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)

The value of exercise thallium scintigraphy in detecting coronary artery disease is well established. However, there are at times situations in which the exercise test cannot be readily used. Isoproterenol (ISP) stress ECG (ISP-ECG) is reportedly a useful method in diagnosing coronary artery disease. In the present study, we assessed the diagnostic value of ISP thallium scintigraphy, comparing it with those of ISP-ECG and exercise thallium scintigraphy. The study population consisted of 24 patients who had histories of chest pain without previous myocardial infarction. ISP was given at increasing doses of 0.02, 0.04, 0.08 micrograms/kg/min at 3-minute intervals, and was terminated for any of the following reasons: angina, significant arrhythmia, significant ST segment depression (greater than or equal to 0.1 mV) or target heart rate. Thallium scintigrams were obtained immediately after terminating ISP infusion, and after a 3-hour delay, redistribution scans were obtained. Scintigrams were considered positive when a reversible defect was present. In nine patients who underwent exercise tests, exercise thallium scintigraphy was also performed. After the stress tests, coronary angiography was performed. According to the presence or absence of significant coronary artery stenosis (greater than or equal to 75%), all subjects were divided into two groups: coronary artery disease (CAD) group (n = 12) and so-called normal coronary (NC) group (n = 12). 1. Among 12 patients in the CAD group, ISP induced anginal pain in six (50%), and ISP-ECG and ISP thallium scintigraphy were positive in 10 (83%) and in 11 (92%), compared with four (33%), four (33%) and two (17%) in the NC group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Isoproterenol stress thallium scintigraphy for detecting coronary artery disease. 264 60

The widespread use of beta-adrenoceptor antagonists against hypertension, angina pectoris and migraine or as a preventive treatment after myocardial infarction has encouraged us to investigate the effects of these drugs on platelet function. The aim of this study was to examine whether beta-blocking drugs interfere with platelet beta- adrenoceptors and whether this dependency is related to their selectivity for beta-adrenoceptor subtypes. Beta-adrenoceptor stimulation of human platelets with isoprenaline increased cyclic AMP (cAMP), which is known to inhibit platelet aggregation. Furthermore, our studies showed that cAMP formation in vitro was stimulated by non-selective and beta 2-selective agonists, but not by the predominant beta 1-agonist prenalterol. Isoprenaline- stimulated cAMP formation was blocked by the non- selective beta-adrenoceptor antagonists propranolol, timolol, and alprenolol, while the beta 1-selective antagonists atenolol and metoprolol had no influence on an isoprenaline-induced cAMP formation. Receptor binding studies using (3H)-dihydroalprenolol revealed an IC50 value for propranolol of 85 nM, while metoprolol only displaced the bound (3H)-dihydroalprenolol at far higher concentrations (IC50, 20 microM). We conclude that the human platelet beta-adrenoceptors are mainly of the beta 2- subtype and that beta-adrenoceptor antagonists, especially the non-selective antagonists interfere with platelet function assessed as platelet cAMP formation.
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PMID:Characterization of human platelet beta-adrenoceptors. 300 61

Antianginal effects of (+/-)-(R*)-2,6-dimethyl-4-(m-nitrophenyl)- 1,4-dihydropyridine-3,5-dicarboxylic acid (R*)-1-benzyl-3-piperidinyl ester, methyl ester hydrochloride (benidipine hydrochloride, KW-3049) in various experimental angina-pectoris models (anesthetized rats, spontaneously hypertensive rats (SHR] were compared with those of nifedipine, propranolol and hydralazine. Furthermore, the effects of these drugs on the pressure-rate product were evaluated. 1. Vasopressin test (SHR): The administration of KW-3049 at 10 micrograms/kg (i.v.) developed an inhibitory effect comparable to that of nifedipine at 200 micrograms/kg (i.v.) against the ischemic ECG changes caused by the intravenous administration of vasopressin at 1 U/kg. The effects of KW-3049 at 3 and 10 mg/kg (p.o.) lasted for 8 h or more. 2. Coronary occlusion test (rat): The rise of T-wave of epicardial ECG following ligation of coronary artery was inhibited by the administration of KW-3049 at doses of 30 and 100 micrograms/kg i.v. Nifedipine at dose of 200 micrograms/kg i.v. was slightly effective. 3. Isoproterenol (isoprenaline) test (rat): The fall of ST in ECG by the continuous infusion of isoprenaline (10 micrograms/kg/min) was almost completely prevented by propranolol (500 micrograms/kg i.v.). Also, KW-3049 (200 micrograms/kg i.v.) and nifedipine (200 micrograms/kg i.v.) significantly inhibited the decline of ST, in which the former was more effective than the latter. 4. Anoxia test (SHR): The fall of ST and rise of T-wave of ECG, induced by stopping artificial respiration of gallamine-immobilized SHR, were suppressed by the administration of KW-3049 at doses of 10 and 30 micrograms/kg i.v.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antianginal effects of the new calcium antagonist benidipine hydrochloride in anesthetized rats and spontaneously hypertensive rats. Electrocardiographic study. 321 44

