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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute colonic ischemia is the most common form of intestinal ischemia. Nonocclusive ischemic colitis contributes to some of these disorders. Heart disease, such as congestive heart failure, myocardial infarction, arrhythmias, aortic valve disease, and atherosclerotic cardiovascular disease, account for many of its risk factors. The majority of cases are associated with severe congestive heart failure with low cardiac output, or disease states resulting in dehydration, or the splanchnic vasoconstrictive effect of some medications. Reactive splanchnic vasoconstriction is responsible for nonocclusive ischemic colitis. Ischemic colitis induced by a cleansing enema has been reported once before. The authors present a case of coronary artery disease complicated by colonic ischemia following glycerin enema in preparation for coronary bypass surgery. Reactive inferior mesenteric artery spasm in response to the enema was noted in this case, rather than diffuse mesenteric artery spasm in response to low cardiac output state and vasoconstrictive drugs.
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PMID:Nonocclusive ischemic colitis following glycerin enema in a patient with coronary artery disease. A case report. 763 24

The epidemiologic approach to investigation of atherosclerotic cardiovascular disease has provided many insights into the preclinical and clinical spectrum of the disease. The hazard of developing atherosclerotic cardiovascular disease is substantial with coronary heart disease (CHD), the most common and most lethal feature. The outlook in those who manage to survive the initial episode is also serious, with a 10-year mortality rate of 37% for persons with angina and a 55% rate for those sustaining a myocardial infarction. Fifteen percent of persons developing CHD present with a fatal event, and 38% of infarctions go unrecognized. The presence of atherosclerosis in one vascular territory imposes an increased risk of its appearing in another area at two to six times the general population rate. The major cardiovascular risk factors adversely affect all arterial vascular territories so that correction of risk factors targeted at one particular atherosclerotic outcome may also favorably influence the other risk factors. Coronary disease is the most prevalent lethal hazard of hypertension, dyslipidemia, glucose intolerance, and cigarette smoking. These risk factors cluster and optimal therapy must improve the whole risk profile. Women share the same risk factors for CHD as men. Although women have a lower absolute risk for most risk factors, a high total/HDL cholesterol ratio, left ventricular hypertrophy, and diabetes each tend to eliminate the female advantage. Menopause also promptly escalates risk threefold. Although women tend to have a lower incidence than men, the initial attack is just as highly lethal in women, and their subsequent outlook as survivors is at least as serious as for men. Sudden death is a pre-eminent feature of coronary disease and cardiac failure. Coronary disease increases sudden death risk 3.3-fold and cardiac failure 4.8-fold. Sudden death incidence varies in relation to the same cardiovascular risk factors as coronary heart disease, with no unique risk factors identified. However, multivariate combinations of these in a profile can identify high-risk candidates for sudden death as well as coronary attacks in general. The key to prevention of sudden death is to prevent coronary attacks and cardiac failure. Despite aggressive cardiac revascularization and treatment of hypertension, congestive heart failure (CHF) has not decreased in prevalence, and innovations in the treatments of overt failure have not substantially improved survival. Median survival is only 1.7 years for men and 3.2 years for women. The conditional probability of developing CHF can be estimated using a logistic function comprised of age, systolic pressure, vital capacity, heart rate, ECG-left ventricular hypertrophy (LVH), glucose intolerance, x-ray enlargement, and presence of CHD and heart murmurs. Eighty percent of CHF events occur in persons in the upper quintile of multivariate risk. Continued clinical, metabolic, and epidemiologic research have expanded and refined atherosclerosis risk factors. The lipid connection is now concerned with the apoprotein makeup of the lipids, subfractions of lipids, and Lp(a). The diabetic influence is now focused on insulin resistance. Ambulatory monitoring is being used to evaluate blood pressure and silent ischemia. Fibrinogen and leukocyte counts have emerged as possible indicators of unstable lesions. Prospects for primary and secondary prevention are good if public health measures, health education, and preventive medicine are implemented based on existing knowledge of correctable or avoidable risk factors. The potential for more effective prevention continues to expand, and great advances have already been made in countries where aggressive preventive measures have been implemented to correct the major established risk factors.
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PMID:Hazards, risks, and threats of heart disease from the early stages to symptomatic coronary heart disease and cardiac failure. 921 Oct 12

