UMLS:C0151744 - FACTA Search

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Query: UMLS:C0151744 (myocardial ischemia)
31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Troponins are highly sensitive and specific biochemical markers of myocardial injury that are released into the circulation during myocardial ischemia. We describe changes in cardiac troponin I (cTnI) prior to and following clinical evidence of severe myocardial dysfunction in a child with hemolytic uremic syndrome (HUS). A previously healthy, 22-month-old girl presented with typical HUS and stool cultures positive for Escherichia coli O157:H7. She required dialysis, blood and platelet transfusions, and insulin for HUS-related diabetes mellitus. On the 6th hospital day she had sudden circulatory collapse with a blood pressure of 70/40 mmHg and an oxygen saturation of 88%. She responded rapidly to emergency resuscitation but had diminished left ventricular function (ejection fraction 18%). Four days after the acute event an echocardiogram showed normal ventricular size and contractility. She underwent hemodialysis for 22 days, and renal function was normal after 33 days. cTnI levels were measured with a microparticle enzyme immunoassay. cTnI was normal (>0.4 microg/l) 32 h prior to cardiac collapse, mildly increased (2.1 microg/l) 8 h before the cardiac collapse, severely elevated shortly after the cardiac event (43.1 microg/l), and peaked (140.6 microg/l) at 24 h. It then fell gradually and was normal at discharge. These results suggest that measurement of cTnI may be a useful predictor of cardiac involvement in severely affected children with HUS.
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PMID:Troponin I levels in a hemolytic uremic syndrome patient with severe cardiac failure. 1468 41

To determine the prevalence of myocardial ischemia before out-of-hospital cardiac arrest (OOHCA), we determined the prevalence of elevated cardiac troponin-T levels in subjects at the time of OOHCA. Plasma was collected from 63 subjects during resuscitation. Troponin levels were elevated (> or =0.03 ng/ml) in 25 subjects (39.7%; 95% confidence intervals [CI] 29% to 52%). Increasing age was associated with elevated troponin (OR 1.10; 95% CI 1.04 to 1.17). Elevated troponin levels did not reliably predict short-term outcome. Because troponin increases hours after the onset of ischemia, these data reveal that about 40% of OOHCA cases can undergo intervention before collapse.
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PMID:Prevalence of troponin-T elevation during out-of-hospital cardiac arrest. 1556 35

Electrical stimulation of the vagal efferent nerve improves the survival of myocardial infarcted rats. However, the mechanism for this beneficial effect is unclear. We investigated the effect of acetylcholine (ACh) on hypoxia-inducible factor (HIF)-1alpha using rat cardiomyocytes under normoxia and hypoxia. ACh posttranslationally regulated HIF-1alpha and increased its protein level under normoxia. ACh increased Akt phosphorylation, and wortmannin or atropine blocked this effect. Hypoxia-induced caspase-3 activation and mitochondrial membrane potential collapse were prevented by ACh. Dominant-negative HIF-1alpha inhibited the cell protective effect of ACh. In acute myocardial ischemia, vagal nerve stimulation increased HIF-1alpha expression and reduced the infarct size. These results suggest that ACh and vagal stimulation protect cardiomyocytes through the PI3K/Akt/HIF-1alpha pathway.
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PMID:Acetylcholine from vagal stimulation protects cardiomyocytes against ischemia and hypoxia involving additive non-hypoxic induction of HIF-1alpha. 1581 27

