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Ischemic Episodes (ischemic + episode)

Distribution by Scientific Domains

Medical Sciences	75%
Life Sciences	25%

Selected Abstracts

POINT: A Prescription to Decrease Left Ventricular Function

PREVENTIVE CARDIOLOGY, Issue 4 2009
Myrvin H. Ellestad MD
The Courage Trial, published in 2007, has significantly reduced the incidence of treating stable angina with angioplasty. The investigators randomized 2297 patients with documented cardiac ischemia to conservative or invasive therapy and concluded that there was no difference in major events during a follow-up of 2.5 to 7 years and that the urge to open the narrowed artery was unjustified. Over the years it has been well documented by myocardial biopsy that repeated ischemic episodes result in replacement of myocardial cells by fibrous tissue, loss of mitochondria, and deterioration of left ventricular function. Ischemic episodes often occur in the absence of angina so that it is impossible to determine whether the therapy is reducing the magnitude or duration of the process. Also, in their study, 32% of the conservatively treated patients crossed over to invasive. The evidence indicated that conservative treatment may result in a progressive decrease in left ventricular function. [source]

Ischemia-induced modifications in hippocampal CA1 stratum radiatum excitatory synapses

HIPPOCAMPUS, Issue 10 2006
Tatiana Kovalenko
Abstract Relatively mild ischemic episode can initiate a chain of events resulting in delayed cell death and significant lesions in the affected brain regions. We studied early synaptic modifications after brief ischemia modeled in rats by transient vessels' occlusion in vivo or oxygen,glucose deprivation in vitro and resulting in delayed death of hippocampal CA1 pyramidal cells. Electron microscopic analysis of excitatory spine synapses in CA1 stratum radiatum revealed a rapid increase of the postsynaptic density (PSD) thickness and length, as well as formation of concave synapses with perforated PSD during the first 24 h after ischemic episode, followed at the long term by degeneration of 80% of synaptic contacts. In presynaptic terminals, ischemia induced a depletion of synaptic vesicles and changes in their spatial arrangement: they became more distant from active zones and had larger intervesicle spacing compared to controls. These rapid structural synaptic changes could be implicated in the mechanisms of cell death or adaptive plasticity. Comparison of the in vivo and in vitro model systems used in the study demonstrated a general similarity of these early morphological changes, confirming the validity of the in vitro model for studying synaptic structural plasticity. © 2006 Wiley-Liss, Inc. [source]

Heterogeneous Regional Endocardial Repolarization is Associated with Increased Risk for Ischemia-Dependent Ventricular Fibrillation after Myocardial Infarction

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2003
Michael H. Swann M.SC.
Introduction: The aim of this study was to investigate whether the characteristics of endocardial ventricular repolarization are associated with differential risk for sudden death. Prolonged surface QT interval is associated with increased arrhythmic risk after myocardial infarction (MI), but the underlying mechanism of QT prolongation and its relation to lethal arrhythmias are unclear. Methods and Results: Ventricular fibrillation (VF) risk was assessed in 12 dogs 1 month after anterior MI during an exercise test coupled with brief circumflex coronary occlusion. Susceptible dogs (n = 5) developed VF during the brief ischemic episode, whereas resistant dogs did not (n = 7). Surface QT interval was measured at rest. Endocardial electroanatomic catheter maps of left ventricular repolarization were obtained in four unique regions identified by echocardiography and compared between groups. Compared to resistant dogs, susceptible dogs were characterized by prolonged surface QT intervals (240 ± 10 msec vs 222 ± 7 msec, P = 0.04). In addition, they had lower baroreflex sensitivity (9.7 ± 1.5 msec/mmHg vs 28 ± 9.8 msec/mmHg, P < 0.01) and a tachycardic response to acute ischemia suggesting higher propensity for stronger sympathetic reflexes. Surface QT interval prolongation in susceptible dogs was due to a marked heterogeneity of endocardial left ventricular repolarization (239 ± 42 msec, basal anterior wall vs 197 ± 35, lateral wall; P < 0.001). Resistant animals had no regional differences in endocardial repolarization. Conclusion: Sympathetic activation following MI not only produces adverse structural remodeling but also contributes to adverse electrophysiologic remodeling resulting in heterogeneous ventricular repolarization and in a myocardial substrate conducive to lethal reentrant arrhythmias. (J Cardiovasc Electrophysiol, Vol. 14, pp. 873-879, August 2003) [source]

Brief, repeated, oxygen-glucose deprivation episodes protect neurotransmission from a longer ischemic episode in the in vitro hippocampus: role of adenosine receptors