The development of atherosclerotic cardiovascular disease is a common comorbidity in patients with the metabolic syndrome, a concurrence of cardiovascular risk factors in one individual. While multiple growth factors and adipokines are identified in atherosclerotic lesions, as well as neurotrophins implicated in both cardiac ischemia and lipid and glucose metabolism, the potential role of neurotrophins in human coronary atherosclerosis and in the metabolic syndrome still remains to be elucidated. Here we describe and discuss our results that represent a novel attempt to study the cardiovascular and metabolic biology of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and mast cells (MC). The local amount of NGF, the immunolocalization of p75 neurotrophin receptor (p75NTR) and the number of MC were correlatively examined in coronary vascular wall and in the surrounding subepicardial adipose tissue, obtained from autopsy cases in humans with advanced coronary atherosclerosis. We also analyzed the plasma levels of NGF, BDNF and leptin and the number of MC in biopsies from abdominal subcutaneous adipose tissue in patients with a severe form of the metabolic syndrome. The results demonstrate that NGF levels are decreased in atherosclerotic coronary vascular tissue but increased in the subepicardial adipose tissue, whereas both tissues express a greater number of MC and a stronger p75NTR immunoreactivity, compared to controls. Metabolic syndrome patients display a significant hyponeurotrophinemia and an increased number of adipose MC; the later correlates with elevated plasma leptin levels. In effect, we provide the first evidence for (i) an altered presence of NGF, p75NTR and MC in both coronary vascular and subepicardial adipose tissue in human coronary atherosclerosis, and (ii) a significant decrease in plasma NGF and BDNF levels and an elevated amount of plasma leptin and adipose MC in metabolic syndrome patients. Together our findings suggest that neuroimmune mediators such as NGF, BDNF, leptin and MC may be involved in the development of cardiovascular disease and related disorders.
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PMID:Neurotrophin presence in human coronary atherosclerosis and metabolic syndrome: a role for NGF and BDNF in cardiovascular disease? 1469 70

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

Spinal cord infarction is a rare complication following thoracic surgery. We present a case who developed paraplegia on the first postoperative day of thoracotomy. A 76-year-old man with a history of atherosclerotic cardiovascular disease was operated for bronchial carcinoma. An epidural infusion of ropivacaine and sufentanil was used for postoperative pain. Eight hours after the surgery, he had an episode of hypotension and respiratory depression. One hour later, he described paraplegia and Ischemia of the spinal cord was found on MRI. There was no recovery during the follow-up.
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PMID:Anterior spinal artery syndrome after thoracic surgery. 1639 81

Atherosclerotic cardiovascular disease (CVD), which includes coronary heart disease (CHD) and stroke, is now the most common cause of death in the middle aged and elderly in all parts of the world except subSaharan Africa. The direct cause of death is frequently an acute thrombotic arterial occlusion. Because atherosclerosis is a diffuse disease, patients with CHD also have a high risk of ischemic stroke. The hemostatic process is a needed defense mechanism to control hemorrhage after injury but at same time, if overactive, may have the potential to precipitate diseases such as myocardial infarction or stroke in the setting of atherosclerosis. In approximately 1% of all patients with ischemic stroke, and in up to 4% of young adults with stroke, the major precipitant of brain ischemia is a hematologic disorder or coagulopathy that predisposes to thrombosis. von Willebrand factor (vWF) plays an important role in platelet adhesion to subendothelial structures and in the intrinsic pathway of coagulation. It is regarded as an indirect measure of endothelial dysfunction. Deficiency of vWF in von Willebrand's disease is well established. However, much less is known regarding the pathophysiologic implications of an elevated level of vWF, particularly in relation to CVD and cerebrovascular disease. The importance of vWF in the pathogenesis of this disease is poorly defined and information is limited and inconsistent. Elevated levels of vWF have been variably linked with risk of CHD; causal criteria are not fully met. Relationships with stroke risk are even less well established. Measurement of vWF adds little to risk prediction after considering the major risk factors--age, sex, smoking, raised blood cholesterol, and hypertension. vWF may have a greater role in predicting outcome in subjects with acute coronary syndromes (ACS), stroke, and perhaps atrial fibrillation. Investigation of the use of vWF level to guide treatment of ACS or stroke is ongoing; however, there is no compelling evidence to date.
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PMID:von Willebrand Factor in CHD and stroke: relationships and therapeutic implications. 1760 81

