Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute ischemic chest pain at rest consistent with unstable angina or non-ST-elevation myocardial infarction is a common problem that may cause death or recurrent myocardial infarction within 30 days unless identified and risk stratified acutely. The latter may be done within 15 minutes by the history, physical exam, and electrocardiogram, and is aided by the measurement of troponin T/I. According to the Agency for Health Care Policy and Research guidelines, low-risk patients can be discharged home and rechecked within 72 hours. Intermediate-risk patients with no ST-segment changes with continuous monitoring and no elevation of troponin should undergo exercise stress testing by electrocardiogram (or nuclear or echocardiographic evaluation if electrocardiogram is non-analyzable). Patients with a negative stress test are low risk (no death or myocardial infarction at 30 days or 6 months) and can be discharged home. Patients with a positive test or who are at high risk according to the Agency for Health Care Policy and Research guidelines should undergo acute invasive testing for possible revascularization. Aspirin and low molecular weight heparin or unfractionated heparin, along with anti-ischemia therapy, is indicated in intermediate- or high-risk patients. The addition of clopidogrel is indicated in these patients, except in those who are potential candidates for coronary artery bypass graft. Platelet glycoprotein IIb/IIIa inhibitors are indicated in high-risk patients likely to undergo percutaneous coronary intervention, should be started early if recurrent ischemia occurs, but are not indicated in lower-risk patients who do not require percutaneous coronary intervention. Intensive secondary prevention should be started before dismissal.
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PMID:Acute coronary syndromes: pathogenesis, acute diagnosis with risk stratification, and treatment. 1553 72

Profound thrombocytopenia after abciximab administration in acute myocardial infarction and stent thrombosis. This article presents a case of a 62-years-old man with acute anterior myocardial infarction, treated with PCI and stent implantation, in whom profound acute thrombocytopenia was observed after abciximab administration. Nadir platelet count was 6 G/L (before treatment: 250 G/L). Pseudothrombocytopenia was excluded. The remaining antiplatelet drugs (heparin, ASA, clopidogrel) were discontinued. There were no symptoms of bleeding, but next morning (platelet count: 14 G/L) a gross hematoma at femoral puncture site was observed. The patient received 5 U transfusion of platelets. On the 4th day, when the platelet count reached 64 G/L, he was started again on ASA (150 mg) and clopidogrel (75 mg). On the 7th day (platelet count: 138 G/L) he developed anterior ischemia and stent reocclusion was diagnosed. After p.o. clopidogrel (300 mg), balloon PCI with i.c. heparin was performed and ischemia symptoms subsided. The platelet value before the patient's discharge, on subsequent therapy with ASA and clopidogrel, increased to 300 G/L. A review of current literature on this topic is provided.
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PMID:[Profound thrombocytopenia after abciximab administration in acute myocardial infarction and stent thrombosis following thrombocytopenia remission--a case report]. 1581 78

We studied the effect of ketamine sedation on oxidative stress during arthroscopic knee surgery with tourniquet application by determining blood and tissue malonyldialdehyde (MDA) and hypoxanthine (HPX) levels. Thirty ASA I-II patients undergoing arthroscopic knee surgery with tourniquet were randomly divided into two groups. Spinal anesthesia induced with 12.5 mg bupivacaine was administered to all patients. In the ketamine group, after IV administration of 0.01 mg/kg midazolam, a continuous infusion of ketamine (0.5 mg . kg(-1) . h(-1)) was used until the end of surgery whereas the placebo group received a volume-equivalent placebo infusion. Ramsey Sedation Scale (RSS) was used for assessing the sedation level. Venous blood and synovial membrane tissue samples were obtained before ketamine infusion, at 30 min of tourniquet ischemia, and at 5 min after tourniquet deflation for MDA and HPX measurements. Tissue MDA and HPX levels were significantly less in the ketamine group than the control group after reperfusion. RSS scores were higher in the ketamine group without any adverse effect. We conclude that ketamine sedation attenuates lipid peroxidation markers in arthroscopic knee surgery with tourniquet application.
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PMID:Ketamine sedation during spinal anesthesia for arthroscopic knee surgery reduced the ischemia-reperfusion injury markers. 1611 12

