[Depression comorbid to ischemic heart disease: a psychometric and molecular-genetic study]

V E Golimbet1, B A Volel2, G I Korovaitseva1

  • 1Mental Health Research Center, Moscow.

Insights

Depression linked to ischemic heart disease (IHD) shows distinct apathy without anxiety or guilt. This psychometric profile correlates with specific genetic markers, including serotonin transporter and receptor genes.

Area of Science:

  • Cardiology
  • Psychiatry
  • Genetics

Background:

  • Depression is a common comorbidity in patients with ischemic heart disease (IHD).
  • Differentiating depression etiologies in IHD patients is crucial for targeted treatment.
  • Psychogenic factors can also precipitate depression in individuals with IHD.

Purpose of the Study:

  • To compare the psychometric profiles of depression associated with IHD versus depression caused by other psychogenic factors in IHD patients.
  • To identify the molecular-genetic characteristics associated with depression specifically linked to IHD.

Main Methods:

  • A cohort of 135 patients with depression comorbid to IHD was analyzed.
  • Patients were divided into two groups: depression associated with IHD (n=71) and depression due to other psychogenic factors (n=64).
  • Depressive symptoms were assessed using the HAMD-21 scale.

Main Results:

  • Patients with IHD-associated depression exhibited a unique psychometric profile characterized by significant apathy.
  • This apathy was not accompanied by pronounced hypothymia, guilt, or anxiety, distinguishing them from the other group.
  • A specific molecular-genetic correlate was identified, involving alleles S (5-HTTLPR) and G (A-1438G), and genotype ValVal (Val66Met).

Conclusions:

  • Depression in the context of IHD presents a distinct psychometric phenotype, primarily marked by apathy.
  • This specific depressive profile in IHD patients is associated with a unique combination of genetic variations in serotonin transporter, serotonin receptor type 2A, and brain-derived neurotrophic factor genes.
Abstract

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