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)

Statins may act rapidly to reverse abnormalities of the arterial wall that may predispose to recurrent ischemic events after acute coronary syndromes. Such abnormalities are endothelial dysfunction, a local inflammatory response. and an exaggerated thrombogenic tendency. In one study almost 20,000 patients with first myocardial infarction were studied with regard to statin treatment (28%) or not. Baseline characteristics were adjusted using multivariate regression analysis including propensity analysis. One year mortality was 3.7/5.0% in statin/not statin groups, respectively, P = 0.001, relative risk 0.75. In another study of more than 20,000 patients, 18% were prescribed statin after an acute coronary syndrome and followed for six months. Propensity analysis was performed in this study as well. Deaths in statin/not statin groups were 1.7/3.5%, P<0.0001, relative risk 0.48. In the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL), a double-blind randomized, placebo-controlled intervention study, 3086 patient with acute non-Q-wave coronary syndromes were allocated immediately in hospital to receive atorvastatin 80 mg daily or placebo for four months. No lower limit for plasma LDL cholesterol was used. Primary endpoint was time to first occurrence of death, non-fatal myocardial infarction, cardiac arrest, and worsening angina with objective evidence of ischemia. This was significantly reduced compared to the placebo group by 2.4% (14.8 versus 17.2%, relative risk 0.84, P= 0.048). Atorvastatin also reduced significantly fatal or non-fatal strokes. Possible mechanisms behind these acute beneficial effects are discussed. The studies highlight the importance of treatment with a statin in the early management of acute coronary syndromes and the need to incorporate this therapeutic strategy in national guidelines and treatment recommendations.
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PMID:Early initiation of treatment with statins in acute coronary syndromes. 1201 32

The extent of brain injury during reperfusion appears to depend on the experimental pattern of ischemia/reperfusion. The goals of this study were: first, to identify the rate of free radicals generation and the antioxidant activity during ischemia and reperfusion by means of biochemical measurement of lipid peroxidation (LPO) and both enzymatic (superoxide dismutase - SOD, catalase - CAT, glutathione peroxidase - GPx) and non-enzymatic antioxidants activity (glutathione - GSH); and second, to try to find out how the pattern of reperfusion may influence the balance between free radical production and clearance. Wistar male rats were subject of four-vessel occlusion model (Pulsinelly & Brierley) cerebral blood flow being controlled by means of two atraumatic arterial microclamps placed on carotid arteries. The level of free radicals and the antioxidant activity were measured in ischemic rat brain tissue homogenate using spectrophotometrical techniques. All groups subjected to ischemia shown an increase of LPO and a reduction of the activity of enzymatic antioxidative systems (CAT, GPx, SOD) and non-enzymatic systems (GSH). For both groups subjected to ischemia and reperfusion, results shown an important increase of LPO but less significant than the levels found in the group with ischemia only. Statistically relevant differences (p<0.01) between continuous reperfusion and fragmented reperfusion were observed concerning the LPO, CAT, SOD and GSH levels, oxidative aggression during fragmented reperfusion being more important.
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PMID:Oxidative damage following cerebral ischemia depends on reperfusion - a biochemical study in rat. 1206 99

Aggressive evaluation and treatment of the patient suffering from lower-extremity ischemia is critical. Vascular reconstruction can be performed to enhance healing and to decrease the incidence of major limb amputation and therefore return these patients to active and productive life.
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PMID:Vascular reconstructive options in the ischemic foot. 1213 78

Severe limb ischemia is a common problem encountered in medical practice. Aggressive attempts at revascularization have extended the limits of limb salvage. However, in certain cases, extended tissue loss compromises the healing process. It often results in amputation despite bypass graft patency. Microvascular free tissue transfer combined with arterial revascularization allows healing of these wounds and limb preservation. This combined approach is the ultimate alternative to amputation.
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PMID:[Arterial revascularization with free tissue transfer for salvage of ischemic limbs with extensive tissue loss: an alternative to amputation]. 1223 21

