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)

Dipyridamole is one of several agents that may be infused intravenously to nonivasively evaluate coronary perfusion without dynamic exercise. Among such agents it is the most investigated, and it is associated with the greatest clinical experience. Its mechanism of action utilizes intrinsic adenosine and does not require the induction of ischemia. Rather, the method tests the coronary flow reserve by dilating the precapillary and arteriolar capillary beds. Vessels with a limited coronary flow reserve demonstrate reduced responsiveness with relative flow reduction and a resultant defect on perfusion scintigraphy. Side effects are common and generally benign, but deaths have been reported and they generally relate to severe hypotension, prolonged dense ischemia and resultant infarction, or bronchospasm. Severe complications are rare and can be avoided by the prompt administration of aminophylline, the dipyridample antedote. Diagnostic accuracy for the identification of coronary disease appears similar to that for exercise perfusion scintigraphy. It should be applied to patients with known or suspected coronary disease who require coronary evaluation, but who cannot exercise adequately for diagnostic or prognostic purposes. In such patients, the method is useful for the preoperative assessment of risk at peripheral vascular and other major noncardiac surgery. It may be of value as well in the assessment of the otherwise uncomplicated patient postinfarction. Not yet established is its application to the patient with unstable angina or in the acute setting, after coronary reperfusion. Similarly, its comparison with direct adenosine infusion or with pharmacological agents whose mechanism rests entirely on ischemia induction, as does dobutamine, has until now been limited. Unlike its use with perfusion scintigraphy, the application of dipyridamole with echocardiography and other functional ischemic indicators is totally dependent on the induction of ischemia. This is likely less frequent than the induction of nonischemic perfusion heterogeneity. The agent is now commonly available and will make a significant beneficial impact on patient evaluation and management.
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PMID:Dipyridamole perfusion scintigraphy. 183 35

Between 1980 and 1988, percutaneous transluminal coronary angioplasty (PTCA) was performed in 1,514 patients. Fifty-five patients (3.6%) underwent emergency coronary bypass surgery because of an acute occlusion of the vessel or a dissection with sustained angina and signs of ischemia on the electrocardiogram. Twenty-five of these 55 patients had a myocardial infarction and 5 patients died, 3 perioperatively, 2 after hospital discharge. The degree of stenosis of the dilated vessel significantly influenced the incidence of infarction, while left ventricular ejection fraction prior to PTCA significantly influenced mortality. Patients who underwent surgery with an occluded vessel experienced myocardial infarction significantly more often (87%) than patients with a patent vessel (24%). The incidence of infarction was 27% when reperfusion of the vessel occluded during PTCA was achieved with a reperfusion catheter, repeated PTCA or intracoronary lysis. The patients' age, presence of unstable angina, left ventricular ejection fraction prior to PTCA, the dilated vessel, the extent of coronary artery disease, collateralization of the dilated vessel, and the time between the onset of the event necessitating bypass surgery and the beginning of extracorporeal circulation were found to have no influence on the incidence of infarction. Patients who died had a significantly lower ejection fraction before PTCA than survivors and all patients who died had experienced a large perioperative myocardial infarction.
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PMID:[Results of emergency bypass operation following percutaneous transluminal coronary angioplasty]. 195 73

For 18 patients consecutively admitted to the coronary care unit for unstable angina, 48-hour electrocardiographic Holter monitoring was performed after they were randomly assigned in a single-blind fashion to 1 of 2 treatment groups. The first group was treated with acetylsalicylic acid (ASA) and intravenous nitroglycerin, the second with ASA and intravenous diltiazem. All of the patients treated with nitroglycerin still had ischemic episodes after 48 hours (33% were symptomatic), in contrast with 11% of the diltiazem group (11% asymptomatic). Maximal ST-segment depressions of symptomatic and asymptomatic episodes were significantly different; and no significant increases in heart rate were observed either during the 15 seconds before ischemia began or during the ischemic episode. During the 48 hours, the diltiazem group had significantly fewer ischemic episodes (17) than did the nitroglycerin group (145). We concluded that "on-line" ST-segment observation is of prime importance for monitoring unstable angina; that the majority of the ischemic episodes associated with unstable angina are silent; and that intravenous diltiazem could be an effective pretreatment for patients who must undergo mechanical or surgical therapy.
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PMID:Intravenous diltiazem versus nitroglycerin for silent and symptomatic myocardial ischemia in unstable angina pectoris. 195 Nov 2

