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)

Interleukin-2 (IL-2) is increasingly used to treat patients with cancers refractory to conventional treatment. Flu-like syndromes are extremely frequent but usually mild. A variety of skin complications (mostly erythema and mucositis) have been reported. Life-threatening skin reactions have also been described. Acute reactivation of psoriasis can also occur. Immediate hypersensitivity reactions have so far not been described, but IL-2 treatment has been shown to predispose to acute hypersensitivity reactions to iodine-containing contrast media. Hypothyroidism is the major endocrine complication and antithyroid antibodies have been detected in approximately 50% of patients. Neurological and psychiatric disturbances with moderate or severe mental status changes are common and sometimes treatment-limiting. The occurrence of peritumoural oedema in patients with brain metastases can also be a major practical problem. Musculoskeletal disorders are transient and resolve spontaneously. The vascular leak syndrome is the most frequent and severe complication of IL-2 of which weight gain, generalised oedema, hypotension and impaired renal function are the main features. Even though a damaging effect on vascular endothelium cells by various cytokines released by activated lymphoid cells or mediated by non-lymphocyte-dependent factors has been proposed to be involved, the mechanism remains unclear. Other cardiovascular injuries, possibly life-threatening, including myocarditis, angina pectoris and myocardial infarction, can occur during the first days of treatment. Supraventricular arrhythmias are the most common rhythmic disorder. Decreases in myocardial contractility and haemodynamic pattern similar to those of septic shock have been encountered in most cases. Acute renal dysfunction is common but resolves with symptomatic management. Intrahepatic cholestasis with hyperbilirubinaemia is observed in most patients but permanent liver damage has not been described. Several cases of pancreatitis have been reported. Anaemia, thrombocytopenia, lymphocytopenia and eosinophilia are frequent and occur in most if not all patients. Some data suggest a high incidence of infectious complications, particularly in patients with surgically tunnelled catheters, but marked flu-like syndromes may be confounding. Finally, death directly related to IL-2 treatment has been noted in less than 1% of all patients. Investigations are under way to minimise IL-2 toxicity with varying dose regimens and combined treatments.
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PMID:Clinical toxicity of interleukin-2. 141 98

We measured levels of tissue plasminogen activator (t-PA) antigen in 100 patients within six hours of the onset of acute myocardial infarction, in 34 patients with chronic angina but no recent infarction, and in 36 normal subjects. We also assayed von Willebrand factor in the acute patients and in the normal subjects. Measurements were repeated in 40 acute patients at three weeks after myocardial infarction. Although resting levels of t-PA antigen were not significantly different from normal during myocardial infarction, the capacity of the vascular endothelium to release t-PA after five minutes of venous occlusion was impaired (p less than 0.01). The acute phase vessel wall release of von Willebrand factor was increased during acute infarction (p less than 0.01). We conclude that impairment of t-PA production is associated with acute coronary thrombosis, although it is not possible to differentiate between a causative role or a secondary response due to exhaustion of the t-PA producing mechanism.
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PMID:Reduced synthesis of tissue plasminogen activator by vascular endothelium during acute myocardial infarction. 149 53

During the past decade, it has become clear that the vascular endothelium critically influences vascular permeability, controls vessel growth, modulates hemostasis, and regulates vasomotion. This latter role of the endothelium is mediated by the liberation of a number of potent vasoactive compounds, including endothelium-derived relaxing factors, one of which is either nitric oxide or a compound that releases nitric oxide, vasoactive prostaglandins, hyperpolarizing factors, and a number of constricting factors. This role of the endothelium is dramatically altered by several diseases, including atherosclerosis, hypertension, and diabetes. Abnormalities of endothelial regulation of vascular tone may contribute to a number of clinical syndromes, including variant angina, unstable angina, syndrome X, and perhaps many others. In this review, several aspects of the endothelium-derived relaxing factor will be considered, including recent concepts regarding its synthesis, its chemical identity, and alterations in atherosclerosis. Finally, its action in the coronary microcirculation as contrasted to that of nitroglycerin will be considered.
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PMID:Normal and pathophysiologic considerations of endothelial regulation of vascular tone and their relevance to nitrate therapy. 152 21

