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Infarction patterns

Koennecke H-C, Bernarding J, Braun J et al (2001) Scattered brain infarct pattern on diffusion-wheighted magnetic resonance imaging in patients with acute ischemic stroke. Cerebrovasc Dis 11 157-163... [Pg.222]

A 13-year-old boy taking lithium developed a pseudo-myocardial infarct pattern on the electrocardiogram this may have been an overinterpretation of nonspecific T-wave changes (118). [Pg.132]

Before the era of reperfusion with fibrinolytics or PCI it was relatively easy to predict the final Q-wave infarction pattern according to the acute phase STE-ACS. Aldrich et al. (1988) described a score (see p. 224) for estimation of the extent of myocardium at risk of infarction in the absence of reperfusion therapy. However, currently with the new strategies of treatment, this is impossible because if the treatment is started on time, the infarction may be aborted (Figure 8.2) or at least decreased. [Pg.287]

Figure 7-11. Normal and pathologic patterns of lactate dehydrogenase (LDH) isozymes in human serum. LDH isozymes of serum were separated by electrophoresis and visualized using the coupled reaction scheme shown on the left. (NBT, nitroblue tetrazolium PMS, phenazine methylsulfate). At right is shown the stained electropherogram. Pattern A is serum from a patient with a myocardial infarct B is normal serum and C is serum from a patient with liver disease. Arabic numerals denote specific LDH isozymes. Figure 7-11. Normal and pathologic patterns of lactate dehydrogenase (LDH) isozymes in human serum. LDH isozymes of serum were separated by electrophoresis and visualized using the coupled reaction scheme shown on the left. (NBT, nitroblue tetrazolium PMS, phenazine methylsulfate). At right is shown the stained electropherogram. Pattern A is serum from a patient with a myocardial infarct B is normal serum and C is serum from a patient with liver disease. Arabic numerals denote specific LDH isozymes.
Cardioembolism Cardioembolism accounts for approximately 30% of all stroke and 25-30% of strokes in the young (age <45 years)." AF accounts for a large proportion of these strokes (15-25%). Symptoms may be suggestive, but they are not diagnostic. Repetitive, stereotyped, transient ischemic attacks (TIAs) are unusual in embolic stroke. The classic presentation for cardioembolism is the sudden onset of maximal symptoms. The size of the embolic material determines, in part, the course of the embolic material. Small emboli can cause retinal ischemic or lacunar symptoms. Posterior cerebral artery territory infarcts, in particular, are often due to cardiac embolism. This predilection is not completely consistent across the various cardiac structural abnormalities that predispose to stroke, and may be due to patterns of blood flow associated with specific cardiac pathologies. [Pg.203]

Stanton LW et al. Altered patterns of gene expression in response to myocardial infarction. Circ Res 2000 86 939-945. [Pg.117]

Austin MA, Breslow JL, Hennekens CH, Buring JE, Willett WC, Krauss RM (1988) Low-density lipoprotein subclass patterns and risk of myocardial infarction. J Am Med Assoc 260 1917-1921... [Pg.237]

In this chapter changes in the distribution of gap junctions within the myocardial tissue, alterations of the distribution of special isoforms in the course of heart disease are described. Thus, changes in gap junction pattern for Cx43 and for Cx40 in the border zone of a chronic infarction are pointed out. Changes with growing age and in the course of heart failure are discussed as well. [Pg.73]

Correct answer = D. The CK isoenzyme pattern at admission showed elevated MB isozyme, indicating that the patient had experienced a myocardial infarction in the previous 12 to 24 hours. [Note 48 to 64 hours after an infarction, the MB isozyme would have returned to normal values.] On day 2, 12 hours after the cardioconversions, the MB isozyme had decreased, indicating no further damage to the heart. However, the patient showed an increased MM isozyme after cardo-conversion. This suggests damage to muscle, probably a result of the convulsive muscle contractions caused by repeated cardioconversion. Angina is typically the result of transient spasms in the vasculature of the heart, and would not be expected to lead to tissue death that results in elevation in serum creatine kinase. [Pg.68]

Nwogu Jl, Geenen D, Bean M, Brenner MC, Huang X, Buttrick PM. Inhibition of collagen synthesis with prolyl 4-hydroxylase inhibitor improves left ventricular function and alters the pattern of left ventricular dilatation after myocardial infarction. Circulation 2001 104 2216-2221. [Pg.344]

Crenshaw BS, Granger CB, Birnbaum Y, et al. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-1 (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. Circulation 2000 101(1 ) 27—32. [Pg.602]

An example of an enzyme which has different isoenzyme forms is lactate dehydrogenase (LDH) which catalyzes the reversible conversion of pyruvate into lactate in the presence of the coenzyme NADH (see above). LDH is a tetramer of two different types of subunits, called H and M, which have small differences in amino acid sequence. The two subunits can combine randomly with each other, forming five isoenzymes that have the compositions H4, H3M, H2M2, HM3 and M4. The five isoenzymes can be resolved electrophoretically (see Topic B8). M subunits predominate in skeletal muscle and liver, whereas H subunits predominate in the heart. H4 and H3M isoenzymes are found predominantly in the heart and red blood cells H2M2 is found predominantly in the brain and kidney while HM3 and M4 are found predominantly in the liver and skeletal muscle. Thus, the isoenzyme pattern is characteristic of a particular tissue, a factor which is of immense diagnostic importance in medicine. Myocardial infarction, infectious hepatitis and muscle diseases involve cell death of the affected tissue, with release of the cell contents into the blood. As LDH is a soluble, cytosolic protein it is readily released in these conditions. Under normal circumstances there is little LDH in the blood. Therefore the pattern of LDH isoenzymes in the blood is indicative of the tissue that released the isoenzymes and so can be used to diagnose a condition, such as a myocardial infarction, and to monitor the progress of treatment. [Pg.75]

In our view, the MRI patterns for identifying the ideal candidate for thrombolysis are straightforward. This particularly applies to treatment beyond the 3-h window. A small infarct core identified by DWI and a large perfusion deficit on PI indicate the potential for a major benefit from thrombolysis. This simple, practical mismatch model has, however, been challenged by partial normalisation of... [Pg.28]


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