks were carefully logged. Over the total forty patient experience, only 15 of 74 (20.3%) angina attacks had corresponding ST segment shifts on the Holter recordings. Nine of 34 (26.5%) angina attacks in the 23 patients who had a cardiac catheterization had corresponding ST segment shifts. A total of 159 ST segment shifts were recorded on these forty patients, but only 15 (9.4%) ST shifts corresponded to a time when the patients were actually experiencing angina attacks. The performance of the test procedure was quantified by use of Youden's J statistic. The aggregate J, over all patients, was 0.203 (J = 1.0 is perfect, J = 0.0 is useless). When consideration was restricted to patients with cardiac catheterization, the aggregate experience J was 0.263. Dealing with only the patients who had angina attacks during the monitoring, and computing the J statistic for each individual patient, the resulting mean J statistic was 0.146, with SEM = 0.0731. The Holter monitoring worked reasonably well in only 2 of the 14 patients who gave clear tests of the procedure. In an attempt to improve the performance of the procedure, 21 Holter recordings in eight patients were reread for ST segment shifts of only +/- 1 mm from baseline, lasting 30 seconds or longer. In these eight patients with rescanned Holter recordings, only five of 17 (29.4%) angina attacks resulted in an ST segment shift. In conclusion, ambulatory Holter recordings proved not to be a suitable method of documenting ST segment shifts during angina attacks in this study.
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PMID:Holter monitor ST segment evaluation in hospitalized patients with unstable angina. 367 5


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