Dietary Flavonoid Intake and Carotid Calcification in Patients with Ischemic Stroke.

INTRODUCTION: Owing to the antioxidant and anti-inflammatory effects, flavonoids can influence the initiation and development of atherosclerosis, but the underlying mechanisms remain largely undetermined. This study aimed to evaluate the associations between dietary flavonoids and carotid calcification in patients with ischemic stroke. METHODS: This study screened consecutive patients with ischemic stroke via Nanjing Stroke Registry Program from February 2016 to April 2021. A semiquantitative food frequency questionnaire was used to evaluate dietary consumption of flavonoids and other nutritional components. Presence and degree of carotid calcification were determined according to Agatston scores on computer tomography angiography. Logistic regression was performed to evaluate the association between dietary flavonoids (total flavonoids, flavonols, flavones, flavanones, flavan-3-ols, anthocyanins, and isoflavones) and carotid calcification. RESULTS: Of the 601 enrolled patients, 368 (61.2%) were detected with carotid calcification. Patients with high intake of total flavonoids (the fifth quintile) had a 52% lower carotid calcification risk than those with low intake (the first quintile; odds ratio [OR] = 0.48; 95% confidence interval [CI], 0.26-0.90; p = 0.007 for trends) after adjusting for major confounders. Patients with high intake of flavan-3-ols (the fifth quintile) had a 51% lower carotid calcification risk than those with low intake (the first quintile; OR = 0.49; 95% CI, 0.25-0.97; p = 0.016 for trends). CONCLUSION: Dietary flavonoid intake is associated with carotid calcification, and, therefore, may influence the risk of stroke occurrence and recurrence.

Association between dietary antioxidant capacity and atherosclerotic carotid stenosis in patients with ischemic stroke.

BACKGROUND AND PURPOSE: The aim of this study was to evaluate the relationship between dietary total antioxidant capacity (DTAC) and atherosclerotic carotid stenosis in patients with ischemic stroke. METHODS: Patients with acute ischemic stroke were consecutively enrolled. Daily food consumption was estimated by a semi-quantitative food frequency questionnaire (FFQ). DTAC was calculated based on classified food intake. Antioxidant potential value was measured by ferric-reducing antioxidant power (FRAP) and oxygen radical absorbance capacity (ORAC) methods. Evaluation of carotid artery stenosis was based on computed tomography angiography (CTA). Logistic regression was used to assess the relationship between DTAC and degree of carotid stenosis. RESULTS: Of the 608 enrolled, 232 patients (38.2%) had moderate or severe carotid stenosis. After adjusting for major confounding factors, FRAP (OR =0.640; 95% CI: 0.410-0.998; P =0.049) and ORAC (OR =0.625; 95% CI: 0.400-0.976; P =0.039) were associated with lower degree of carotid artery stenosis (third vs first tertile). Spearman analysis indicated that FRAP (r =-0.121, P =0.003) and ORAC (r =-0.147, P <0.001) were correlated with degree of carotid stenosis. CONCLUSIONS: DTAC may influence the initiation and development of atherosclerosis, and, therefore, the risk of ischemic stroke.

High Dietary Inflammatory Index Is Associated With Increased Plaque Vulnerability of Carotid in Patients With Ischemic Stroke.

BACKGROUND AND PURPOSE: Long-term dietary patterns can influence the intensity of systemic inflammation and, therefore, the development of atherosclerosis. This study aimed to evaluate the association between dietary inflammatory index (DII) and vulnerability characteristics of carotid atherosclerotic plaques in patients with ischemic stroke. METHODS: Patients with ischemic stroke within 7 days of onset were enrolled. DII was calculated from 32 food components with the help of a food frequency questionnaire. Vulnerable plaque was defined as presence of artery positive remodeling (remodeling index >1.1) and low CT attenuation plaques (<35 HU) on carotid arteries by computed tomography angiography. RESULTS: Of the 398 enrolled patients, 144 (36.2%) were detected with vulnerable plaque. Their DII ranged from -4.58 to 4.18. Patients with vulnerable plaques consumed less nutrients with anti-inflammatory properties, less fruits and vegetables (85.6±64.3 versus 94.6±74.4 g/d, P=0.027), and less nuts (5.66±7.14 versus 8.84±15.9 g/d, P=0.024) than patients without vulnerable plaques. Patients with vulnerable plaque had higher DII than patients without vulnerable plaque (-0.26±1.54 versus -0.64±1.53, P=0.018). Logistic regression analysis revealed that DII was associated with vulnerable plaques after adjusted for major confounding factors (odds ratio=1.307; 95% CI, 1.113-1.533). CONCLUSIONS: DII is associated with the vulnerability of carotid plaques in patients with ischemic stroke. Considering a possible causal relationship, the mechanisms underlying the association between diet and atherosclerosis warrant further study.

Dietary Glycemic Index and Glycemic Load in Relation to Atherosclerotic Stenosis of Carotid and Cardiovascular Risk Factors in Ischemic Stroke Patients.

