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)

In the course of 1 year 130 patients were examined who had survived myocardial infarction and were alive 2 months after the onset of the disease and were included into the Myocardial Infarction Registry. After 2,3,6,9 and 12 months ECG of various duration was recorded. The prolongation of ECG recording permits to give a more precise characteristics of the incidence and nature of the rhythm disorders observed in chronic ischaemic heart disease patients. Repeated heart rhythm examinations at rest during 1 hour, or during physical exercises (bicycle test) permitted to reveal rhythm disorders in 72.2--66.7% of the patients, and among them ventricular extrasystole in 62.6--66.7% of those examined, respectively. The appearance of ventricular extrasystoles correlates with the state of the patients surviving myocardial infarction A higher incidence of ventricular extrasystoles is observed in pateints with distinct tecg changes, with angina pectoris and elevated blood pressure (larger than or equal to140/90mm Hg).
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PMID:[Incidence and characteristics of cardiac rhythm disorders after myocardial infarct]. 6 35

Although ventricular tachycardia is a well-known complication of myocardial ischaemia and may be provoked by exercise, many patients may appreciate only the angina and be unaware of the unduly rapid heart rate that precipitates it. Exercise testing is needed to show this arrhythmia and to enable treatment to be started.Twenty-three patients were found to have chronic ischaemic heart disease complicated by ventricular tachycardia. Six patients with old myocardial infarction had ventricular tachycardia at rest which required conversion to sinus rhythm; 17 patients developed ventricular tachycardia only when they exercised. In 12 of these 17 patients coronary angiography showed disease of the anterior descending branch of the left coronary artery; other vessels were usually also affected. Although beta-adrenergic blocking drugs increased exercise tolerance, ventricular tachycardia still occurred when the heart rate on exercise reached a level similar to that before treatment. In five patients coronary artery bypass surgery was performed because of angina and exercise-induced ventricular tachycardia. Exercise tolerance was increased in all three patients who underwent exercise tests after operation, and in two of these patients, both of whom were known to have patent grafts, ventricular tachycardia was abolished.If part of the beneficial effect of coronary bypass surgery is preventing life-threatening ventricular arrhythmias it is essential to detect these, and ambulatory monitoring and stress testing have a complementary role.
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PMID:Ventricular tachycardia due to cardiac ischaemia: assessment by exercise electrocardiography. 30 27

Seventy-seven patients with chronic ischemic heart disease were treated in single-seater oxygen hyperbaric chambers; 52 patients had angina pectoris of effort or angina of effort and at rest while 25 patients with macrofocal postinfarction cardiosclerosis had insufficiency of pulmonary or systemic circulation. Treatment consisted of 12--15 procedures. The use of hyperbaric oxygenation in a complex with drug therapy makes it possible to alleviate or arrest the attack of angina pectoris and relieve considerably the symptoms of cardiac decompensation. The initial condition of central hemodynamics affects greatly the results of barotherapy. Normal parameters of hemodynamics hardly change after treatment. At the same time, in patients with markedly reduced myocardial contractility hyperbaric oxygenation causes evident positive changes in hemodynamics. The combination of hyperbaric oxygenation with drug therapy improves the effect of treatment significantly.
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PMID:[Hyperbaric oxygenation in the overall therapy of chronic ischemic heart disease]. 51 59

It may be established that the complex cardiopulmonary functional diagnostics in patients with chronic ischaemic heart disease obtained the following essential results: 1. The ergometrically achieved total functional capacity is clearly decreased in all age groups compared with the healthy persons, the differences are highly significant. 2. The proof of a coronary insufficiency got by the electrocardiogram after work is to be regarded as a factor limiting the functional capacity. 3. 72% of the patients reveal under load a PAEDP increased more than the normal of 25 Torr. After exclusion of a respiratory insufficiency these findings must be regarded as a disturbed myocardial function. 4. Thus the increased PAEDP under load apart from the well-known triad (angina pectoris under load, decreased total functional capacity, pathological ECG after work) is a sensitive and decisive factor for proving the disturbed cardial function in chronic ischaemic heart disease.
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PMID:[Cardiopulmonary diagnosis in patients with ischemic heart disease]. 96 Aug 85

