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)

This study compares remifentanil/propofol (remi/prop) with isoflurane/fentanyl (iso/fen) anesthesia to determine which provides the greater hemodynamic stability, lesser myocardial ischemia, and morbidity with better postoperative outcomes after carotid endarterectomy. Sixty patients undergoing unilateral carotid endarterectomy were randomized to receive either a remi/prop or iso/fen anesthetic. Hemodynamic variables were recorded during the surgical procedure. In addition, transesophageal echocardiography was used to assess evidence of intraoperative regional wall motion abnormalities suggestive of cardiac ischemia. Emergence and extubation times, recovery from anesthesia, hemodynamic instability, nausea, vomiting, and pain in post anesthesia recovery, discharge delays, ICU admittance, hospital discharge, and preoperative and postoperative troponin levels were compared using appropriate statistical methods with P < 0.05 considered significant. The groups were demographically alike. Hemodynamic variables were similar during intubation and throughout surgery. Twenty-two percent of patients receiving iso/fen developed intraoperative regional wall motion abnormalities suggestive of ischemia, whereas no remi/prop patients had changes (P < 0.05). There was no difference in ST-T wave changes after surgery, and no patient had an elevation in troponin I levels. Postoperative variables were similar except that patients who received iso/fen had lower Stewart recovery scores during the first 15 minutes after post anesthesia care unit admission and a higher incidence of nausea and vomiting the day after surgery, whereas patients receiving remi/prop had discharge delays secondary to hypertension. ICU admittance, time to first void, oral intake, and time to hospital discharge were similar between the groups. At 9 times the cost of an iso/fen anesthesia technique, remi/prop offers little advantage over inhalational anesthesia for carotid endarterectomy.
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PMID:Hemodynamic stability, myocardial ischemia, and perioperative outcome after carotid surgery with remifentanil/propofol or isoflurane/fentanyl anesthesia. 1282 64

The aim of our study was to evaluate whether a single dose of cerivastatin at the time of admission of patients with unstable angina pectoris (UAP) or non-Q-wave myocardial infarction (NQMI) can influence the serum level of C-reactive protein (CRP), interleukin-6 (IL-6) and interleukin-8 (IL-8) 24 h later. Forty-four patients with rest chest pain and subendocardial ischemia on ECG were randomized to receive cerivastatin 0.3 mg at the time of admission (group C+) to standard therapy or to remain just on standard therapy (group C-). Blood samples for determination of troponin I (TI), CRP, IL-6 and IL-8 were collected at admission (entry level) and 24 h later (final level). Patients with non-physiological baseline levels of TI, as well as patients with progression to Q wave MI were excluded. All baseline, clinical and demographic data and final values of TI were comparable in the two groups. In patients treated with cerivastatin (group C+, n = 13) we observed decrease in the CRP level (-6.73 +/- 3.93 mg/L); on the other hand, in group C- (n = 17) the CRP level increased (+7.92 +/- 2.77 mg/L, p = 0.004). Similar differences were observed also in IL-6: in group C+ the level was significantly reduced as compared with the increase in group C- (-0.76 +/- 0.52 vs. 4.58 +/- 1.49 ng/L, p = 0.005). The level of IL-8 was not affected. Our results suggest that early treatment with cerivastatin can decrease the serum level of CRP and IL-6 in patients with UAP/NQMI; this might positively influence their prognosis. Nevertheless, further studies are needed to support this hypothesis.
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PMID:The effect of early treatment by cerivastatin on the serum level of C-reactive protein, interleukin-6, and interleukin-8 in the patients with unstable angina and non-Q-wave myocardial infarction. 1284 42

The physiopathological mechanisms resulting in increased left ventricular pressures in acute cardiac failure with normal systolic function are not well understood. Although coronary artery disease is commonly associated with acute episodes, the diagnostic value of troponin I measurement and the prevalence of ischaemia as the predisposing factor are not known. Twenty coronary patients (mean age 77 +/- 9 years) in acute cardiac failure with left ventricular ejection fractions of 50% or over and without angina, were studied retrospectively. The diagnostic value of troponin I (cTnI, AxSYM, method) was assessed by comparing with a control group of 16 acute cardiac failure patients without coronary disease. The frequency of hypertension and diabetes in the coronary group was 50 and 45% respectively. At the time of investigation, the pulmonary capillary and systemic arterial pressures were comparable in the coronary patients irrespective of the cTnl value. At threshold levels of 0.5 microgram/l, cTnl had a specificity of 100% and confirmed ischaemia in 60% of the coronary patients. Ischaemia was the commonest predisposing factor for increased cardiac pressures. Over a 268 +/- 101 days follow-up period, half the coronary patients were readmitted for acute cardiac failure and a third of them died. The authors conclude that silent ischaemia is a common predisposing factor for acute cardiac failure in coronary patients with normal systolic function and troponin I measurement is a useful diagnostic help.
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PMID:[Silent ischemia and acute cardiac insufficiency with normal systolic function: diagnostic value of troponin I measurement]. 1457 38

