Disease relevance of Infarction

• Ventricular tachycardia terminated a mean of 10 minutes after injection in six of nine lidocaine-treated patients with acute myocardial infarction but in none of five control patients with infarction (P less than 0.02) [1].
• In contrast, VEGF transcripts were seen in specimens with evidence of acute ischemia or evolving infarction (onset, 24 to 120 hours before surgery) [2].
• CONCLUSIONS: An increase in the level of HIF-1alpha is an early response to myocardial ischemia or infarction [2].
• Hypoxia induces severe right ventricular dilatation and infarction in heme oxygenase-1 null mice [3].
• Overexpression of insulin-like growth factor-1 in mice protects from myocyte death after infarction, attenuating ventricular dilation, wall stress, and cardiac hypertrophy [4].

Psychiatry related information on Infarction

• A patient, SL, who had a profound anterograde amnesia following posterior cerebral artery infarction, performed a measure of complex emotion-based learning (the Iowa Gambling Task) on three separate occasions [5].
• We used antibodies against ApoE and phosphorylated neurofilament (pNF) to investigate the immunohistochemical features of ballooned neurons (BNs) in infarction and in various chronic degenerative disorders, including Pick body disease, corticobasal degeneration/progressive supranuclear palsy, Alzheimer's disease, and frontotemporal dementia [6].
• In contrast, no anti-GQ1b antibody was found in sera from patients with other neurologic diseases which were able to produce transient brain stem disturbance: multiple sclerosis, neuro-Behçet's disease, brain stem infarction, herpes simplex virus encephalitis, and Wernicke's encephalopathy [7].
• We encountered unexpected accumulation of thallium-201 in a patient with thalamic dementia resulting from bithalamic venous infarction induced by arteriovenous fistula in the posterior fossa The site and degree of abnormal accumulation varied between early and delayed thallium-201 SPECT images [8].
• Transient mutism after brain stem infarction (ref. Acta Neurochirurgia 1999, 141: 209-213) [9].

High impact information on Infarction

• Patients with normal ventricles or evidence of infarction in the distant past had no detectable levels of either VEGF mRNA or HIF-1alpha mRNA [2].
• On days 3 to 7 after infarction, 1749 patients were randomly assigned to receive oral trandolapril (876 patients) or placebo (873 patients) [10].
• Thus, the findings in the MILIS population do not support the assertion that digoxin therapy is excessively hazardous after infarction, but the existence of an undetected harmful effect can only be excluded with a randomized study [11].
• The relation between fibrinogen and infarction, and between fibrinogen and stroke, became weaker when blood pressure, serum cholesterol, and smoking habits were taken into account, but was still significant for stroke [12].
• The results indicate that infusion of nitroprusside in the early phase of acute infarction limits complications, possibly by reducing infarct size [13].

Chemical compound and disease context of Infarction

• One hundred sixty-eight patients (47 per cent), who were without major complications, elevation of total serum creatine phosphokinase, or electrocardiographic evidence of transmural infarction during the first day, could be designated "low-risk" patients [14].
• A comparison of digoxin and dobutamine in patients with acute infarction and cardiac failure [15].
• We conclude that diltiazem was effective in preventing early reinfarction and severe angina after non-Q-wave infarction and that it was also safe and generally well tolerated [16].
• In six patients with infarction shortly after these studies and in two in whom the infarction developed during hemodynamic monitoring or during angiography the onset of infarction was indistinguishable from the onset of anginal attacks [17].
• In 417 patients in whom treatment was started within four months of infarction oxprenolol increased the six-year cumulative survival rate from 77 to 95 per cent (P less than 0.001) [18].

