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

Within a relatively short period of time, nitroglycerin patches have come into widespread use for treatment of coronary artery disease in the absence of sufficient clinical data in support of their efficacy. Presently, there is still considerable controversy regarding the extent and duration of action as well as the dosage requirements. Accordingly, a study was carried out in six patients with angiographically-documented coronary artery disease, stable exercise-induced angina pectoris and reproducible ST-segment depression to analyze the effects of nitroglycerin patches, formulated to deliver 5 mg, 10 mg, 20 mg as well as 30 mg per 24 hours, respectively, on the extent of ST-segment depression. In a further study, the extent and duration of antianginal and anti-ischemic effects of nitroglycerin patches delivering 30 mg/24 hours were investigated in ten patients according to a randomized, double-blind, crossover placebo-controlled protocol. In seven of these patients, testing was again performed at 2.5 hours after repeated application (second application at 24 hours) (Figure 1). Nitroglycerin patches delivering 5 mg, 10 mg, 20 mg as well as 30 mg/24 hours, respectively, led to significant reductions in ST-segment depression at 2.5 hours of 59% (range 25 to 100%; p less than 0.025), 63% (0 to 100%, p less than 0.01), 77% (50 to 100%, p less than 0.001) as well as 82% (50 to 100%, p less than 0.005) as compared with control values (Figure 2).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[High-dose transdermal nitroglycerin therapy: loss of effect within 24 hours?]. 392 12

Antianginal efficacy and improved exercise performance with timolol, a new beta-adrenergic blocking agent, was assessed in 23 patients with chronic stable angina pectoris in an 11-week double-blind, placebo-controlled study. Twenty-two of the 23 subjects completed the open-label phase of this investigation (weeks 0 to 6) while receiving 10 to 30 mg of timolol twice daily to optimize exercise capacity. Weekly anginal episodes and nitroglycerin consumption declined from 8.9 +/- 9.1 episodes/week and 8.1 +/- 10.6 tablets/week, respectively, with placebo to 2.7 +/- 5.2 episodes/week and 2.6 +/- 6.0 tablets/week with optimal timolol dose (p less than 0.05). Resting heart rate (HR) and systolic blood pressure (SBP) also decreased from 75.2 +/- 14.0 beats/min and 139.1 +/- 15.7 mm Hg with placebo to 55.1 +/- 8.9 beats/min and 130.5 +/- 15.9 mm Hg with timolol (p less than 0.05). Peak exercise HR, peak exercise SBP, and peak exercise double product (HR X SBP) were significantly (p less than 0.05) reduced when evaluated 12 to 13 hours after administration of timolol compared with placebo (101.5 +/- 21.1 beats/min verus 193.3 +/- 96.2 beats/min, 161.5 +/- 26.7 mm Hg versus 175.6 + 20.8 mm Hg, and 16.6 +/- 5.1 X 10(-3) versus 21.7 +/- 5.4 X 10(-3), respectively). Exercise duration was prolonged from 263.3 +/- 90.2 seconds to 330.3 +/- 73.9 seconds (p less than 0.05), while time to onset of 1 mm S-T segment depression was delayed in 15 patients from 231.8 +/- 86.4 seconds to 298.7 +/- 68.4 seconds (p less than 0.05). During the double-blind phase (weeks 7 to 10), 8 subjects received timolol and 11 patients received placebo. Nitroglycerin consumption at weeks 8 and 10 and anginal frequency at week 8 were unchanged compared with initial placebo treatment. Resting HR, peak exercise HR, and peak exercise double product were significantly attenuated at weeks 8 and 10 in timolol patients compared with their initial placebo exposure. However, these variables were unchanged in placebo subjects compared with their initial placebo therapy. Exercise duration was again prolonged at week 8 in timolol subjects compared with initial placebo results (315.1 +/- 61.2 seconds versus 261.3 +/- 68.8 seconds, p less than 0.05), but not at week 10. Placebo patients demonstrated no difference at week 8 or 10 in exercise performance compared with initial placebo treatment. Timolol twice daily, therefore, is potentially useful in some patients with angina pectoris. Other patients may, however, require a shorter dose interval for optimal angina control and maximal improvement in exercise capacity.
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PMID:Antianginal efficacy and improved exercise performance with timolol. Twice-daily beta blockade in ischemic heart disease. 612 94

We performed a double-blind controlled crossover trial of perhexiline maleate versus identical placebo in daily doses of 100-400 mg in 20 male patients who were severely limited with angina pectoris despite therapy with beta-adrenoreceptor blockers. All patients had documented coronary artery disease and were awaiting coronary artery bypass grafting. Beta-blocker therapy was continued unchanged. A significant response compared to placebo was evident after 100 mg of perhexiline, and incremental therapeutic effects were evident up to 400 mg. The mean weekly angina rate fell from 18.2 +/- 2.8 basal to 6.2 +/- 1.5 on 200 mg (P less than 0.05) to 2.8 +/- 0.9 on 400 mg perhexiline (P less than 0.05). Nitroglycerin consumption fell in parallel. The mean exercise duration increased from 261 +/- 57 sec to 384 +/- 75 sec (P less than 0.05). Five patients became asymptomatic on perhexiline, and the number of pain-free days increased 100% (P less than 0.01) compared to placebo. No patient experienced hypotension or heart failure. This study shows that the addition of perhexiline to beta-adrenoreceptor antagonists in patients with severe angina pectoris is effective and represents an alternative therapy.
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PMID:Antianginal efficacy of perhexiline maleate in patients refractory to beta-adrenoreceptor blockade. 613 84

