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

Myocardial ischemia of short duration (15 to 20 min) produces myocardial "stunning" during reperfusion. The vasoregulatory and contractile status of reperfused myocardium during normal and reduced perfusion pressures is of interest in the treatment of patients with unstable angina. In the present study the effects of 15 min of reversible ischemic injury on several aspects of coronary vasoregulation were assessed with use of pressure-flow curves in anesthetized open chest dogs. The left anterior descending coronary artery was cannulated and perfused with arterial blood with use of a servo-controlled roller pump. The autoregulatory gain and an adenosine dose-response curve for coronary flow before and after ischemia and reperfusion were obtained. The maximal autoregulatory gain values in the pressure range of 140 to 60 mm Hg were not significantly different before and after ischemia and reperfusion (0.41 +/- 0.08 vs. 0.5 +/- 0.06, p greater than 0.1). The adenosine dose-response curve was significantly shifted to the right after reperfusion; however, coronary blood flows during maximal adenosine vasodilation over a large range of perfusion pressures (140 to 60 mm Hg) were significantly greater after ischemia and reperfusion. The pressure-dependent decrease in segment shortening (sonomicrometry) over the coronary pressure range of 160 to 30 mm Hg was similar in myocardium before and after stunning. Contractile function in the stunned myocardium at normal (100 mm Hg) and low (40 mm Hg) coronary perfusion pressures was similarly and significantly enhanced by the administration of adenosine. It is concluded that 1) coronary autoregulation is unchanged after brief ischemia and reperfusion; 2) although maximal coronary vascular conductance assessed with adenosine is greater after ischemia, the coronary circulation shows a decreased coronary sensitivity to exogenous adenosine; 3) the relation of contractile function to coronary pressure before and after stunning is unchanged; and 4) enhancement of function in stunned myocardium by vasodilation with adenosine occurs at low and normal perfusion pressures.
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PMID:Effect of transient coronary occlusion on coronary blood flow autoregulation, vasodilator reserve and response to adenosine in the dog. 186 50

The immediate and delayed effects of urokinase and heparin on minimal cross-sectional area of a patent ischemia-producing coronary artery were prospectively investigated in 43 patients with unstable angina. After baseline angiography, patients were randomized to 3 different treatment groups: group I--urokinase (1,000,000 U intravenous bolus dose), followed by heparin infusion 3 hours later; group II--heparin (10,000 U intravenous bolus, followed by continuous infusion); and group III--conventional therapy only (intravenous nitroglycerin, beta blockers and calcium antagonists). Angiography was repeated at 1 hour and at 8 days of treatment and minimal cross-sectional area was determined in the 35 patients who completed the study. In group I, minimal cross-sectional area increased from 0.84 +/- 0.48 mm2 at baseline to 0.94 +/- 0.49 mm2 at 1 hour (p less than 0.05), and to 1.00 +/- 0.51 mm2 at 8 days (p less than 0.01 vs baseline). In group II, a significant increase in minimal cross-sectional area was observed only at the 8-day angiography (0.64 +/- 0.39 mm2 at baseline; 0.67 +/- 0.37 mm2 at 1 hour [p = not significant]; and 0.79 +/- 0.48 mm2 at 8 days [p less than 0.01] vs baseline). In group III, no significant changes in minimal cross-sectional area occurred either at 1 hour or at 8 days. Thus, both urokinase and heparin improved lesion geometry in patients with unstable angina, although a large individual variation was noticed. The effect occurred earlier with urokinase than with heparin.
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PMID:Effects of urokinase and heparin on minimal cross-sectional area of the culprit narrowing in unstable angina pectoris. 187 70

