UMLS:C0022116 - FACTA Search

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Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To know whether the pathogenesis of impending myocardial infarction(IMI) could be predicted by the direction of ST segment shifts during an ischemic chest pain, we studied 62 patients with IMI and undergoing emergent coronary angiography(CAG). They were selected from a consecutive number of 474 patients with unstable angina. IMI was defined when patients had more than 2 episodes of chest pain at rest under intensive pharmacological interventions after their CCU admission, and at least one of those was not relieved by nitroglycerin given intravenously. They were divided into 2 groups according to ST segment shifts during chest pain; 35 patients with ST elevation (G-1) and 27 patients with ST depression (G-2). The time of CAG was individually determined in each patient according to the severity of illness. Those with acute MI within 3 months before the study and 24 hours following the chest pain just before CAG were excluded from the study. New onset angina accounted for 49% in G-1 and 4% in G-2(p less than 0.01). Average history length of IMI, frequency of symptoms after CCU admission, and interval from the last symptom to CAG were similar in each groups. Single vessel disease was more predominant in G-1 than in G-2 (54% vs 11% p less than 0.01). Intracoronary thrombus(IT) in an ischemia related artery(IRA) was found in 97% of G-1 and 22% of G-2(p less than 0.001), while complex lesions(CL) proposed by Ambrose as another genesis of IMI were in 26% of G-1 and 74% of G-2(p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical significance of ST segment shifts during chest pain in predicting the pathogenesis of impending myocardial infarction]. 202 79

The average annual mortality in unselected patients with chronic stable angina is 4%. Mortality is increased in male patients and in patients who have risk factors such as hypertension, previous MI, or abnormal ECGs. We do not routinely recommend cardiac catheterization in the initial management of patients with stable angina unless the patient exhibits evidence for severe myocardial ischemia on non-invasive testing or has symptoms that are refractory to treatment. In patients who undergo cardiac catheterization, the most important determinant of survival is left ventricular function followed by the number of diseased vessels. Noninvasive testing provides important additional prognostic information to cardiac catheterization data and should be used in the decision to treat a patient medically or surgically. Mortality is increased in patients who have low exercise tolerance, exercise-induced ischemia, or a poor hemodynamic response to exercise. Unstable angina in medically treated patients is associated with a 3% to 5% hospital mortality and 7% to 8% mortality in the first year. The rate of nonfatal MI is about 8% to 10% in the first 2 weeks. We routinely recommend coronary angiography unless patients have had recent cardiac catheterization or there is a major contraindication. Mortality is increased in those who fail to respond to initial therapy, who have severe left ventricular dysfunction, and who have multivessel CAD, particularly left main CAD. The question of whether all patients with unstable angina require coronary angiography for risk stratification and possible revascularization is being addressed in the TIMI III trial.
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PMID:The prognosis in stable and unstable angina. 202 4

The prognostic value of information derived from clinical characteristics and exercise treadmill tests performed before discharge and repeated at three months was evaluated in 205 consecutive patients followed for five years. Recurrent myocardial infarction, unstable angina and mortality were tabulated. Survival was analyzed by the Kaplan-Meier life-table method and the Cox regression model. The major difference between the predischarge and three month intervals was the failure of exercise-induced ST depression to predict mortality from the predischarge test. However, it was predictive of mortality at three months when 76% survived five years with a positive ischemic response compared to 94% with a negative response (P less than 0.0005). In contrast, resting ST depression of at least 1 mm was associated with a very poor five year survival rate of 58.3% and 50% when assessed at both predischarge and three months (P less than 0.0005 and P less than 0.004, respectively). Selected univariately at the predischarge interval, the following characteristics were ranked in descending order of predictive power for five year mortality by discriminant analysis: history of previous infarction; exercise capacity; and ST depression on resting ECG greater than 1 mm. At three months, the same characteristics were selected. However, recurrent infarction and unstable angina were not predictable at either interval by any clinical or treadmill variable. Characteristics tending to reflect poor exercise capacity are stronger predictors of five year outcome than exercise-induced ischemia. While predischarge exercise testing for ST segment response failed to predict survival, this variable showed improved predictive power with repeat testing at three months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Importance of timing of treadmill predictors for risk stratification after myocardial infarction: a five year follow-up study. 204 85

