Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The causes of unstable angina are still largely unknown. However, some facts deriving from angiographic, postmortem, and pathophysiologic studies are well established. Angiographic findings: coronary thrombi and complicated stenoses are more frequent in unstable than in stable angina. Conversely, the severity of coronary atherosclerosis and the development of collateral circulation is similar in both coronary syndromes. Postmortem findings: the following features are more frequent in unstable than in stable angina: (1) mural thrombi, which often represent out-growth from the inside of a fissured plaque; (2) inflammatory cells at the site of plaques and in perivascular nerves; and (3) contraction bands in smooth muscle cells of the media surrounding plaques. However, fissured plaques can be found in 10% of individuals dying of noncardiac causes, and fissured plaque may occasionally be missing under the coronary thrombus in unstable angina. Pathophysiologic findings: patients with unstable angina compared with those with stable angina exhibit: (1) higher levels of serotonin in the coronary sinus; (2) higher systemic levels of fibrino-peptide A; (3) higher urinary levels of thromboxane A2 metabolites; and (4) a greater coronary reactivity to constrictor stimuli. A critical analysis of these established facts is required to set the stage for a better comprehension of the causes which can cause a coronary segment to progress in a stuttering way toward acute persistent coronary occlusion and myocardial infarction. Plaque fissure is likely to be an important background thrombogenic stimulus in many cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The elusive cause of instability in unstable angina. 189 62

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

The feasibility of using a flexible, steerable angioscope to perform coronary angioscopy before and after percutaneous coronary angioplasty was tested. The microangioscope fits through an 8F coronary angioplasty guiding catheter and contains a multifiber viewing bundle incorporated into the body of a 4.3F balloon catheter with a central lumen for distal flushing and guide-wire passage. Angioscopy was performed without complications 45 times in 24 patients, including 6 patients with stable and 18 with unstable angina. Circumferential visualization of the target lesion was successful in 20 (83%) of the 24 patients and improved with operator experience. Excellent visualization of the target lesion was achieved in 16 (94%) of the last 17 patients. Plaque, thrombus and dissection were among the abnormal findings in the 20 patients (4 with stable, 16 with unstable angina) in whom circumferential viewing of the target lesion was achieved. In four patients with restenosis after angioplasty, the lesion morphology was distinctly different from that of lesions in arteries without prior angioplasty. In patients with stable angina, no thrombus or dissection was seen by angiography or angioscopy before angioplasty. In patients with unstable angina, thrombus was detected more frequently by angioscopy than by angiography before angioplasty (8 versus 2 of 16) and after (15 versus 2 of 16) angioplasty. Intimal dissection was also seen much more frequently by angioscopy than by angiography before angioplasty (7 versus 0 of 16) and after angioplasty (16 versus 7 of 16). It is concluded that high resolution percutaneous coronary angioscopy can be performed safely in conjunction with balloon angioplasty. Further investigation is needed before this diagnostic tool can be applied clinically.
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PMID:Percutaneous angioscopy during coronary angioplasty using a steerable microangioscope. 198 10

Coronary lesion morphology was analyzed in 72 patients 1 to 8 days after streptokinase treatment for acute myocardial infarction and compared with lesion morphology in a control group of 24 patients with stable angina. In the streptokinase group the infarct-related artery was patent in 55 patients (76%). Compared with stenoses in the stable angina group, there were no differences in the stenosis length, severity, calcification or in the proportion located at an acute bend or at a branch point. However, lesions in the streptokinase group were more often irregular (p less than 0.005) and eccentric (p less than 0.01), had a shoulder (p less than 0.0001), globular filling defects (p less than 0.01), linear filling defects (p less than 0.00005) and contrast staining (p less than 0.05). Plaque ulceration index was higher in the streptokinase than in the stable angina group (6.2 +/- 7.9 versus 3.5 +/- 3.4, p less than 0.001). Of the 72 streptokinase-treated patients, 35 were maintained on heparin infusion until angioplasty 2 to 10 days later. At repeat angiography before angioplasty, globular lesion filling defects seen in eight patients had disappeared, whereas linear filling defects persisted in 7 of 14 cases. Fewer lesions were irregular (p less than 0.0001) and the ulceration index decreased from 7.4 +/- 10.4 to 3.0 +/- 1.6 (p less than 0.001). These data show that the lesion in the infarct-related artery after streptokinase treatment is irregular and often associated with filling defects, perhaps corresponding to plaque fissuring and intraluminal thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coronary lesion morphology in acute myocardial infarction: demonstration of early remodeling after streptokinase treatment. 222 52

