Altered left ventricular diastolic function in subjects with spinal cord injury.

STUDY DESIGN: This is cross-sectional study. OBJECTIVES: The aim of this study is to investigate the cardiac structure and function of subjects with spinal cord injury (SCI) and the impact of metabolic, hemodynamic and inflammatory factors on these parameters. SETTING: São Paulo, Brazil. METHODS: Sixty-five nondiabetic, nonhypertensive, sedentary, nonsmoker men (34 with SCI and 31 healthy subjects) were evaluated by medical history, anthropometry, laboratory tests, analysis of hemodynamic and inflammatory parameters and echocardiography. RESULTS: Subjects with SCI had lower systolic blood pressure and higher levels of C-reactive protein and tumor necrosis factor receptors than the healthy ones. Echocardiography data showed that the SCI group presented similar left ventricular (LV) structural and systolic parameters, but lower initial diastolic velocity (Em) (9.2 ± 0.5 vs 12.3 ± 0.5 cm s(-1); P<0.001) and higher peak early inflow velocity (E)/Em ratio (7.7 ± 0.5 vs 6.1 ± 0.3; P = 0.009) compared with the able-bodied group, even after adjustment for systolic blood pressure and C-reactive protein levels. Furthermore, injured subjects with E/Em >8 had lower peak spectral longitudinal contraction (Sm) (9.0 ± 0.7 vs 11.6 ± 0.4 cm s(-1); P<0.001) and cardiac output (4.2 ± 0.2 vs 5.0 ± 0.2 l min(-1); P = 0.029), as well as higher relative wall thickness (0.38 ± 0.01 vs 0.35 ± 0.01; P = 0.005), than individuals with SCI with E/Em<8, but similar age, body mass index, blood pressure, injury level, metabolic parameters and inflammatory marker levels. CONCLUSION: Subjects with SCI presented impaired LV diastolic function in comparison with able-bodied ones. Moreover, worse LV diastolic function was associated with a pattern of LV concentric remodeling and subclinical decreases in systolic function among injured subjects. Overall, these findings might contribute to explain the increased cardiovascular risk reported for individuals with SCI.

Subclinical atherosclerosis is related to injury level but not to inflammatory parameters in spinal cord injury subjects.

STUDY DESIGN: Cross-sectional. OBJECTIVES: Individuals with spinal cord injury (SCI) exhibit increased carotid intima-media thickness (IMT) and are reported to be exposed to higher circulating levels of inflammatory mediators. This study evaluated the relationship between inflammatory markers and carotid surrogates of cardiovascular risk in subjects with SCI. SETTING: São Paulo, Brazil. METHODS: A total of 65 nondiabetic, nonhypertensive, sedentary, nonsmoker men (34 with SCI; 31 healthy subjects) were evaluated by medical history, anthropometry, routine laboratory tests, analysis of hemodynamic, inflammatory parameters and ultrasound examination of carotid arteries. RESULTS: Subjects with SCI (18 tetraplegic and 16 paraplegic) had lower systolic blood pressure (P = 0.009), higher serum C-reactive protein (P = 0.001), tumor necrosis factor (TNF) receptor-II (P = 0.02) and TNF receptor-I (P = 0.04) levels and increased in vitro production of interleukin-6 by mononuclear cells (P = 0.04), compared to able-bodied individuals. No differences in serum interleukin-6, e-selectin, intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and transforming growth factor-ß levels, or in vitro release of interleukin-10, interleukin-17 and interferon-γ by mononuclear cells, were detected between the studied groups. Common carotid IMT, but not internal carotid resistive index, was significantly higher in subjects with SCI (P<0.0001 adjusted for C-reactive protein and TNF receptor-II levels). In addition, tetraplegic subjects exhibited increased IMT (P = 0.002 adjusted for systolic blood pressure and body mass index), but similar levels of inflammatory mediators compared to paraplegic ones. CONCLUSIONS: Individuals with SCI exhibit a clustering of vascular and inflammatory surrogates of increased cardiovascular risk. Nevertheless, subclinical carotid atherosclerosis is related to injury level but not to increased inflammatory status in these subjects.