Leukocyte ß-adrenergic receptor sensitivity and depression severity in patients with heart failure

Clinical outcomes are worse for patients with heart failure (HF) and elevated depression symptoms. Depression-related sympathoimmune dysregulation may be one mechanism leading to poorer HF prognosis. Sympathetically mediated adrenergic activity is known to regulate immune activity via β-adrenergic receptors (β-ARs). However, studies show conflicting relationships between leukocyte β-AR sensitivity and depression symptoms. The aim of this study was to determine in patients with HF the relationship of leukocyte β-AR sensitivity with two diverse measures of depression, self-report questionnaire versus clinical diagnostic interview.

Patients with HF (N = 73, mean [standard deviation] age = 56.3 [13.0]) completed the Beck Depression Inventory-1A and a modified Structured Clinical Interview for the DSM-IV. Leukocyte β-AR sensitivity was determined from isoproterenol-stimulated cyclic adenosine monophosphate levels; plasma norepinephrine and epinephrine were also assessed.

Patients with major depression determined by Structured Clinical Interview for the DSM-IV had significantly higher β-AR sensitivity than did nondepressed patients (F(6,72) = 9.27, p = .003, η = 0.12). The Beck Depression Inventory-1A revealed a more complex relationship. Minimal, mild, and moderate-to-severe depression symptom groups had significant differences in β-AR sensitivity (F(7,72) = 7.03, p = .002, η = 0.18); mild symptoms were associated with reduced β-AR sensitivity and moderate-to-severe symptoms with higher β-AR sensitivity compared with patients with minimal depressive symptoms.

Clinical depression was associated with elevated β-AR sensitivity in patients with HF. By deconstructing depression measurements, a greater depth of information may be garnered to potentially reveal subtypes of depression symptoms and their relation to β-AR sensitivity.