Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients with coronary artery disease, angina pectoris provides an unreliable underestimation of disease activity and risk. Unheralded myocardial infarction and sudden death are common clinical presentations. Furthermore, objective testing, in hospital and more recently during the patient's normal daily activities, has demonstrated frequent and asymptomatic episodes of ischemia, as indicated by transient ST-segment depression. Since the underlying pathophysiologic disturbances of myocardial perfusion appear to be similar in painful and painless episodes, it seems appropriate to consider them together as the "total ischemic burden" on the myocardium. Research into this functional expression of coronary disease has indicated that active ischemia is associated with an increased risk of morbid events in all clinical subgroups of patients, including those with stable angina, unstable angina, peripheral vascular disease and following myocardial infarction. If this is confirmed in prospective trials, the assessment of total ischemic burden is likely to become part of the clinical investigation of patients with coronary disease. Clinical trials testing the efficacy of interventions will need to examine the effect on ischemic activity during normal daily life, in addition to symptoms and exercise tolerance. Evidence is still required to demonstrate whether therapy aimed at reducing the total ischemic burden will prolong life. The total ischemic burden provides a marker to follow the dynamic changes of the atherosclerotic lesion. Future research may have to concentrate on treatment aimed at altering the natural history of obstructive coronary atherosclerosis in order to affect the long-term outlook for patients with coronary artery disease.
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PMID:Total ischemic burden in patients with coronary artery disease. 209 78

Patients with unstable angina pectoris who remain symptomatic despite medical treatment are at high risk of death and myocardial infarction. The incidence of refractory unstable angina was examined in a consecutive series of 103 patients who received conventional medical treatment with nitrates, beta blockers, calcium antagonists and aspirin. During 48 hours of continuous electrocardiographic monitoring, 24 patients had greater than or equal to 1 anginal attack, 5 of whom had both painful and painless ischemic episodes. In these 24 patients with unstable angina refractory to conventional medical treatment, the short-term efficacy of recombinant tissue-type plasminogen activator (rt-PA) followed by heparin was assessed and compared with heparin alone in a randomized double-blind trial. Recurrences of ischemic attacks during a 72-hour follow-up period were documented in 9 of the 12 patients given heparin alone. All patients experienced at least 1 symptomatic ischemic episode and 1 patient had both painful and painless ischemia. No patient given rt-PA plus heparin had either symptomatic or asymptomatic ischemic attacks during follow-up. Kaplan-Meier curves analysis demonstrated a significantly higher probability of being ischemia free in the group of patients treated with rt-PA followed by heparin than in the group treated with heparin alone (p less than 0.01). Quantitative coronary arteriography failed to reveal any significant changes of ischemia-related lesions before and after each treatment. This study demonstrates that the combination of rt-PA and heparin has a greater protective effect than heparin alone in treating recurrent ischemic episodes in patients with refractory unstable angina.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Recombinant tissue-type plasminogen activator followed by heparin compared with heparin alone for refractory unstable angina pectoris. 212 Oct 16

Unstable angina can manifest as an array of symptom complexes. In some patients, medical therapy will stabilize the episodes of angina, and only predismissal exercise testing or angiography (or both) will be necessary. At the other end of the spectrum are patients with rest angina or multiple episodes of silent ischemia who are refractory to medical therapy and experience undetected microinfarction. Most of these patients require immediate catheterization and subsequent intervention with intra-aortic balloon pulsation, percutaneous transluminal coronary angioplasty, or coronary artery bypass grafting. An entire spectrum of manifestations exists between these two extremes. One challenge during the 1990s will be better stratification of patients with unstable angina so that safe, efficient, cost-effective treatment strategies can be appropriately applied to all patients.
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PMID:Unstable angina. 217 45

