Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight cases of acute pustular bacterid preceded by angina of beta-streptococcal origin are summarized. Although this disease appears to be an acute type of pustular bacterid Andrews, the elevated antistreptolysin titers and the histological features of vasculitis with perivascular deposits of C3 and IgM seem to be remarkable findings. One of the patients' skin symptoms were complicated by a glomerulonephritis. The skin lesions improved rapidly after systemic administration of glucocorticosteroids.
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PMID:[Acute generalized pustular bacterid: a variety of pustular Andrew's bacterid]. 43 70

The importance of inflammatory phenomena in atherosclerosis is now appreciated. Here, a clinical trial to be conducted using anti-inflammatory drugs (sulfasalazine, griseofulvin and colchicine) in angina pectoris, myocardial infarction and coronary restenosis after angioplasty and bypass grafting is proposed. Patients who have both atherosclerosis and a disease responsive to anti-inflammatory drugs (ulcerative colitis or Crohn's disease, dermatomycosis, necrotizing vasculitis, Behcet's disease, gout or other colchicine-sensitive diseases), are desirable targets of the present proposal.
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PMID:Proposal for clinical trials using anti-inflammatory drugs in the therapy of angina pectoris, myocardial infarction and coronary restenosis after angioplasty and bypass grafting. 135 49

A 23-year-old male with bronchial asthma developed eosinophilia (eosinophils greater than 2,000/mm3) and was observed at our hospital. After using a prescribed indomethacin suppository for fever at home, he experienced an attack of acute chest pain and severe dyspnea. He suffered cardiac arrest while being transferred to the ward. After resuscitation, he was diagnosed as having acute myocardial infarction on the basis of electrocardiographic and ultrasonic cardiographic findings, and marked elevation of serum concentrations of myocardial enzymes. Thereafter, he often complained of precordial pain and abdominal pain. When he was administered an analgesic in another hospital, he developed severe precordial pain, and marked ST elevation was recorded on the electrocardiogram. Coronary angiography revealed no stenosis nor atherosclerotic changes, suggesting that severe spasm of the coronary arteries and direct myocardial injury by eosinophils were the causes of the myocardial infarction-like symptoms and angina pectoris-like attacks. He was diagnosed as having Churg-Strauss syndrome (allergic granulomatous angiitis) on the basis of the clinical findings; skin biopsy and transbronchial lung biopsy findings were consistent with the diagnosis. Following steroid administration, his angina-like attacks and abdominal pain ceased. This patient developed two episodes of acute cardiovascular symptoms upon administration of antipyretic analgesics. This suggests that in cases of Churg-Strauss syndrome with aspirin-induced asthma, physicians must be aware of the cardiovascular complications, and such drugs should be administered with caution.
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PMID:[Acute myocardial injury and repeated angina pectoris-like attacks in a young patient with Churg-Strauss syndrome]. 180 89

Most ischemic heart disease in associated with severe coronary atherosclerosis. A small subset of patients, however, had angina pectoris despite angiographically normal coronary arteries and absence of inducible coronary spasm. Coronary microcirculation (i.e. arteries too small to be visualized by current angiographic techniques) has been identified as the weak point of these patients. Small coronary vessel involvement may be due to organic conditions (such as diabetes, vasculitis, systemic collagen-vascular diseases, infectious processes) that act through coronary thrombosis or embolism and related alteration in coronary vasomotion; alternatively, the vascular abnormality appears to be entirely functional (no ultrastructural myocardial changes) such as the case of hypertension, hypertrophic cardiomyopathy and syndrome X. Whatever the cause(s) and mechanism(s) of the small coronary artery involvement, this leads to myocardial ischemia and to the related complications as in classic atherosclerotic heart disease. Syndrome X is characterized by effort-induced angina pectoris, ST-segment changes during exercise testing, negative ergonovine test and reduced coronary reserve. A pre-arteriolar hypersensitivity to vasoconstrictor influences (elicited by cold pressor test or ergonovine) and a reduced vasodilator capacity (unmasked by metabolic and pharmacological studies) have been proposed as potential pathogenetic substrate. This dynamic alteration in vasomotion would answer for both symptoms and signs of myocardial ischemia, that, however, appear to be contemporarily elicitable in a minority of patients. Treatment with beta-blockers and calcium-antagonists has been found to be effective. The long-term follow-up shows favorable outcome with a high survival rate and a low incidence of cardiovascular events.
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PMID:[Angina due to microvascular pathology]. 184 63

