Baseline characteristics
In all, 2206 consecutive patients with ischaemic stroke within 7 days were admitted to our hospital during the study period and 2043 patients were included in this study (Figure 1). Of these 2043 patients, the mean age was 65 ± 14 years, and 63.1% were males.
Demographic and clinical characteristics of participants based on Non-HDL-C quartiles are summarized in Table 1. Non-HDL-C levels ranged from 0.59 to 10.03 mmol/L (mean value, 3.14 mmol/L). Patients were divided into four categories based on Non-HDL-C quartiles: Q1, <2.35 mmol/L; Q2, 2.35–3.06 mmol/L; Q3, 3.07-3.83 mmol/L and Q4 3, >3.83 mmol/L. As shown in table 1, patients in the lowest quartile were more likely to be older, have a higher proportion of atrial fibrillation, have higher NIHSS scores and HDL-C compared with those in the highest quartile of Non-HDL-C. In addition, patients in the highest quartile were more likely to be have a higher proportion of hypertension, diabetes mellitus, have higher SBP, DBP, glucose, TG, TC and LDL-C compared with those in the lowest quartile of Non-HDL-C.
Of the 2043 patients, 232 (11.4%) were identified as HT, of whom 34 (1.7%) were symptomatic HT. Incidence of HT was 14.0% in quartile1, 11.5% in quartile2, 12.3% in quartile3, and 7.1% in quartile4 for LDL-C (P=0.003), and was 14.8% in quartile1, 13.1% in quartile2, 11.2% in quartile3, and 6.3% in quartile4 for Non-HDL-C (P<0.001).
Association of Non-HDL-C and LDL-C with HT, symptomatic HT
In the univariate analysis, age (P<0.001), males (P<0.001), atrial fibrillation (P<0.001), smoking (P=0.033), alcohol consumption (P=0.049), TOAST classification (P<0.001), NIHSS scores on admission (P<0.001), SBP (P<0.001), DBP (P=0.048), thrombolysis (P<0.001), thrombectomy (P<0.001), TG (P<0.001), TC (P=0.003), HDL-C (P=0.005), LDL-C (P<0.001) and Non-HDL-C (P<0.001) were significantly associated with HT (Table 2). In addition, only age (P=0.017), atrial fibrillation (P<0.001), NIHSS scores on admission (P<0.001), TC (P=0.047) and Non-HDL-C (P=0.028) were significantly related to symptomatic HT (Supplemental Table 1).
Table 3 shows the association between quartiles of Non-HDL-C or LDL-C and HT. After adjusting for age and sex in model 1, patients in the lower Non-HDL-C quartiles were associated with increased risks of HT (P for trend <0.001). Compared with the highest quartiles, the first, second and third quartiles of Non-HDL-C were associated with increased risk of HT (adjusted ORs 1.74 [95% CI 1.09-2.78], 2.01[95% CI 1.26-3.20], and 1.76 [95% CI 1.10-2.83], respectively) after adjusting for age, sex, NIHSS scores on admission, atrial fibrillation, smoking, alcohol consumption, SBP, thrombolysis, thrombectomy and TOAST classification in model 2. However, the only significant association was found between the third quartiles of Non-HDL-C and symptomatic HT (adjusted ORs 3.82 [95% CI 1.05-13.85]) after adjusting for age and NIHSS scores on admission (Supplemental Table 2).
After adjusting age and sex in model 1, patients in the lower LDL-C quartiles were associated with increased risks of HT (P for trend <0.001). Compared with the highest quartiles, the first and third quartiles of LDL-C were associated with increased risks of HT (adjusted ORs 1.57 [95%CI 1.00-2.47] and 1.82 [95%CI 1.16-2.87]), but not the second quartiles (adjusted ORs 1.51 [95%CI 0.95-2.40]) after adjusting for age, sex, NIHSS scores on admission, atrial fibrillation, smoking, alcohol consumption, SBP, thrombolysis, thrombectomy and TOAST classification in model 2 (Table 3). No obvious relationship was found between LDL-C and symptomatic HT after adjusting for age and NIHSS scores on admission (Supplemental Table 2).
Using a multiple-adjusted spline regression, no nonlinear trend was found between Non-HDL-C, LDL-C and HT (Figure 2). When adding Non-HDL-C or LDL-C to Model2, the c-statistics were 0.79 (95%CI 0.77-0.80, P<0.001) for Non-HDL-C and 0.78 (95%CI 0.77-0.80, P<0.001) for LDL-C (Table 4). In addition, when adding Non-HDL-C, LDL-C to model 2 containing conventional risk factors significantly improved predictive ability (Non-HDL-C, net reclassification index 0.24, 95%CI 0.17-0.31, P<0.001; LDL-C, net reclassification index 0.15, 95%CI 0.08-0.22, P=0.03) (Table 4).
Patients Age Affects the Relationship between Non-HDL-C and HT
Age is an interaction factor between Non-HDL-C and HT(P=0.021). Limiting the analysis to younger patients (<60) showed a significant negative relationship between Non-HDL-C and HT (OR 0.64, 95%CI 0.47-0.87), P<0.01), whereas this relationship was no longer significant in older patients (≥60) (Table 5). After adjustment for potential confounding variables, we found that the relationship between Non-HDL-C and HT did not change by sex, base NIHSS score, atrial fibrillation, smoking, alcohol consumption, SBP, reperfusion therapy (thrombolysis/thrombectomy) and stroke subtype (all P for interaction > 0.05) (Table 5).