A 24-hour ECG monitoring was performed in 30 patients with unstable angina. Ten patients had episodes of transient ST-segment displacement only in the presence of anginal attacks (Group 1), 10 had ST-segment displacement episodes in the presence of both anginal attacks and silent myocardial ischemia (Group 2), and 10 with the displacements concurrent with only silent ischemia (Group 3). The patients from the groups were not significantly different in terms of major clinical, history, and angiographic data. Following an average of 1 year, death and acute myocardial infarction were observed in 1 (10%) and 2 (22.2%) in Group 1; 1 (10%) and 3 (33.3%) in Group 2; and 2 (20%) and 5 (62.5%) patients, respectively. It was concluded that episodes of silent myocardial ischemia are prognostically more hazardous than those of transient hypoxic ECG changes concomitant with anginal attacks.
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PMID:[Prognostic significance of "silent" myocardial ischemia in patients with unstable stenocardia]. 187 91

The majority (greater than 75%) of major coronary thrombi are precipitated by a sudden rupture of the surface of an atherosclerotic plaque (plaque fissuring) causing platelet aggregation where thrombogenic subendothelial tissue has been exposed. Whether the thrombus remains mural and limited, just sealing the rupture, or evolves into an occlusive thrombus seems to depend on: (1) the amount and character of exposed thrombogenic material; (2) the actual thrombotic-thrombolytic equilibrium; and (3) local flow disturbances due to preexisting atherosclerotic stenosis. Thrombus formation may take place within the stenosis, where blood velocity and shear forces are highest, or it may take place or extend poststenotically, where flow separation, recirculation, and turbulence prevail. Platelet aggregation within the stenosis is responsible for the primary flow obstruction, but fibrin subsequently enmeshes the platelets and thus stabilizes the thrombus. Most thrombi have a layered structure, indicating an episodic growth that may alternate with thrombus fragmentation and peripheral embolization: thrombosis and thrombolysis are dynamic processes occurring simultaneously. If the platelet-rich thrombus at the rupture site evolves into an occlusive thrombus, the blood proximal and distal to the occlusion may stagnate and coagulate, giving rise to a secondarily formed red stagnation thrombosis consisting predominantly of erythrocytes held together by fibrin membranes. A ruptured plaque with a dynamic thrombosis superimposed (with or without spasm) seems to underlie the great majority of acute ischemic syndromes: unstable angina, acute infarction, and sudden death. The clinical presentation and the outcome depend on the severity and duration of ischemia: whether the obstruction is occlusive or nonocclusive, transient or persistent--modified by the magnitude of collateral flow.
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PMID:Coronary thrombosis: pathogenesis and clinical manifestations. 189 65

We investigated incidence, severity, and distribution of coronary atherosclerosis, acute thrombosis, and plaque fissuring in ischemic heart disease (both unstable-acute syndromes and chronic ischemia) and in nonischemic controls. We also studied the structural, immunohistochemical, and biochemical profile of plaques, with and without thrombus, including morphometry, immunophenotyping of inflammatory infiltrates, cytokine presence, and ultrastructural features. Critical coronary stenosis was almost the rule in both acute and chronic ischemic series (greater than 90%) whereas it reached 50% in control subjects. Thrombosis was principally characteristic of unstable-acute ischemic syndromes (unstable angina, 32%; acute myocardial infarction, 52%; cardiac sudden death, 26%) but was also found in chronic ischemia (stable angina, 12%; ischemic cardiomyopathy, 14%) and in control subjects (4%). Plaque fissuring without thrombus occurred in low percentages in lipid-rich, severe eccentric plaques in most series. Major differences were found between pultaceous-rich versus fibrous plaques rather than between plaques with or without thrombus. Pultaceous-rich plaques were frequent in sites of critical stenosis, thrombosis, and ulceration. Inflammatory infiltrates, i.e., T cells, macrophages, and a few beta cells, mostly occurred in lipid-rich, plaques unrelated to thrombus. In adventitia, infiltrates were a common finding unrelated to any syndrome. Necrotizing cytokines such as alpha-TNF were immunohistochemically detected in macrophages, smooth muscle, and intimal cells and detected by immunoblotting in 67% of pultaceous-rich plaques, either with or without thrombus. Immune response mediators such as IL-2 were also expressed in analogous plaques but in a minor percentage (50%-40%). Media were extensively damaged in severely diseased vessels with and without thrombus. Ultrastructural study showed that the fibrous cap was either highly cellular or densely fibrillar. Intimal injury with collagen exposure was often associated with platelet adhesion, whereas foamy cell exposure was not. In conclusion, investigated parameters were essentially similar in plaques, both with and without thrombus, whereas major differences were found between pultaceous-rich and fibrous plaques. Since platelets adhere to exposed collagen and not to foam cells, the type of exposed substrates could play a major role in thrombosis.
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PMID:Coronary atherosclerotic plaques with and without thrombus in ischemic heart syndromes: a morphologic, immunohistochemical, and biochemical study. 189 66

