Depression Predicts Elevated Endothelin-1 in Patients With Coronary Artery Disease

Abstract

Objective: 

To examine the relationship of depression severity to circulating endothelin-1 (ET-1), which has previously been linked to plaque rupture and postacute coronary syndrome (ACS) survival. Depression carries an independent two- to four-fold increased risk of early morbidity and mortality after ACS. The pathway(s) linking depression to event-free survival remains to be determined.

Methods: 

Patients with documented history of coronary artery disease (n = 101) provided a resting morning blood sample that was assayed for ET-1, and they completed the Beck Depression Inventory (BDI). ET-1 was treated as a log-transformed continuous variable (logET-1), and as a dichotomous variable using a post-ACS risk threshold previously reported (≥1.16 fmol/mL).

Results: 

BDI score was related to logET-1 in both unadjusted and adjusted models. In addition, unadjusted and adjusted logistic regression models with dichotomous ET-1 revealed that, for each point increase in BDI score, there was approximately a 14% increased likelihood of being at or above ET-1 risk threshold. Secondary logistic regression models demonstrated a >3.5-fold likelihood of being at or above this risk threshold in association with a BDI score of ≥10.

Conclusions: 

Depression symptom severity predicts ET-1 elevation that has previously been linked to post-ACS survival, with the greatest risk of elevation among those patients with worse depression symptoms. This link may identify a vulnerability to triggered ACS and poorer survival associated with depression. Future research should establish whether the observed relationship of depressive symptoms to ET-1 level mediates the link between depression and survival.

ACS = acute coronary syndrome;

BDI = Beck Depression Inventory;

β blocker = beta-blocking medication;

CAD = coronary artery disease;

ET-1 = endothelin-1;

logET-1 = log transformed endothelin-1;

SAS = statistical analysis software;

TNF-α = tumor necrosis factor-α.