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Biomedical subjects

M E Lewis

Publications and source records attributed to M E Lewis.

129 records · Page 8Linked to original sources
PubMedDate not supplied

Coronary artery surgery for ischemic heart failure: risks, benefits, and the importance of assessment of myocardial viability.

Heart failure and left ventricular dysfunction are common and are most often caused by myocardial ischemia/infarction secondary to occlusive coronary artery disease. Although recent refinements in medical therapy have resulted in improved survival, morbidity and mortality remain high in patients with advanced heart failure. Heart transplantation remains an option for selected patients, and implantable left ventricular assist devices may soon provide another treatment strategy for such patients. However, patients with established postischemic heart failure, significant myocardial viability, and coronary artery anatomy amenable to surgical revascularization can derive significant functional and survival benefit after coronary artery surgery, albeit with an increased perioperative risk. We discuss the role of coronary artery surgery in ischemic heart failure and review the evidence for such an approach.

Algorithms↗
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Enhanced lipolysis in normal mice expressing liver-derived human lipoprotein lipase after adenoviral gene transfer.

The authors previously demonstrated that the gene for human lipoprotein lipase (hLPL), an enzyme crucial to the breakdown of triglyceride (TG)-rich dietary fats, corrects the hypertriglyceridemia in lipoprotein lipase (LPL)-deficient knockout mice after adenoviral (Ad)-mediated LPL gene transfer. They have now extended their observations to primary cultured mouse hepatocytes and intact animals of normal LPL genotype, and confirm effective overexpression of hLPL from the liver and a sustained TG-lowering effect in plasma over 60 days. A typical first-generation Ad-vector containing the hLPL cDNA (Ad-LPL) resulted in efficient gene transfer into isolated mouse hepatocytes and significant de novo synthesis of active hLPL protein. In this experiment, 5 x 10(9) viral particles (5 x 10(7) pfu) of either Ad-LPL or an Ad-LacZ control vector were injected into CD1 mice of normal LPL genotype. Hepatic expression of hLPL was confirmed at Day 7 postinjection by in situ hybridization and direct measurement of LPL in the liver. This correlated with a total LPL activity (human + mouse) in postheparin plasma (PHP) of 1020.5 standard deviation [SD] 93.6 mU/mL, versus 479.5 SD 129.7 mU/mL (p < 0.001) in Ad-LacZ controls at Day 7. Respective hLPL activity comprised 49% of the total. Significantly raised levels of hLPL protein mass persisted until Day 60. Corresponding plasma TGs decreased to 39% of Ad-LacZ controls at Day 7, and, despite absent hLPL activity from Day 28 on, serum TGs remained significantly lower in Ad-LPL mice up to Day 42. Fast phase liquid chromatography analysis showed a dramatic depletion in TG-rich lipoproteins, mainly very low density lipoproteins (VLDL) and chylomicron fractions. Therefore, Ad-mediated overexpression of hepatic LPL was found to significantly decrease plasma TG levels unrelated to primary LPL deficiency.

Adenoviridae↗