Biological context of Infarction

• After ischemia, minocycline inhibits caspase-1 and inducible nitric oxide synthetase upregulation, and reduces infarction [19].
• OVX increased ischemic damage in +/? mice; estrogen reduced tissue injury and enhanced antiapoptotic gene expression (bcl-2 and bfl-1). db/db mice demonstrated more damage, without increased bcl-2 mRNA; bfl-1 expression appeared at 48 hours of recovery associated with infarction [20].
• Genetic polymorphisms of apolipoprotein C-III (apo C-III) and insulin were studied in 48 Caucasian post-myocardial infarction patients [21].
• There were significantly more patients with anterior infarction, congestive heart failure, higher level of maximal creatine kinase-MB isoenzyme, and lower left ventricular ejection fraction in the biphasic group than in the monophasic group [22].
• Long-term therapy with captopril, which we had previously shown to improve left ventricular function and lessen dilatation in the chronic phase of infarction, also had a pronounced effect on prolonging survival in this preparation of chronic infarction [23].

Anatomical context of Infarction

• In support of this hypothesis, NMDA receptor antagonists reduce the volume of infarction produced by occlusion of the middle cerebral artery in vivo and attenuate Ca2+ influx and neuronal death elicited by L-glutamate or NMDA in vitro [24].
• Thus, high-dose methylprednisolone given within 24 h after transmural infarction worsens infarct expansion before collagen is laid down by promoting the slippage of necrotic myocytes [25].
• Total body irradiation followed by transplantation with bone marrow from PKCdelta-null mice donors reduced infarct size and improved neurological outcome in WT mice, whereas marrow transplantation from WT donors increased infarction and worsened neurological scores in PKCdelta-null mice [26].
• Two patients undergoing hemodialysis for 19 and 13 yr, respectively, developed intestinal infarction with extensive amyloid deposits in the muscle layer and blood vessels [27].
• Letter: Infarction of fallopian tube after tubal diathermy [28].

Gene context of Infarction

• Thus, our investigation revealed a previously uncharacterized role for c-kit signaling after infarction by mediating bone marrow-derived NK and angiogenic cell mobilization, which contributes to improved remodeling and cardiac function after MI [29].
• Systemic administration of EPO (5,000 units/kg of body weight, i.p.) after middle-cerebral artery occlusion in rats dramatically reduces the volume of infarction 24 h later, in concert with an almost complete reduction in the number of terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling of neurons within the ischemic penumbra [30].
• Preeclamptic patients with extensive placental infarction exhibited higher plasma PAI activity (24.1 U/mL v 11.6 U/mL) and PAI-1 values (305 ng/mL v 80.9 ng/mL) than preeclamptic patients without extensive placental infarction [31].
• In contrast, PAI-2 levels were reduced in preeclamptic patients with infarction in comparison with those of patients without infarction (141 ng/mL v 212.9 ng/mL) [31].
• Structural analysis 1, 2, and 5 weeks after infarction revealed that infarct healing was virtually abolished in Plg-/- mice, indicating that the plasminogen system is required for the repair process of the heart after infarction [32].

Analytical, diagnostic and therapeutic context of Infarction

• Northern blot analysis showed an increase in beta-myosin heavy chain expression in the hearts of the sedentary infarction group soon after infarction when compared to sham controls [33].
• BACKGROUND: Diltiazem reduces non-fatal reinfarction and refractory ischaemia after non-Q-wave myocardial infarction, an acute coronary syndrome similar to the incomplete infarction that occurs after successful reperfusion [34].
• 135 patients already had ECG evidence of infarction at entry; 72 received atenolol which significantly decreased subsequent enzyme release (atenolol and control means = 121 IU, SE +/- 10 and 177 IU, SE +/- 17; 2p < 0.005) and enhanced R-wave preservation (atenolol and control means = 46% +/- 3 and 36% +/- 3; 2p < 0.02) [35].
• Fourteen of 19 documented infarctions were demonstrated by PCT to have concordantly decreased glucose utilization and perfusion [36].
• Five (25%) of 20 patients in the placebo group and 14 (73.7%) of 19 patients with confirmed infarction in the timolol group developed a left ventricular apical thrombus as detected by two-dimensional echocardiography from 2 to 10 days after inclusion (p less than .005) [37].

References