Effects of beta blockade on physiologic regulation, depressive symptoms, and heart failure severity

Over 5 million Americans are diagnosed with chronic heart failure (CHF) each year. Despite advances in CHF treatment, mortality rates continue to rise. Compared to the general population, the coexistence of depression is high in persons with CHF. Depression is a strong predictor of morbidity and mortality in persons with CHF and is associated with higher health care costs and utilization of medical resources. Because beta (β)-blockers inhibit sympathetic nervous system (SNS) pathways, and SNS activation stimulates the expression of proinflammatory cytokines that contribute to depressive symptoms, 13-blockers may inhibit cytokine-induced depressive symptoms in persons with CHF. The purpose of this study was to explore the relationship between β-blocker medication therapy and, autonomic nervous system activity via heart rate variability (HRV), levels of proinflammatory cytokines, depressive symptoms, and CHF severity in persons with CHF. A convenience sample of eight subjects was enrolled in this prospective, descriptive study. Measures of HRV; plasma levels of tumor necrosis factor-alpha, interleuken-6, and brain natriuretic peptide; Beck Depression Inventory (BDI); and CHF severity, measured by the New York Heart Association HF classification and the Specific Activity Scale were evaluated prior to β-blocker medication optimization and then again after 12 weeks of β-blocker titration. Descriptive statistics demonstrated a mean BDI score of 11 indicating mild to moderate depressive symptoms within this sample. Wilcoxon\u27s matched-pairs signed-ranks test was used to evaluate differences in the variables pre- and post-optimal β-blocker medication titration. Trends indicating a possible improvement in the time domain measures of HRV were identified suggesting an increase in parasympathetic nervous system activity. A statistically significant decrease in depressive symptoms was found indicating improvements in depressive symptoms 12 weeks post β-blocker medication titration. No other significant findings were identified. Findings corroborate the presence of depressive symptoms in persons with CHF and provide preliminary support for national guidelines for the use of β-blocker medications in this population, while further dispelling the myth of β-blocker induced depressive symptoms. Replication of this study is warranted to fully explore the possible pathophysiological links between the ANS, proinflammatory cytokines, CHF severity, and depressive symptoms in the CHF population