The recent discovery of endothelium-derived relaxation factor (EDRF) has altered the traditional classification of vasodilators used in angina pectoris and heart failure. If a vasodilator induces release of EDRF from the epithelium it is classified as endothelium-dependent, if not it is independent. Sodium nitroprusside and SIN-1 (active metabolite of molsidomine) are the main independent vasodilators since the endothelium relaxation factor appears to be principally a nitric oxide radical in these synthetic vasodilators. In contrast, calcium-channel blockers and a good number of endogenous chemical mediators (acetylcholine, bradykinin, serotonin, etc.) are endothelium-dependent. Furthermore, simple increase in blood flow through the large vessels can result in endothelium-dependent vasodilation (flow rate-dependence) the extent of which depends on the drug examined. The fact that the pharmacologic response of a vasodilator can be altered under certain pathologic conditions (atherosclerosis, hypertension, diabetes, etc.) further increases the importance of the role of the vascular endothelium in the action of vasodilators since endothelial modulation may then be completely diverted to secretion of endothelium-derived contracting factors (EDCFS).
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PMID:[Vasodilator agents and the vascular endothelium]. 262 13

If myocardial ischemia always results from an imbalance between the needs and supplies in oxygen of the myocardium cells, the physiopathology of this process seems today infinitely more complex than the mere diminution or interruption of the output in a coronary artery. The extension of atheromatous lesions, the platelets aggregation, thrombosis, the coronary spasm, the release of products from the arachidonic cascade, the reactivity of the vascular endothelium, the profibrinolytic activity of the tissues are many of the intricate factors inducing myocardial ischemia. Cellular alterations, of which some are triggered by the release of oxygenated free radicals, lead then to an irreversible necrosis. The medications used until now in the treatment of angina are oxygen scavengers and research goes on in this direction with vaso-dilators beta-blockers, prolonged action nitro-compounds (nicorandil) or nitro-compounds with an action reinforced by N-acetyl-cysteine, bradycardiac derivates of alinidine and the new calcium antagonists dihydropyridine. However, the new physiopathological concepts of ischemia have opened new directions for the research: products which modify the arachidonic cascade by increase of synthesis or release of PGI2 (nafazatrom, defibrotide), by inhibition of TXA2 synthesis or blocking of TXA2 receptors, and similar products of PGI2 (iloprost); thrombolytic agents more specific of thrombin (PTA) or fibrinolysis activators (defibrotide), and anticoagulants with extended action; chelating agents of oxygenated free radicals (peroxide dismutase, catalase, peroxidase) or xanthine oxidase inhibitors; platelets anti-aggregates like ticlopidine which blocks the platelets receptors to fibrinogen, or inhibitors of the synthesis of pro-aggregating agents.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Current therapeutic concepts in the treatment of myocardial ischemia. Current and future drugs]. 287 4

Different patho-anatomical and functional factors are considered to be involved in patients with unstable angina pectoris. Among these are a pre-existing plaque based on coronary atherosclerosis, the development of fissures or dissections of the plaque (often combined with thrombus formation at the site of the plaque) coronary vascular tone, and theoretically primary aggregation of platelets at a site of apparently normal vascular endothelium. Several comprehensive studies on patients who died from acute myocardial infarction or unstable angina, have convincingly shown that complications of an atherosclerotic plaque like fissures, dissections and thrombus formation may be present in 60 to 90% of cases. In addition, two groups of investigators, who have applied coronary angioscopy for direct visualization of offending coronary arteries, have confirmed these results, since in about 60-80% of patients with unstable angina complicated atheromata, i.e. rupture, ulceration, thrombus formation, could be documented, whereas in all patients with stable angina an uncomplicated atheroma was seen angioscopically. On the basis of these results a hypothetical sequence of events in patients with stable angina, unstable angina and acute myocardial infarction has been proposed. Stable angina pectoris may be seen in patients with uncomplicated atheroma in one of the major coronary artery branches. When dissections, ulcerations and thrombus formation occur as a complication of a formerly smooth plaque, patients show the clinical syndrome of unstable angina. If an occlusive thrombus develops, the patient will run into a fresh myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathophysiology of unstable angina pectoris--correlations with coronary angioscopic imaging. 324 55

