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

Recent clinical observations have extended our classification of unstable angina to include new groups of patients now recognized at high risk of subsequent infarction. Patients with non-Q wave myocardial infarction and those with early postinfarction ischemia share a prognosis similar to that of patients with crescendo angina or with acute coronary insufficiency. Unstable angina after coronary angioplasty and after coronary artery surgery also form particular subsets of patients. Pathologic, coronary angiographic, and coronary angioscopic studies have extended the role of the obstructive atherosclerotic plaque to include a dynamic component to explain the unstable state. Recognized dynamic components are rapid progression of the disease, active vasomotion, plaque fissuring, and thrombus formation. Activation of platelets and blood coagulation factors may play a major role in triggering the syndrome. Our therapeutic approach has also become more specific for the correction of the cause of the disease. Our understanding of unstable angina now appears to be at a turning point, and a pathophysiologic basis for its clinical classification and for its management may soon be available.
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PMID:A pathophysiologic basis for the clinical classification and management of unstable angina. 288 69

Guiding catheters used in coronary angioplasty can make coronary angioplasty potentially hazardous when they become positionally unstable, induce myocardial ischemia, or impair angiographic visualization. In order to avoid this problem, a double catheter technique was employed in seven patients involving nine procedures consisting of a standard 8 or 9 French angioplasty guiding catheter and a standard 7 French angiographic catheter to prevent coronary flow reduction and to permit improved coronary artery visualization. In two of the procedures, the second diagnostic catheter also permitted the prevention of potential plaque disruption by the guide catheter in the proximal right coronary artery. The predilatation stenosis was 88 +/- 12%; the postdilatation stenosis was 28 +/- 9%. The use of the diagnostic catheter as a second catheter prevented damping and permitted the stable disengagement of the guiding catheter from the coronary artery. This technique is most useful in patients who have proximal right coronary artery stenoses because it provides optimal visualization of the segment undergoing dilatation, avoids the potential for ischemia in more distal stenoses, and thereby allows the procedure to be performed in a controlled, unhurried manner.
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PMID:Improved stability and visualization during coronary artery angioplasty using a double catheter technique. 294 47

Post-infarction angina includes a syndrome of ischemic chest pain occurring either at rest or during minimal activity 24 hours or more following an acute MI. It develops in approximately 10 to 15 per cent of patients and is particularly common in non Q-wave infarcts involving the anterior myocardial wall. Post-infarction angina may result from ischemia either within the infarct zone or at a distance and frequently portends a poor long term prognosis. Platelet aggregation, coronary vasospasm, and thrombus formation at the site of a ruptured atherosclerotic plaque are each involved in its pathogenesis. The initial treatment of post-infarction angina includes identification and correction of factors that increase myocardial demand including congestive heart failure and arrhythmias. beta-Adrenergic blockers, calcium channel blockers, and nitrate preparations constitute the first line of medical therapy. The role of heparin is controversial, yet it continues to be used in clinical practice. Although thrombolytic agents are currently being investigated, early experience suggests that they may accelerate clinical stabilization and allow time for elective revascularization when required. Antiplatelet therapy with aspirin has proven benefit in the long term management of unstable angina. Patients unresponsive to medical therapy should be considered for intra-aortic balloon pump placement and early coronary angiography. Revascularization with either coronary angioplasty or coronary artery bypass grafting may then be performed as dictated by the overall clinical status, available facilities, and coronary anatomy.
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PMID:Management of post-infarction angina. 304 72

The extracranial carotid systems of 105 patients with retinal ischemia were examined using B-mode ultrasonography with integrated pulsed Doppler. Sixty-four patients had amaurosis fugax (AF), 17 central retinal artery occlusions (CRAO), and 21 branch retinal artery occlusions (BRAO). The prevalence of carotid stenosis (greater than or equal to 60%) ipsilateral to the symptomatic eye was low (16%). Eighty-six percent of AF patients had either no plaque causing less than a 60% stenosis. A significant proportion of subjects with normal duplex scans had alternative explanations for their retinal ischemia (eg, migraine, cardiac embolus). Patients with Hollenhorst plaques were more likely to have stenotic or ulcerated plaque (p = 0.04). The degree of carotid stenosis correlated significantly with the number of vascular risk factors identified in individual patients (p = 0.02). The presence of risk factors was more common in CRAO and BRAO patients compared with the AF group. Combined ultrasound-Doppler investigations of the carotid bifurcation are valuable noninvasive tools for the screening of patients with retinal ischemia.
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PMID:Atherosclerotic carotid artery disease in patients with retinal ischemic syndromes. 328 40

