Fibrous tissue appears as echo dense areas on conventional ultrasound images; however, the determinants of such echo brightness have not been assessed. We demonstrated previously, using 600-MHz ultrasound images, that collagen fiber morphology determines echo brightness. In the current study, we tested the hypothesis that collagen fiber morphology also determines echogenicity of myocardial scar at the lower transducer frequencies used in conventional ultrasound. We examined both the infarcted and noninfarcted regions of rat hearts 1 and 3 weeks after permanent coronary artery occlusion. Ultrasound images obtained from excised hearts were digitized to quantify echocardiographic brightness. The hearts were then sectioned, stained with picrosirius red, and examined with polarized light microscopy. We found that myocardial scar tissue appeared either hyperechoic or normoechoic depending on collagen fiber morphology. Specifically, the hyperechoic areas corresponded to the 3-week-old infarcted regions containing thick collagen fibers that appeared predominantly orange when viewed with polarized light. In contrast, normoechoic areas corresponded to the 1-week-old infarcted regions containing thin collagen fibers that appeared predominantly green and also to noninfarcted myocardium. We conclude that the echogenicity of tissue early after infarction is similar to that found in normal, noninfarcted myocardium, thus compromising the ability of echocardiography to distinguish between these two states based on echotexture. (ECHOCARDIOGRAPHY, Volume 23, February 2006) collagen, echocardiography, infarct, myocardium, scar
contributed to the smaller difference in peak VO 2 between diabetics and nondiabetics in the Guazzi et al. (5) study. Glycosylated hemoglobin was Ͻ7% in every one of the Guazzi et al. (5) patients, whereas it averaged 7.5% in our patients. Insulin therapy improves peak VO 2 in patients with diabetes and CHF (6,7). Diabetes is associated with cardiac, vascular, metabolic, and skeletal muscle alterations that all tend to reduce peak VO 2 (8). High-energy phosphate metabolism is impaired in skeletal muscles from patients with diabetes in the absence of CAD or LV dysfunction (2). Phosphocreatinine loss, pH decline, and deoxygenation occur sooner in exercising skeletal muscles of diabetics than in controls. Alterations in energy metabolism contribute to reduce peak aerobic capacity in CHF (9,10). The coexistence of diabetes and CHF may further alter skeletal muscle energy metabolism and reduce peak aerobic capacity. A major limitation of our study is the absence of longitudinal data with tighter diabetes control.In summary, diabetes negatively impacts on and is an independent determinant of peak aerobic capacity in patients with CHF. Diabetes needs to be taken into consideration when evaluating functional capacity in patients with CHF.
Amit S. Tibb, MD
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