Anxiety disorders following percutaneous coronary intervention for acute myocardial infarction: A comprehensive review of clinical manifestations and interventions

Table 1 Differential protein expression in post-percutaneous coronary intervention anxiety pathophysiology

Protein/pathway	Regulation	Cell/tissue type	Mechanism	Functional impact	Potential as target
Inflammation-related proteins
IL-6	Increased (high)	Circulating monocytes	Upregulated via NF-κB signaling post-PCI	Enhances systemic inflammatory response, promotes BBB permeability	High (anti-IL-6 antibodies)
TNF-α	Increased (moderate)	Activated macrophages	Activated through TLR4 pathway following myocardial injury	Activates microglia, promotes neuroinflammation	Moderate (TNF inhibitors)
CRP	Increased (very high)	Hepatocytes	Acute phase response to cardiac tissue injury	Correlates with anxiety severity (r = 0.62, P < 0.001)	Low (biomarker only)
ICAM-1	Increased (moderate)	Endothelial cells	Activated by inflammatory cytokines	Facilitates leukocyte infiltration across BBB	Moderate
NLRP3 inflammasome	Increased (moderate)	Cardiac tissue, microglia	Activated by DAMPs released during myocardial injury	Mediates IL-1β production, promotes neuroinflammation	High (NLRP3 inhibitors)
Autonomic regulation proteins
Neuropeptide Y	Increased (high)	Sympathetic neurons	Released with catecholamines during sympathetic activation	Potentiates anxiety, promotes vasoconstriction	Moderate (Y1 antagonists)
α1-adrenergic receptors	Increased (moderate)	Vascular tissue, amygdala	Upregulated in response to chronic sympathetic activation	Enhances peripheral vasoconstriction and amygdala excitability	High (α-blockers)
Muscarinic M2 receptors	Increased (moderate)	Cardiac tissue	Downregulated following autonomic imbalance	Reduces parasympathetic control of heart rate	Moderate (M2 agonists)
COMT enzyme	Increased (moderate)	Prefrontal cortex	Epigenetic modifications following stress exposure	Impairs catecholamine metabolism, sustains arousal	Moderate (COMT enhancers)
β2-adrenergic receptors	Increased (moderate)	Immune cells	Receptor desensitization following chronic activation	Reduces anti-inflammatory effects of β-signaling	High (β-agonists)
HPA axis-related proteins
Glucocorticoid receptor	Increased (moderate)	Hippocampus, PFC	Receptor downregulation following cortisol exposure	Impairs negative feedback of HPA axis	High (GR modulators)
CRH[50]	Increased (moderate)	Paraventricular nucleus	Enhanced expression via CREB phosphorylation	Drives HPA axis hyperactivity	High (CRH antagonists)
FKBP5	Increased (moderate)	Multiple CNS regions	Upregulated by cortisol exposure	Inhibits GR function, promotes HPA axis dysregulation	Moderate
11β-HSD1	Increased (moderate)	Adipose tissue, CNS	Upregulated in response to inflammation	Increases local cortisol regeneration	Moderate (11β-HSD1 inhibitors)
Mineralocorticoid receptor	Increased (moderate)	Hippocampus	Downregulated following chronic stress	Alters HPA axis sensitivity	Moderate (MR agonists)

PCI: Percutaneous coronary intervention; HPA: Hypothalamic-pituitary-adrenal.