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The Influence of Current Depressive Symptomology on Cerebrovascular Function in Young Adults with Major Depressive Disorder
Author(s) -
Darling Ashley,
Akins John,
Richey Rauchelle,
Saunders Erika,
Brothers R. Matthew,
Greaney Jody
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2021.35.s1.03499
Subject(s) - major depressive disorder , transcranial doppler , cardiology , medicine , cerebral blood flow , hypercapnia , middle cerebral artery , blood pressure , cerebral autoregulation , arterial stiffness , photoplethysmogram , anesthesia , autoregulation , ischemia , acidosis , filter (signal processing) , amygdala , computer science , computer vision
Major depressive disorder (MDD), characterized by persistently depressed mood and/or anhedonia, is episodic in nature and highly recurrent. Importantly, MDD is directly linked to an increased risk for the development of cerebrovascular disease and neurocognitive deficits. In older adults with depression, cerebral vasodilatory responsiveness—an index of cerebrovascular health—is blunted, likely mechanistically contributing to depression‐cerebrovascular disease comorbidity. Previous research has demonstrated peripheral vascular dysfunction in young adults with MDD that is graded in relation to symptom severity. However, whether active depressive symptomology influences cerebrovascular function in young adults with MDD has not been examined. We tested the hypothesis that adults with symptomatic MDD (sMDD) would have blunted cerebral vasodilatory reactivity to a hypercapnic stimulus compared to adults with MDD in remission (euthymic MDD; eMDD). Six adults with sMDD (5 women; 21±3 yrs; PHQ‐9 13±7), 8 adults with eMDD (5 women; 22±3 yrs; PHQ‐9 9±6), and 14 healthy non‐depressed adults participated (HA; 5 men; 22±3 yrs; PHQ‐9 3±3). End‐tidal carbon dioxide concentration (PETCO 2 ; capnograph), beat‐to‐beat mean arterial pressure (MAP; finger photoplethysmography), middle cerebral artery blood velocity (MCAv; transcranial Doppler ultrasound), and internal carotid artery (ICA) diameter and blood velocity (Doppler ultrasound) were continuously measured during baseline (i.e., normocapnia) and rebreathing‐induced hypercapnia. Cerebral vascular conductance index (CVCi= MCAv/MAP) and ICA blood flow (V mean •π(d/20) 2 •60) and conductance (CVC= ICA blood flow/MAP) were calculated at baseline and at the highest common magnitude of hypercapnia achieved during rebreathing (∆PETCO 2 =9 Torr). The hypercapnia‐induced increase in CVCi and ICA blood flow were expressed as a relative change from baseline (% baseline ). At baseline, there were no differences in any outcome variable between groups (all p>0.05). The hypercapnia‐induced increases in MAP (sMDD: ∆4±5; eMDD: ∆2±2; HA: ∆4±3 mmHg; p=0.60) and MCAv (sMDD: ∆23±10; eMDD: ∆29±8; HA: ∆29±6 cm/s; p=0.28) were also not different between groups. Further, there were no group differences in either CVCi (sMDD: ∆24±15; eMDD: ∆36±11; HA: ∆36±12% baseline ; p=0.13) or ICA CVC (sMDD: ∆31±13; eMDD: ∆35±25; HA: ∆34±23% baseline ; p=0.95). Despite a ~10% reduction in the middle cerebral artery vasodilatory response to hypercapnia, these preliminary data suggest that cerebrovascular function is not altered by active depressive symptomology.