Sleep-disordered breathing is very common and is associated with an increased risk of cardiovascular disease, cardiac arrhythmia and stroke. There are two types of sleep apnea: obstructive and central. The objective of this review is to provide a broad perspective of the pathophysiological and clinical aspects of the two types of apnea and to discuss their cardiovascular adverse effects. The diagnosis of sleep apnea syndrome is based on polysomnography, and severity is measured with an apnea-hypopnea index that counts the total number of apneas per hour of sleep. Recent large epidemiologic studies have shown that sleep apnea affects about 16% of men and 5% of women between 30 and 65 years of age. Obstructive sleep apnea is characterized by abnormal collapse of the pharyngeal airway during sleep, snoring, vigorous inspiratory efforts causing frequent arousal, and excessive daytime drowsiness. Central sleep apnea with Cheyne-Stokes respiration is a form of periodic breathing with frequent periods of hyperventilation, and carries a poor prognosis in patients with heart failure. Obstructive apnea can also have substantial health consequences. Although the exact mechanism linking sleep apnea with cardiovascular disease is unknown, there is evidence that obstructive apnea is associated with a group of proinflammatory and prothrombic factors that are also important in the development of atherosclerosis. Nocturnal and daytime sympathetic activity is elevated after sleep apnea. Autonomic abnormalities include an increased resting heart rate, decreased cardiac rhythm activity, and increased blood pressure variability. Obstructive apnea is associated with endothelial dysfunction, increased C-reactive protein and cytokine expression, elevated fibrinogen levels and decreased fibrinolytic activity. Enhanced platelet activity and aggregation, leukocyte adhesion and accumulation of endothelial cells are common in both obstructive apnea and atherosclerosis. Surges in sympathetic activity, blood pressure, ventricular wall tension and afterload adversely affect ventricular function. Many studies have shown that patients with obstructive apnea have an increased incidence of daytime hypertension, and this syndrome is recognized as an independent risk factor for hypertension. Obstructive apnea is associated with myocardial ischemia (silent or symptomatic), acute coronary events, stroke and transient ischemic attacks, cardiac arrhythmia, pulmonary hypertension and heart failure. Central sleep apnea is frequent in severe heart failure. Most heart failure patients with pulmonary congestion chronically hyperventilate because of stimulation of vagal irritant receptors and central and peripheral chemosensitivity. When PaCO2 falls below the threshold required to stimulate breathing, the central drive to respiratory muscles and air inflow ceases and central apnea ensues. Apnea, hypoxia, CO2 retention and arousals provoke elevated sympathetic activity, increased afterload and elevated left ventricular transmural pressure, and promote the progression of heart failure. Tentative relationships have been identified between central apnea and markers of inflammation, oxidative stress and endothelial dysfunction. Recent mid-terms trials showed that nocturnal use of positive airway pressure in patients with the two types of apnea alleviates symptoms, reduces sympathetic activity, improves ventricular function and quality of life, and reduces daytime drowsiness. More studies are needed to understand the mechanisms underlying the relationship between sleep apnea and cardiovascular disease, but clinicians should be aware of this link and should attempt to identify patients with these syndromes.
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PMID:[Sleep apnea syndromes and cardiovascular disease]. 1614 10

Sudden cardiac death accounts for more than half of all cardiovascular deaths in the US, and a large proportion of these deaths are attributed to ischemia-induced ventricular fibrillation. As such, the mechanisms underlying the initiation and maintenance of these lethal rhythms are of significant clinical and scientific interest. In large animal hearts, regional ischemia induces two phases of ventricular arrhythmia. The first phase (1A) occurs between 5 and 7 min after arrest of perfusion. This phase is associated with membrane depolarization, a mild intracellular and extracellular acidification and a small membrane depolarization. A second phase (1B) of ventricular arrhythmia occurs between 20 and 30 minutes after arrest of perfusion. This phase occurs at a time when ischemia-induced K+ and pH changes are relatively stable. The arrhythmia is presumed to relate to the process of cell-to-cell electrical uncoupling because a rapid increase of tissue impedance precedes the onset of the arrhythmia. Of note is that tissue resistance is primarily determined by the conductance properties of the gap junctions accounting for cell-to-cell coupling. Impulse propagation in heart is determined by active and passive membrane properties. An important passive cable property that is modulated by ischemia is intercellular resistance and is determined primarily by gap junctional conductance. As such changes in Impulse propagation during myocardial ischemia are determined by contemporaneous changes in active and passive membrane properties. Cellular K loss, intracellular and extracellular acidosis and membrane depolarization are important factors decreasing excitatory currents, while the collapse of the extracellular compartment and cell-to-cell electrical uncoupling increase the resistance to current flow. The time-course of cellular coupling is closely linked to a number of physiological processes including depletion of ATP, and accumulation of intracellular Ca2+. Hence, interventions such as ischemic preconditioning attenuate the effect of subsequent ischemia, delay the onset of cell-to-cell electrical uncoupling and likewise delay the onset of ischemia-induced arrhythmia.
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PMID:Ischemia-induced arrhythmia: the role of connexins, gap junctions, and attendant changes in impulse propagation. 1622 75