Drug-induced cardioprotection, that is, protection of the heart from injuries of all kinds, is of particular importance in coronary heart disease, especially in fresh myocardial infarction including unstable angina pectoris, within the framework of secondary prevention after infarction, and in chronic coronary insufficiency (stable angina pectoris, silent ischemia). In the case of fresh infarctions, functional myocardium can be protected or salvaged in particular by early thrombolysis, early administration of calcium antagonists or beta blockers (in particular the combination of calcium antagonists with beta blockers). In the area of secondary prevention, beta blockers predominate. In chronic coronary insufficiency, calcium antagonists, nitrates and beta blockers are the first-choice cardioprotective agents.
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PMID:[Cardioprotection with drugs. 1: Coronary heart disease]. 196 78

Unstable angina is a clinical syndrome characterized by increased rate and severity of angina pectoris attacks and, sometimes but not always, accompanied by ECG changes similar to those seen in coronary insufficiency. According to the present conception of the pathogenesis, ruptures at points of high-grade stenosis in the epicardial coronary arteries with simultaneous apposition of thrombi and vasoconstriction cause critical narrowing of the vascular lumen, which means that with the same level of oxygen consumption, coronary blood flow might be inadequate even at rest. In this way the development of severe ischemia, sudden cardiac death or myocardial infarction is programmed. Therapy must accordingly aim at avoiding or eliminating the progression of thrombosis and at increasing the reduced coronary blood flow. The prognosis is unequivocally improved by aspirin. In addition, heparin, 400 units/kg body weight, should be given. Thrombolysis may be possible after mechanical recanalization, depending on the individual results of coronary angiography. Providing the adverse reactions are monitored, nitroglycerin given intravenously is the basic drug therapy, although comparative studies against other drugs are not available and some data show the development of tolerance during prolonged use. Therefore, an early change to sustained-release nitrates or mononitrates can be justified. beta-receptor blockers reduce the frequency of silent ischemia and of myocardial infarction. By these means, in 80% of the patients affected, unstable angina will be converted to the stable form of the disease. If symptoms persist coronary angiography is urgently indicated, to allow the selection of PTCA or aortocoronary bypass surgery according to the findings.
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PMID:Unstable angina: pathophysiology and drug therapy. 197 60

Because of the absence of a generally accepted definition of unstable angina, the clinical context of drug trials for this condition has varied from trial to trial. Early- versus late-entry trials must be distinguished, and the possibility of a modification of effect caused by the nature of drug therapy already given when the patient became unstable or by concomitant treatment in addition to experimental treatment must be taken into account. These factors cannot be overlooked when the results from a limited number of reported trials are pooled together. The largest early-entry trial with a beta-blocker and a calcium antagonist was the Holland Interuniversity Nifedipine/metoprolol Trial (HINT), which enrolled patients with suspected unstable angina diagnosed at coronary care unit admission. HINT results showed that unstable angina cannot be reliably differentiated from evolving myocardial infarction (MI) in this particular context and that there are few early MIs that could have been prevented. In patients who were not already taking a beta-blocker, metoprolol reduced the incidence of acute MI or recurrent ischemia, and there was no benefit of nifedipine. On the other hand, the addition of nifedipine was effective in patients whose conditions became unstable despite maintenance treatment with a beta-blocker. Thus, previous beta-blockade modified the effect of the calcium antagonist studied. Based on evidence from HINT and other trials, it is concluded that beta-blockers should be used as the first-line treatment in patients with unstable angina and that a calcium antagonist should be added when patients remain unstable despite beta-blockade.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Medical management of unstable angina. What have we learned from the randomized trials? 197 26

Questionnaires were sent to 61 Norwegian hospitals treating acute coronary syndromes, and 90% replied. Thrombolytic drug treatment is now the routine when the history of chest pain is short and ischemia appears in ECG. Use of glyceryl trinitrate and beta blocking drugs varies considerably, as does the use of oral anticoagulants and platelet inhibitors. Practice also varies in unstable angina. However, a combination of aspirin, intravenous nitrate, and betablockers is common. Several treatment regimens have an uncertain scientific foundation. The varying practice reflects international scientific debate.
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PMID:[Drug therapy of acute myocardial infarction and unstable coronary syndrome]. 197 6

