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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The medicamentous therapy of the angina pectoris vera and of the chronic ischaemic heart disease is at present based on three groups of medicaments: nitrate compounds, beta-blocking agents and calcium antagonists. The underlying therapeutic principle which is common for them consists in the reduction of the oxygen requirement of the myocardium so that an improvement of the complaints and a larger load capacity may be achieved. The improvement may be objectified also at the behaviour of the haemodynamics and the ECG under load. The so-called coronary dilating remedies and the beta-stimulators did not prove clinically. In the acute attack rapidly acting nitroglycerin compounds remain the remedies of choice. Also the permanent treatment should at first again use longer acting nitrate preparations. When despite a sufficient dosage no satisfying improvement takes place an additional prescription of beta-blocking agents is recommended. Calcium antagonists are suitable particularly for the vasospastic form of the angina pectoris. They can be used also as basis medicaments, however, according to the hitherto yielded experiences they do not possess any advantages in contrast to the proved nitrates and beta-blocking agents. When apart from the ischaemic heart disease a hypertension exists, the beta-blocking agents are particularly indicated. This is further important for certain forms of tachycardiac disturbances of rhythm, which partly also well response to calcium antagonists. In patients with disturbances of conduction (sinus node and atrioventricular nodes, bifascicular block) beta-blocking agents are contraindicated. If there are no signs of cardiac decompensation and radiologically the heart proves to be normally large, so there is no indication for the prescription of glycosides.
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PMID:[Actual and theoretical points of view in the application of coronary therapeutic agents]. 610 22

We observed 70 male patients with a seriously proceeding Chronic myocardial ischemia. They were hospitalised because of frequent, permanent and serious attacks of stenocardia at rest and in stress situations. More than 2/3 of these patients had suffered from a myocardial infarct. In the course of two weeks an intensive therapy with all modern preparations for vasodilatation was made. This therapy proved to be unsuccessful. Nearly all patients were administered more than 10 tables of nitroglycerin per day and, in addition, they were injected analgetics as a compensation of attack. The ultraviolet own blood irradiation (UVB) had a positive therapeutic effect in all patients. There was a good success in 46 patients, in all patients satisfactory results could be registered. The effect of therapy was evident by the decrease of administration of nitroglycerin required, by an increase in the degree of stress capacity, and by an easier treatment of stenocardia attacks. The observation time for patients amounted to 2-8 months. The success of therapy remained in 38 patients. After this time the success of therapy could partially be regained by a repeated number of irradiation series. Then, it remained positive in 9 of 22 patients who had been followed-up for 10 months. The half decay period of eliminating 131I from an intradermal depot could be normalised under the influence of ultraviolet own blood irradiation. This ultraviolet own blood irradiation had no significant influence on the fibrinogen level, fibrinolytic activity, and erythrocyte aggregation (examined in 11 patients). A 2 1/2-fold diminution of monomer fibrin complexes in the blood could be observed. The titre of antistreptolysin-O was increased in all patients who had got over the infarct. It had completely normalised a week after finishing the ultraviolet own blood irradiation. Spectroscopic examinations of the blood and plasma made after ultraviolet own blood irradiation revealed that this irradiation will not only affect the properties of Hb, but will also cause a photochemical transformation accompanied by a destruction of some plasma proteins, of the membrane of formed blood elements, and a photosynthesis of biochemically active compounds. The mechanism of action of ultraviolet own blood irradiation is complicated and requires further exact investigations. Even today, however, this method can be recommended as a complex therapy in patients with severe myocardial ischemia.
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PMID:[Therapy of severe stenocardia with ultraviolet blood irradiation (UVB) and various action mechanisms of this therapy]. 618 67

The cardiovascular responses to combined static-dynamic effort, postprandial dynamic effort and dynamic effort alone were evaluated by upright bicycle ergometry during equilibrium-gated blood pool scintigraphy in 24 men, mean age 59 +/- 8 years, with chronic ischemic heart disease. Combined static-dynamic effort and the postprandial state elicited a peak cardiovascular response similar to that of dynamic effort alone; work load 643 +/- 156 and 638 +/- 161 vs 650 +/- 153 kg-m/min, respectively; heart rate 147 +/- 14 and 145 +/- 14 vs 143 +/- 17 beats/min; systolic pressure 195 +/- 26 and 200 +/- 25 vs 197 +/- 25 mm Hg; and rate-pressure product 286 +/- 48 and 292 +/- 55 vs 282 +/- 52. Heart rate, intraarterial systolic and diastolic pressures, rate-pressure product and ejection fraction were similar for the three test conditions at the onset of ischemia and at peak effort. The prevalence and extent of exercise-induced ischemic left ventricular dysfunction, ST-segment depression, angina pectoris and ventricular ectopic activity were also similar during the three test conditions. Direct and indirect measurements of systolic and diastolic blood pressure were highly correlated. The onset of ischemic ST-segment depression and angina pectoris correlated as strongly with heart rate alone as with the rate-pressure product during all three test conditions. The cardiovascular response to combined static-dynamic effort and to postprandial dynamic effort becomes more similar to that of dynamic effort alone as dynamic effort reaches a symptom limit. If significant ischemic and arrhythmic abnormalities are absent during symptom-limited dynamic exercise testing, they are unlikely to appear during combined static-dynamic or postprandial dynamic effort. This simplifies, the task of formulating guidelines for physical effort in patients with chronic ischemic heart disease, especially in providing "clearance" to perform avocational and vocational tasks involving combined static-dynamic and postprandial dynamic effort.
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PMID:Comparison of cardiovascular response to combined static-dynamic effort, postprandial dynamic effort and dynamic effort alone in patients with chronic ischemic heart disease. 628 Aug 92

