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)

Postinfarction angina carries a poor prognosis, with a 20-70% incidence of recurrent myocardial infarction (MI) or death within the subsequent 3-6 months. The pathophysiologic mechanisms causing postinfarction angina may include thrombus, complex coronary arterial lesions that form a nidus for thrombus formation, inadequate collateral supply following acute MI, or intimal endothelial dysfunction. The role of thrombus has been established in the pathophysiology of Q-wave MI, and thrombolytic treatment of patients presenting with acute transmural MI has been shown to salvage left ventricular function and to reduce mortality. However, thrombolytic therapy for the acute MI does not reduce the incidence of recurrent ischemia or infarction, as is evident from the 18-26% incidence of recurrent ischemia reported in the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) and Thrombolysis in Myocardial Infarction (TIMI) trials. In the Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI) study the incidence of reinfarction was documented as 4% in the streptokinase group, which was actually significantly greater than in the placebo group (2%). In a randomized placebo-controlled study of thrombolysis for postinfarction angina, 29 patients were randomized to placebo (P group, n = 17) or to thrombolytic therapy (T group, n = 12). Patient groups were similar with respect to age, location of MI, ejection fraction, severity of coronary artery disease, and antianginal therapy. Patients underwent coronary angiography 6 +/- 1 days postinfarction. Filling defects consistent with intracoronary thrombus was seen in 11 of 12 T group patients and in 11 of 17 P group patients prior to treatment. Lysis occurred in 7 of 11 T patients and 1 of 11 P (p less than 0.02). Holter-detected silent ischemia was compared pre- and posttherapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thrombolysis in postinfarction angina. 189 59

The impact of postinfarction angina pectoris on the course of myocardial infarction (MI) was studied in the hospital setting in 359 patients who had sustained large MI, 247 of them being followed for a year after their discharge. In the group of patients with postinfarction angina pectoris, the course of the disease was found to be more severe in hospital and during a year-follow-up after MI. They more frequently developed acute and chronic heart failure, rhythm and conduction disturbances, recurrent MI. A statistic relationship was not established between the development of postinfarction angina and late fatality. Postinfarction angina was demonstrated to increase a risk for an unfavorable course of a postinfarction period. No significant difference was found in the prognostic significance of the time angina occurred following MI.
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PMID:[Post-infarction stenocardia (clinical and prognostic significance)]. 204 41

To elucidate the pathophysiology of angina pectoris after myocardial infarction, we analyzed the coronary stenoses in 45 subjects (28 men, 17 women, aged 33 to 67 years) with recent (less than or equal to 60 days) infarction, significant narrowing of only the infarct-related artery, and residual anterograde flow in this artery. Postinfarction angina was absent in 19 (group I) and present in 26 (group II). The groups were similar in age, left ventricular function, incidence with which each coronary artery was involved, as well as stenosis diameter (1.0 +/- 0.3 vs 0.9 +/- 0.4 mm [mean +/- standard deviation], respectively, difference not significant), stenosis area (0.9 +/- 0.4 vs 0.8 +/- 0.8 mm2, respectively, difference not significant), percent diameter narrowing (65 +/- 5 vs 66 +/- 9, respectively, difference not significant), and stenosis eccentricity. However, those with postinfarction angina had longer stenoses (group I, 4.3 +/- 1.4 mm; group II, 10.3 +/- 4.0 mm; p less than 0.001). Thus, patients with postinfarction angina and residual anterograde flow in the infarct artery may have angina due to a marked reduction in anterograde flow, caused by a long stenosis. There is no apparent relation between stenosis eccentricity and postinfarction angina.
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PMID:Angiographic characteristics of the infarct-related coronary artery in patients with angina pectoris after myocardial infarction. 275 70

To examine the vasospastic cause of myocardial infarction (MI) we studied 1) the incidence of rest angina before MI, 2) clinical features of postinfarction angina and 3) the occurrence of MI in variant angina. 1) Of 178 patients with MI, 60 (34%) experienced rest angina for 1 day to 10 years before the onset of MI. The incidence of rest angina was significantly higher in patients having milder coronary stenosis of 75% or less (15/30, 50%) than in others having severe stenosis of 90% or more (45/148, 30%), p less than 0.05. 2) Postinfarction angina with ST elevation was observed in 16 patients (9%) and ST elevation developed in leads with pathological Q waves in all patients. The incidence of postinfarction angina was significantly higher in those having milder coronary stenosis than in others having severe stenosis, (27% versus 5%, p less than 0.005). Patients with postinfarction angina experienced rest angina before MI more frequently (81%) than others (29%, p less than 0.005). Sublingual nitroglycerin was effective in relieving postinfarction angina attacks and oral calcium antagonist prevented attacks in all patients. 3) MI developed in 9 of 97 patients with variant angina. Six patients had transmural and 3, non-transmural MI. Pathological Q waves and/or coronary T waves appeared in leads where ST elevation was observed during anginal attack. In 7 patients MI developed when antispastic agents were not used and in 2, when angina persisted even under treatment with calcium antagonist. These data strongly suggest that the coronary spasm can be a cause of MI in some patients.
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PMID:Clinical evidence suggesting vasospastic cause of myocardial infarction. 372 79