Physiologic concepts relating to reperfusion of ischemic areas of myocardium may be applied both to acute coronary insuficiency, manifested by angina pectoris, and to restoration of coronary blood flow by coronary bypass procedures, currently employed both in acute myocardial infarction and in chronic myocardial ischemia for relief of angina pectoris. Of the information currently available from experimental studies, much may be applicable to the clinical situation. After acutr transient coronary occlusion mechanical and electrical properties of the ischemic area rapidly return to normal, but there is prolongation of tension development and occurrence of ventricular arrhythmias; implications of these phenomena for clinical coronary ischemia deserve exploration. Following more prolonged coronary ischemia, results of experimental reperfusion appear to be variable and, although restoration of function following several hours of ischemia is possible, certain deleterious effects are often observed in the form of myocardial edema and hemorrhage. Clinical use of bypass procedures in acute myocardial infarction suggests that results may be good, but that deleterious effects are occasionally observed; occurrence of the later requires definition and explanation. Restoration of myocardial blood flow in the presence of normal left ventricular function in chronic coronary artery disease, and failure to reverse functional abnormalities when left ventricular damage has already ensued in the clinical situation, appears to be well established; however, better methods to assess the potential for recovery of function following revascularization are needed in both acute and chronic coronary artery diseases. It is anticipated that more careful exploration of pathophysiology both in the catheterization laboratory and in the operating room may aid this process.
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PMID:Effect of reperfusion in acute ischemia and infarction. 115 38

The efficacy of amlodipine, a long half-life dihydropyridine calcium antagonist, at the dosage of 5-10 mg/day in a single daily administration, has been compared with that of nifedipine R, a short half-life dihydropyridine, at the dosage of 20-40 mg b.i.d. in 29 patients with chronic ischemic heart disease. After a one week placebo period, patients were assigned to the treatment with amlodipine or nifedipine R, according to a randomized sequence and a cross-over, single-blind design, for two control periods of four weeks and without a wash-out interval between these two phases. During the stress test, a significant increase from baseline in test duration and in time to onset of ischemia and of angina have been obtained with both treatments; moreover amlodipine increased significantly the time to onset of ST segment deviation (-1 mm) and the time to maximum ST segment deviation compared with nifedipine R changes. Also with Holter monitoring and in the angina diary there was a significant reduction of anginal episodes. As regards safety profile, amlodipine treatment was associated with a significantly lower incidence of side effects compared with nifedipine R. This is probably due to the particular pharmacokinetics of amlodipine which, besides the long half-life which allows a single daily administration, shows a retarded peak (between the 6th and the 12th hour) with consequent reduction of phenomena connected with fast and excessive peripheral vasodilatation. In conclusion, amlodipine was as effective in reducing the signs of ischemia as nifedipine R, but compliance was better due to the single daily administration and so was tolerability.
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PMID:Amlodipine versus nifedipine retard in the treatment of chronic ischemic heart disease. 138 15

Recent studies suggest that granulocytes (PMNs) play a role in the pathogenesis of acute and chronic myocardial ischemia and extension of myocardial injury. Rabbit-derived antiserum-dependent reduction of circulating PMNs in the dog or using monoclonal antibody anti-CD11b/CD18 of PMNs resulted in smaller myocardial infarcts. Experience in humans shows the modification of PMN function in angina and during myocardial ischemia. In our studies, patients affected by coronary artery disease presented an increase in granulocyte aggregability in coronary sinus and showed a related higher expression of CD11b/CD18 in coronary sinus with respect to aorta leukocytes. The potential role of this modification of PMNs was analyzed.
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PMID:Correlation between CD11b/CD18 and increase of aggregability of granulocytes in coronary artery disease. 152 63