Recovery of the mitochondrial inner membrane potential (DeltaPsi(m)) is a key determinant of postischemic functional recovery of the heart. Mitochondrial ROS-induced ROS release causes the collapse of DeltaPsi(m) and the destabilization of the action potential (AP) through a mechanism involving a mitochondrial inner membrane anion channel (IMAC) modulated by the mitochondrial benzodiazepine receptor (mBzR). Here, we test the hypothesis that this mechanism contributes to spatiotemporal heterogeneity of DeltaPsi(m) during ischemia-reperfusion (IR), thereby promoting abnormal electrical activation and arrhythmias in the whole heart. High-resolution optical AP mapping was performed in perfused guinea pig hearts subjected to 30 minutes of global ischemia followed by reperfusion. Typical electrophysiological responses, including progressive AP shortening followed by membrane inexcitablity in ischemia and ventricular fibrillation upon reperfusion, were observed in control hearts. These responses were reduced or eliminated by treatment with the mBzR antagonist 4'-chlorodiazepam (4'-Cl-DZP), which blocks depolarization of DeltaPsi(m). When applied throughout the IR protocol, 4'-Cl-DZP blunted AP shortening and prevented reperfusion arrhythmias. Inhibition of ventricular fibrillation was also achieved by bolus infusion of 4'-Cl-DZP just before reperfusion. Conversely, treatment with an agonist of the mBzR that promotes DeltaPsi(m) depolarization exacerbated IR-induced electrophysiological changes and failed to prevent arrhythmias. The effects of these compounds were consistent with their actions on IMAC and DeltaPsi(m). These findings directly link instability of DeltaPsi(m) to the heterogeneous electrophysiological substrate of the postischemic heart and highlight the mitochondrial membrane as a new therapeutic target for arrhythmia prevention in ischemic heart disease.
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PMID:The mitochondrial origin of postischemic arrhythmias. 1628 48

According to guidelines established by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists, life-threatening hemodynamic disturbances are classified as a category I indication for the intraoperative use of transesophageal echocardiography (TEE). However, the usefulness of TEE during intraoperative cardiac arrest and its impact on patient management have not been rigorously investigated. Using our departmental TEE database, we identified a population of 22 patients who underwent noncardiac surgical procedures and experienced unexpected intraoperative hemodynamic collapse requiring the initiation of Advanced Cardiac Life Support procedures between the time of induction of general anesthesia and the termination of the surgical procedure. Results of TEE examinations, patient records, detailed operative records, and outcome of patients were reviewed for the utility of TEE to diagnose the etiology of the hemodynamic collapse. Furthermore, the impact on subsequent patient management was evaluated. A primary suspected diagnosis of the underlying pathological process was established in 19 of 22 patients with TEE, including 9 with thromboembolic events, 6 with acute myocardial ischemia, 2 with hypovolemia, and 2 patients with pericardial tamponade. A definitive diagnosis could not be made in 3 patients with TEE. In 18 patients, TEE guided specific management beyond implementation of Advanced Cardiac Life Support protocols, including the addition of surgical procedures in 12 patients. Fourteen patients survived to leave the operating room, and 7 of these patients were eventually discharged from the hospital. Thus, TEE may provide additional diagnostic information in patients with intraoperative cardiac arrest and may directly guide specific, potentially life-saving therapy.
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PMID:The usefulness of transesophageal echocardiography during intraoperative cardiac arrest in noncardiac surgery. 1671 2

