Reductions in Cardiac Structure and Function 24 Months After Spinal Cord Injury

Abstract

Smaller heart structures and reduced cardiac function are documented in cross‐sectional comparisons of individuals with spinal cord injury (SCI) and age/weight matched able bodied controls. The smaller heart structures and reduced function may result from progressive cardiac atrophy similar to that observed with diminished physical activity, extended periods of bed rest, and space flight. It is unknown if there is progressive cardiac atrophy in the months following SCI. Additionally, slightly larger hearts and greater retention of function are found in individuals with thoracic compared to cervical injuries, suggesting that the level of spinal injury may differentially affect reductions in heart structure and function after SCI. Therefore, the purpose of this research was to 1) quantify cardiac structure and function of individuals within the first 24 months after injury, 2) identify the relationship between cardiac structure and function and time since injury, and 3) examine injury level’s effect on heart structure/function and time since injury. A cross‐sectional assessment of cardiac structure and function was made using transthoracic echocardiography (Vivid‐Q; GE Healthcare) on twenty‐nine (4F) volunteers who were 3‐ to 24‐months post‐injury. Myocardial structure and function were assessed using 2D, speckle‐tracking, and tissue Doppler in accordance with contemporary clinical echocardiographic guidelines. Heart rate and blood pressures were assessed simultaneously using a combination of a standard lead II electrocardiogram (ECG) and brachial oscillometric blood pressure monitor (Dash 5000 patient monitor, GE). The relationship between cardiac structure/function and time since injury were analyzed using linear regression. Neurological and sensory level of injury were entered into the model as covariates to determine whether or not the relationships differed with time since injury. Time since injury was most strongly associated with a reduction in left ventricular end‐diastolic volume (Δ= −2.07±0.70 ml·mo−1, r2=0.266, p=0.007), end‐systolic volume (Δ= −1.05±0.38 ml·mo−1, r2=0.237, p=0.012), and left ventricular mass (Δ= −3.0 ± 1.2 g·mo−1, r2=0.192, p=0.018). These changes in left ventricular structure were paralleled by a reduced stroke volume (Δ= −1.03±0.50 ml·mo−1, r2=0.154 p=0.048) and cardiac output (Δ= −0.12±0.04 L·min−1·mo−1, r2=0.322, p=0.002). There were no significant associations of blood pressures, wall thickness, or measures of diastolic function with time since injury (p>0.050). The reductions in left ventricular structure and systolic function were not differentially affected by neurological or sensory level of injury (p= 0.412–0.973). These results suggest there are gradual reductions in left ventricular structure and systolic function over the 24 months following spinal cord injury which are not affected by the neurological or sensory level of injury. Although there is loss of left ventricular structure and function, blood pressure appears maintained suggesting peripheral compensatory adjustments. This information indicates that cardiac rehabilitation interventions should occur relatively soon after spinal cord injury to mitigate cardiac atrophy.Support or Funding InformationFunded by NIH Grant (R01‐HL‐117037) and The Spaulding Research Institute Leadership Catalyst