Prostacyclin belongs to the family of prostaglandins, which are derived from arachidonic acid. It is secreted by vascular endothelium and possesses vasodilator and platelet anti-aggregant properties. This paper shows that molsidomine, a new anti-angina agent with vasodilator effects, is able to induce the secretion of prostacyclin by vascular endothelial cells in the aorta of the piglet. Molsidomine, via its stable metabolite SIN 1, induces very rapid and early secretion of prostacyclin followed by a refractory effect on vascular endothelium. At the same time, SIN 1 inhibits the platelet synthesis of thromboxane A2, which suggests that part of the action of molsidomine is related to an improvement in the prostacyclin/thromboxane A2 equilibrium, which has been shown to be disturbed in the course of certain cardiovascular diseases.
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PMID:[Cellular mechanism of action of molsidomine. Bioinduction of prostacyclin]. 642 Dec 23

Nitrates have been used in the pharmacological treatment of cardiac diseases for over hundred years, at the beginning in the treatment of angina pectoris. Later on the scale of clinical indications has widened towards other diseases where the vasodilating effect of these drugs could be of benefit. The increased interest in nitrates is based on new knowledge about their pharmacokinetics, pharmacodynamics and development of tolerance as well as the new idea of their cellular mode of action. They release nitric oxide, vasodilator and vasorelaxant physiologically originating from the vascular endothelium (EDRF). Nitrates and other NO-donors can substitute for this endogenous factor in the case of diseases endothelium or on other occasions where the production of NO is reduced or abnormally changed to toxic products. It is evident that totally new type of NO-donors like molsidomine and others will appear on the market for the treatment not only of cardiovascular diseases but also other disorders where smooth muscle relaxation is necessary. This review deals with the present status of nitrates in the cardiology and predicts some future aspects in this field.
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PMID:NO-donors in cardiology. 762 May 15

Clinical and experimental observations have confirmed that an episodic increase in the vasomotor tone of a major coronary artery may play a pathogenetic role not only in "variant angina" but also in other, more common anginal syndromes. In chronic stable angina, dynamic changes of vascular smooth muscle tone at the site of eccentric atheromatous plaques are responsible for "mixed angina." Abnormal coronary vasomotion contributes to myocardial ischemia in acute coronary syndromes as well. Studies have shown that a "primary" reduction of coronary blood flow, usually associated with plaque fissuring and thrombus formation, causes infarction and unstable angina. Abnormal vasoconstriction associated with the release of vasoactive substances by platelets and other constituents of the thrombus can contribute to coronary flow reduction in patients with unstable angina and myocardial infarction. Better understanding of the complex interactions among atherosclerotic coronary obstructions, the vascular smooth muscle, and the vascular endothelium has resulted in novel therapeutic approaches and has stimulated the search for more efficacious and safer coronary vasodilators. Recently interest has focused on vasodilator agents such as nicorandil that influence coronary arterial tone by acting through potassium channel activation. Nicorandil appears to be effective for treatment of vasospastic angina, as suggested by studies in Japan and Europe. In addition to its "antivasospastic" properties, nicorandil dilates coronary artery stenoses in patients with stable angina pectoris.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Management of vasospastic angina--role of nicorandil. 764 26

The seronin or 5-hydroxytryptamine (5-HT) is a biogenic amine involved in diverse physiologic and physiopathological processes in the cardiovascular system. 5-HT may lower the arterial blood pressure by an action on central 5-HT1A receptors, or may increase it by stimulation of 5-HT2 receptors located in vascular smooth muscle. It has been postulated that hypofunction of 5-HT1A receptors, or the exaggerated stimulation of 5-HT2 receptor may be associated with arterial hypertension and that agonists of the first type (indorenate or 8-OH-DPAT) or antagonists of the second type (ketanserin or pelanserin) allow the control of arterial hypertension. On the other land, ketanserin and pelanserin attenuated the hemodynamic manifestations in an experimental model of thromboembolism, suggesting that 5-HT is involved in such phenomenon. Finally, 5-HT could be related with the presence of angor pectoris during hypertension or atherosclerosis, diseases that are associated with a lesional of the vascular endothelium, a condition that favors the 5-HT induced vasoconstriction in coronary arteries.
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PMID:[Serotoninergic receptors and cardiovascular diseases]. 765 75


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