Nuclear factor-kappaB (NF-kappaB) plays an essential role in the intracellular signal transduction of the second window of protection (SWOP). Acetylsalicylic acid (ASA) blocks NF-kappaB-dependent gene activation in leukocytes and endothelial cells through preventing phosphorylation and subsequent degradation of the inhibitor IkappaB-alpha. This study investigated the effect of ASA on the late phase of ischemic preconditioning (PC) against myocardial infarction and on the activation of NF-kappaB in the preconditioned myocardium. Conscious rabbits were subjected to 4 cycles of 5 minutes of coronary occlusion and 5 minutes of reperfusion together with 3 different doses of ASA (5 mg/kg; 25 mg/kg; 130 mg/kg). After 30 minutes of reperfusion we determined the activation of NF-kappaB with an electrophoretic mobility shift assay (EMSA). Twenty-four hours later, after 30 minutes of test ischemia, we performed infarct size analysis using triphenyltetrazolium-chloride (TTC) staining. Neither 5 mg/kg (antithrombotic dose) nor 25 mg/kg (analgesic/antipyretic dose) of ASA interfered with the NF-kappaB activation and the protective effect of late preconditioning against myocardial infarction. In contrast, NF-kB activation and late PC effect were completely abrogated by 130 mg/kg of ASA. Our results suggest that nonselective doses of NSAIDs should be used with caution in patients with atherosclerotic cardiovascular disease because they may deprive the heart of its innate defensive response.
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PMID:Effect of acetylsalicylic acid on nuclear factor-kappaB activation and on late preconditioning against infarction in the myocardium. 1611 34

Since Robert discovery that pretreatment with prostaglandin (PG) applied in non-antisecretory dose can prevent the injury of gastric mucosa induced by necrotizing agents, much attention was paid to the role of these cyclooxygenase (COX) products in the mechanism of gastric mucosal integrity and ulcer healing. The ability of exogenous PG to attenuate or even completely prevent mucosal damage caused by corrosive substances such as absolute ethanol, hyperosmolar solutions or concentrated bile has been termed "cytoprotection". Increased generation of endogenous PG in the gastric mucosa exposed to the topical contact with "mild irritant" such as 20% ethanol, 1 mM NaCl or 5 mM taurocholate also prevented gastric injury caused by strong irritants via phenomenon of adaptive cytoprotection. Other mediators such as growth factors, nitric oxide (NO) or calcitonin gene related peptide (CGRP) as well as some gut hormones including gastrin and cholecystokinin (CCK), leptin, ghrelin and gastrin-releasing peptide (GRP) have been also found to protect gastric mucosa against the damage induced by corrosive substances. This protective action of gut hormones has been attributed to the release of PG or activation of sensory nerves because it could be abolished by the pretreatment with indomethacin or large neurotoxic dose of capsaicin and restored by the addition of exogenous PGE(2) or CGRP, respectively. Short (5 min) ischemia of the stomach applied before prolonged ischemia-reperfusion (I/R) attenuated markedly the gastric lesions produced by this I/R and also prevented the mucosal damage provoked by necrotizing substances. This protection could be abolished by the pretreatment with non-steroidal anti-inflammatory drugs (NSAID) and was accompanied by an enhancement of gastric mucosal COX-2 expression and activity. Exposure of gastric mucosa to single insult of acidified aspirin (ASA) causes severe mucosal damage with occurrence of multiple haemorrhagic lesions but with repeated application of ASA, the attenuation of mucosal lesions is observed, despite the profound inhibition of PGE(2) generation. This phenomenon called "gastric adaptation" does not appear to depend upon endogenous biosynthesis of PG but possibly involves enhanced production of growth factors increasing cell proliferation and mucosal regeneration. Unlike short lived gastroprotection by PG, NO, CGRP, mild irritants or short ischemia, gastric adaptation appears to be long-lasting phenomenon accompanied by increased resistance of the adapted mucosa to subsequent damage induced by corrosive agents.
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PMID:Role of prostaglandins in gastroprotection and gastric adaptation. 1624 88

