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Heart failure echocardiogram

Fig. 7. Displacement of endogenous PI3K from 3-ARK prevents the development of heart failure after pressure overload. (A) Representative echocardiograms in conscious wild-type (WT) and transgenic mice overexpressing a catalytically inactive mutant of PI3Kyafter4, 8, and 12 wk of pressure overload. (B) (1-ARK-associated PI3K activity in membrane fractions from hearts of WT and transgenic mice overexpressing a catalytically inactive mutant of PI3Ky. (From ref. 109, with permission.)... Fig. 7. Displacement of endogenous PI3K from 3-ARK prevents the development of heart failure after pressure overload. (A) Representative echocardiograms in conscious wild-type (WT) and transgenic mice overexpressing a catalytically inactive mutant of PI3Kyafter4, 8, and 12 wk of pressure overload. (B) (1-ARK-associated PI3K activity in membrane fractions from hearts of WT and transgenic mice overexpressing a catalytically inactive mutant of PI3Ky. (From ref. 109, with permission.)...
Although the history, physical examination, and laboratory tests can provide important clues to the underlying cause of heart failure, imaging is required to identify any structural abnormality of the heart. In most patients, an echocardiogram is used to detect any valvular, pericardial, or myocardial abnormalities. The echocardiogram also can determine the presence of systolic and/or diastolic dysfunction and the left ventricular ejection fraction (LVEE). [Pg.228]

A case of frastuzumab-associated cardiomyopathy presenting as an acute coronary syndrome was reported in a 58-year-old man with metastatic adenocarcinoma who developed chest tightness and shortness of breath immediately following his third trastuzumab infusion. An echocardiogram demonstrated new anterior and anteroseptal wall motion abnormalities and an ejection fraction of 40%. Trastuzumab was witiidrawn but lOweeks later left ventricular dys-fxmction persisted with ejection fractions of 40% apparently demonstrating irreversible cardiac damage despite withdrawal of the drug, minimal epicardial disease and standard heart failure treatmenf [213 ]. [Pg.583]

A 64-year-old woman with systemic lupus erythematosus took chloroquine for 7 years (cumulative dose 1000 g). She developed sjmcope, and the electrocardiogram showed complete heart block a permanent pacemaker was inserted. The next year she presented with biventricular cardiac failure, skin hyperpigmentation, proximal muscle weakness, and chloroquine retinopathy. Coronary angiography was normal. An echocardiogram showed a restrictive cardiomyopathy. A skeletal muscle biopsy was characteristic of chloroquine myopathy. Chloroquine was withdrawn and she improved rapidly with diuretic therapy. [Pg.723]


See other pages where Heart failure echocardiogram is mentioned: [Pg.300]    [Pg.202]    [Pg.60]    [Pg.341]    [Pg.889]    [Pg.200]    [Pg.82]    [Pg.591]    [Pg.12]   
See also in sourсe #XX -- [ Pg.228 , Pg.359 ]




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Echocardiogram

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