We report on a patient who was admitted to the hospital because of severe angina pectoris. During hospitalization extensive ECG alterations and intermittent ventricular fibrillation were observed. However, coronary angiography showed normal coronary arteries and left ventricular function. Treatment with high-dose nitrates and Ca-antagonists gradually improved the patient's clinical situation. Although a Prinzmetal angina seemed likely, a vasculitis of the coronary arteries could not be excluded with certainty. Therefore, additional corticoid therapy was administered to the patient. After 5 weeks the patient was discharged from the hospital without any pathological clinical symptoms.
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PMID:[Recurrent ventricular fibrillation in a patient with angiographically normal coronary arteries and intermittent ST segment elevation]. 212 Aug 57

The clinical syndrome "coronary insufficiency with normal coronary arteriogram" is found in approximately 10% to 20% of patients with exercise-induced coronary insufficiency. In most of these cases, disturbances of the coronary microcirculation are present. They can appear in vascular diseases (arterial hypertension, systemic immunopathies, immune complex vasculitis), in rheologic diseases (paraproteinemia, hyperlipoproteinemia, polyglobulia) and in disturbances of transport and diffusion of oxygen (carbon monoxide intoxication, methemoglobinemia). The clinical diagnosis is based on the usual diagnostic procedures (electrocardiogram, exercise electrocardiogram, responsiveness to nitroglycerin), as well as on newer functionally oriented diagnostic procedures (determinations of coronary blood flow and coronary vascular reserve, production of lactate, serologic findings, histology and immune histology of peripheral arteries, measurements of viscosities in both plasma and blood). Many clinically relevant disturbances in the coronary microcirculation can thus be detected and treated on a rational basis by management of the underlying main disease, that is, by treatment of the vascular, rheologic and metabolic disorders. Persistent angina pectoris in the presence of a normal coronary arteriogram does not represent an end to coronary diagnostic procedures, but introduces the clinical task of using all diagnostic possibilities to enable functional and therapeutic assessment of the coronary microcirculation.
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PMID:The significance of coronary reserve in clinical heart disease. 230 86

The generation of toxic oxygen metabolites is more usually associated with inflammation. However, pathological free radical reactions can cause tissue damage by adversely affecting prostacyclin (PGI2) synthesis allowing initiation of coagulation. We have assessed changes in the red cell defence to toxic oxygen metabolite generation, viz measurement of glutathione concentration (GSH) and superoxide dismutase activity (SOD). GSH and SOD were measured in 20 patients with peripheral arterial disease, 22 patients with vasculitis, and 11 patients with angina, and compared to 17 matched controls. The 53 subjects with arterial disease had significantly lower SOD levels: in contrast GSH levels were significantly higher. Extracellularly plasma thiol levels (PSH) were low and caeruloplasmin (Cp) levels were high. We suggest that free radical pathology exists not only in inflammatory vascular disease but also in atherosclerosis.
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PMID:Free radical pathology in chronic arterial disease. 270 21