In the heart, the contractile apparatus is adapted to the specific demands of the organ for continuous rhythmic contraction. The specialized contractile properties of heart muscle are attributable to the expression of cardiac-specific isoforms of contractile proteins. This review describes the isoforms of the thin filament proteins actin and tropomyosin and the three troponin subunits found in human heart muscle, how the isoform profiles of these proteins change during development and disease, and the possible functional consequences of these changes. During development of the heart, there is a distinctive switch of isoform expression at or shortly after birth; however, during adult life, thin filament protein isoform composition seems to be stable despite protein turnover rates of 3 to 10 days. The pattern of isoforms of actin, tropomyosin, troponin I, troponin C, and troponin T is not affected by aging or heart disease (ischemia and dilated cardiomyopathy). The evidence for proteolysis of thin filament proteins in situ during ischemia and stunning is evaluated, and it is concluded that C-terminal cleavage of troponin I is a feature of irreversibly injured myocardium but may not play a role in reversible stunning.
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PMID:Modulation of thin filament activation by breakdown or isoform switching of thin filament proteins: physiological and pathological implications. 1467 Aug 32

Myocardial stunning is a form of acute reversible cardiac dysfunction that occurs after brief periods of ischemia and reperfusion. In several animal models, stunning is associated with proteolytic truncation of troponin I (TnI). Mice expressing the same proteolytic TnI fragment [TnI-(1-193)] demonstrate cardiac depression with a decreased maximal calcium-activated tension. We therefore hypothesized preferential improvement in mice expressing TnI-(1-193) treated with the calcium-sensitizing drug EMD-57033. TnI-(1-193) and nontransgenic myofibrils exhibited significant sensitization to calcium in Mg-ATPase assays after EMD-57033 exposure. However, only transgenic myofibrils exhibited an increase in maximal activity (P = 0.023). EMD-57033 also increased maximal calcium-activated force in TnI-(1-193) muscle, such that it was comparable to nontransgenic cardiac muscle. EMD-57033 enhanced in vivo systolic function modestly in controls but had a marked effect in transgenic mice, with an almost threefold greater leftward shift of the end-systolic pressure-volume relation (P = 0.0005). These data indicate a targeted efficacy of EMD-57033 in offsetting the contractile defect in TnI-(1-193) mice, and this may have therapeutic implications in models displaying this myofilament defect.
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PMID:Augmented systolic response to the calcium sensitizer EMD-57033 in a transgenic model with troponin I truncation. 1469 78

We report on three patients with acute myocardial ischemia syndrome, without significant coronary artery disease, who were admitted within one year in our hospital and presenting an atypical balloon-like, reversible left ventricular apical wall motion abnormality. The reported cases showed the following similarities: 1) elderly women (age >65 years), 2) triggered by physical or emotional stress, 3) dynamic reversible ST-T segment abnormalities and 4) positive troponin I. During a one year follow-up, all patients remained asymptomatic. As compared to the usual forms of the acute coronary ischemia syndrome, this syndrome showed a unique balloon-like left ventricular (LV) wall motion abnormality at the apex, which did not correlate with the coronary supply of a major coronary vessel. The etiology and pathophysiological basis of this coronary syndrome, which has previously been described in Japan, is still not well understood.
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PMID:[Atypical acute myocardial ischemia syndrome with reversible left ventricular (LV) wall motion abnormalities ("apical ballooning") without significant coronary artery disease]. 1496 82

Several glycosaminoglycans (GAGs) have been demonstrated to protect the ischemic heart against reperfusion injury, in part, by modulating activation of the complement cascade. The present study assessed the cardioprotective effects of sulodexide (KRX-101), a mixture of GAGs composed of 80% low-molecular mass heparin and 20% dermatan sulfate. KRX-101 differs from other GAGs (e.g., heparin) in that it has limited anticoagulant efficacy and can be administered orally. The experimental protocol was designed to determine whether KRX-101 could protect the ischemic myocardium. Anesthetized New Zealand white rabbits underwent 30 min of coronary artery occlusion. Intravenous doses of KRX-101 (0.5 mg/kg, n = 10) or drug diluent (n = 10) were administered at the end of regional ischemia and at each hour of reperfusion. Infarct size, as a percentage of the area at risk, was calculated for both groups. Myocardial infarct size was 31.3 +/- 4.1% in the vehicle- and 17.3 +/- 3.2% in the KRX-101-treated animals (p < 0.05 versus vehicle). Activated partial thromboplastin times determined at baseline (preischemia) and at each hour of reperfusion (n = 4) were not significantly different between vehicle- and KRX-101-treated groups (p = N.S.). Myocardial injury was further assessed by measuring serum levels of cardiac-specific troponin I. KRX-101 administration significantly reduced (p < 0.05) the serum concentration of troponin I during reperfusion. The results suggest that KRX-101 may be an effective adjunctive agent in myocardial revascularization procedures, without the risk of increased bleeding.
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PMID:Sulodexide attenuates myocardial ischemia/reperfusion injury and the deposition of C-reactive protein in areas of infarction without affecting hemostasis. 1536 91

