Publications

OBJECTIVE

To estimate the effect of hormone therapy on risk of stress and urge urinary incontinence.

METHODS

The Heart Estrogen/progestin Replacement Study was a randomized, placebo-controlled, double-blinded trial to evaluate daily oral conjugated estrogen (0.625 mg) plus medroxyprogesterone acetate (2.5 mg) therapy for the prevention of heart disease events in women with established heart disease. The 1,208 participants in Heart Estrogen/progestin Replacement Study who reported no loss of urine in the previous 7 days at baseline are included in this analysis.

RESULTS

During 4.2 years of treatment, 64% of women randomly assigned to hormone therapy compared with 49% of those assigned to placebo reported weekly incontinence (P < .001). The higher risk of incontinence in the hormone group was evident at 4 months, persisted throughout the treatment period, and was independent of the age of the women. The odds ratios for weekly incontinence among women on hormone therapy compared with placebo were 1.5 for urge incontinence (95% confidence interval [CI] 1.2-1.8; P < .001) and 1.7 for stress incontinence (95% CI 1.5-2.1; P < .001). Four years of treatment with hormone therapy caused an excess risk of 12% for weekly urge incontinence and 16% for weekly stress incontinence; the corresponding numbers needed to harm were 8.6 (95% CI 5.8-16.6) and 6.2 (95% CI 4.6-9.4).

CONCLUSION

Estrogen plus progestin therapy increases risk of urge and stress incontinence within 4 months of beginning treatment.

LEVEL OF EVIDENCE

I.

OBJECTIVE

Depressive symptoms are associated with an increased risk of cardiac events in patients with heart disease. Elevated catecholamine levels may contribute to this association, but whether depressive symptoms are associated with catecholamine levels in patients with heart disease is unknown.

METHOD

The authors examined the association between depressive symptoms (defined by a Patient Health Questionnaire score > or =10) and 24-hour urinary norepinephrine, epinephrine, and dopamine excretion levels in 598 subjects with coronary disease.

RESULTS

A total of 106 participants (18%) had depressive symptoms. Participants with depressive symptoms had greater mean norepinephrine excretion levels than those without depressive symptoms (65 microg/day versus 59 mug/day, with adjustment for age, sex, body mass index, smoking, urinary creatinine levels, comorbid illnesses, medication use, and cardiac function). In logistic regression analyses, participants with depressive symptoms were more likely than those without depressive symptoms to have norepinephrine excretion levels in the highest quartile and above the normal range. Depressive symptoms were not associated with dopamine or epinephrine excretion levels.

CONCLUSIONS

In patients with coronary disease, depressive symptoms are associated with elevated norepinephrine excretion levels. Future longitudinal studies are needed to determine whether elevations in norepinephrine contribute to adverse cardiac outcomes in patients with depressive symptoms.

BACKGROUND

To evaluate whether depressive symptoms are independently predictive of mortality and hospitalization among patients with acute myocardial infarction (AMI) complicated by heart failure.

METHODS

The EPHESUS trial enrolled patients with AMI complicated by heart failure. Patients from Canada, the UK, and the United States completed a Medical Outcomes Study-Depression questionnaire at baseline in addition to a comprehensive clinical examination. Cox proportional hazards regression was used to determine the relationship between depressive symptoms and outcomes, including 2-year all-cause mortality and cardiovascular death or hospitalization, adjusting for baseline clinical variables.

RESULTS

Overall, 143 of 634 patients (22.6%) had significant depressive symptoms at baseline (Medical Outcomes Study-Depression score > or = 0.06). Depressed patients had higher 2-year mortality (29% vs 18%; P = .004) and cardiovascular death or hospitalization (42% vs 33%; P = .016). After risk adjustment, depressive symptoms remained significantly associated with mortality (hazard ratio 1.75, 95% CI 1.15-2.68, P = .01) and cardiovascular death or hospitalization (hazard ratio 1.41, 95% CI 1.03-1.93, P = .03). Results were consistent across demographic and clinical subgroups.

CONCLUSIONS

Depression is an independent predictor of all-cause mortality and cardiovascular death or hospitalization after AMI complicated by heart failure. Although many factors may mediate outcomes in patients with AMI, studies are warranted to evaluate whether a depression intervention can improve survival and/or reduce hospitalizations.

While tissue engineering has long been thought to possess enormous potential, conventional applications using biodegradable scaffolds have limited the field's progress, demonstrating a need for new methods. We have previously developed cell sheet engineering using temperature-responsive culture dishes in order to avoid traditional tissue engineering approaches, and their related shortcomings. Using temperature-responsive dishes, cultured cells can be harvested as intact sheets by simple temperature changes, thereby avoiding the use of proteolytic enzymes. Cell sheet engineering therefore allows for tissue regeneration by either direct transplantation of cell sheets to host tissues or the creation of three-dimensional structures via the layering of individual cell sheets. By avoiding the use of any additional materials such as carrier substrates or scaffolds, the complications associated with traditional tissue engineering approaches such as host inflammatory responses to implanted polymer materials, can be avoided. Cell sheet engineering thus presents several significant advantages and can overcome many of the problems that have previously restricted tissue engineering with biodegradable scaffolds.