One hundred and ninety five patients who underwent successful percutaneous transluminal coronary angioplasty (PTCA) for single vessel disease and have been followed up for more than 6 months are being reported. Angiography was done routinely in first 20 patients (Group 1) 8 to 15 weeks (mean 9.6 weeks) after PTCA. Restenosis (loss of 50% of the initial improvement in luminal diameter) was seen in 4 patients (20%). The remaining 175 patients (Group II) have been followed up clinically and subjected to serial exercise testing. Coronary angiography was performed only if symptoms and/or objective evidence of ischemia recurred. In this group, restenosis suspected clinically and confirmed by angiography occurred in 37 patients (21%), 2 to 23 weeks (mean 12.5 weeks) after PTCA. The restenosis rate for the entire patient population was 21%. In general the restenosed lesions were longer and tighter than the lesions before PTCA. A comparison of 41 patients with restenosis with those who did not have clinical restenosis revealed a proximal left anterior descending artery (LAD) involvement (66% vs 31%, p = 0.01), crescendo unstable angina (37% vs 16% p = 0.05), length of pre PTCA stenotic lesion greater than or equal to 1 cm (41% vs 27.5%, p less than 0.05), absence of intimal haziness in immediate post PTCA angiogram (27% vs 16%, p less than 0.05) and residual stenosis greater than or equal to 25%, (34% vs 14% p less than 0.05) in the restenosis group. Repeat PTCA was done in 30 patients with a 96% success rate; 4 patients required coronary artery bypass grafting (CABG). Restenosis after PTCA is a significant problem in our experience.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Restenosis after successful coronary angioplasty in single vessel disease. 189 94

This study was designed to determine in patients with unstable angina whether specific electrocardiographic abnormalities associated with ischemia, the presence of coronary lesions consistent with thrombosis on angiography or the presence of recurrent ischemia reflects increases in thrombin activity as manifested by increased plasma concentrations of fibrinopeptide A. The concentration of fibrinopeptide A in plasma was increased to 6.7 +/- 3.1 nM for the group as a whole (n = 29). Increases were greater in the 17 patients who exhibited reversible ST segment shifts (10.2 +/- 5.2 nM) than in the 12 patients exhibiting reversible T wave abnormalities alone (1.6 +/- 0.2 nM) (p less than 0.01). Nine of the 17 patients with reversible ST segment shifts who underwent coronary angiography had lesions with morphologic characteristics consistent with atherosclerotic plaque complicated by thrombosis compared with only 2 of 9 patients with T wave changes only (p less than 0.05). Plasma concentrations of fibrinopeptide A were markedly elevated in 7 of the 11 patients in whom complex lesions were noted on angiographic examination. Thus, the occurrence of reversible ST segment shifts identifies a group of patients with unstable angina in whom ongoing thrombosis is likely and who may be particularly likely to benefit from antithrombotic therapy.
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PMID:Relation between ST segment shifts during ischemia and thrombin activity in patients with unstable angina. 189 62