During 1979 to 1987, we collected 84 consecutive cases of juvenile sudden death which occurred in the Veneto Region, northeast Italy. Death was attributed to cardiovascular disease in 79 cases. Nineteen of these (24%), consisting of 17 males and two females, from 18 to 35 years of age, had 70% or greater atherosclerotic coronary stenosis, in the absence of other cardiac pathology and previous clinical evidence of angina pectoris or myocardial infarction. In 13 cases (68%), sudden death was the first manifestation of coronary artery disease; the remaining six patients had experienced atypical, non-diagnostic prodromal symptoms. At the moment of death, 16 patients were engaged in sedentary activity. Pathological examination disclosed that in 15 cases (79%), only one major vessel was stenosed, and in 12 cases it was the proximal descending coronary artery: the other four patients had three-vessel disease. Histologic study revealed uncomplicated, obstructive fibromatous plaques in 16 cases, and a preserved tunica media in all cases. Plaque fissuring with superimposed mural or occlusive thrombosis was present in only three cases. Overt myocardial infarction was not observed. Our findings indicate that coronary atherosclerosis is an important cause of sudden death in young persons. In this series, coronary disease was 'silent', and sudden death was its first clinical manifestation. The occurrence of death at rest, in the absence of an acute coronary lesion, with preservation of the coronary tunica media suggests that fatal outcome might be due to coronary vasomotor tone abnormalities culminating in ischaemia-induced cardiac arrest.
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PMID:Sudden death as the first manifestation of coronary artery disease in young people (less than or equal to 35 years). 324 45

The Lipid Research Clinic Coronary Primary Prevention Trial was a randomized, double-blind, placebo-controlled intervention trial performed in 3806 hypercholesterolaemic (greater than 265 mg dl-1) but asymptomatic men aged 35-59 at entry. The bile acid sequestrant cholestyramine was used to achieve the cholesterol differential in the treatment group. Both groups received a modest low cholesterol-low fat diet. All subjects were followed for at least seven years (mean duration 7.4 years) during which time a mean fall of 8% and 12% in plasma total cholesterol and LDL cholesterol levels respectively relative to levels in placebo controls were achieved and maintained. The cholestyramine group experienced a 19% reduction in risk (P greater than 0.05) of the primary end point-definite coronary heart disease death and/or definite non-fatal myocardial infarction. In addition, the incidence rates for new positive exercise tests, angina, and coronary bypass surgery were all significantly reduced by 25%, 20% and 21%, respectively, in the cholestyramine group. In the treated group, risk reduction was related directly to reduction in total and LDL cholesterol. In a similar but considerably smaller double blind, placebo-controlled, secondary prevention trial where coronary artery lesion change as determined by serial coronary angiography was the end point (The NHLBI Type II Intervention Trial), cholestyramine treatment significantly delayed the progression of atherosclerotic lesions. Plaque progression related directly to both a fall in low density lipoprotein and a rise in high density lipoprotein.
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PMID:Report on the Lipid Research Clinic trials. 331 77

Plaque rupture with the exposure of a tissue factor-rich procoagulant surface is considered the common pathogenetic mechanism of unstable angina and myocardial infarction. Activated factor VII, the key enzyme for initiating blood coagulation under resting conditions, is increased in pathological situations associated with tissue factor exposure. We measured the plasma levels of activated factor VII and studied their relation with signs of coagulation enzyme activity in patients with acute coronary syndromes. The plasma levels of activated factor VII, prothrombin fragment 1 + 2, and fibrinopeptide A were measured on admission in consecutive patients presenting with acute myocardial infarction (n = 28), unstable angina (n = 32), and stable angina (n = 17) and in age- and sex-matched healthy individuals (n = 33). Plasma determinations of the same markers were also repeated at 15 days and 3 and 6 months. On admission, the patients with unstable angina or myocardial infarction had significantly higher plasma levels of prothrombin fragment 1 + 2 (P < .0001) and fibrinopeptide A (P < .0001) than those with stable angina or healthy individuals, whereas no differences were detected in the plasma levels of activated factor VII. During follow-up there was a significant decrease in the plasma levels of fibrinopeptide A both in patients with unstable angina (P < .001) and in those with myocardial infarction (P < .001), whereas no changes in plasma prothrombin fragment 1 + 2 or activated factor VII levels were observed. Hence, in the acute and chronic phases of myocardial infarction and unstable angina, heightened coagulation enzyme activity is not accompanied by an increase in activated factor VII.
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PMID:Heightened thrombin formation but normal plasma levels of activated factor VII in patients with acute coronary syndromes. 758 43