The essential social and academic task of legal medicine is to devote itself to a multidisciplinary approach to problems at the interface of medicine and law. It includes forensic medical activity, in which one of the social concerns is to investigate the fatal mechanisms, survival time and physical activity, especially in traumatic and unexpected sudden death, by means of forensic pathological procedures. To meet the social requirements through reliable interpretation of those issues, systematic practical investigations are necessary, establishing the evidence-based assessment in forensic pathology. For that purpose, an approach based on the pathophysiochemistry of fatal mechanisms may be useful to aid or support pathomorphological observations. Essential markers in forensic pathophysiochemistry are the indicators of systemic responses involving acute phase reaction to traumas, i.e., circulatory, respiratory and central nervous system (CNS) functions. A comprehensive study based on previous investigations is necessary to establish practical markers and to promote their use in routine forensic casework. In the present paper, reviewing the literature, our data in routine casework are summarized. Routine forensic casework at our institute includes biochemistry on automated analyzer systems, immunohistochemistry using commercial kits and molecular biology by means of RT-PCR: 1) blood and urine biochemistry in general, 2) oxymetry, 3) serum and pericardial myocardial markers (creatine kinase MB, troponin I and T), 4) serum pulmonary surfactants (SP-A and -D), 5) other serum markers including C-reactive protein, neopterin, catecholamines, cortisol, erythropoietin and S-100 protein, 6) pericardial natriuretic peptides, 7) urinary myoglobin, 8) immunohistochemistry of a pulmonary surfactant (SP-A) in the lungs, ubiquitin, S-100 protein and ssDNA in the brain, and 9) RT-PCR for a pulmonary surfactant (SP-A) in the lungs, ischemia- and hypoxia-related factors (hypoxia-inducible factor 1A, vascular endothelial growth factor and erythropoietin) in the brain, heart and kidneys. Further accumulation of practical data may be essentially important to establish evidence for medico-legal assessment in individual cases and to renew forensic pathology in response to potential social requirements.
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PMID:[Pathophysiochemistry of acute death: an approach to evidence-based assessment in forensic pathology]. 1552 66

Patients with renal insufficiency can have elevations of serum troponin without suspected clinical coronary ischemia. Although cardiovascular disease is the main cause of death in patients with renal failure, the process of elevation of serum troponin is not well known. Troponin T is more frequently elevated than troponin I in these patients which leads to uncertainty in the clinical interpretation of results. There are studies suggesting that troponin elevations are associated with a higher risk and increased mortality. To explain the process leading to troponin increases in this kind of pathology and to confirm its usefulness in the diagnosis, evolution and prognosis it would be necessary to carry out more clinical studies monitoring troponin and studying the stratification of risk.
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PMID:[Value of troponins in acute coronary syndrome in patients with renal failure]. 1553 31

We studied the role of ischemia-modified albumin (IMA) with standard biomarkers (myoglobin, creatine kinase-MB [CK-MB], troponin I [TnI]) in assessment of 200 patients with suspected myocardial ischemia admitted to the emergency department. Every case was reviewed by a cardiologist. A clinical diagnosis of ischemia was assigned and correlated with biomarker test results. Of the patients, 25 (13.0%) had myocardial ischemia. Receiver operating characteristic curves demonstrated IMA as highly sensitive but somewhat poorly specific for the presence of ischemia (area under curve, 0.63; P = .01). With a cut point of 90 U/mL, the Albumin Cobalt Binding Test had 80% sensitivity and 31% specificity for diagnosing ischemia and a negative predictive value of 92%. IMA was positive in 4 of 5 patients with electrocardiographic (ECG) evidence of ischemia and 16 of 20 patients with coronary ischemia but negative ECG. Among the same patients, the myoglobin-CK-MB-TnI triad had a sensitivity of 57%. The combination of IMA-myoglobin-CK-MB-TnI increased the sensitivity for detecting ischemia to 97%, with a negative predictive value of 92%. IMA is highly sensitive and has a high negative predictive value, which might improve the usefulness of standard biomarkers of myocardial ischemia.
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PMID:Ischemia-modified albumin improves the usefulness of standard cardiac biomarkers for the diagnosis of myocardial ischemia in the emergency department setting. 1627 Apr 50


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