Synchronized coronary venous retroperfusion was used during coronary balloon angioplasty to support the ischemic myocardium of 20 patients with unstable angina and anatomy at high risk of a coronary event. Hemodynamics and left ventricular function were the major end points of the study. Coronary venous catheterization and retroperfusion were successfully performed in 15 patients. The target vessel was an unprotected left main artery in 2, left anterior descending artery in 10, left circumflex coronary artery in 1 and right coronary artery in 2 patients. A nonsupported balloon inflation (mean 44 +/- 13 s) was compared with a later retroperfusion-supported inflation (mean 145 +/- 21 s). Right anterior oblique left ventriculograms, aortic blood pressure, pulmonary artery pressure and thermodilution cardiac output were obtained before and during peak untreated and treated balloon inflations and on completion of angioplasty. All patients had either a baseline left ventricular ejection fraction less than 0.40 or greater than 40% of contracting myocardium estimated to be at risk for severe ischemia during angioplasty. The cardiac (liters/min per m2) and stroke work (g.m/m2) indexes decreased from mean baseline values of 2.5 +/- 0.52 and 52 +/- 15 to 1.7 +/- 0.47 and 27 +/- 12 (mean +/- SD), respectively, during nonsupported balloon inflations but decreased only to 2.1 +/- 0.52 (p less than 0.01 vs. nonsupported) and to 36 +/- 14 (p = 0.01 vs. nonsupported), respectively, during retroperfusion-supported inflations. Ejection fraction (n = 8) decreased from a baseline value of 55 +/- 13% to 27 +/- 7.3% during nonsupported inflations but only to 39 +/- 10% during retroperfusion-supported inflations (p = 0.01 vs. nonsupported). Regional wall motion (area change) in the ischemic (target) region was reduced from a baseline value of 49 +/- 17% to 11 +/- 16% during nonsupported inflations but only to 27 +/- 15% during retroperfusion-supported inflations (p less than 0.01 vs. nonsupported). All but two patients had a favorable hemodynamic response to retroperfusion. There were no serious adverse effects related to the procedures and no hospital deaths. It is concluded from this preliminary study that coronary venous retroperfusion appears to be safe, to provide hemodynamic support and to improve left ventricular function during angioplasty in patients with unstable angina and anatomy at high risk of a coronary event.
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PMID:Coronary venous retroperfusion support during high risk angioplasty in patients with unstable angina: preliminary experience. 205 Sep 32

The clinical and angiographic findings of 17 resuscitated victims of exercise-related sudden ischemic death are reported in an attempt to elucidate the mechanism(s) of these deaths. Ten survivors developed cardiac arrest during or after sporting activities (group A) and 7 others during or after an exercise stress test (group B). There were 15 men and 2 women. The mean age of group A was 46 years and of group B 55 years. Coronary risk factors, as well as previous angina and myocardial infarction, were more frequent in group B. Only 3 of the 17 survivors had anginal symptoms before sudden death. Sudden death in group A was associated with acute myocardial infarction in 8 and unstable angina in 2 and was associated in group B with acute myocardial infarction in 2, unstable angina in 3 and silent ischemia in 2. Coronary angiography was acutely performed in 15 patients. In most patients the ischemia-related coronary artery was totally or subtotally occluded. Clinical and angiographic findings indicate that exercise-related sudden ischemic death was due to an acute coronary event--in most cases unexpected and unpredictable. It is suggested that exercise-induced intracoronary changes were probably responsible for the development of acute coronary (sub)occlusion and sudden death.
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PMID:Clinical and angiographic observations on resuscitated victims of exercise-related sudden ischemic death. 205 59

A 68-year-old man who presented with unstable angina had had cardiac bypass surgery 12 years earlier and successful angioplasty of a native circumflex lesion 18 months previously. Repeat catheterization showed a widely patent angioplasty site but interval closure of a saphenous vein graft to a large marginal branch that was totally occluded proximally. A stress test revealed significant myocardial ischemia. Severe peripheral peripheral vascular disease with known bilateral iliac artery occlusions mandated a brachial approach. Because of his high risk for repeat cardiac surgery, it was elected to attempt saphenous graft angioplasty following a prolonged urokinase infusion. After an infusion of urokinase for 36 hr, antegrade flow was restored and angioplasty was carried out successfully on a discrete mid-graft legion. Subsequent stress testing showed resolution of the ischemia. There were no vascular complications.
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PMID:Successful angioplasty of a chronically occluded saphenous vein graft using a prolonged urokinase infusion from the brachial route. 207 Mar 99

The relation between the results of the early submaximal symptom-limited bicycle ergometry [correction of veloergometric] test and coronary angiography were examined in 127 patients with unstable angina pectoris stabilized by medicaments. In 19 (15.0%) patients the test was negative and in 108 (85%) patients the test was positive (angina pectoris and/or ST depression greater than or equal to 0.1 mV at 80 ms after the point J of the ECG). Between the results of the early bicycle ergometry [correction of veloergometric] test and the coronary angiography, performed soon after the test, there was a close correlation. By using strict criteria or a combination of criteria for assessment of residual ischemia the test can with great accuracy differentiate the patients with multivascular from those with monovascular disease or with healthy coronary vessels.
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PMID:[The early bicycle ergometry test in drug-stabilized patients with unstable angina pectoris--the correlation with coronary angiography]. 208 Jun 9