The treatment of patients with stable angina has three goals: 1) minimize or eliminate ischemia (silent or symptomatic), 2) reduce morbidity, and 3) decrease mortality. Surgical and now angiographic revascularization procedures are increasingly popular approaches to the management of these patients. The results of randomized, controlled trials suggest that revascularization may not improve survival, but is useful to improve symptoms and exercise capacity. However, these trials are of limited value because they do not reflect current state of the art revascularization techniques or optimal medical management. Because many of these studies were conducted more than a decade ago, patients were recruited before the survival benefits of antiplatelet therapy, b-blockers, angiotensin-converting enzyme inhibitors, and aggressive lipid lowering were accepted. The Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) trial should help us determine the best approach in these patients. It is a multicenter, randomized trial comparing aggressive medical therapy with aggressive medical therapy with current state of the art percutaneous coronary intervention (PCI) for patients with stable coronary disease. The COURAGE protocol targets global risk reduction emphasizing 1) lifestyle modification, 2) maximal use of drugs to lower blood pressure to Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC) VI goals, 3) maximal use of drugs to lower cholesterol to below National Cholesterol Education Program Adult Treatment Panel III goals for secondary prevention, and 4) maximal use of drug to alleviate anginal symptoms with or without the best interventional devices to conduct PCI.
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PMID:Aggressive medical management of coronary artery disease versus mechanical revascularization. 1257 97

Brain areas involved in heart autonomic control are not well characterized. Insulae have been proposed as control centers. A lesion in these areas may induce a cardiac autonomic dysfunction (arrhythmias, atrioventricular conduction abnormalities). Asystolia has not been previously reported. A 65-year-old man suffered an acute ischemia of the right middle cerebral artery (MCA) territory. NIHSS score was 19 points. Brain CT scan was normal. Transcranial Doppler (TCD) showed occlusion of the right MCA. Fibrinolysis was initiated 135 minutes after stroke onset with TCD monitoring. Twenty minutes later he suffered cardiac arrest with asystolia trace in the ECG monitor. Fibrinolysis was stopped during resuscitation. Four minutes later, he recovered with the same NIHSS score. Aggressive resuscitation maneuvers were not necessary. A repeated brain CT scan showed infarct signs in the whole MCA territory and a new TCD did not show any change. Serial blood analyses including cardiac nzymes were normal. The patient experienced four brief cardiac arrests in the next nine hours, so a temporary cardiac pacemaker was placed for four days. He was treated with aspirin and was discharged 14 days after admission. He has not experienced recurrences during a 6-month follow-up. We could not diagnose the etiology of the cardiac arrests. All the episodes occurred in the acute stroke stage and arrhythmia, atrioventricular block, myocardial ischemia or structural lesions were not found in the cardiac study. We propose that ischemia in the right insula induced sudden and transitory interruptions of the sympathetic cardiac tone.
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PMID:[Asystolias in the acute phase of brain stroke. Report of a case]. 1267 86

Calciphylaxis is a confusing disease process that affects people with end-stage renal disease. The prognosis of this increasingly common condition is poor and mortality rates range from 60% to 80% related to wound infection, sepsis, and organ failure. Its presenting sign is skin necrosis related to calcification of the arteriole microvasculature. The disease is painful and debilitating, particularly due to the necrotic wounds. Aggressive wound care to prevent infection is vital when eschar does not protect the wound and drainage is present, but debridement is contraindicated for wounds covered with dry, noninfected eschars. The decision to debride is based on the patient's total clinical picture. Patients with calciphylaxis have poor healing potential due to ischemia and comorbidity factors such as diabetes mellitus, peripheral vascular disease, and obesity. The goal of care is prevention of infection and pain management. Some of the sensitizers and challengers responsible for the chemical imbalance leading to the arteriole calcification, as well as risk factors and clinical manifestations of calciphylaxis, are reviewed. A discussion of treatment focuses on wound care of stable necrotic ulcers and a case report illustrating the progression of calciphylaxis is presented.
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PMID:Mysterious calciphylaxis: wounds with eschar--to debride or not to debride? 1525 2

