Recovery of normal ventricular function in patients with dilated cardiomyopathy: predictors of an increasingly prevalent clinical event.

BACKGROUND: This investigation was designed to identify clinical variables associated with recovery of normal ventricular function in patients with dilated cardiomyopathy treated with medical therapy. Recovery of normal ventricular function with medical treatment of patients with dilated cardiomyopathy is observed with increasing frequency. However, the clinical variables associated with such dramatic improvement of ventricular performance are poorly defined. METHODS: Fifty-three patients with dilated cardiomyopathy and reduced ejection fractions who achieved an increase in ejection fraction to > or = 40% with medical therapy were identified during follow-up in a dedicated heart failure clinic. A cohort of patients frequency-matched on baseline ejection fraction who did not recover ventricular systolic function to this magnitude constituted the control group. Clinical variables characterizing the 2 groups were compared by univariable analysis. Variables that significantly differed between the 2 groups were entered in a stepwise logistic regression analysis to identify factors independently associated with recovery of ejection fraction to > or = 40%. RESULTS: In the final logistic regression model, QRS duration, sex, etiology of cardiomyopathy, diabetes, and systolic blood pressure were significantly associated with improvement of ejection fraction to > or = 40%. CONCLUSIONS: Five clinical variables that are independently associated with improvement of left ventricular ejection fraction to normal or near-normal values with medical therapy alone were identified by this modeling process. These variables may be used to discriminate between patients in whom ventricular function will normalize with medical therapy alone and those who will require more aggressive pharmacologic or device therapy.

Depressive symptoms and inflammation among heart failure patients.

BACKGROUND: Psychological depression has been linked to heart failure, both an antecedent to and as a risk factor for poor outcomes among patients with existing heart failure. Elevated levels of proinflammatory cytokines have been proposed as a possible physiological link between the 2 conditions. The objective of this study was to examine the proinflammatory cytokines interleukin (IL)-6, IL-1beta, and tumor necrosis factor-alpha (TNFalpha) in heart failure patients with and without elevated symptoms of depression. METHODS: Thirty-two heart failure patients were recruited from an outpatient heart failure clinic. Depressive symptoms were measured with the Beck Depression Inventory (BDI), and a patient was classified as having elevated symptoms of depression if he/she scored > or = 10. The cognitive-affective subscale score of the BDI, which measures depressed mood independent of physical symptoms, was also examined. RESULTS: In the multiple linear regression models controlling for age, sex, smoking, and antidepressant medication use, there was no relation between BDI score and IL-6 (P = .7612) or IL-1beta (P = .8261). However, there was a statistically significant positive relation between BDI score and TNFalpha (P = .0374). There was also a significant relation between an elevated cognitive-affective score and TNFalpha (P = .0322) but no association with IL-6 (P = .8593) or IL-1beta (P = .3737). CONCLUSIONS: The association between TNFalpha and the cognitive-affective subscale, which eliminates the physical signs and symptoms that are shared by depression and heart failure, demonstrates a depression-specific activation of proinflammatory cytokines that may promote disease progression and mortality in patients with heart failure.