New insights into fibrous cap thickness of vulnerable plaques assessed by optical coherence tomography.

OBJECTIVE: Vulnerable plaques with fibrous cap thickness (FCT) of ≤65 µm are prone to rupture and/or thrombosis. However, plaques with FCT > 65 µm cause acute myocardial infarction and even sudden death. We aimed to investigate the relationship between 65 < FCT ≤ 80 µm and plaque rupture and/or thrombosis using optical coherence tomography (OCT). METHODS: OCT was performed on culprit lesions in 502 consecutively enrolled patients to identify FCT. Patients were classified into three groups according to FCT: Group A (FCT ≤ 65 µm, n = 147), Group B (65 < FCT ≤ 80 µm, n = 84) and Group C (FCT > 80 µm, n = 271). Clinical and laboratory data was collected from the inpatient medical record system. RESULTS: Plaques with thinner FCT, especially < 65 µm, were more susceptible to rupture and/or thrombosis (P < 0.001). Plaques with FCT between 65 and 80 µm had a higher probability of rupture and/or thrombosis than those with FCT > 80 µm (P < 0.001). In multivariable analysis, FCT ≤ 65 µm and 65 < FCT ≤ 80 µm were independent predictors for plaque rupture ([FCT ≤ 65 µm vs. FCT > 80 µm]: OR = 8.082, 95% CI = 4.861 to 13.435, P < 0.001; [65 < FCT ≤ 80 µm vs. FCT > 80 µm]: OR = 2.463, 95% CI = 1.370 to 4.430, P = 0.003), thrombosis ([FCT ≤ 65 µm vs. FCT > 80 µm]: OR = 25.224, 95% CI = 13.768 to 46.212, P < 0.001; [65 < FCT ≤ 80 µm vs. FCT > 80 µm]: OR = 3.675, 95% CI = 2.065 to 6.542, P < 0.001) and plaque rupture with thrombosis ([FCT ≤ 65 µm vs. FCT > 80 µm]: OR = 22.593, 95% CI = 11.426 to 44.674, P < 0.001; [65 < FCT ≤ 80 µm vs. FCT > 80 µm]: OR = 4.143, 95% CI = 1.869 to 9.184, P < 0.001). CONCLUSIONS: OCT-assessed 65 < FCT ≤ 80 µm was independently associated with increased risk of plaque rupture and/or thrombosis compared with FCT > 80 µm.

The association between nutritional risk and contrast-induced acute kidney injury in patients undergoing coronary angiography: a cross-sectional study.

BACKGROUND: Nutritional risk is prevalent in various diseases, but its association with contrast-induced acute kidney injury (CI-AKI) remains unclear. This study aimed to explore this association in patients undergoing coronary angiography (CAG). METHODS: In this retrospective cross-sectional study, 4386 patients undergoing CAG were enrolled. Nutritional risks were estimated by nutritional risk screening 2002 (NRS-2002), controlling nutritional status (CONUT), prognostic nutritional index (PNI), and geriatric nutritional risk index (GNRI), respectively. CI-AKI was determined by the elevation of serum creatinine (Scr). Multivariable logistic regression analyses and receiver operator characteristic (ROC) analyses were conducted. Subgroup analyses were performed according to age (< 70/≥70 years), gender (male/female), percutaneous coronary intervention (with/without), and estimated glomerular filtration rate (< 60/≥60 ml/min/1.73m2). RESULTS: Overall, 787 (17.9%) patients were diagnosed with CI-AKI. The median score of NRS-2002, CONUT, PNI, and GNRI was 1.0, 3.0, 45.8, and 98.6, respectively. Nutritional risk was proven to be associated with CI-AKI when four different nutritional tools were employed, including NRS-2002 ([3-7 vs. 0]: odds ratio [95% confidence interval], OR [95%CI] = 4.026 [2.732 to 5.932], P < 0.001), CONUT ([6-12 vs. 0-1]: OR [95%CI] = 2.230 [1.586 to 3.136], P < 0.001), PNI ([< 38 vs. ≥52]: OR [95%CI] = 2.349 [1.529 to 3.610], P < 0.001), and GNRI ([< 90 vs. ≥104]: OR [95%CI] = 1.822 [1.229 to 2.702], P = 0.003). This is consistent when subgroup analyses were performed. Furthermore, nutritional scores were proved to be accurate in predicting CI-AKI (area under ROC curve: NRS-2002, 0.625; CONUT, 0.609; PNI, 0.629; and GNRI, 0.603). CONCLUSIONS: Nutritional risks (high scores of NRS-2002 and CONUT; low scores of PNI and GNRI) were associated with CI-AKI in patients undergoing CAG.