BRITISH JOURNAL OF PHARMACOLOGY, Issue 2 2003
Anna Maria Pugliese
Ischemic preconditioning in the brain consists of reducing the sensitivity of neuronal tissue to further, more severe, ischemic insults. We recorded field epsps (fepsps) extracellularly from hippocampal slices to develop a model of in vitro ischemic preconditioning and to evaluate the role of A1, A2A and A3 adenosine receptors in this phenomenon. The application of an ischemic insult, obtained by glucose and oxygen deprivation for 7 min, produced an irreversible depression of synaptic transmission. Ischemic preconditioning was induced by four ischemic insults (2 min each) separated by 13 min of normoxic conditions. After 30 min, an ischemic insult of 7 min was applied. This protocol substantially protected the tissue from the irreversible depression of synaptic activity. The selective adenosine A1 receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 100 nM), completely prevented the protective effect of preconditioning. The selective adenosine A2A receptor antagonist 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3- a][1,3,5]triazin-5-ylamino]ethyl)phenol (ZM 241385, 100 nM) did not modify the magnitude of fepsp recovery compared to control slices. The selective A3 adenosine receptor antagonists, 3-propyl-6-ethyl-5[ethyl(thio)carbonyl]-2-phenyl-4-propyl-3-pyridinecarboxylate (MRS 1523, 100 nM) significantly improved the recovery of fepsps after 7 min of ischemia. Our results show that in vitro ischemic preconditioning allows CA1 hippocampal neurons to become resistant to prolonged exposure to ischemia. Adenosine, by stimulating A1 receptors, plays a crucial role in eliciting the cell mechanisms underlying preconditioning; A2A receptors are not involved in this phenomenon, whereas A3 receptor activation is harmful to ischemic preconditioning. British Journal of Pharmacology (2003) 140, 305,314. doi:10.1038/sj.bjp.0705442 [source]

POINT: A Prescription to Decrease Left Ventricular Function

Circulating endothelial microparticles as a marker of cerebrovascular disease,

ANNALS OF NEUROLOGY, Issue 2 2009
Keun-Hwa Jung MD
Objective Circulating endothelial microparticles (EMPs) have been reported to reflect vascular damage. Detailed profiling of these blood endothelial markers may adumbrate the pathogenesis of stroke or enable determination of the risk for stroke. We investigated EMP profiles in patients at risk for cerebrovascular disease. Methods We prospectively examined 348 consecutive patients: 73 patients with acute stroke and 275 patients with vascular risk factors but no stroke events. We quantified various types of EMPs by flow cytometry using CD31, CD42b, annexin V (AV), and CD62E antibodies in the peripheral blood of patients. This method allowed fractionation of CD31+/CD42b,, CD31+/AV+, and CD62E+ EMPs. Clinical and laboratory factors associated with EMPs were assessed. Results Recent ischemic episodes were found to be more strongly associated with greater CD62E+ EMP levels than with levels of other phenotypes. Increased National Institutes of Health Stroke Scale scores and infarct volumes in acute stroke patients were significantly associated with greater CD62E+ EMP levels. In the risk factor group, patients with extracranial arterial stenosis had greater CD62E+ EMP levels, whereas those with intracranial arterial stenosis had greater CD31+/CD42b, and CD31+/AV+ EMP levels. The ratio of CD62E+ to CD31+/CD42b, or CD31+/AV+ EMP level significantly discriminated extracranial and intracranial arterial stenosis. Interpretation Circulating EMP phenotypic profiles reflect distinct phenotypes of cerebrovascular disease and are markers of vascular pathology and an increased risk for ischemic stroke. Ann Neurol 2009;66:191,199 [source]

White Blood Cell Count and the Occurrence of Silent Ischemia after Myocardial Infarction

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2003
gorzata Kurpesa
Background: Inflammation plays a role in the pathogenesis of atherosclerosis. Attempts are made to use markers of inflammation as prognostic factors in coronary artery disease and acute coronary syndromes. The correlation between inflammation and silent postinfarction ischemia is unknown. Methods: The study population consists of 104 asymptomatic patients who had uncomplicated Q-wave myocardial infarction within 6 months prior to the enrollment. After the white blood cell (WBC) count was assessed, the population was divided into two groups: group I comprising 48 patients with WBC , 7.0 × 103/,l and group II comprising 56 patients with WBC > 7.0 × 103/,l. Twenty-four-hour Holter monitoring was performed to detect the presence of silent ischemia. Results: Eighty-eight silent ischemic episodes were recorded. Ischemia on Holter monitoring was detected in 47 patients (84%) from group II and in five patients (9%) in group I (P < 0.01). We have found a significant positive correlation between WBC count and the number of ischemic episodes (r = 0.25), their maximal amplitude (r = 0.39), duration (r = 0.34), and total ischemic burden (r = 0.36). In multivariate analysis leucocytosis proved to be the only parameter independently correlated with the presence of silent ischemia. Conclusion: Postinfarction asymptomatic patients with increased WBC count are more likely to have residual ischemia. [source]

Observer Variability and Optimal Criteria of Transient Ischemia During ST Monitoring with Continuous 12-lead ECG

