Ventricular-arterial coupling in community-dwelling individuals and athletes with cervical spinal cord injury.

Cervical spinal cord injury (SCI) removes descending sympathetic control over the heart and vasculature, which alters cardiovascular function. Ventricular-arterial coupling (VAC) provides insight into the heart's mechanical and energetic efficiency by evaluating the interaction between cardiac contractility (end-systolic elastance; Ees) and arterial elastance (Ea). This study investigated VAC in nonathletes (SCI-NA) and athletes (SCI-A) with cervical SCI, and able-bodied (AB) controls. We additionally validated noninvasive estimation of Ees with catheter-derived assessments in rodents with SCI. Data were collected on SCI-NA (9 M, 2 F), SCI-A (12 M, 2 F), and AB (10 M, 5 F) individuals. Cardiac contractility was estimated using single-beat Ees(sb) and an alternative assessment of contractility derived from the left ventricle outflow tract [contractility(LVOT)]. Ea was determined with the standard Simpson's biplane method [Ea(Simp)] and with Doppler [Ea(Doppl)]. VAC was determined for each method as: VAC(sb) = Ea(Doppl)/Ees(sb) and VAC(LVOT) = Ea(Simp)/contractility(LVOT). Associations between contractility(LVOT) and catheter Ees in rats were assessed with linear regression and intraclass correlation coefficient (ICC). Compared with AB, contractility(LVOT) was lower in SCI-NA (P < 0.001) and SCI-A (P = 0.04). Ea(Simp) was higher in SCI-NA versus SCI-A and AB (all P < 0.01). As such, SCI-NA exhibited a higher VAC(LVOT) versus AB (P < 0.001) and SCI-A (P = 0.002). In rodents, we found excellent agreement between contractility(LVOT) and Ees (ICC 0.880; P = 0.002). SCI-NA exhibit an elevated VAC due to lower contractility(LVOT) and higher Ea, suggesting an uncoupling of the heart and vasculature. SCI-A exhibit preserved VAC despite a lower contractility(LVOT) than AB, suggesting that chronic exposure to exercise maintains coupling between the heart and vasculature.NEW & NOTEWORTHY The present study provides the first demonstration that VAC is impaired in humans with SCI, which may further contribute to the poor exercise tolerance often observed in this population. Our findings in the SCI-A group imply that chronic exposure to exercise increases VAC, suggesting that adherence to a long-term exercise program may optimize ventricular-vascular interaction postinjury.