Architectural and dynamic features are important in breast MR imaging interpretation. Multivariate models involving feature assessment have a diagnostic accuracy superior to that of qualitative characterization of the dynamic enhancement pattern.

MR imaging findings are a stronger predictor of pathologic response to NACT than clinical assessment, with the greatest advantage observed with the use of volumetric measurement of tumor response early in treatment.

AMMOGRAPHY IS THE PRImary imaging modality used to detect clinically occult breast cancer. However, mammography has limitations in both sensitivity and specificity that have led to exploration of other imaging techniques. Magnetic resonance imaging (MRI) has been evaluated for breast imaging because of its value for assessing soft tissues of the body. Breast MRI is performed before and after injection of a gadoliniumbased contrast agent. 1,2 Additional lesions seen by MRI that are not visible on the mammogram have been reported to be present in between 27% and 37% of patients. 3,4 The use of MRI to evaluate women with mammographically or clinically suspicious breast lesions who are undergoing biopsy has shown high potential, with the reported sensitivities of MRI for breast cancer from larger single center studies ranging from 88% to 95%. 5-12 Thus, there has been considerable enthusiasm for breast MRI and use of the procedure for Medicare patients increased almost 3-fold between 2001 (3440 examinations) and 2003 (10 115 examinations). 13 However, the reported specificity of MRI is variable, ranging from 30% to For editorial comment see p 2779.

Cardiac muscle adapts well to changes in loading conditions. For example, left ventricular (LV) hypertrophy may be induced physiologically (via exercise training) or pathologically (via hypertension or valvular heart disease). If hypertension is treated, LV hypertrophy regresses, suggesting a sensitivity to LV work. However, whether physical inactivity in nonathletic populations causes adaptive changes in LV mass or even frank atrophy is not clear. We exposed previously sedentary men to 6 (n = 5) and 12 (n = 3) wk of horizontal bed rest. LV and right ventricular (RV) mass and end-diastolic volume were measured using cine magnetic resonance imaging (MRI) at 2, 6, and 12 wk of bed rest; five healthy men were also studied before and after at least 6 wk of routine daily activities as controls. In addition, four astronauts were exposed to the complete elimination of hydrostatic gradients during a spaceflight of 10 days. During bed rest, LV mass decreased by 8.0 +/- 2.2% (P = 0.005) after 6 wk with an additional atrophy of 7.6 +/- 2.3% in the subjects who remained in bed for 12 wk; there was no change in LV mass for the control subjects (153.0 +/- 12.2 vs. 153.4 +/- 12.1 g, P = 0.81). Mean wall thickness decreased (4 +/- 2.5%, P = 0.01) after 6 wk of bed rest associated with the decrease in LV mass, suggesting a physiological remodeling with respect to altered load. LV end-diastolic volume decreased by 14 +/- 1.7% (P = 0.002) after 2 wk of bed rest and changed minimally thereafter. After 6 wk of bed rest, RV free wall mass decreased by 10 +/- 2.7% (P = 0.06) and RV end-diastolic volume by 16 +/- 7.9% (P = 0.06). After spaceflight, LV mass decreased by 12 +/- 6.9% (P = 0.07). In conclusion, cardiac atrophy occurs during prolonged (6 wk) horizontal bed rest and may also occur after short-term spaceflight. We suggest that cardiac atrophy is due to a physiological adaptation to reduced myocardial load and work in real or simulated microgravity and demonstrates the plasticity of cardiac muscle under different loading conditions.