The nervous tissue and the myocardium have in common many denominators, such as: the inability to renew to substitute the severely damaged or dead cells, the role of the membrane electric activity, the presence of similar systems for antioxidation protection, which are obviously involved in pathologic events a.s.o. Aggressive factors mainly act by free radicals injury and increase in cytosolic calcium level. Magnesium orotate molecule includes two synergic protective components: orotic acid and magnesium. Moreover, the orotic acid behaves as a transporter, carrying magnesium into the cells. The antioxidation protective effect of the orotic acid is mainly due to the pirimidinic bases that favor and increased synthesis of enzymes which act as free radical scavengers. The cell antioxidation protective system is dramatically impaired following heavy aggressions such as the ischemia-reperfusion process. Magnesium orotate improves the survival of cells situated within the perinecrotic areas as well as of the cells secondarily damaged during the so-called "second wind".
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PMID:Magnesium orotate in myocardial and neuronal protection. 1552 49

During the past decade, our understanding of the pathophysiology of coronary artery disease (CAD) has undergone a remarkable evolution. We review here how these advances have altered our concepts of and clinical approaches to both the chronic and acute phases of CAD. Previously considered a cholesterol storage disease, we currently view atherosclerosis as an inflammatory disorder. The appreciation of arterial remodeling (compensatory enlargement) has expanded attention beyond stenoses evident by angiography to encompass the biology of nonstenotic plaques. Revascularization effectively relieves ischemia, but we now recognize the need to attend to nonobstructive lesions as well. Aggressive management of modifiable risk factors reduces cardiovascular events and should accompany appropriate revascularization. We now recognize that disruption of plaques that may not produce critical stenoses causes many acute coronary syndromes (ACS). The disrupted plaque represents a "solid-state" stimulus to thrombosis. Alterations in circulating prothrombotic or antifibrinolytic mediators in the "fluid phase" of the blood can also predispose toward ACS. Recent results have established the multiplicity of "high-risk" plaques and the widespread nature of inflammation in patients prone to develop ACS. These findings challenge our traditional view of coronary atherosclerosis as a segmental or localized disease. Thus, treatment of ACS should involve 2 overlapping phases: first, addressing the culprit lesion, and second, aiming at rapid "stabilization" of other plaques that may produce recurrent events. The concept of "interventional cardiology" must expand beyond mechanical revascularization to embrace preventive interventions that forestall future events.
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PMID:Pathophysiology of coronary artery disease. 1598 62

The pathophysiological mechanisms underlying a diabetic foot disease are complex and multifactorial, including neuropathy, ischemia, infection and abnormal foot biomechanics. All these factors are often intricated and source of delayed wound healing. Insight in the pathophysiology of the diabetic foot provides a comprehensive basis for a protocol of primary and secondary preventive care. Since non-enzymatic glycosilation of proteins and of connective tissue underlies structural changes in vessels, nerves and osteo-articular structures, a rigid control of blood glucose levels is of paramount importance. Early recognition of the etiology of foot lesions and prompt management of foot ulcers are essential for successful outcome. Aggressive treatment of infections, clinical assessment and correction of vascular occlusive disease (diabetic macroangiopathy), adequate wound care and appropriate off-loading (pressure relief) of the ulcer are essential steps in the treatment protocol. It is not surprising that optimal management of the diabetic foot requires a multidisciplinary approach in a Diabetic Foot Clinic, coordinating care-provisions by a team of diabetologist, infectiologist, vascular surgeon, interventional radiologist, plastic surgeon, podiatrist and specialized nurse. Applying evidence-based multidisciplinary treatment results in a 50% reduction of major lower-limb amputation in this high risk group.
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PMID:[The diabetic foot]. 1603 20


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