Glaucoma is a common blinding disease worldwide. Although traditionally considered as a disease of elevated intraocular pressure, it is now clear that glaucoma is primarily a distinctive optic neuropathy with many proposed pathogenic mechanisms. Impaired blood flow resulting in ischemia has been proposed to be involved in the retinal ganglion cell loss seen in glaucoma. Aspirin might improve optic nerve head perfusion by stabilizing microcirculatory flow. Evidence also indicates that apoptosis may be the final common pathway for ganglion cell death in glaucoma. Aspirin has been shown to exhibit neuroprotective properties. Prostaglandins play an important role in the regulation of intraocular pressure. Aspirin is well known to inhibit cyclooxygenase mediated prostaglandin synthesis. The NSAID-inhibition of PGs synthesis up-regulates the concentration prostaglandin receptors in retinovascular tissues. Based on the body of evidence implicating ocular blood flow disturbances, apoptotic cell death, and also the role of prostaglandins in the pathogenesis of glaucoma we hypothesize that aspirin could be potentially useful drugs in the treatment of glaucoma. Hypothetical pathophysiologic mechanisms explaining potential beneficial effects of aspirin on glaucomatous optic neuropathy include: increasing optic nerve blood flow, preventing retinal ganglion cell death through neuroprotective mechanisms, and upregulating prostaglandin receptors.
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PMID:Therapeutic potentials of aspirin in glaucomatous optic neuropathy. 1652 27

NCX 4016, 2-(acetyloxy)benzoic acid 3-[(nitrooxy)methyl]phenyl ester, is a new molecule in which a nitric oxide (NO)-releasing moiety is covalently linked to aspirin. After enzymatic metabolism, NCX 4016 releases both components. In vitro and in some animal models, these components exert their pharmacologic effects simultaneously. Nitric oxide (NO) is a small gaseous molecule that exerts several activities which may prevent atherothrombotic disorders. Moreover, it displays a protective activity on the gastric mucosa. NCX 4016 has been shown to inhibit platelet activation in vitro more effectively than aspirin, to inhibit smooth muscle cell proliferation, to exert an endothelial cell protective activity and to suppress the function of several inflammatory cells potentially involved in atherothrombosis. In animal models, NCX 4016 protected from platelet thromboembolism, prevented restenosis in atherosclerosis-prone animals, protected the heart from ischemia/reperfusion injury, and induced neoangiogenesis in critically ischemic limbs. Moreover, it displayed little or no gastric toxicity and appeared to protect stomach from noxious stimuli, including aspirin. NCX 4016 has been evaluated in healthy volunteers and found to inhibit platelet cyclo-oxygenase-1 (COX-1) similarly to or slightly less than aspirin, to raise the circulating levels of NO-degradation products, and to have little or no gastric toxicity in short term studies. In particular, in phase II studies, NCX 4016 had favorable effects on effort-induced endothelial dysfunction in intermittent claudication and on platelet-activation parameters elicited by short-term hyperglycemia in type II diabetics. In patients with type II diabetes the effects of NCX 4016 on microalbuminuria and on some hemodynamic parameters were promising. The pharmacokinetics of in vivo aspirin- and NO- released by NCX 4016, as well as the bioavailability of the two molecules, were not yet adequately studied. Also, the long-term tolerability of NCX 4016, as well as its possible effectiveness in preventing ischemic cardiovascular events and progression of atherosclerosis, should be explored.
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PMID:Pharmacologic profile and therapeutic potential of NCX 4016, a nitric oxide-releasing aspirin, for cardiovascular disorders. 1696 26

According to the new definition proposed by the TIA working group, transient ischemic stroke (TIA) is "a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction." Patient presenting with a TIA should be investigated and treated urgently because the risk of ischemic stroke is about 10% at one month with 50% of these events occurring during the first 48 hours. Atherosclerosis, cardioembolism and small vessel disease account for the majority of TA. Aspirin should be started as soon as possible after brain imaging has been performed. Other treatment such as oral anticoagulants or carotide surgery may be necessary, depending on the result of the electronical work up.
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PMID:[Transient ischemic stroke]. 1700 66