Numerical and functional impairment of circulating endothelial progenitor cells (EPCs) is thought to contribute to endothelial dysfunction and the associated increase in cardiovascular risk. Increased EPCs number and activity are associated with the inhibition of EPCs senescence, which involved activation of telomerase. Telomerase activity can be regulated by phosphatidylinositol-3-kinase/Akt (PI3K/Akt) signaling pathway which also modulates the activity of endothelial nitric oxide synthase (eNOS). Increased oxidative stress induces telomerase inactivity whereas nitric oxide (NO) can reduce oxidative stress, thus activates telomerase. Plasma high-density lipoprotein (HDL) cholesterol levels have an inverse correlation with incidence of ischemic heart disease as well as other atherosclerosis-related ischemic conditions. However, the exact mechanism by which HDL prevents ischemic disease is not fully understood. HDL not only increases NO by activating eNOS through PI3K/Akt signaling pathway, but also directly stimulates EPCs differentiation via PI3K/Akt pathway. Moreover HDL can increase circulating EPCs number and enhances ischemia-induced angiogenesis. On the basis of recent findings, this manuscript proposed a new hypothesis that HDL could against atherosclerotic cardiovascular disease partially through slowing down EPCs senescence by increasing NO and promoting telomerase activity via PI3K/Akt signaling pathway.
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PMID:HDL slowing down endothelial progenitor cells senescence: a novel anti-atherogenic property of HDL. 1764 Aug 24

Post-hoc analyses of the GREACE and the LIFE trials have renewed the interest in elevated serum uric acid (SUA) as a factor contributing to atherosclerotic cardiovascular disease (CVD) and in the possible benefit derived from its pharmacological reduction. The results of these trials are consistent with reports indicating favourable effects of SUA lowering treatment with allopurinol on the rate of cardiovascular complications in patients with coronary heart disease, congestive heart failure and dilated cardiomyopathy. Two recent overviews have concluded that, while in population samples at relatively low risk of CVD, SUA is at best a very weak predictor of CVD, by contrast it is a significant independent predictor among subjects at high or very high risk. This raises the question of a different meaning of excess SUA levels under different circumstances. Whereas in uncomplicated obese, insulin-resistant and hypertensive patients SUA levels increase mainly as a consequence of impaired renal excretion, in conditions of local ischemia an increased production of uric acid occurs in parallel with that of reactive oxygen species (ROS). Thus, although clinical and experimental evidence suggest that uric acid has actually antioxidant properties, it is conceivable that under these conditions its antioxidant activity is overcome by the pro-oxidant and pro-inflammatory effects of ROS accumulation. At present, there is no solid evidence to recommend treatment of the mild asymptomatic hyperuricemia associated with obesity, diabetes and/or hypertension (up to 10mg/dL). By contrast, similar SUA elevations in patients at higher cardiovascular risk should be taken more seriously. A controlled trial to investigate the effects of SUA reduction in these patients, while monitoring concomitant changes in parameters of oxidative stress and inflammation, is warranted.
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PMID:Uric acid and oxidative stress: relative impact on cardiovascular risk? 1764 80

Ischemic insult to the splanchnic vasculature can jeopardize bowel viability and lead to devastating consequences, including bowel necrosis and gangrene. Although acute mesenteric ischemia (AMI) may occur at any age, the elderly are most commonly affected due to their higher incidence of underlying systemic pathology, most notably atherosclerotic cardiovascular disease. Treatment options include pharmacology-based actions, endovascular, and surgical interventions. AMI remains a life-threatening condition with a mortality rate of 60% to 80%, especially if intestinal infarction has occurred and surgical intervention becomes emergent. Early recognition and an aggressive therapeutic approach are essential if the usually poor outcome is to be improved. Anesthetic management is complex and must account for comorbid disease as well as the patient's presumptive acute deterioration. Blood pressure support typically involves careful, but often massive, fluid resuscitation and may also additionally require pharmacologic support.
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PMID:Anesthetic management of acute mesenteric ischemia in elderly patients. 1982 92

In the early moments of ischemic stroke, the processes of thrombosis, ischemia, and inflammation are intimately interrelated, setting in motion an injury that leads to infarction and permanent damage. Of these, the potential roles that innate inflammation can play in the evolution of brain tissue damage in response to the ischemic injury are not well understood. Observations in the settings of atherosclerotic cardiovascular disease and cerebral ischemia have much to teach each other. The following provides an introductory overview of the conference "Innate Inflammation as the Common Pathway of Risk Factors Leading to Transient Ischemic Attacks and Stroke: Pathophysiology and Potential Interventions," which took place May 9-10, 2010 at the New York Academy of Sciences. This meeting was convened to explore aspects of the cellular and tissue responses to innate inflammation. A faculty of leading experts was assembled to discuss the role of inflammation in laboratory models of stroke and myocardial infarction, define possible novel means from laboratory evidence to alleviate or prevent inflammation underlying stroke and cardiovascular disease, and present information on current examples of clinical translation of these understandings in relation to human stroke and myocardial infarction.
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PMID:Innate inflammation as the common pathway of risk factors leading to TIAs and stroke. 2095 19


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