Ambulatory blood pressure monitoring in spinal cord injury: clinical practicability

Abstract

Trauma to the spinal cord often results not only in sensorimotor but also autonomic impairments. The loss of autonomic control over the cardiovascular system can cause profound blood pressure (BP) derangements in subjects with spinal cord injury (SCI) and may therefore lead to increased cardiovascular disease (CVD) risk in this population. The use of ambulatory blood pressure monitoring (ABPM) allows insights into circadian BP profiles, which have been shown to be of good prognostic value for cardiovascular morbidity and mortality in able-bodied subjects. Past studies in SCI subjects using ABPM have shown that alterations in circadian BP patterns are dependent on the spinal lesion level. Tetraplegic subjects with sensorimotor complete lesions have a decreased daytime arterial BP, loss of the physiological nocturnal BP dip, and higher circadian BP variability, including potentially life-threatening hypertensive episodes known as autonomic dysreflexia (AD), compared with paraplegic and able-bodied subjects. The proposed underlying mechanisms of these adverse BP alterations mainly are attributed to a lost or decreased central drive to sympathetic spinal preganglionic neurons controlling the heart and blood vessels. In addition, several maladaptive anatomical changes within the spinal cord and the periphery, as well as the general decrease of physical daily activity in SCI subjects, account for adverse BP changes. ABPM enables the identification of adverse BP profiles and the associated increased risk for CVD in SCI subjects. Concurrently, it also might provide a useful clinical tool to monitor improvements of AD and lost nocturnal dip after appropriate treatments in the SCI population.

Figures

FIG. 1.

Autonomic control of cardiovascular systems. Various nuclei within the medulla oblongata coordinate cardiovascular control and are under control of the cerebral cortex and the hypothalamus. Descending sympathetic projections provide tonic control to spinal sympathetic pre-ganglionic neurons (SPNs) located within the lateral horn of spinal segments T1–L2. Axons of SPNs exit the spinal cord via the ventral root and synapse with post-ganglionic neurons located in the paravertebral ganglia. The post-ganglionic fibers then synapse directly with smooth muscle in the heart and blood vessels. Parasympathetic pre-ganglionic fibers exit the brainstem via the vagus nerve and synapse with post-ganglionic parasympathetic neurons in the cardiac ganglia. Figure adapted with permission from Krassioukov.

FIG. 2.

Differences in daytime and nighttime systolic blood pressure (SBP) between three groups: tetraplegia (C4-C8, American Spinal Injury Association Impairment Scale [AIS] A, n=51), paraplegia (T6-L4, AIS A, n=32), and able-bodied subjects (n=36). Mean±standard deviation of SBP was calculated from values of sensorimotor complete SCI and able-bodied subjects from studies presented in Table 1.

FIG. 3.

Nocturnal dip differences of systolic blood pressure among tetraplegic (C4-C8, American Spinal Injury Association Impairment Scale [AIS] A, n=51), paraplegic (T6-L4, AIS A, n=32), and able-bodied subjects (n=36). Values are shown in mean±standard deviation. Nocturnal dip was calculated as (systolic blood pressure [SBP] nighttime – SBP daytime)/SBP daytime x 10042 from values of sensorimotor complete (AIS A) SCI and able-bodied subjects of studies presented in Table 1. Significant differences in nocturnal SBP dip were found between tetraplegic and paraplegic subjects (p=0.02), and tetraplegic and able-bodied subjects (p=0.03; Mann-Whitney U test).

FIG. 4.

(A) Ambulatory blood pressure monitoring (ABPM) profiles from an able-bodied subject (female, 29 years) with preserved physiological nocturnal dip (>10% drop in systolic blood pressure [SBP] from day- to nighttime) and normal daily blood pressure and heart rate variability due to increased physical bouts, such as walking upstairs. (B) Recordings from a subject with complete tetraplegia (C5, American Spinal Injury Association Impairment Scale B, male, 58 years) showing loss of nocturnal dip, multiple episodes of autonomic dysreflexia and hypotension ranging from 180 to 71 mm Hg SBP. Shaded time section represents nighttime. These ABPM profiles are examples from our laboratory.