Estimated pulse wave velocity as a marker of major adverse cardiovascular events in essential thrombocythaemia and polycythaemia vera.
Key claim: Higher baseline estimated pulse wave velocity independently predicts major adverse cardiovascular events, driven by arterial thrombosis, in patients with essential thrombocythemia and polycythemia vera.
Abstract
Estimated pulse wave velocity (ePWV), a simple surrogate of arterial stiffness, predicts cardiovascular events in general and oncology populations, but its relevance in myeloproliferative neoplasms (MPN) is unknown. We evaluated the association of baseline ePWV with major adverse cardiovascular events (MACE) and overall survival (OS) in 664 patients with essential thrombocythaemia (n = 477) or polycythaemia vera (n = 187). Median ePWV was 11.1 m/s (interquartile range [IQR], 9.2-12.9), and 72.1% met criteria for early vascular ageing (≥9.4 m/s). Over a median follow-up of 67.4 months, 58 first MACE (8.7%) and 58 deaths (8.7%) occurred. In multivariable cause-specific Cox models, each 1 m/s higher baseline ePWV was independently associated with MACE (hazard ratio [HR] 1.16, 95% confidence interval [CI] 1.02-1.32; p = 0.025). The adjusted HRs were 1.18 (95% CI 1.00-1.39; p = 0.054) for arterial thrombosis and 0.98 (95% CI 0.74-1.28; p = 0.860) for venous thromboembolism. For OS, ePWV lost significance after adjustment for age (HR 0.92, p = 0.670). Among JAK2-mutated patients, JAK2 V617F variant allele fraction showed a significant correlation with ePWV (ρ = 0.134; p = 0.022). These findings identify ePWV as a scalable marker of vascular ageing associated with cardiovascular risk in MPN, warranting prospective validation.
Why this matters
Arterial thrombosis is the leading cause of morbidity in ET and PV, yet current risk stratification (IPSET-thrombosis, ELN PV criteria) leans on age, prior thrombosis, and JAK2 status without incorporating vascular biology directly. Showing that estimated pulse wave velocity — computable from age and blood pressure without specialized equipment — independently predicts MACE in these subtypes introduces a scalable arterial-stiffness axis to subtype-specific cardiovascular risk assessment and complements the emerging JAK2-vasculopathy narrative (thoracic aortic aneurysm, cardiac microvascular disease).