Cardiovascular manifestations develop in the majority of SLE patients at some time during the course of their illness, the most common being acute fibrinous pericarditis and pericardial effusion. Echocardiography has demonstrated an increased incidence of pericardial effusion, even in those who have minimal symptoms. Chronic adhesive pericarditis, pericardial tamponade, and constrictive pericarditis occur rarely. While myocarditis is commonly noted at autopsy, it is often silent clinically. Diagnosis during life can be confirmed only by endomyocardial biopsy. Electrocardiographic changes are often nonspecific. Endocarditis with superimposed nonbacterial verrucous vegetations (Libman-Sacks) is noted in more than 40% of hearts at autopsy, but is rarely diagnosed during life. Valve dysfunctions, such as aortic stenosis, aortic insufficiency, mitral stenosis, and mitral insufficiency, occasionally manifest during life and rarely may necessitate surgery. Atrial and ventricular arrhythmias, first degree AV block, and acquired CHB occur in association with pericarditis, myocarditis, vasculitis, and myocardial fibrosis, respectively. CCHB developing in newborns of mothers with SLE, particularly those who have an antibody to soluble tissue ribonuclear protein RO(SS-A), is increasingly being appreciated by both pediatric cardiologists and rheumatologists. Recently, severe coronary atherosclerosis resulting in angina pectoris and/or myocardial infarction in young adults has been noted, particularly in those who had developed risk factors such as hypertension and hyperlipidemia while receiving prolonged corticosteroid therapy. Rarely, coronary arteritis may produce similar symptoms. Congestive heart failure of either single or multiple etiologies carries an ominous prognosis. It remains a cause of high morbidity and mortality unless recognized early and treated properly. Extracardiac vascular manifestations of SLE include telangiectasia, vasculitis, livedo reticularis, Raynaud's phenomena, and thrombophlebitis, all of which may occur either alone or in different combinations. Evidence is now slowly accumulating that substantiates that immune complex deposition, complement activation and subsequent inflammatory reaction is responsible for the majority of the cardiovascular manifestations of SLE, for example, pericarditis, myocarditis, endocarditis, coronary arteritis, coronary atherosclerosis, and systemic and pulmonary vasculitis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiovascular manifestations of systemic lupus erythematosus: current perspective. 286 Jun 99

The clinical syndrome "coronary insufficience at normal coronary arteriogram" is found in approximately 10-20% of patients with exercise-induced coronary insufficience. In most of these cases disturbances of coronary microcirculation are present. They can appear in vascular diseases (arterial hypertension, systemic immunopathies, immune complex vasculitis, etc.), in rheological diseases (paraproteinemia, hyperlipoproteinemia, polyglobulia, etc.), and in disturbances of transport and diffusion of oxygen (carbon monoxide intoxication, methemoglobinemia, hyperlipoproteinemia). The clinical diagnosis is based on usual diagnostic programs (electrocardiogram, exercise electrocardiogram, responsiveness to nitroglycerin, etc.), as well as on newer, functionally orientated diagnostic procedures (determinations of coronary blood flow and of coronary vascular reserve, production of lactate, serological findings, histology and immune histology of peripheral arteries, measurements of viscosities in both plasma and blood, etc.). Many clinically relevant disturbances in coronary microcirculation can thus be detected and treated on a rational basis by the management of the internal main disease, that is, by the treatment of the vascular, rheological, and metabolic disorders. Persistent angina pectoris in the presence of normal coronary arteriogram represents no termination of coronary diagnostics, but moreover implies the clinical task for using diagnostic possibilities to enable functional and therapeutical assessment of coronary microcirculation.
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PMID:[Angina pectoris and coronary insufficiency with a normal coronary angiogram: pathophysiological principles, diagnosis and therapeutic consequences]. 306 40

A 40 year-old male presented symptoms of angina pectoris for about nine years and expired with symptoms of unstable angina, changing pattern at the terminal stage. At autopsy, both right and left coronary arteries of the subepicardial region were grayish white and elastic hard. Histologically, inflammatory infiltration was localized in adventitia of coronary arteries located in the subepicardial region. Inflammatory cells infiltrated into the adventitia were mostly eosinophiles. The medial smooth muscle cells were well preserved and the intima showed irregular thickening with fibrosis. Vascular obstruction or recanalization could not be observed. As a result of these findings, it was considered that these inflammatory changes of the coronary arteries could be termed eosinophilic periarteritis. These inflammatory changes could not be found in the intramural coronary arteries. Rather extensive fibrosis could be seen in the muscle layer centering about the posterior wall of the left ventricle. No findings of angiitis could be detected in the blood vessels except subepicardial coronary arteries.
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PMID:Periarteritis of coronary arteries with severe eosinophilic infiltration. A new pathologic entity (eosinophilic periarteritis)? 323 70


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