Complex stenosis morphology frequently occurs in patients with unstable angina pectoris. However, its relation to transient myocardial ischemia and hospital outcome has not been ascertained. To address this issue, 88 patients with significant (greater than or equal to 50%) coronary artery disease presenting with angina--new onset (n = 38), worsening (n = 20) or at rest (n = 30)-were studied. Patients with left main artery disease, normal coronary arteries or occlusion of the ischemia-related arteries were not included in the study. Continuous electrocardiographic recordings were obtained during the first 24 hours. Angiography was performed within 1 week from admission. Complex morphology was defined as any stenosis with irregular borders, overhanging edges or intracoronary thrombus. Only data referring to the in-hospital outcome were considered in this study. Adverse end points were sudden death, myocardial infarction and emergency revascularization. Analysis of the angiograms revealed a complex morphology in 58 patients (group 1). The remaining 30 patients served as control subjects (group 2). Thirty-two of the 58 group 1 patients had an unfavorable clinical outcome (positive predictive value, 55%). A similar outcome occurred in only 2 of the 30 group 2 patients (negative predictive value, 93%). Of the 32 group 1 patients who had an unfavorable clinical outcome, 29 had a cumulative duration of transient myocardial ischemia of greater than or equal to 60 minutes per 24 hours. A similar duration of ischemia, however, was observed in another 6 group 1 and in 8 group 2 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Angiographic morphology in unstable angina and its relation to transient myocardial ischemia and hospital outcome. 199 76

Experimental studies demonstrate that short-term regional perfusion-contraction matching, in which the energy demands of regional myocardial contraction are reduced to match the diminished myocardial substrate supply, occurs during states of low coronary blood flow under resting conditions and during exercise-induced ischemia. This phenomenon is rapidly reversible and appears to occur in several clinical settings. Sustained perfusion-contraction matching is observed in states of partial experimental ischemia of intermediate duration lasting several hours. This condition might be called short-term hibernation and resembles clinical conditions such as unstable angina pectoris or myocardial infarction with some residual perfusion in which the contractile defect can be improved by reperfusion provided the ischemia is not severe enough to cause transmural necrosis. Such experimental and clinical observations may or may not relate to the setting of regional dysfunction at rest in patients with chronic coronary heart disease, in whom manifestations of acute ischemia may be absent but improvement of wall motion abnormalities occurs after CABG or balloon angioplasty. This condition may constitute the hypothetical state of chronic myocardial hibernation, for which tentative evidence exists from metabolic and perfusion studies using PET. Whether such a condition of prolonged perfusion-contraction matching might be associated with adaptive processes that could allow its persistence for long periods without manifest ischemia remains to be investigated.
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PMID:Myocardial perfusion-contraction matching. Implications for coronary heart disease and hibernation. 199 10

The purpose of the study was to evaluate the effect of antiischemic treatment on left ventricular function in selected patients with unstable angina pectoris that was due to severe proximal left anterior descending coronary artery narrowing and to identify subgroups liable to an adverse outcome (mean term 2.7 years). Effect of antiischemic treatment on systolic and diastolic left ventricular wall motion was studied in 35 patients who had unstable angina pectoris and an electrocardiogram that indicated severe proximal left anterior descending coronary artery narrowing. Treatment consisted of either a revascularization procedure (17 patients) or antianginal drug therapy (18 patients). All patients underwent a two-dimensional echocardiographic study within 48 hours (mean 20 hours) of entry into the study. This study semiquantitatively analyzed systolic performance of the ischemia-related segments by calculation of a total wall motion score. In 16 patients this investigation was combined with a continuous detailed recording of only the apical interventricular septal wall motion. This detailed study included measurements for regional function by providing a typification of the pattern of systolic and early diastolic excursion of the endocardial border of the apical interventricular septum. A repeat ultrasonic study was performed at least 1 month (median 2 months, 7 days) after admission. Results of the systolic wall motion analyses of all 35 patients showed, in both treatment groups, a significant improvement in systolic wall motion of the anterior and apical segments (mean total wall motion score at early study vs late study: revascularization, 6.9 vs 2.2 and medical therapy, 4.6 vs 1.0).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Improvement of systolic and diastolic left ventricular wall motion by serial echocardiograms in selected patients treated for unstable angina. 200 Jul 45


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