Angiographic studies in patients with unstable angina indicate that intracoronary thrombus is present in a substantial proportion of patients with unstable angina who have early angiography and that these patients often have distinctive coronary lesion morphology that may represent a marker for instability. These studies, in conjunction with recent histopathologic studies demonstrating plaque defects and overlying thrombosis in patients with unstable ischemia and sudden death, suggest a common mechanism for unstable angina and myocardial infarction and strongly support the rationale for antithrombotic therapy with heparin and with aspirin in the management of patients with unstable angina.
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PMID:Thrombosis in unstable angina: angiographic aspects. 330 Sep 81

Thrombosis is an important pathogenetic factor in acute coronary syndromes, including unstable angina, myocardial infarction and sudden death. In all of these conditions, atherosclerotic plaque fissuring is a key inciting event. Minor injury to the vessel wall brings into play interactions between platelets and the wall. Platelet adhesion and aggregation ensue, modulated by a number of factors and substances. More severe injury to the vessel wall exposes the blood to other thrombogenic substances. Platelet deposition is also affected by rheologic (blood flow) factors at the site of injury, depending on the degree of stenosis and the resulting shear rates. The mechanism of unstable angina appears to be related to these factors in the following sequence: mild stenosis and minor injury with plaque fissuring, platelet responses, labile thrombosis, intermittent ischemia and pain at rest. Vasoconstriction may contribute to the symptoms. Although developing from the same origin, infarction may stem from a greater degree of vessel wall damage resulting in more permanent thrombus. Such considerations provide a focus for preventive strategies, including the optimal use of current inhibitors of platelet adhesion and aggregation and the application of peptide receptor blockers and monoclonal antibodies. Also important is control of rheologic factors by preventing stenosis or correcting it with angioplasty and thrombolytic therapy. Further elucidation of the critical role of thrombosis in coronary syndromes will facilitate progress toward the ultimate goal of primary prevention.
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PMID:Platelet/vessel wall interactions, rheologic factors and thrombogenic substrate in acute coronary syndromes: preventive strategies. 331 54

Atheromatous embolism disease is a recently defined entity of still to be determined prevalence. This complication can develop during the course of any arterial disease by overload or dystrophy in lower limbs, and is certainly responsible for many cases of worsening of subacute ischemias occurring during arterial disease for which it is not always possible to affirm the embolic origin. It is in no way a rare syndrome and the true frequency of this affection can only be underestimated. If arterial dystrophies are excluded, the primum movens is ulceration of an atherosclerotic plaque. Two types of emboli have been described as originating in these plaques. First, small cholesterol crystal emboli containing fibrino-platelet material that are the cause of very distal arterial occlusion, notably in the foot: the most typical corresponding clinical condition is the so-called blue toe syndrome. Second, larger emboli due to formation and migration of a fibrino-platelet thrombus in contact with the atheromatous ulcer. They consist mainly of fibrino-platelet material with variable quantities of atheromatous debris. They may be of moderate size, occluding a collateral of the deep femoral artery or a leg artery usually in an asymptomatic manner, or larger and provoking occlusion of main trunks. Diagnostic difficulties emphasize the importance of referring all embolectomy products for histopathology. One of the essential problems of this disease is that of diagnostic criteria. When confronted with the previously evoked picture of peripheral ischemia and/or a peripheral arterial occlusive lesion, how can this distal accident be related to a subjacent arterial lesion suspected of possessing an emboli-forming nature?(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Emboli-forming arteriopathies of the limbs]. 332 Feb 45