The term coronary artery spasm should not be used interchangeably with the specific clinical syndrome "variant angina" since it does occur in other acute and chronic ischemic heart disease syndromes. The term coronary artery spasm should not be applied to patients with ischemic heart disease unless there is clinical, angiographic, and physiologic evidence of its presence. The diagnosis of coronary artery spasm is confirmed by angiography, i.e. change in caliber of the coronary arteries plus evidence of ischemia. Probable diagnosis is in patients who have the syndrome of variant angina, i.e. rest angina associated with ST segment elevation on the electrocardiogram. One can be highly suspicious that the spasm is at work in patients who have rest angina, especially those with unstable angina. One can be suspicious of patients who have variable effort angina or walk-through angina. Coronary artery spasm is a possibility in patients with an acute myocardial infarction or acute re-infarction and is also possible that sudden death in patients with normal coronary arteries can be related to coronary artery spasm. Coronary artery spasm is the usual cause of myocardial ischemia in patients with rest angina without effort angina. This has also commonly been documented in patients with rest and effort angina. There are isolated reports suggesting that patients with effort angina pectoris also develop coronary artery spasm. Coronary artery spasm has been documented to occur in association with acute myocardial infarction. Whether coronary artery spasm is the cause or the result of myocardial infarction has not been determined at this time. However, the recent combined use of intracoronary nitroglycerin and intracoronary streptokinase in patients with acute myocardial infarction has shown reversal of totally obstructed arteries and suggests the relationship between coronary artery disease, coronary artery spasm, and in situ coronary thrombosis. The incidence of sudden death in patients with documented coronary artery spasm is unknown. But, since complete heart block and/or ventricular tachycardia occur during episodes of coronary artery spasm, it is not unreasonable to assume that some patients have died as a result of these rhythm disturbances. The prognosis of patients with coronary artery spasm seems to depend on the presence or absence of severe coronary atherosclerosis, i.e. those with severe disease have a worse prognosis. Current therapy of patients with coronary artery spasm involves the use of nitrates and calcium antagonists.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of coronary artery spasm in ischemic heart disease. Therapeutic implications. 633 45

To compare acute effects of nitroglycerin (0.8 mg sublingually), nifedipine (5 ng/kg/min i.v.) and metoprolol (0.15 mg/kg i.v.) on normal, ischemic and scarred myocardial segments in man, we performed simultaneous hemodynamic and radionuclide measurements of left ventricular functions. Sixteen patients with isolated left anterior descending (LAD) disease were studied at rest and during exercise. Nine patients had angina and exercise-induced ischemia (LAD stenosis) and seven patients had previous transmural myocardial infarction and no ischemic changes during thallium imaging (LAD occlusion). The effects of the drugs on regional ejection fraction of the involved anteroseptal region and the normal posterolateral area were compared. Global ejection fraction at rest did not change after nitroglycerin, increased after nifedipine and decreased after metoprolol. In patients with ischemia, the exercise ejection fraction improved after all drugs due to increased regional ejection fraction in ischemic segments: i.e., a regional antiischemic effect evidenced by improved regional function could be demonstrated with all three agents. Regional ejection fraction increased from 35.8 +/- 19.5% to 66.2 +/- 15.2% (+/- SD) after nitroglycerin (p less than 0.001), to 61.7 +/- 8.7% after nifedipine (p less than 0.001), and to 48.4 +/- 7.0% after metoprolol (p less than 0.01). In regions of myocardial scar, regional ejection fraction was not changed after any drug. In normal areas, regional ejection fraction remained unchanged after nitroglycerin and nifedipine, but decreased after metoprolol. Despite similar antiischemic effects of all three drugs, underlying hemodynamic mechanisms were quite different and may provide a rationale for combined forms of treatment. These results may help to select optimal drug combinations to improve myocardial performance in patients with chronic ischemic heart disease.
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PMID:Comparative effects of nitroglycerin, nifedipine and metoprolol on regional left ventricular function in patients with one-vessel coronary disease. 640 Dec 30

