| Intervention | HR (95% CI) | Mechanism | Recan.% | Bleed% | Evidence | E-Value | N (studies) | Key Sources |
|---|
Bayesian Causal Analysis Methodology
Framework: Judea Pearl's Structural Causal Model (SCM) with do-calculus. The causal DAG (Directed Acyclic Graph) for PVT includes the following structural equations:
Treatment = g(Thrombus_extent, Cirrhosis_severity, MPN_status, Timing) + ε₂
Outcome = h(Thrombus(t), Treatment, Portal_Pressure, Baseline_LF) + ε₃
Backdoor Criterion: The set {Cirrhosis_severity, Thrombus_extent, Etiology, Timing} d-separates Treatment from Outcome in the causal graph. Adjustment is applied via the backdoor formula:
Cross-Correlation Adjustment: Interventions sharing causal pathways inflate the apparent combined effect. The Pearl-adjusted log-HR is computed as:
where ρ̄ = (2/n(n−1)) × Σᵢ<ⱼ ρᵢⱼ (mean pairwise cross-correlation)
E-Value (Unmeasured Confounding): For each intervention HR < 1, the minimum risk ratio an unmeasured confounder must have with both exposure and outcome to fully explain away the observed association:
Dose–Response: Saturation modeled via 4-parameter Hill equation:
Antithesis (Commandment 7): Key limitations include: (1) Most PVT anticoagulation evidence is from observational cohorts; RCT data are limited to n<100. (2) TIPS data include strong selection bias toward suitable anatomy and Child-Pugh A/B. (3) Cross-correlations derived from mechanistic overlap, not empirical data. (4) Combined HR floors at biological minimum (~0.15) due to spontaneous fibrinolysis. (5) Thrombus age (acute <3m vs. chronic) is a major effect modifier not fully captured by the composite endpoint.