Unstable angina can be defined by the development of chest pain at rest, usually with reversible S-T segment changes. It has been found in patients in whom angina developed at rest in the cardiac catheterization laboratory that a decrease in coronary sinus oxygen saturation preceded changes in left ventricular relaxation and contractility that preceded the development of chest pain and/or electrocardiographic changes. Increases in heart rate and/or blood pressure followed, rather than preceded, these ischemic episodes. These findings suggest that a decrease in oxygen supply, rather than an increase in oxygen demand, is the cause of episodes of angina at rest. Although principles of treatment of effort angina have emphasized the reduction of myocardial oxygen demand, treatment of rest angina should logically emphasize therapies that improve oxygen supply. A stepwise approach to the treatment of patients admitted to the Coronary Care Unit with unstable angina is proposed. The initial step consists of replacing oral and/or transcutaneous nitrates with an intravenous infusion of nitroglycerin while maintaining beta-blockers and calcium blockers at their previous doses. Nitroglycerin dilates coronary arteries and intercoronary collateral channels in addition to reducing preload and afterload. Intravenous administration allows faster titration to an effective dose and also more rapid reversal of hemodynamic effects, if the patient's status changes. The second step would consist of maintaining the nitroglycerin infusion and beta-blockers and adding or increasing the dose of calcium channel blockers. Slow channel calcium blockers dilate coronary arteries and prevent or reverse coronary spasm in addition to reducing afterload. The third step consists of adding or increasing the dose of beta-blockers in subgroups of patients with resting tachycardia and/or arterial hypertension. The fourth and final step would be to employ intra-aortic balloon counterpulsation therapy and/or to perform urgent coronary angiography. In patients with suitable coronary anatomy, angiography could be followed by percutaneous transluminal angioplasty or coronary artery bypass surgery.
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PMID:Unstable angina. Rational approach to management. 614 57

By manually assigning pulmonary regions of interest and deriving pulmonary time-activity (volume) curves, we were able to make count estimates of pulmonary blood volume (PBV) from gated cardiac blood pool scans. Five patients with coronary heart disease developed angina spontaneously while under a gamma camera. This produced an increase in cardiac volumes (p less than 0.05), a reduction in left ventricular ejection fraction (p less than 0.01), along with a marked increase in PBV (0.010 +/- 0.003 to 0.015 +/- 0.002 units, p less than 0.05). Nitroglycerin was then administered and reduced PBV in association with a return to normal in cardiac systolic function and size. In patients with stable chronic ischemic heart disease, sublingual nitroglycerin also reduced PBV (p less than 0.05), although not as much as when administered during an anginal episode. We conclude that gated imaging of the chest can be utilized to follow changes in PBV serially. These changes can be utilized to evaluate clinically important changes in hemodynamic status and the response to pharmacologic interventions.
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PMID:Radionuclide analysis of pulmonary blood volume: the response to spontaneous angina pectoris and sublingual nitroglycerin in patients with coronary artery disease. 640 7

Nitroglycerin has been the mainstay of the medical management of angina pectoris for over 100 years. The long-held clinical impression of the efficacy of nitroglycerin has now been clearly documented in controlled clinical trials designed to evaluate objective response to antianginal agents. Advances in scientific methodology and improved experimental design have contributed to continuing interest in nitrates. Newer uses of nitroglycerin and other nitrates in congestive heart failure and acute myocardial infarction are the result of a developing understanding of the pharmacology of nitrates.
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PMID:The transdermal administration of nitrates: an overview. 640 50

