Hypertension. 2026 Feb 24. doi: 10.1161/HYPERTENSIONAHA.125.26543. Online ahead of print.
ABSTRACT
Blood pressure (BP) instability is a hallmark of disrupted autonomic cardiovascular control after spinal cord injury (SCI). Individuals frequently experience hypertensive surges during autonomic dysreflexia and hypotensive drops during orthostatic hypotension, yet the commonly used thresholds for defining these events are derived from expert consensus rather than outcome-based evidence. Similarly, arterial stiffness, typically assessed by pulse wave velocity, is consistently elevated in SCI, but no validated cut points exist to guide clinical intervention. This lack of outcome-anchored thresholds limits risk stratification and leaves clinicians without tools to evaluate the cumulative cardiovascular burden imposed by chronic hemodynamic instability. Accumulating data indicate that individuals with SCI demonstrate profound BP variability, particularly those with cervical or high thoracic injuries, and exhibit higher rates of ischemic heart disease, stroke, and sudden cardiac death compared with the general population. Pulse wave velocity values are also markedly increased across multiple cohorts, indicating the presence of accelerated vascular aging. However, the long-term consequences of BP instability and increased pulse wave velocity remain unquantified. A comprehensive, multicenter prospective framework is urgently needed to link BP fluctuations and pulse wave velocity changes to hard cardiovascular end points. Advances in registry-based longitudinal cohorts now make this achievable. Establishing outcome-validated thresholds, whether based on absolute BP levels, frequency of BP excursions, or degree of arterial stiffness, would enable the development of SCI-specific cardiovascular risk calculators and shift clinical practice from reactive management to proactive prevention. Closing this evidence gap is essential to reducing the disproportionate cardiovascular burden faced by individuals living with SCI.
PMID:41732873 | DOI:10.1161/HYPERTENSIONAHA.125.26543