In 14 patients with obstructive hypertrophic cardiomyopathy and angiographically normal coronary arteries, 8 with angina (group B) and 6 without (group A), the effects of intravenous isoproterenol, 2 to 4 micrograms/min, followed by intravenous propranolol, 0.2 mg/kg, were studied. An intraventricular systolic gradient less than 50 mm Hg, high-quality echocardiograms and cineangiograms and high-fidelity pressure tracings were selection criteria. Hemodynamic and metabolic variables were assessed during basal conditions, after 5 minutes of isoproterenol infusion or at angina and ST-segment depression, and 5 and 10 minutes after intravenous propranolol infusion. Isoproterenol increased the intraventricular systolic gradient more significantly in group B than in group A (102.4 +/- 8.3 vs 52.2 +/- 8.2, p less than 0.0001). Group B also had higher left ventricular end-diastolic pressure (32.5 +/- 3.9 vs 20.2 +/- 5.7), lower mean arterial pressure (69.7 +/- 3.5 vs 84.7 +/- 4.8) and a smaller increase in coronary sinus flow (176.1 +/- 9.2 vs 261.5 +/- 33.9, all p less than 0.0001), concomitant with lactate release and ST-segment depression. Propranolol promptly reversed hemodynamic and metabolic changes caused by isoproterenol, except for a further coronary sinus flow increase (from 176.1 +/- 9.2 to 219 +/- 14.2 ml/min, p less than 0.001), and heart rate decrease below basal values (57.8 +/- 7.5 vs 79.9 +/- 9.8 beats/min, p less than 0.001) in group B.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of isoproterenol-induced angina pectoris in patients with obstructive hypertrophic cardiomyopathy and normal coronary arteries. 366 32

1 Haemodynamic changes have been studied in cats after the chronic oral administration of oxyfedrine (14 mg/kg for 3-4 weeks) or of placebo (lactose). The initial part of the study was carried out under double-blind conditions. The arterial blood pressure was between 19 mmHg (diastolic) and 27 mmHg (systolic) higher in the oxyfedrine treated animals, but there were no differences between the two groups with regard to cardiac output, left ventricular dP/dt max, heart rate or systolic ejection time.2 In cats similarly treated with propranolol (4 mg/kg) there was a slight (12%), but significant, reduction in cardiac output.3 Isoprenaline dose-response curves were shifted to the right in the cats administered oxyfedrine as well as in those administered propranolol. The degree of shift was five-fold (positive chronotropic response) and 20-fold (decrease in diastolic blood pressure) in the oxyfedrine group and 10- and 80-fold, respectively, in the propranolol group.4 In contrast to the partial blockade of the effects of isoprenaline, the haemodynamic response to oxyfedrine was largely unaltered, both in the cats pretreated with propranolol and in those pretreated with oxyfedrine. The pressor response to noradrenaline was potentiated in the cats pretreated with oxyfedrine.5 These results provide an explanation for the anti-anginal action of oxyfedrine. Some degree of beta-adrenoceptor blockade is achieved without a reduction in cardiac output or left ventricular dP/dt max. The relevance of these findings to the haemodynamic situation in angina is discussed.
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PMID:The haemodynamic effects of prolonged oral administration of oxyfedrine, a partial agonist at beta-adrenoceptors: comparison with propranolol. 415 36

Myocardial oxygen consumption (MVO2) is defined by the equation: MVO2 = coronary blood flow x arteriovenous difference in O2 content. The average value for a heart of 300 g is 30 to 35 ml/min. In the absence of physiological variations in the arteriovenous difference in O2 content, MVO2 is related to coronary blood flow and the typical anti-anginal agent is one which prevents or reduces increases in MVO2. MVO2 depends on several factors: 1. intraparietal tension, which depends on intraventricular pressure and volume and in which the oxygen demands of pressure overload are much higher than those of volume overload; 2. contractility or myocardial inotropism: 50 per cent increase in the velocity of left ventricular contraction increases MVO2 by 40 per cent; 3. heart rate; 4. external cardiac work--the work accomplished during the ejection phase; this represents about 15 per cent of the MVO2; 5. the energy of electrical activation; this represents about 0,5 per cent of the MVO2; 6. the oxygen requirements of basal myocardial metabolism which represent about 20 per cent of the MVO2; 7. ventricular relaxation: is a factor to be added to those described above; this consumes about 15 per cent of the total energy of a cardiac beat; it may be increased with Isoproterenol or decreased by increasing the calcium concentration. This mechanism may explain the physiopathological impact of calcium inhibitors in effort angina or angina due to increased MVO2.
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PMID:[Oxygen requirements of the myocardium]. 630 99