The coronary haemodynamic effects of nifedipine and glyceryl trinitrate were compared in 22 patients undergoing investigations for suspected coronary artery disease. Myocardial blood flow was estimated by the coronary sinus thermodilution technique. In sinus rhythm nifedipine increased mean coronary sinus flow from 135 ml/min to 152 ml/min, and reduced arterio-coronary sinus oxygen difference from 12.4 to 10.96 ml/100 ml without causing a significant change in coronary vascular resistance or in myocardial oxygen consumption. Glyceryl trinitrate reduced mean coronary sinus flow from 165 to 111 ml/min, myocardial oxygen consumption from 19.2 to 11.9 ml/min, and arterio-coronary sinus oxygen difference from 11.7 to 10.9 ml/100 ml. There was a rise in coronary vascular resistance from 54 355 to 74 364 dynes s cm-5. During atrial pacing nifedipine reduced the arterio-coronary sinus oxygen difference from 11.99 to 11.0 ml/100 ml but had no significant effect on the other variables measured. Glyceryl trinitrate caused a fall in mean coronary sinus flow from 207 ml/min to 168 ml/min; myocardial oxygen consumption fell from 24 ml/min to 18 ml/min, while coronary vascular resistance rose from 41 714 to 51 234 dynes s cm-5. Direct comparison of the two drugs showed a significant difference in effects on coronary sinus flow and coronary vascular resistance in sinus rhythm. Both drugs appeared effective in relieving ischaemia as judged by a reduction of the incidence of pacing induced angina and an improvement in lactate status.
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PMID:Coronary haemodynamic effects of nifedipine. Comparison with glyceryl trinitrate. 640 88

The orthostatic changes in heart rate (HR) and blood pressure (BP) were recorded in ten patients with stable angina pectoris before and after simultaneous sublingual nitroglycerin administration. All patients were examined three times: without other medication, during chronic metoprolol treatment, and during chronic verapamil treatment. Under control conditions, only minor changes were found in systolic BP following vertical tilting, while diastolic BP increased by approximately 10%. Nitroglycerin augmented these changes to some extent, while neither metoprolol nor verapamil caused significant changes. The orthostatic HR increase was considerably augmented by nitroglycerin. Verapamil treatment did not influence this response, while metoprolol caused significant reductions. These findings seem to explain why some few patients have observed severe orthostatic symptoms while taking nitroglycerin during treatment with beta-adrenergic blocking agents.
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PMID:Orthostatic response before and after nitroglycerin in metoprolol- and verapamil-treated angina pectoris. 641 53

Ten patients with stable angina pectoris and obstructed coronary arteries (greater than 75% reduction in diameter) were studied before and during two periods of pacing, the second of which was preceded by sublingual administration of glyceryl trinitrate (mean dose 0.78 mg). Coronary sinus blood flow measurements and aortocoronary sinus blood sampling for metabolite determinations were carried out. Although the rate of pacing was increased by 10 beats/minute after glyceryl trinitrate administration, the onset of angina was delayed in eight patients during pacing. Drug administration decreased coronary sinus blood flow by 42% and myocardial oxygen uptake by 41% during pacing and induced a shift in mean lactate extraction towards a net release (from 3.1% to -12.6%). It increased the number of patients producing lactate from three to five. Glyceryl trinitrate administration decreased myocardial glucose uptake throughout the study, decreased lactate extraction during recovery, and increased the aortocoronary sinus citrate gradient at rest and during recovery, while the exchange of free fatty acids remained unchanged. A decrease in aortocoronary sinus lactate difference during pacing after glyceryl trinitrate administration correlated positively with the fall in coronary sinus blood flow. The metabolic data do not indicate an augmented myocardial lactate production after glyceryl trinitrate administration. A decrease in coronary sinus blood flow seems, therefore, to be of primary importance in explaining the elevated coronary sinus lactate concentration. Our finding that coronary sinus lactate concentration increased during pacing after glyceryl trinitrate administration despite clinical improvement questions the validity of its use as a quantitative index of ischaemia.
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PMID:Increased coronary sinus lactate concentration during pacing induced angina pectoris after clinical improvement by glyceryl trinitrate. 641 79

The influence of indomethacin therapy on the circulatory and antianginal effects of nitroglycerin were studied in six patients with stable angina pectoris. Indomethacin 50 mg or identical placebo capsules were administered three times a day for 1 week each in a double-blind, random manner. Heart rate, blood pressure, and ST-segment depression were measured at rest and during exercise before and after the administration of 0.6 mg sublingual nitroglycerin during indomethacin and placebo therapy. Nitroglycerin lowered standing systolic blood pressure by 38 mm Hg during placebo therapy (p less than 0.001) and by 36 mm Hg during indomethacin therapy (p less than 0.001). This was accompanied by a reflex increase in heart rate (p less than 0.001) which was of similar magnitude during placebo and indomethacin therapy. The increase in exercise duration to the onset of angina post nitroglycerin was similar during placebo and indomethacin therapy (128 vs 84 s; NS). Similarly, the increase in the total duration of exercise post nitroglycerin was similar during placebo and indomethacin therapy. Reduction in ST-segment depression post nitroglycerin was more pronounced during placebo than indomethacin therapy, but did not achieve statistical significance. The results show that indomethacin did not modify the circulatory effects of nitroglycerin at rest or during exercise and did not attenuate the increase in exercise tolerance produced by sublingual nitroglycerin. Since indomethacin is a potent prostaglandin inhibitor, the findings indirectly suggest that the vasodepressor and antianginal effects of nitroglycerin are in all probability not mediated by prostaglandins.
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PMID:Interaction of indomethacin and nitroglycerin on hemodynamics and exercise tolerance in patients with angina pectoris. 642 Oct 13


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