In a prospective study the significance of silent ischemia was evaluated in 66 patients with a clinical diagnosis of unstable angina (no requirement for reversible ST-T changes during pain on 12-lead electrocardiograms before entry), and the results of continuous 2-channel electrocardiographic (ECG) recordings, begun within 24 hours of admission, were compared with other clinical and ECG predictors of adverse outcome. Ischemic changes were detected in 7 patients (11%) during a mean of 41 hours of recording. There were 37 episodes of transient ST-segment change (16 ST elevation, 21 ST depression) of which 11 (30%) were symptomatic and 26 (70%) were silent. All 7 patients had at least 1 silent episode and 5 also had symptomatic episodes during the recording but only 2 patients had exclusively silent episodes. During a mean follow-up of 13.3 months, 3 patients died, 5 had a nonfatal myocardial infarction and 32 required revascularization. Although transient myocardial ischemia during the continuous ECG recording, whether silent or symptomatic, was a specific predictor of subsequent nonfatal myocardial infarction or death (specificity 92%), its sensitivity for these events was low (25%). In contrast, recurrent rest pain (greater than or equal to 1 episode) occurred in all patients with these serious adverse events (sensitivity 100%, specificity 49%). Transient ischemia occurs infrequently during continuous ECG recordings in patients with unstable angina not selected by reversible ST-T changes on a 12-lead electrocardiogram at entry. Recurrent rest pain after hospital admission is a more sensitive predictor of serious events in this group.
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PMID:Clinical significance of silent ischemia in unstable angina pectoris. 218 94

Rupture of an atherosclerotic plaque associated with partial or complete thrombotic vessel occlusion is fundamental to the development of ischemic coronary syndromes. Plaques that produce only mild-to-moderate angiographic luminal stenosis are frequently those that undergo abrupt disruption, leading to unstable angina or acute myocardial infarction. Plaques with increased lipid content appear more prone to rupture, particularly when the lipid pool is localized eccentrically within the intima. Macrophages appear to play an important role in atherogenesis, perhaps by participating in the uptake and metabolism of lipoproteins, secretion of growth factors, and production of enzymes and toxic metabolites that may facilitate plaque rupture. In addition, the particular composition or configuration of a plaque and the hemodynamic forces to which it is exposed may determine its susceptibility to disruption. Exposure of collagen, lipids, and smooth muscle cells after plaque rupture leads to the activation of platelets and the coagulation cascade system. The resulting thrombus may lead to marked reduction in myocardial perfusion and the development of an unstable coronary syndrome, or it may become organized and incorporated into the diseased vessel, thus contributing to the progression of atherosclerosis. In unstable angina, plaque disruption leads to thrombosis, which is usually labile and results in only a transient reduction in myocardial perfusion. Release of vasoactive substances, arterial spasm, or increases in myocardial oxygen demand may contribute to ischemia. In acute myocardial infarction, plaque disruption results in a more persistent thrombotic vessel occlusion; the extent of necrosis depends on the size of the artery, the duration of occlusion, the presence of collateral flow, and the integrity of the fibrinolytic system. Thrombi that undergo lysis expose a highly thrombogenic surface to the circulating blood, which has the capacity of activating platelets and the coagulation cascade system and may lead to thrombotic reocclusion. Measurements aimed at reversing the process of atherosclerosis via cholesterol reduction and enhanced high density lipoprotein activity are encouraging. Active research is being focused on the development of new antithrombotic tools, such as inhibitors of thrombin, thromboxane, and serotonin receptor antagonists, and monoclonal antibodies aimed at blocking platelet membrane receptors or adhesive proteins. These compounds may prove useful when immediate and potent inhibition of the hemostatic system is desired. Intensive research is still needed in the areas of pathogenesis and therapeutic intervention in atherosclerosis.
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PMID:Atherosclerotic plaque rupture and thrombosis. Evolving concepts. 220 64