Although parthenolide was reported to reduce cardiovascular damage in endotoxic shock and have beneficial effects in myocardial ischemia, its actions on cardiac myocytes have not been reported. Because parthenolide possesses an alpha-methylene-gamma-lactone ring and epoxide residue, we hypothesized that it would induce oxidative stress in cardiac myocytes. Superoxide production and sources, viability, glutathione levels, and mitochondrial membrane potential were studied in neonatal rat ventricular myocytes treated with parthenolide. Parthenolide, dose dependently, induced oxidase activity as assessed by superoxide generation in cell lysates. Superoxide formation was increased more than 4-fold with 50 microM parthenolide. At concentrations >5 microM, parthenolide decreased cell viability in a dose-and time-dependent manner, and activated the stress MAP kinases JNK and p38. Over 6 h, parthenolide at concentrations >5 microM markedly depleted intracellular glutathione and led to collapse of the mitochondrial membrane potential. At lower parthenolide concentrations (<5 microM) the source of superoxide was mitochondria; at higher concentrations (>5 microM) the primary source was NADPH oxidase. We conclude that parthenolide causes oxidative stress in cardiac myocytes by inducing superoxide formation by mitochondrial and NADPH oxidase in a dose-dependent manner. Parthenolide may be a useful tool for studying the roles of oxidative stress and mitochondrial dysfunction in the pathogenesis of cardiac hypertrophy and failure.
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PMID:Parthenolide induces a distinct pattern of oxidative stress in cardiac myocytes. 1727 79

Death due to hemorrhage from ruptured peripheral varicose veins is an uncommon event. A review of the files of Forensic Science SA (FSSA) in Adelaide, South Australia, was undertaken over a 10-year period from January 1996 to December 2005 for such cases. A total of 8 cases were found out of a total of 10,686, representing <0.01% of autopsy cases. The male to female ratio was 1:3, with an age range of 58-84 years (mean = 78 years). The victims were all located at their home addresses, where they had been alone at the time of their deaths. Scene investigations revealed considerable blood loss, with pooling around the victims' bodies, and also in other parts of the house, particularly the bathroom/toilet areas. Four ulcers were of an acute perforative type and 2 were of a chronic ulcerative type. In 2 cases, bleeding followed trauma. Toxicologic evaluation was performed in only 3 of the cases, revealing blood alcohol levels of 0.06% and 0.14% in 2 cases, respectively. A further victim had been prescribed anticoagulant drugs for an unrelated condition. Additional findings of significance were ischemic heart disease in 3 cases and deep venous thrombosis of the calf veins on the side of the fatal hemorrhage in another case (with no evidence of pulmonary thromboembolism). One victim had acute gastric erosions, suggesting that hypothermia following collapse played a role in the terminal event. Autopsy evaluation of such cases should include careful layer dissection of the area of hemorrhage to confirm the presence of the ruptured varix and to enable directed histologic sampling.
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PMID:The incidence and characteristic features of fatal hemorrhage due to ruptured varicose veins: a 10-year autopsy study. 1804 15

Sickle cell trait, which affects approximately 8% of American blacks, is generally felt to be a benign condition. Exercise-related collapse in persons with sickle cell trait is a rare but serious complication. It occurs most often in military recruits and deconditioned athletes undergoing intense physical training, but can also occur in other situations in which an individual exerts himself beyond his limits of endurance. Local hypoxia causes intravascular sickling, in turn causing vascular occlusion and organ and tissue damage. This can result in rhabdomyolysis, myocardial ischemia, arrhythmias and sudden death. Risk factors include poor physical conditioning, inadequate hydration, excess heat and/or altitude, heat-retaining clothing and febrile illness. Seven cases are presented, and the implications of the diagnosis of sickle trait-associated collapse and sudden death are discussed.
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PMID:Sudden death and sickle cell trait: medicolegal considerations and implications. 1946 21

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