Coronary heart disease (CHD) was followed up in 239 patients with rheumatic heart disease. According to the clinical data 40 (16.73%) patients had myocardial infarction (MI), 100 (41.84%) cardiosclerosis (CS), 185 (77.4%) angina pectoris (AP). AP (44.35%) prevailed among the isolated (66.1%) forms of valvular disease, associated AP and CS (23%) among the combined (33.9%) forms. In the majority of patients, AP originated and ran its course as stable throughout many years; in one-fifth of patients, the disease occurred as unstable. The incidence of AP was significantly higher in the senior age group, in women with aortic valvular disease, in men with stage III circulatory failure, and in cardiomegaly, AP aggravated the disease and life prognosis. MI was manifested by a moderately pronounced painful attack; it was frequently complicated by acute or incremental chronic circulatory failure. Small-focal MI was seen more frequently while the electrocardiographic changes associated with the disease resembled those seen in rheumatic carditis. Postinfarction CS stimulated the onset and progress of chronic congestive heart failure in 93.02% of patients.
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PMID:[The course of ischemic heart disease in rheumatic defects in persons over 45]. 401 13

An important question facing the profession each and every day is whether to recommend cardiac catheterization to a patient who has just had an acute myocardial infarction. Criteria have been proposed and ongoing studies are helping to establish guidelines to determine which survivors of an uncomplicated myocardial infarction can benefit from a knowledge of the coronary anatomy and ventricular function. In the case presented in this vignette the problem is related to angina recurring during the early stages of an acute myocardial infarction. Postinfarction angina often reflects subtotal obstruction of a major coronary artery that supplies either a portion of the myocardium that had infarcted or myocardium distant from the zone of the infarction. This is a high-risk group. Here the criteria are firmly established. Coronary angiography should be performed promptly to help determine whether coronary artery bypass surgery or balloon angioplasty is indicated.
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PMID:Cardiac catheterization after an acute myocardial infarction. 660 29

Recurrent ischemia after acute myocardial infarction (AMI) has been largely associated with a poor prognosis. This study was carried out to analyze the relationship among different clinical variables and both postinfarction angina and reinfarction after AMI. A total of 452 consecutive patients (mean age 58.2 +/- 12 years) were admitted to the coronary care unit and were studied prospectively. More than half of the patients received some type of thrombolytic therapy. Death occurred in 45 patients (9.9%) during hospital stay. Postinfarction angina was diagnosed in 81 patients (17.9%) and reinfarction in 22 (4.9%). Patients who developed reinfarction had a high mortality rate (45.5%) compared with those who did not develop such an event (8.1%) (p < 0.0001; odds ratio: 9.4; 95% confidence interval 3.5-25.4). On the other hand, postinfarction angina had no significant association with mortality. Multivariate analysis revealed that a history of angina (> 1 week) was predictive of the occurrence of postinfarction angina and that the use of fibrinolytic treatment, prodromal symptoms, and postinfarction angina were significantly related to reinfarction. We conclude that several simple clinical variables are clear independent predictors of postinfarction angina and reinfarction following AMI and should be taken into account in routine clinical practice or when planning intervention trials.
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PMID:Prognostic value of clinical variables for recurrent ischemic events after acute myocardial infarction. 774 87

Postinfarction left ventricular aneurysm is a serious disorder that can lead to congestive heart failure, lethal ventricular arrhythmia, and premature death. Surgical treatment is indicated in established cases of congestive heart failure, angina pectoris, malignant ventricular arrhythmia, or recurrent embolization from the left ventricle. The goal of surgical intervention is to correct the size and geometry of the left ventricle, reduce wall tension and paradoxical movement, and improve systolic function. Surgical techniques for repair of left ventricular aneurysm have evolved over the last five decades. Aneurysmectomy and linear repair of the left ventricle was introduced by Cooley and colleagues in 1958 and remained the standard procedure until the late 1980s. Endoventricular patch plasty (EVPP) was then introduced as a more physiologic repair than the linear closure technique, especially when the aneurysm extends into the septum. However, there is still controversy whether EVPP is superior to simple linear resection in terms of impact on early and late clinical outcomes. In the current era of evidence-based medicine, the best strategy to resolve a controversy is through the explicit and conscientious assessment of current best evidence. This review article attempts to evaluate the current best available evidence on the impact of technique of left ventricular aneurysm repair on postoperative clinical outcomes.
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PMID:Impact of technique of left ventricular aneurysm repair on clinical outcomes: current best available evidence. 1943 91