PTCA is a widely used technique in patients post-acute myocardial infarction (AMI) as well as in unstable angina (UA). The precise timing of its application and some aspects of the indication nowadays remains a matter of controversy. Primary PTCA is not generally considered to be the initial treatment of AMI. In contrast, immediate PTCA after thrombolysis has been proposed attempting to decrease the incidence of early reocclusion, improve myocardial salvage, decrease the incidence of postinfarction angina and improve survival. Nevertheless, three recent controlled studies (TAMI, TIMI II and ECSG) have demonstrated that an "aggressive" strategy with obligatory, invasive intervention following thrombolysis does not provide any advantage in terms of survival, rate of reocclusion or improved ventricular function and is, in fact, likely to be harmful. Emergent coronary arteriography after AMI should be reserved for unstable patients with continued or recurrent ischemia in the CCU. In elective basis it should be indicated in all patients with spontaneous or provocable ischemia prior to hospital discharge. If high grade coronary stenoses are identified, the patient should be considered for PTCA or surgical revascularization. In our own experience with coronary arteriography 24 hours to 15 days after intravenous thrombolysis with SK, PTCA is anatomically feasible in 44% of all the patients and in 60% of those showing a patent vessel. However, when indicated because of postinfarction angina or a positive stress test, PTCA was performed only in 22%, some of them presenting with a totally occluded vessel. In case of stenosis lesser than 100% the dilation success rate is slightly lower than that of out entire series (84% vs 88%), but the incidence of acute occlusion is significantly higher (10% vs 6%), particularly in patients with angiographic evidence of intracoronary thrombi. The incidence of "non-significant" (less than 70%) stenosis spontaneously increases when the coronary arteriography is performed late during hospitalization (34% vs 17% when the patient is studied in the first 24-48 hours).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Coronary angioplasty in acute coronary syndrome]. 220 92

Silent (asymptomatic) myocardial ischemia (SMI) is defined as a transient alteration in myocardial perfusion in the absence of chest pain or the usual anginal equivalents. Patients may be classified as having one of the three types of SMI: type A--totally asymptomatic patients with no history of angina or myocardial infarction; type B--asymptomatic patients with previous myocardial infarction; type C--patients with angina and asymptomatic ischemic episodes. SMI has been found in 2.5% of all healthy males aged 40-59 and in 20% of all postinfarction patients. In type C-patients, 80% has been found to have asymptomatic ischemic episodes in addition to typical angina pectoris. The frequency of SMI may be up to three or four times that of anginal attacks. SMI patients have generally reduced sensitivity to pain an differences in severity an duration of ischemic episodes. Diagnosis is based on screening by means of exercise testing in patients working in specific professions (like pilots, busdrivers etc.), in postinfarction patients and in patients after unstable angina pectoris and after coronary bypass surgery or coronary angioplasty. Prognosis is the same as in asymptomatic ischemia. SMI is an indicator of instability in certain groups of patients (post infarction, after unstable angina pectoris). SMI persisting after medical therapy of unstable angina is associated with adverse short-term-prognosis, therefore coronary surgery or angioplasty is indicated.
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PMID:[Asymptomatic myocardial ischemia]. 223 47

In a prospective pilot trial of antithrombotic therapy in the acute coronary syndromes (ATACS) of resting and unstable angina pectoris or non-Q-wave myocardial infarction, 3 different antithrombotic regimens in the prevention of recurrent ischemic events were compared for efficacy. Ninety-three patients were randomized to receive aspirin (325 mg/day), or full-dose heparin followed by warfarin, or the combination of aspirin (80 mg/day) plus heparin and then warfarin. Trial antithrombotic therapy was added to standardized antianginal medication and continued for 3 months or until an end point was reached. Analysis, by intention-to-treat, of the 3-month end points, revealed the following: recurrent ischemia occurred in 7 patients (22%) after aspirin, in 6 patients (25%) after heparin and warfarin, and in 16 patients (43%) after aspirin combined with heparin and then warfarin; coronary revascularization occurred in 12 patients (38%) after aspirin, in 12 patients (50%) after heparin and warfarin, and in 22 patients (60%) after aspirin combined with heparin and then warfarin; myocardial infarction occurred in 1 patient (3%) after aspirin, in 3 patients (13%) after heparin and warfarin, and in no patient after aspirin combined with heparin and then warfarin; no deaths occurred after aspirin or after aspirin combined with heparin and then warfarin, but 1 patient (4%) died after warfarin alone; major bleeding occurred in 3 patients (9%) after aspirin, in 2 patients (8%) after heparin and warfarin, and in 3 patients (8%) after aspirin combined with heparin and then warfarin. Recurrent myocardial ischemia occurred at 3 +/- 3 days after randomization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Usefulness of antithrombotic therapy in resting angina pectoris or non-Q-wave myocardial infarction in preventing death and myocardial infarction (a pilot study from the Antithrombotic Therapy in Acute Coronary Syndromes Study Group). 224 56