The Association of Nutritional Risk Screening 2002 With 1-Year Re-hospitalization and the Length of Initial Hospital Stay in Patients With Heart Failure.

Backgrounds and Aims: Nutritional Risk Screening 2002 (NRS-2002) has been widely recommended for identifying the nutritional risk. However, the association between NRS-2002 and the prognosis of heart failure has not been fully addressed. This study aimed to explore the association of NRS-2002 with 1-year re-hospitalization and the length of initial hospital stay in heart failure patients. Methods: This retrospective study included 2,830 heart failure patients. The primary endpoint was 1-year re-hospitalization for heart failure. The secondary endpoint was the length of initial hospital stay. The Log-binomial regression analysis was performed to determine the association between NRS-2002 and re-hospitalization. The Cox regression model was fitted to estimate hazard of discharge. The cumulative incidence curves of discharge were plotted using Kaplan-Meier method and log-rank test was performed. Exploratory analysis was also conducted according to the classification of heart failure and the level of N-terminal pro-B-type natriuretic peptide (NT-proBNP) fold-elevation. Results: Among 2,830 heart failure patients, the mean age was 64.3 years and 66.4% were male. A total of 122 (4.3%) patients were considered at high nutritional risk. Log-binomial regression analysis demonstrated that higher NRS-2002 score was an independent risk factor of re-hospitalization ([1 vs. 0]: relative risks [RR] = 1.383, 95% CI = 1.152 to 1.660; [2 vs. 0]: RR = 1.425, 95% CI = 1.108 to 1.832; [3-7 vs. 0]: RR = 1.770, 95% CI = 1.310 to 2.393). Kaplan-Meier curve showed that the cumulative incidence of discharge was lower in high nutritional risk group (Log rank p < 0.001). Cox regression analysis also found that higher NRS-2002 score (2 or ≥3) was strongly associated with longer length of initial hospital stay ([2 vs. 0]: Hazard ratios [HR] = 0.854, 95% CI = 0.748 to 0.976; [3-7 vs. 0]: HR = 0.609, 95% CI = 0.503 to 0.737). Exploratory analysis showed that such association still remained irrespective of NT-proBNP fold-elevation, but only existed in patients with heart failure with preserved ejection fraction (HFpEF). Conclusion: In patients with heart failure, high NRS-2002 score was strongly and independently associated with the incidence of 1-year re-hospitalization and the length of initial hospital stay.

The regulation effect of ulinastatin on the expression of SSAT2 and AQP4 in myocardial tissue of rats after cardiopulmonary resuscitation.

OBJECTIVE: This study aims to investigate the regulation effects of ulinastatin (UT1) on the expression of spermidine/spermine -N1-acetyltransferase 2 (SSAT2) and aquaporin 4 (AQP4) in myocardial tissue of rats after cardiopulmonary resuscitation (CPR) and their correlations. METHODS: A total of 90 adult SD rats were divided into sham operation group (A, n=30), model group (B, n=30) and UT1 group (C, n=30). The cardiac arrest (CA) and CPR model was established by asphyxia method. Left ventricular fractional shortening (LVFS), left ventricular ejection fraction (LVEF) and E/A peak ratio of mitral valve in three groups were collected by ultrasonic echocardiography. Apoptosis of myocardial cells was detected by DAPI staining. The expression levels of SSAT2 and AQP4 were detected by RT-PCR, Western blotting and immunohistochemical methods. RESULTS: UT1 could significantly improve the levels of LVFS, LVEF and E/A ratio and decrease myocardial cell apoptosis. As compared with group B, the expression level of SSAT2 increased and the expression level of AQP4 decreased in group C (P<0.01). SSAT2 was the most in group A and the least in group B while AQP4 was the least in group A and the most in group B (P<0.01). There was positive correlation between SSAT2 and cardiac function in CRP model while there was negative correlation between AQP4 and cardiac function (P<0.01). The expression of SSAT2 and AQP4 protein in myocardial tissue was negatively correlated in CRP model (r=-0.920, P<0.01). CONCLUSIONS: UT1 can effectively reduce the cardiac function damage caused by CRP, which could be related with the increased SSAT2 and decreased AQP4.