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2002
Ph.D., Tomas Jernberg M.D.
Background: ST monitoring with continuous 12-lead ECG is a well-established method in patients with unstable coronary artery disease (CAD). However, the method lacks documentation on optimal criteria for episodes of transient ischemia and on observer variability. Methods: Observer variability was evaluated in 24-hour recordings from 100 patients with unstable CAD with monitoring in the coronary care unit. Influence on ST changes by variations in body position were evaluated by monitoring 50 patients in different body positions. Different criteria of transient ischemia and their predictive importance were evaluated in 630 patients with unstable CAD who underwent 12 hours of monitoring and thereafter were followed for 1 to 13 months. Two sets of criteria were tested: (1) ST deviation , 0.1 mV for at least 1 minute, and (2) ST depression , 0.05 mV or elevation , 0.1 mV for at least 1 minute. Results: When the first set of criteria were used, the interobserver agreement was good (kappa = 0.72) and 8 (16%) had significant ST changes in at least one body position. Out of 100 patients with symptoms suggestive of unstable CAD and such ischemia, 24 (24%) had a cardiac event during follow-up. When the second set of criteria were used, the interobserver agreement was poor (kappa = 0.32) and 21(42%) had significant ST changes in at least one body position. Patients fulfilling the second but not the first set of criteria did not have a higher risk of cardiac event than those without transient ischemia (5.3 vs 4.3%). Conclusions: During 12-lead ECG monitoring, transient ischemic episodes should be defined as ST deviations , 0.1 mV for at least 1 minute, based on a low observer variability, minor problems with postural ST changes and an important predictive value. A.N.E. 2002;7(3):181,190 [source]

Acute effect of antidiabetic 1,4-dihydropyridine compound cerebrocrast on cardiac function and glucose metabolism in the isolated, perfused normal rat heart

CELL BIOCHEMISTRY AND FUNCTION, Issue 2 2008
Janina Briede
Abstract Diabetes mellitus (DM) is an important cardiovascular risk factor and is associated with abnormalities in endothelial and vascular smooth muscle cell function, evoked by chronic hyperglycemia and hyperlipidemia. Chronic insulin deficiency or resistance is marked by decreases in the intensity of glucose transport, glucose phosphorylation, and glucose oxidation, plus decreases in ATP levels in cardiac myocytes. It is important to search for new agents that promote glucose consumption in the heart and partially inhibit extensive fatty acid beta-oxidation observed in diabetic, ischemia. When the oxygen supply for myocardium is decreased, the heart accumulates potentially toxic intermediates of fatty acid beta-oxidation, that is, long-chain acylcarnitine and long-chain acyl-CoA metabolites. Exogenous glucose and heart glycogen become an important compensatory source of energy. Therefore we studied the effect of the antidiabetic 1,4-dihydropyridine compound cerebrocrast at concentrations from 10,10,M to 10,7,M on isolated rat hearts using the method of Langendorff, on physiological parameters and energy metabolism. Cerebrocrast at concentrations from 10,10,M to 10,7,M has a negative inotropic effect on the rat heart. It inhibits L -type Ca2+channels thereby diminishing the cellular Ca2+ supply, reducing contractile activity, and oxygen consumption, that normally favors enhanced glucose uptake, metabolism, and production of high-energy phosphates (ATP content) in myocardium. Cerebrocrast decreases heart rate and left ventricular (LV) systolic pressure; at concentrations of 10,10,M and 10,9,M it evokes short-term vasodilatation of coronary arteries. Increase of ATP content in the myocytes induced by cerebrocrast has a ubiquitous role. It can preserve the integrity of the cell plasma membranes, maintain normal cellular function, and inhibit release of lactate dehydrogenase (LDH) from cells that is associated with diabetes and heart ischemia. Administration of cerebrocrast together with insulin shows that both compounds only slightly enhance glucose uptake in myocardium, but significantly normalize the rate of contraction and relaxation (,±,dp/dt). The effect of insulin on coronary flow is more pronounced by administration of insulin together with cerebrocrast at a concentration of 10,7,M. Cerebrocrast may promote a shift of glucose consumption from aerobic to anerobic conditions (through the negative inotropic properties), and may be very significant in prevention of cardiac ischemic episodes. Copyright © 2007 John Wiley & Sons, Ltd. [source]

Percutaneous Intervention of Superior Mesenteric Artery Stenosis in Elderly Patients

CLINICAL CARDIOLOGY, Issue 5 2009
Neelima Penugonda MD
This review article focuses on stent placement in mesenteric arteries in older patients with an increasingly common diagnosis of chronic mesenteric ischemia (CMI). We reviewed the articles that focused on the treatment of this gastrointestinal disorder by stenting/open surgical revascularization to avoid further ischemic episodes and bowel infarction and necrosis. The advantages of stent placement in mesenteric arteries are discussed in comparison to open surgical revascularization. In summary, the low morbidity and high technical success rate of catheter-based techniques have made this approach the first line of therapy for CMI due to superior mesenteric artery stenosis for many elderly patients especially high-risk operative candidates. Copyright © 2009 Wiley Periodicals, Inc. [source]