The incidence and prognostic significance of silent myocardial ischemia were assessed in 175 patients who survived a first acute myocardial infarction (AMI). This was done by means of a 24-hour continuous ECG monitoring which was performed before discharge. Twenty-six out of 175 patients (14.8%) showed one episode or more of S-T segment depression; 19 of these reported no pain at all while the other 7 reported both painful and painless episodes. A total of 65 ischemic episodes were registered; of these 53 (81.5%) were painless and 12 (18.5%) were painful. No difference in the duration of ischemic episodes or in heart rate at the onset of S-T segment depression was detected for painless or painful episodes. The S-T segment depression episodes showed a peak in the morning but were higher in the afternoon and this circadian pattern was statistically significant both with regard to duration (p less than 0.05) and to the number of episodes (p less than 0.05). Cardiac death occurred in 5 of the 26 patients (19.2%) with S-T segment depression during continuous ECG monitoring, and in 5 of the 149 (3.4%) without S-T segment depression (p less than 0.01). In patients with ischemia duration greater than 60 min/24 hours, the mortality rate was higher (p less than 0.05). No cardiac events (unstable angina, non-fatal re-infarction, balloon angioplasty and/or coronary by-pass) occurred in 117 out of 149 patients (78.5%) without ST-segment depression, while these events were observed in 13 out of the 26 patients (50%) with ischemic episodes during Holter monitoring (p less than 0.01). Sensitivity and specificity of S-T segment depression was respectively 29.3 and 89.5% for cardiac death and cardiac events considered together.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The clinical characterization and prognostic significance of episodes of transient myocardial ischemia in patients with a recent myocardial infarct]. 224 97

The clinical characteristics and coronary angiographic findings of 42 well-conditioned subjects with an acute ischemic event related to sport are reported. Five patients had unstable angina, 25 had acute myocardial infarction (AMI), and 12 were resuscitated victims of sudden ischemic death. Twenty-two events occurred during sport (group A) and 20 after sport (group B). There were two women and 40 men. The mean age was 46 years (range 25 to 65). Twelve out of 30 patients who smoked cigarettes had an adjunctive risk factor for coronary artery disease. Twelve others (28%) had no identifiable risk factor. Prodromal cardiac symptoms were detected in three patients (group A). Two patients had previous myocardial infarction (group B). Coronary angiography was performed acutely in 39 patients. The distribution of the ischemia-related coronary artery was comparable in both groups. The lesion morphology of 35 culprit coronary arteries was described as concentric in six patients and eccentric with regular borders (type I lesion) in 11 and irregular borders (type II lesion) in 18. Eccentric lesions consistent with ruptured plaques prevailed in both groups. Associated coronary artery disease was present in 10 patients. There was no relationship between the number of risk factors and the extent of diseased coronary arteries. Clinical characteristics and coronary angiographic findings of patients with unstable angina, AMI, and sudden death either during or after sport are similar and indicate a common pathogenesis. The probable mechanism of a coronary event related to sport is exercise-induced plaque rupture. In most instances such an event is unexpected and unpredictable. Identification of some subjects at risk is possible.
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PMID:Clinical characteristics and coronary angiographic findings of patients with unstable angina, acute myocardial infarction, and survivors of sudden ischemic death occurring during and after sport. 224 76


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