Regardless of the factor assumed responsible for precipitation of myocardial ischemia - varying from coronary occlusion in acute myocardial infarction to increased oxygen demand in exertional angina pectoris and reduced myocardial oxygen supply due to plaque rupture or changes in vasomotor tone in unstable angina - its incurrence may or may not be associated with pain. In the vast majority of cases, silent myocardial ischemia is observed in patients with established symptomatic coronary artery disease. Interindividual comparisons have not enabled reliable differentiation between those with painful and those with silent ischemia based on the anatomic extent of coronary artery disease, left ventricular function or previous myocardial infarction. Similarly, functional parameters such as exercise capacity, exercise duration, time to onset of ST-segment depression during exercise as well as heart rate and blood pressure both at rest and during exercise have failed to reveal differences between the symptomatic and the asymptomatic patients. Intraindividual differences have also been noted, but not consistently corroborated, and postulated as responsible for the fact that ischemia in a given patient alternates in its presence with and without pain. Since most patients with silent ischemia either have, or at some time in the past have experienced, painful ischemia, the integrity of the appropriate nervous system function can be assumed to be intact and neurocardiologic factors seem most likely to account for apparent discrepancies in pain perception. Prior to precipitation of pain, myocardial ischemia must elicit an adequate stimulus. According to some investigators, the adequate stimulus is that associated with a duration of the ischemic episode of at least three minutes and with increase in left ventricular filling pressure of more than 7 mm Hg. This threshold, consequently, represents a prerequisite but not invariably sufficient criteria for the occurrence of pain. The next step in the sequence of pain is generation of an action potential, that is, transduction by means of chemical or mechanical stimuli. During this process, a latency of 20 to 40 seconds is incurred such that the appearance of pain usually has its onset after derangement of relaxation and contraction, increased filling pressure and the observation of ECG changes. Through conduction, the information is forwarded to the central nervous system after coding of the details with regard to intensity. The intensity, in turn, is determined by the number of receptors (free nerve endings) in the field activated by the ischemic event.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pathophysiology of painful and silent myocardial ischemia]. 332 3

The coronary morphology of ischemia-related arteries in unstable angina and Q-wave acute myocardial infarction (AMI) has been described. An eccentric stenosis with overhanging edges or irregular borders (type II eccentric) was seen in most lesions less than 100% occluded and probably represented plaque disruption, nonocclusive thrombus or both. The coronary morphology of non-Q AMI has not been described. Thus, the angiograms of 106 consecutive patients catheterized with either unstable angina (n = 73) or non-Q AMI (n = 33) and an identifiable ischemia-related artery were prospectively analyzed. Non-Q AMI was diagnosed by prolonged chest pain and new and persistent ST-T changes or creatine phosphokinase twice the normal level. The results showed a higher incidence of total occlusion of the ischemia-related artery in non-Q AMI (21%) compared with unstable angina (8%) (p = 0.1). The coronary morphology of nonoccluded ischemia-related arteries was similar with preponderance of type II eccentric lesions in both unstable angina and non-Q AMI. These lesions were found in 65% of ischemia-related arteries in non-Q AMI but were uncommon (3%) in nonischemia-related arteries with significant (50% to 100%) stenoses. Therefore, the type II eccentric lesion is a sensitive and specific marker of less than 100% occluded ischemia-related arteries in both unstable angina and non-Q AMI. These similarities in coronary morphology suggest a similar pathogenesis, which, as previously suggested, may relate to plaque disruption with or without thrombus. Unstable angina and non-Q AMI appear to represent part of a continuous spectrum of acute coronary artery disease. Further, the management of patients with non-Q AMI should be similar to patients with unstable angina and possibly include anticoagulation and consideration for early catheterization.
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PMID:Angiographic demonstration of a common link between unstable angina pectoris and non-Q-wave acute myocardial infarction. 334 Dec 1

To investigate the clinical significance of lucent defects in computed tomography (CT) scans of the cervical carotid artery plaque, we studied 95 patients with recent symptoms of hemispheric ischemia. Using multiple linear regression analysis, we estimated the strength of the association of symptoms with laterality of carotid artery lucent lesions, stenoses, and ulcerations observed in CT scans. Hemispheric symptoms correlated strongly with ipsilateral carotid lucent lesions (partial p less than 0.025) and with ipsilateral severe (greater than 75%) carotid stenosis (partial p less than 0.025). Carotid artery ulcerations had a weaker association (partial p less than 0.1), and stenoses of mild and moderate degrees showed none. The overall performance of all three plaque complications was highly significant (p less than 0.005). The lucent defect indicates a morphologic change in the carotid plaque that plays an important role in the development of symptoms of hemispheric ischemia. This is in agreement with the notion that the lucent defect is the image of intraplaque hemorrhage and/or necrosis, which are complications central to the development of symptomatic carotid disease.
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PMID:Computed tomography of the cervical carotid artery: significance of the lucent defect. 337 63


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