From April 1980 to January 1990, among 2,576 percutaneous transluminal coronary angioplasty (PTCA) procedures, 100 patients (82 men and 18 women; mean age, 54 +/- 10 years [3.9%]) underwent emergency coronary artery bypass graft surgery. Before PTCA 56 had unstable angina, 34 had prior myocardial infarction, and 60 had single-vessel coronary artery disease. The mean time period from the onset of ischemia to surgical reperfusion was 147 +/- 16 minutes; 155 grafts were placed (1.5 grafts per patient). In-hospital mortality was 19%; operative mortality was significantly related to older age (59 +/- 9 versus 53 +/- 10 years, p less than 0.05), presence of unstable angina (74% versus 53%, p less than 0.05), and development of cardiogenic shock or necessity of cardiac massage before surgery (53% versus 16%, p less than 0.0001). In addition, 57 patients developed a Q wave myocardial infarction. For hospital survivors, overall survival at 7 years was 94% (Kaplan-Meier method), with three cardiac deaths during follow-up; two additional patients had late myocardial infarction, and four had late PTCA. At a mean follow-up of 55 +/- 38 months, 78% of the patients had no chest pain, and 80% reported no dyspnea. All patients received antiplatelet agents or oral anticoagulants; 34% had no antianginal medications. Among the 40 previously employed patients, 73% resumed work after surgery. All patients with cardiogenic shock or cardiac massage who survived the initial hospital period were alive at follow-up. After an initial critical period, the long-term clinical outcome of patients with emergency coronary bypass surgery after failed PTCA is satisfactory.
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PMID:Early and long-term outcome after emergency coronary artery bypass surgery after failed coronary angioplasty. 193 17

Coronary disease is the main cause of mortality and morbidity among long-term survivors on renal replacement therapy (RRT). Despite the additional risk factors, myocardial revascularization has been recently attempted with various success in some patients on RRT. We report on 26 patients (13 dialyzed and 13 transplanted, mean age: 50 years [range 38-66]) who have undergone either surgical aorto-coronary bypass (CABG) (n = 16) with mammary artery grafts, or percutaneous coronary angioplasty (PTCA) (n = 9), or both procedures (n = 2). Indication was angina pectoris in all but three patients with painless ischemia. Eight patients had unstable angina (NYHA class IV). A previous myocardial infarction was documented in 11 cases. Coronary angiography disclosed mainly multiple vessel disease (81%). Post CABG complications consisted of severe intrathoracic bleeding (n = 3) resulting in death in 2 cases. PTCA entailed no major complication. After the critical postoperative period, the long-term survival was the same as that of non-uremic patients and the clinical improvement, according to the NYHA classification, was highly satisfactory at 6 months and persists up to 2 years. We conclude that coronary angiography and myocardial revascularization should be considered in patients on long-term RRT developing coronary disease.
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PMID:Myocardial revascularization in patients on renal replacement therapy. 193 71

Today many patients admitted with an acute coronary syndrome are already taking aspirin. Because they have symptoms despite antithrombotic therapy, these patients are presumed to be at higher risk for subsequent clinical events. In a pilot trial of antithrombotic therapy in patients with unstable angina at rest or non-Q wave infarction, 93 patients admitted within 48 h of pain were prospectively followed up for 12 weeks. On admission, 29 patients (31%) were already taking daily aspirin; 64 (68%) were receiving no antiplatelet agent. After enrollment all patients received antithrombotic therapy with either aspirin or heparin according to protocol regardless of prior aspirin use. The two groups (prior users versus nonusers of aspirin) were similar with regard to age, gender, coronary risk factors, prior antianginal medication, duration of symptomatic coronary disease, presentation with non-Q wave infarction and extent of electrocardiographic changes on admission. Quantitative analysis of coronary arteriograms (on a 0 to 10 scale) showed similar myocardium-in-jeopardy scores (JS). Follow-up events (recurrent ischemia [Isch], infarction [MI] and revascularization [Revasc]) were: (formula: see text) Aspirin users experiencing rest angina are similar to other patients with ischemic rest pain. The "resistant to aspirin" group does not constitute a subgroup that is at higher risk for cardiac events or revascularization.
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PMID:Clinical and angiographic characteristics and outcome of patients with rest-unstable angina occurring during regular aspirin use. 193 46


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