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

In order to assess acute effects of nitroglycerin, nifedipine and metoprolol on normal, ischemic and scar myocardial segments in man, non-invasive hemodynamic and radionuclide measurements of left ventricular function were performed. Sixteen patients with single left anterior descending (LAD) disease were studied at rest and during exercise: 9 patients with angina and exercise-induced ischemia (LAD stenosis) and 7 patients with previous transmural myocardial infarction and no ischemic changes at thallium imaging (LAD occlusion). Effects on regional ejection fraction were compared between involved antero-septal and normal postero-lateral areas. Global ejection fraction at rest was unchanged after nitroglycerin, increased after nifedipine and decreased after metoprolol. In patients with ischemia, improvement in exercise ejection fraction after all drugs was due to increased regional ejection fraction in ischemic segments, i.e. a real anti-ischemic effect could be demonstrated. In regions of myocardial scar, regional ejections fraction was not changed after either drug. In normal areas, regional ejection fraction remained unchanged after nitroglycerin and nifedipine but decreased after acute beta-blockade. Despite the very similar anti-ischemic effects of all drugs, underlying hemodynamic mechanisms were quite different: Reduction in preload and afterload after nitroglycerin, vasodilatation and reflex sympathetic activity after nifedipine and reduction in double product and contractility after metoprolol. Thus, the mode of action of nitroglycerin, nifedipine and metoprolol on normal, ischemic and scar myocardial segments could be demonstrated in man. Non-invasive antianginal drug testing as shown in this study should allow optimal medical therapy for patients with chronic ischemic heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antianginal drug effects on normal, ischemic and scar myocardial segments in man. 644 4

We have explored the systolic time intervals of 52 patients with angina pectoris at the time of their hospitalization in our wards. Our results are in close agreement with published data, essentially indicating prolongation of the preejection time and shortening of the ejection time. These alterations of systolic times can be interpreted pathophysiologically as as expressing reduced myocardial contractility. The long PEP-short LVET polygraph picture, occurring in the course of chronic ischemic heart disease, reveals the deficit of myocardial contractility at a stage of the disease at which clinical evidence of left ventricular failure is usually not yet detectable.
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PMID:Evaluation of systolic time intervals in patients with angina pectoris. 684 20

The evidence on the clinical relevance of the behaviour of the R-amplitude under load for the non-invasive diagnosis of the chronic ischaemic heart disease is contradictory in literature. One of the causes for the variable estimation is possibly to be found in the different localization of the lead electrodes. With the help of the ECG mapping using 30 electrodes at the anterior thoracic wall 15 males were examined with typical syndrome of angina pectoris and a clearly pathological reaction of the ST-distance in a preceding usual bicycle ergometry. The ECG mapping was carried out before, during and after an ergometer load in lying position with 50 Watt. The most frequent pathological reactions of the R-amplitude were found below the chest wall electrodes V4, V5 and V6 after Wilson. The estimation of the valency of this first observation must be performed in further examinations.
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PMID:[ECG mapping studies for optimal electrode placement for the detection of stress-induced changes in R-amplitude in the diagnosis of chronic ischemic heart disease]. 685 73

The workup of a patient with chronic ischemic heart disease (IHD) before the selection of medical-surgical or medical therapy depends on multiple objective and subjective factors. These include symptoms, extent of anatomic disease (degree of coronary arteriosclerosis and left ventricular abnormalities), objective evidence of ischemia, extent of left ventricular dysfunction, and recent intercurrent ischemic events. In a minority of patients, a single factor is of overwhelming importance; e.g., the presence of severe left main coronary artery narrowing in a symptomatic patient indicates surgery is a better choice, whereas evidence of advanced left ventricular dysfunction suggests that surgery is likely to be risky and of limited help to the patient. In most instances, multiple factors should be considered before making a recommendation. The patient should be placed in the appropriate clinical subset and the objective factors that are most important in determining survival should be evaluated. Hence, an exercise electrocardiographic study to evaluate symptoms and exercise tolerance in a patient with angina pectoris and radioventriculographic studies with exercise to estimate left ventricular performance in a patient who complains of fatigue and breathlessness are superior to the subjective interpretations of routine clinical examinations. Asymptomatic patients and those with excellent exercise tolerance pose the most difficult decisions. Perhaps serial (even annual) noninvasive evaluation is appropriate in such patients in light of the current uncertainty about how to manage them. Laboratory tests should be used selectively, systematically and sequentially. The high cost of many of the examinations is reason to avoid duplication. When noninvasive evaluation can answer the question being posed and the cost of hospitalization avoided, this should be done. However, there is little reason to perform noninvasive examinations that do not answer the clinical question being asked; hence, in many patients it is appropriate to proceed directly to coronary arteriography rather than to perform a variety of "screening" examinations before this procedure.
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PMID:The reasonable workup before recommending medical or surgical therapy: an overall strategy. 697 29


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