The decision to offer patients with myocardial ischemia a coronary artery bypass graft (CABG) surgery has been largely determined by extent of coronary artery disease (CAD) and left ventricular function, since the early 1970's. Based upon subset analyses, and long-term follow-up, of three moderate-sized trials of stable patients and two small trials of unstable angina (excluding recent myocardial infarction, MI) patients, the notion has persisted that patients with left main narrowing >50% or three-vessel stenoses >70%, or even two-vessel stenoses >70%, where one of the vessels is the proximal left anterior descending, derive a "survival benefit" relative to medical therapy (MED), from CABG (anatomic paradigm). The MED of the original CABG versus MED trials consisted of little more than anti-anginal medications, used on an as-needed basis. In the ensuing 3 decades, multiple large, well done, randomized clinical trials have established a survival benefit for 4 different forms of MED among a broad spectrum of CAD patients. Aspirin; lipid lowering, especially with statins; b-blockers; and angiotensin-converting-enzyme inhibitors and/or angiotensin receptor blocking agents; have all been shown to enhance survival, as well as reduce other objective adverse outcomes of CAD. The advances in MED, coupled with the small but significant mortality and morbidities of both CABG and percutaneous coronary intervention (PCI), are among the reasons to skeptically consider potential "survival benefit" of revascularization. A more common and far more easily justified reason to consider revascularization is to relieve "medically refractory" myocardial ischemia, particularly when the ischemia is accompanied by symptoms. Accordingly, documentation of medically refractory myocardial ischemia provides the answer to the first question of myocardial revascularization, "Is this patient likely to derive clinical benefit from revascularization, at this time?" It is only after this question has been answered that one needs to consider the relative advantages and disadvantages of PCI versus CABG (physiologic paradigm). Two of the relative advantages of PCI, namely speed of reperfusion, and relatively low morbidity, are among the reasons that most randomized trial data, and most clinical application of revascularization to patients with MI (ST-elevation MI [STEMI], and non-STEMI) have been by PCI. In contrast, for stable patients with medically refractory ischemia, anatomic considerations continue to be relevant to the choice between CABG and PCI. Specific advantages of CABG include: its potential to revascularize chronically occluded vessels with collaterals supplying viable myocardium; the fact that conduits protect territories rather than simply treating lesions; and the greater durability of conduits compared to bare-metal stents (drug-eluting stents may change the picture). Based on these principles, physiologic, rather than anatomic, considerations are most useful in determining whether to revascularize, and how urgently to revascularize (STEMI is an emergent indication and high-risk non-STEMI an urgent indication). Coronary anatomy, including both number of vessels and lesion characteristics, continues to help decide between CABG and PCI, and in formulating patient specific strategies.
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PMID:PCI versus CABG versus medical therapy in 2006. 1701

Nitric oxide (NO) plays a protective role in myocardial ischemia-reperfusion (I/R) injury. However, the concomitant production of superoxide and other reactive oxygen species (ROS) during I/R may diminish the bioavailability of NO and hence compromise the beneficial effects. The objective of this study was to investigate the protective effect of the coadministration of NCX-4016 [2-(acetyloxy)benzoic acid 3-(nitrooxymethyl)phenyl ester] (an NO donor) with antioxidants Tempol, superoxide dismutase (SOD), or urate on I/R injury. Isolated rat hearts, perfused with Krebs-Henseleit buffer, were subjected to 30 minutes of global ischemia, followed by 45 minutes of reperfusion. Before the induction of ischemia, the hearts were infused for 1 minute with NCX-4016 (100 microM) either alone or in combination with Tempol (100 microM), SOD (200 U/mL), or urate (100 microM). Hearts pretreated with NCX-4016 showed a significantly enhanced recovery of function and decreased infarct size and LDH/CK release compared with the controls. However, treatment of hearts with NCX-4016 + Tempol, SOD, or urate showed a significantly enhanced recovery of heart function compared with NCX-4016 alone. The treatment of hearts with NCX-4016 + Tempol showed significantly enhanced NO generation and decreased ROS and dityrosine (a marker of peroxynitrite) formation. In conclusion, NCX-4016 in combination with Tempol demonstrated significant cardioprotection and, thus, may offer a novel therapeutic strategy to prevent I/R-mediated myocardial injury.
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PMID:Prevention of postischemic myocardial reperfusion injury by the combined treatment of NCX-4016 and Tempol. 1703 Dec 60


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