Celiprolol is a novel beta 1 selective adrenoreceptor blocker with partial beta 2 agonism and direct vasodilator activity. These ancillary properties may reduce symptomatic breathlessness and fatigue and modify respiration during exercise. To test this hypothesis 20 men with stable effort angina were enrolled in a double-blind crossover study to investigate the effects of atenolol 100 mg once daily (A) and celiprolol 400 mg once daily (C) on cardiorespiratory and symptomatic variables during maximal and submaximal exercise. Total exercise time on a modified Bruce protocol was similar on both treatments: C12.5 min, A 13.1 min. During steady state submaximal exercise at 60-75% (mean 68%) of maximum work capacity, minute ventilation (C33.81 min-1, A 33.51 min-1), oxygen uptake (C14.6 ml.kg-1.min-1, A15.1 ml.kg-1.min-1), respiratory exchange ratio (C 0.89, A 0.87), ratio of VE/VCO2 (C 33.6, A 33.4), ratio of VE/VO2 (C 2.34, A 2.72), Borg perceived exertion score (C 11.2, A 10.9) and visual analogue scores for breathlessness (C 29.5, A 25.9) and muscle fatigue (C 28.9, A 26.0) were all similar on both treatments. At maximal exercise capacity on the modified Bruce protocol, minute ventilation (C 58.31 min-1, A 60.41 min-1), oxygen uptake (C 21.3 ml.kg-1.min-1, A 21.7 ml.kg-1.min-1), respiratory exchange ratio (C 1.02, A.1.05), ratio VE/VCO2 (C 34.8, A 35.9), and ratio VE/VO2 (C 2.80, A 2.83) were also similar on both drugs. Over a 10 day period anginal attacks (C 10.1 +/- 10.4, A 5.4 +/- 5.9) and sublingual GTN use (C 5.9 +/- 10.3, A 4.4 +/- 9.8) were both more frequent on celiprolol).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiorespiratory and symptomatic variables during maximal and submaximal exercise in men with stable effort angina: a comparison of atenolol and celiprolol. 783 73

Congenital anomalies of the coronary arteries are relatively uncommon conditions with an incidence of approximately 2% in the adult population. Although less common than acquired coronary artery disease, these anomalies may be associated with myocardial ischemia and its consequences; angina, arrhythmia, infarction, and sudden death. A 21-year-old female patient with no significant prior medical history was found dead at home. Postmortem examination revealed high take-off of the right coronary artery with acute down-ward angulation of the proximal right coronary artery and acute downward angulation of the left main coronary artery. Microscopic examination revealed global myocardial ischemia consistent with a terminal ventricular dysrhythmia. There was no evidence of any other disease processes. Detailed toxicological investigation was negative. The Regional Forensic Pathology Unit experience with sudden death due to congenital coronary artery anomalies is presented along with a review of the current literature.
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PMID:Sudden death due to coronary artery anomalies: a case report and clinical review. 811 4

Percutaneous cardiopulmonary bypass support was electively instituted prior to coronary angioplasty in 16 patients at high risk for hemodynamic collapse. In all cases the dilated artery supplied greater than 2/3 of the functioning myocardium. Eight patients had moderate LV dysfunction with ejection fraction 25-40%. Eight patients had an ejection fraction less than 20%. A 21 French cannula and a 17 French cannula were percutaneously inserted into the femoral vein and artery. Cardiopulmonary bypass support was instituted using a Bio-Medicus centrifugal pump just prior to coronary angioplasty at flow rates of 3.5-5 liters/minute. Thirteen patients had single vessel angioplasty and three patients had multivessel angioplasty. Complete loss of systolic function was observed in 9 (56%) patients. This finding when present confirms the absolute requirement for cardiopulmonary support. Technical success was achieved in all 16 patients (100%), clinical success was achieved in 14 patients (88%). Patient followup (mean 10 months) revealed 3 patients with class I-II angina and 10 patients were asymptomatic. There was one late death. In conclusion, percutaneous cardiopulmonary bypass support for carefully selected high risk patients may allow coronary angioplasty to be performed safely and effectively despite complete loss of systolic function during balloon inflation.
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PMID:Clinical application of percutaneous cardiopulmonary bypass for high risk coronary angioplasty. 1014 76

A 21-year-old man with angina-like chest pain and syncope related to ischemic ECG changes due to an anomalous origin of the right coronary artery. The patient was submitted to surgical correction with myocardial revascularization with internal thoracic artery. A literature review of this rare congenital heart disease is presented.
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PMID:Myocardial revascularization in anomalous origin of the right coronary artery: case report. 1848 22


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