The term unstable angina encompasses heterogeneous clinical syndromes. Fissuring of an atherosclerotic coronary artery plaque with superimposed platelet deposition, with or without additional thrombus formation, is invariably responsible for a prolonged episode of angina at rest, increasing frequency of angina at rest, or with minimal exertion of less than 4 weeks in duration and early postinfarction angina. Plaque progression, rather than plaque fissuring, is the most likely mechanism for progressive reduction in walking distance due to angina in patients who previously have stable angina. Coronary artery spasm is responsible for Prinzmetal's variant angina, but its exact role in other forms of unstable angina is unknown. The mainstay of treatment of unstable angina (prolonged episode of angina at rest and recent onset angina at rest, or with minimal exertion with a crescendo pattern) is aspirin, heparin, or both. Both aspirin and intravenous (i.v.) heparin or their combination reduce early mortality and the incidence of acute myocardial infarction in patients hospitalized with unstable angina. However, these agents do not promptly relieve chest pain. There are no placebo-controlled studies evaluating the usefulness of nitrates in unstable angina. In open-label studies, continuous therapy with i.v. nitroglycerin (NTG) for 24 hours or longer has been shown to relieve chest pain in patients with rest angina refractory to therapy with other antianginal agents, including long-acting nitrates. Recurrence of chest pain in patients receiving i.v. NTG is a common problem and probably represents development of pharmacologic tolerance, but this can be overridden by dose escalation; protracted tolerance during short-term use of i.v. NTG is usually not a problem.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nitrates for unstable angina. 787 68

Complex coronary morphologic abnormalities with thrombus and ulceration have been recognized in acute ischemic syndromes by angiography, angioscopy, and autopsy. However, in vivo histopathologic correlates of unstable ischemic syndromes have not been described. The purpose of this study was to characterize intracoronary lesion morphologic abnormalities by analyzing specimens excised by directional atherectomy in patients with different ischemic syndromes. Tissue specimens removed by directional coronary atherectomy of primary lesions in native vessels were matched blindly to the clinical status of 130 patients representing 43% of a consecutive directional coronary atherectomy population of 300 patients; 824 specimens (range per patient 1 to 30, mean 6.3) were obtained. Clinical subgroups were prospectively classified as recent myocardial infarction (< or = 15 days, mean 6, range 1 to 15 days), 48 patients; prolonged rest angina, 34 patients; crescendo angina, 29 patients; and stable angina, 19 patients. Shavings were prospectively analyzed for presence of thrombus, ulceration, or chronic inflammatory cells. Thrombus was observed in 33 (69%) patients with recent myocardial infarction, 17 (50%) with rest angina, 12 (41%) with crescendo angina, 7 (37%) with stable angina (p = 0.048). Plaque ulceration was identified in 12 (25%) patients with recent myocardial infarction, 4 (12%) with rest angina, 2 (7%) with crescendo angina, and 1 (5%) with stable angina (p = 0.09). Inflammatory cells were noted in the specimens of 32 (67%) patients with recent myocardial infarction, 16 (45%) with rest angina, 12 (41%) with crescendo angina, and 9 (45%) with stable angina.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Histopathologic correlates of unstable ischemic syndromes in patients undergoing directional coronary atherectomy: in vivo evidence of thrombosis, ulceration, and inflammation. 807

Angina pectoris is a significant risk predictor in patients with atherosclerotic heart disease. The major complications are myocardial infarction, heart failure, and arrhythmias. Plaque rupture turns stable angina pectoris into acute coronary syndrome by provoking platelet aggregation and thereby thrombus formation. Verapamil significantly inhibits platelet aggregation and thrombus formation, which may be one of several reasons for the protective effect of verapamil on reinfarction in patients recovering from myocardial infarction. Ischemia may lead to left ventricular dilation and diastolic dysfunction, and thereby heart failure. In postinfarction patients intervention with verapamil significantly reduced the use of diuretics compared with placebo, indicating that anti-ischemic intervention may prevent heart failure. Ventricular arrhythmias are significantly associated with arrhythmic as well as non-arrhythmic death. The lack of preferential association of ventricular arrhythmias with arrhythmic death rather than nonarrhythmic death may imply that arrhythmias are provoked by ischemia. Antiarrhythmic intervention in postinfarction patients significantly increases death and arrhythmic events compared with placebo, especially in patients with residual ischemia. This may be due to a significant slowing of conduction during ischemia in patients treated with antiarrhythmic agents. In animal studies anti-ischemic agents prevent or suppress ventricular arrhythmias during ischemia, whereas traditional antiarrhythmic drugs have no effect or even worsen the arrhythmias, especially during episodes with elevated sympathetic activity. Verapamil significantly reduces plasma norepinephrine levels and the norepinephrine release during ischemia, whereby ventricular arrhythmias may be prevented. Also, supraventricular arrhythmias are significantly associated with myocardial ischemia and are prevented by verapamil. In patients with atherosclerotic heart diseases, angina pectoris is a significant risk predictor, but anti-ischemic intervention should be considered even in patients in whom the major problem is heart failure or arrhythmias.
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PMID:Anti-ischemic intervention as prognosis improvement in patients with coronary artery disease, with special focus on verapamil. 867 96


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