AIM: Glycemic index (GI) and glycemic load (GL) influence postprandi al glucose concentrations and insulin responses. This study aims to ascertain the connection between GI, GL, and carotid atherosclerotic stenosis and cardiovascular disease (CVD) risk factors. METHODS: A total of 669 patients with ischemic stroke within 7 days were enrolled. GI and GL were assessed with a validated food frequency questionnaire from patients. Computed tomography angiography (CTA) was used for the evaluation of carotid atherosclerotic stenosis. Traditional risk factors such as total cholesterol, triglycerides, LDL-C, HDL-C, C-reactive protein, homocysteine, neutrophil to lymphocyte ratio (NLR), fasting plasma glucose, and hemoglobin A1c were measured. GI/GL and its association with CVD risk factors and carotid stenosis were explored with Spearman analysis and multivariable logistic regression, respectively. RESULTS: The prevalence of carotid stenosis was 63.2% of all 669 participants. The mean value of GI/GL was 49.3/137. Spearman test did not detect significant relationships between GI/GL and CVD risk factors. In multivariable regression models, GI (4th vs. 1st quartile, OR=2.11; 95% CI, 1.30-3.42) and GL (4th vs. 1st quartile, OR=1.82; 95% CI, 1.12-2.96) were observed a significant association with carotid stenosis after adjustment for major confounding factors. The association between GL and carotid stenosis became more pronounced among yo ungers (4th vs. 1st quartile, OR=2.42; 95% CI, 1.13-4.76) and women (4th vs. 1st quartile, OR=3.81; 95% CI, 1.45-5.05). CONCLUSION: Higher GI and GL were positively associated with a higher degree of carotid stenosis in these Chinese cerebral infarction patients, especially in younger patients and women.

Socioeconomic Status and the Risk of Stroke Recurrence in Chinese Patients.

BACKGROUND: The association between socioeconomic status (SES) and the risk of stroke recurrence has been rarely studied, especially in a developing country. OBJECTIVE: This study aimed to evaluate the association between SES and the risk of stroke recurrence in Chinese stroke patients. METHODS: Patients with first-ever ischemic stroke registered in the Nanjing Stroke Registry Program from 2013 to 2015 were enrolled and followed in this study. Information about SES, measured by disposable income and educational level, was collected at baseline. The primary endpoint was defined as fatal or nonfatal recurrent stroke after 7 days of the index stroke. The association between SES and the risk of stroke recurrence was analyzed with multivariate Cox regression model. RESULTS: A total of 2,294 patients with first-ever stroke were included in the study. During a mean follow-up of 2.8 ± 1.2 years, 298 (13.0%) patients had stroke recurrence. After adjusting for potential confounding factors, compared with patients with a monthly family income of USD ≥1,539, those with an income of USD 769-1,538, USD 462-768, and USD 1-461 had an adjusted hazard ratio (HR) of 1.87 (95% CI 1.11-3.17), 2.40 (95% CI 1.43-4.03), and 2.79 (95% CI 1.65-4.69) for recurrence, respectively. Compared with those with an educational level of ≥13 years, patients with an educational level of 7-12 years and 0-6 years had adjusted HRs of 1.21 (95% CI 0.79-1.86) and 1.73 (95% CI 1.11-2.70), respectively. CONCLUSIONS: Chinese stroke patients with lower SES bear higher recurrent risk. These results are suggestive for secondary stroke prevention in Chinese patients.

Impact of Smoking Status on Stroke Recurrence.

Background Smoking is a well-established risk factor of stroke and smoking cessation has been recommended for stroke prevention; however, the impact of smoking status on stroke recurrence has not been well studied to date. Methods and Results Patients with first-ever stroke were enrolled and followed in the NSRP (Nanjing Stroke Registry Program). Smoking status was assessed at baseline and reassessed at the first follow-up. The primary end point was defined as fatal or nonfatal recurrent stroke after 3 months of the index stroke. The association between smoking and the risk of stroke recurrence was analyzed with multivariate Cox regression model. At baseline, among 3069 patients included, 1331 (43.4%) were nonsmokers, 263 (8.6%) were former smokers, and 1475 (48.0%) were current smokers. At the first follow-up, 908 (61.6%) patients quit smoking. After a mean follow-up of 2.4±1.2 years, 293 (9.5%) patients had stroke recurrence. With nonsmokers as the reference, the adjusted hazard ratios for stroke recurrence were 1.16 (95% CI , 0.75-1.79) in former smokers, 1.31 (95% CI , 0.99-1.75) in quitters, and 1.93 (95% CI , 1.43-2.61) in persistent smokers. Among persistent smokers, hazard ratios for stroke recurrence ranged from 1.68 (95% CI , 1.14-2.48) in those who smoked 1 to 20 cigarettes daily to 2.72 (95% CI , 1.36-5.43) in those who smoked more than 40 cigarettes daily ( P for trend <0.001). Conclusions After an initial stroke, persistent smoking increases the risk of stroke recurrence. There exists a dose-response relationship between smoking quantity and the risk of stroke recurrence.