Patients with unstable angina and/or non-Q-wave infarction constitute a group that is at high risk for progression to acute myocardial infarction or sudden death. Furthermore, in spite of maximal medical therapy, a large fraction of these patients experience recurrent episodes of myocardial ischemia prompting surgical revascularization or coronary angioplasty. In prior studies of patients with unstable angina, the incidence of myocardial infarction within 1 month of hospitalization was 8-13%, and the incidence of death was about 4%. Between 3 months and 1 year after presentation, the cumulative rate of infarction or death increased to 10-14 and 8-10%, respectively. That is, most recurrent ischemic events occur within the first 3 months after the onset of symptoms. In the subset of patients with pain at rest or with electrocardiographic changes at the time of admission, the prognosis is even worse. The rate of myocardial infarction or death in such patients ranged between 14 and 21% during the first 3-4 months after onset of symptoms. Crossover to surgical therapy because of recurrent ischemic pain was also common, occurring in 30-50% of the patients at 3 months. Recent advances in understanding the pathophysiology of these two syndromes suggest that an aggressive antithrombotic regimen could be of great benefit in preventing progression to acute coronary occlusion and death. Pathologic investigations strongly suggested that plaque fissuring and subsequent overlying thrombosis were the major components in the process of unstable angina progressing to myocardial infarction and/or sudden death. This hypothesis has been substantiated by recent pathologic studies of patients who died shortly after the onset of unstable angina. Examination of the coronary arteries revealed not only plaque fissuring with superimposed layers of thrombus in the majority of the cases, but also evidence of distal thromboembolism from these foci. In vivo coronary arteriography in patients with unstable angina highlighted the progression of prior coronary stenoses, even to total occlusion, and the eccentric and irregular angiographic morphology of the ischemia-producing lesions. Furthermore, intracoronary thrombus is often seen at these sites, especially when arteriography is carried out soon after rest pain. These observations also suggested that plaque rupture may have occurred. Intraoperative angioscopy has revealed ruptured plaques in patients with progressive unstable angina, while those with rest pain had complicating thrombi. Patients with unstable angina also have biochemical evidence of activation of both the coagulation systems and platelets.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Insights into the pathogenetic mechanisms of unstable angina. 208 62

We tested the safety and the usefulness of intravenous fibrinolysis in 44 patients with refractory unstable angina, defined as persistence of ischemic episodes during 48-hour Holter monitoring (phase 1) despite maximal medical therapy. After fibrinolysis, recurrence of ischemia was recorded during 1 week of observation in CCU including 2 24-hour Holter monitoring at the beginning and at the end of this week (phase 2): 17 patients completed the observation period without either symptomatic or asymptomatic ischemic episodes (Group A); the remaining 27 patients continued to manifest ischemia (Group B). No bleeding complications occurred. Within a 6-month follow-up, 2 patients of Group A had recurrence of unstable angina while in Group B, 10 patients underwent CABG or PTCA for refractory angina, 6 other patients with refractory angina continued medical therapy, 1 patient had a myocardial infarction and 2 patients died (p less than 0.001). Phase 1: the duration of total ischemia (min/24 hours) was a relevant prognostic marker: higher duration correlated with adverse clinical outcome (p less than 0.01). Phase 2: in comparison with phase 1, duration of total ischemia was significantly reduced (p less than 0.001). A percent value expressing this variation was calculated for each patient: (min of ischemia in phase 2 - min of ischemia in phase 1/min of ischemia in phase 1). The variation thus obtained again gave information on the clinical outcome: the greater was the reduction, the lower was the risk of cardiac events (p less than 0.001). Our data suggest that: clinical stabilization may be obtained with the addition of fibrinolysis to conventional treatment; Holter monitoring bears prognostic information helpful in identifying patients who need further intervention.
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PMID:[Systemic fibrinolysis in patients with refractory unstable angina]. 209 25

The very first presentation of ischemic heart disease--acute infarction, sudden death, or unstable angina--most often occurs abruptly. The first approximation that it occurs as a random event only when a certain "threshold severity" of coronary atherosclerosis has gradually developed, although widely accepted, should perhaps be reconsidered and expanded on the basis of the following considerations. Acute coronary occlusion leading to myocardial infarction often occurs at the site of mild or noncritical coronary stenoses. Conversely, in patients with chronic angina severe coronary stenoses can remain unchanged for years with no detectable progression. When a coronary artery occludes, the size of infarction can vary greatly, and when ischemia and infarction occur, malignant arrhythmias occur in some patients but not in others. Thus, in a second approximation, ischemic heart disease should be considered as the result of the variable combination of three major components: a) A very variable chronic atherosclerotic background, which can result from a variety of pathologic processes; b) A number of acute ischemic stimuli, which can unpredictably impair myocardial blood flow as a result of coronary thrombosis and/or vasoconstriction; c) A variable response of the heart to a sudden reduction of coronary blood flow in terms of collateral perfusion and malignant arrhythmias. Therefore, at one extreme end of the spectrum in any individual, ischemic syndromes may present predominantly as a result of an extremely large chronic background component. At the other extreme, powerful acute ischemic stimuli can unexpectedly impair blood supply by coronary thrombosis, constriction, or their combination, in the presence of a mild chronic atherosclerotic background.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of myocardial ischemia. 209 77

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