Recent studies suggest that granulocytes (PMNs) play a role in the pathogenesis of acute and chronic myocardial ischemia and extension of myocardial injury. A positive correlation was also found between leukocyte count and severity of coronary artery disease. Rabbit derived antiserum dependent-reduction of circulating PMNs in the dog or using monoclonal antibody anti-CD11b/CD18 of PMNs resulted in smaller myocardial infarcts. Granulocytes can release a variety of mediators tissue injury and synergize with these different mediators and other cells resulting in amplification of neutrophil stimulation and rising to additional products with enhanced endothelial injury. This paper reviews "in vivo" studies that have been instrumental in demonstrating this role of granulocytes as a mediator of myocardial ischemia. Experience in humans shows the modification of PMNs function in angina and during myocardial ischemia, and data from our group demonstrated that their aggregability is increased in the coronary sinus of patients with angiographically documented coronary disease. Upon re-perfusion PMNs accumulate and produce an inflammatory response resulting in endothelial injury. Free radicals formed during ischemia or re-perfusion produce deleterious effects on cell membranes, endothelial cell and myocardium. On the other hand the PMNs activation occurring during coronary angioplasty (PTCA) by the release of proteolytic enzymes and the generation of oxygen-free radicals, may aggravate the endothelial damage induced by PTCA and further stimulate platelets having potential implications in subsequent development of restenosis. An other aspect of PMNs function is related to leukotriene C4 release; the vasoconstrictor effect of this leukotriene on coronary arteries is synergistic with that induced by platelet-released thromboxane A2, as well as the decrease in coronary flow produced by the combination of both substances is greater than the sum of changes caused by the two eicosanoids separately administered. The potential role of leukocytes, oxygen radicals, leukotrienes and granulocyte enzymes in pathophysiology of myocardial injury due to a regional ischemia and reperfusion is an area of intense investigation. Experimental and clinical studies to elucidate these events should not only provide insights into acute and chronic pathologic tissue damage, but may also lead to the identification of important new targets of pharmacologic intervention.
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PMID:Role of granulocytes in endothelial injury in coronary heart disease in humans. 181 45

To compare the natural history of patients with new onset ischemic heart disease with that of patients with exacerbations of chronic ischemic heart disease, short- and long-term outcomes of 3,465 emergency room patients with acute ischemic heart disease at four community and three university hospitals were evaluated. Acute myocardial infarction was diagnosed in 598 (33%) of the 1,835 patients with a prior history of infarction or angina and 934 (57%) of the 1,630 without such a history (p less than 0.001). Patients with new onset ischemic heart disease with acute myocardial infarction were more likely than patients with infarction and exacerbated chronic ischemic heart disease to have Q wave infarction (57% versus 36%) and to receive thrombolytic therapy (11% versus 5%); they also had higher maximal creatine kinase levels (1,088 +/- 1,299 versus 733 +/- 906 U/liter) (p less than 0.0001 for all three). After adjustment for differences in clinical presentation and initial triage, patients with new onset ischemic heart disease with acute myocardial infarction were less likely than the comparison group to have congestive complications (odds ratio 0.63, 95% confidence interval 0.47 to 0.84, p less than 0.01) but not less likely to have arrhythmic, ischemic or overall complications. Among patients with angina without acute myocardial infarction, patients with new onset ischemic heart disease were less likely to have recurrent ischemic pain and congestive heart failure. In multivariate analysis of long-term follow-up data on 457 patients from one hospital, patients with new onset ischemic heart disease had better cardiovascular survival rates.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of the natural history of new onset and exacerbated chronic ischemic heart disease. The Chest Pain Study Group. 219 11

The serum level of myoglobin (Mb) was determined in 11 male patients with chronic ischemic heart disease (angiographically studied) by the mean of an enzyme immunoassay (EIA). By a second EIA we could detect in all our patients autoantibodies (autoAB) to Mb. While the level of Mb in all cases was normal (less than 100 ng/ml) we found differences in the level of autoAB to Mb (normal value 90-100%). 7 patients with unstable Angina pectoris exhibited decreased levels of autoAB to Mb (65%). In 4 patients with stable Angina pectoris autoAB to Mb were 93%. The physiological role of the autoAB to Mb remains still unclear. The simultaneous determination of Mb and the autoAB to Mb may be helpful in differential diagnosis of stable and unstable Angina pectoris.
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PMID:Determination of serum level of myoglobin and plasma level of autoantibodies to myoglobin in patients with angina pectoris. 246 75


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