Triglyceride glucose-body mass index as a novel predictor of slow coronary flow phenomenon in patients with ischemia and nonobstructive coronary arteries (INOCA).

BACKGROUND: The triglyceride glucose-body mass index (TyG-BMI index) has been suggested as a novel predictor of insulin resistance. However, its predictive value for slow coronary flow phenomenon (SCFP) in patients with ischemia and nonobstructive coronary arteries (INOCA) remains unclear. METHODS: We consecutively recruited 1625 patients with INOCA from February 2019 to February 2023 and divided them into two groups based on thrombolysis in myocardial infarction (TIMI) frame counts (TFCs): the SCFP group (n = 79) and the control group. A 1:2 age-matched case-control study was then performed. The TyG-BMI index was calculated as ln [plasma triglyceride (mg/dL) × fasting blood glucose (mg/dL)/2] × BMI. RESULTS: TyG-BMI index in the SCFP group (218.3 ± 25.2 vs 201.0 ± 26.5, P < .001) was significantly higher than in the normal controls. TyG-BMI index also increased with the number of coronary arteries involved in the SCFP. Multivariate logistic regression analysis showed that TyG-BMI, BMI, and TG were independent predictors for SCFP. Receiver operating characteristic (ROC) curve analysis showed that when the TyG-BMI index was above 206.7, the sensitivity and specificity were 88.6% and 68.5%, respectively, with an AUC of 0.809 (95% CI: 0.756-0.863, P = .027). Combined BMI with TG, the TyG-BMI index had a better predictive value for SCFP than BMI and TG (P < .001). CONCLUSION: The TyG-BMI index was an independent predictor for SCFP in INOCA patients, and it had a better predictive value than BMI and TG.

Assessment of the relationship between plasma fibrinogen-to-albumin ratio and slow coronary flow phenomenon in patients without obstructive coronary artery disease.

BACKGROUND: Prior studies have suggested that the chronic inflammatory response has an important role in the pathophysiology of slow coronary flow phenomenon (SCFP). However, data are scarce regarding the role of plasma fibrinogen-to-albumin ratio (PFAR) in patients having SCFP without obstructive coronary artery disease (CAD). In this study, we investigated the relationship between PFAR and the presence of SCFP in patients without obstructive CAD. METHODS: From January 2021 to January 2023, we consecutively recruited 1085 patients without obstructive CAD according to the diagnostic and exclusion criteria. In total, SCFP was diagnosed in 70 patients. A 1:2 age-matched case-control study was then conducted using comparators without SCFP. Ultimately, this study enrolled 70 patients with angiographically normal coronary arteries and SCFP, along with 140 comparators with angiographically normal coronary arteries and normal coronary flow. Plasma fibrinogen and albumin levels were measured, and the PFAR was then calculated for each patient. RESULTS: PFARs were significantly greater in the SCFP group than in the comparators with normal coronary flow (82.8 ± 15.4 vs 73.1 ± 19.5, p < 0.001). PFAR increased with increasing numbers of vessels affected by SCFP. Multivariate logistic regression analysis showed that PFAR was an independent predictor of SCFP (odds ratio: 1.818, p = 0.015). Receiver operating characteristic (ROC) curve analysis indicated that PFAR showed a better predictive value of SCFP than fibrinogen or albumin, although not significantly (p > 0.05). CONCLUSION: PFAR is an independent predictor of SCFP in patients without obstructive CAD. PAFR could improve the predictive value of SFCP than albumin or fibrinogen alone, but not significantly.

Prevalence, predictors, and management for balloon uncrossable or undilatable lesions in patients undergoing percutaneous coronary intervention with in-stent restenosis chronic total occlusion.

Background: Percutaneous coronary intervention for in-stent restenosis (ISR) chronic total occlusion (CTO) has been a great challenge. There are occasions when the balloon is uncrossable or undilatable (BUs) even though the guidewire has passed, leading to failure of the procedure. Few studies have focused on the incidence, predictors, and management of BUs during ISR-CTO intervention. Methods: Patients with ISR-CTO were recruited consecutively between January 2017 and January 2022 and divided into two groups based on the presence of BUs. The clinical data of the two groups (BUs group and non-BUs group) were retrospectively analyzed and compared to explore the predictors and clinical management strategies of BUs. Results: A total of 218 patients with ISR-CTO were included in this study, 23.9% (52/218) of whom had BUs. The percentage of ostial stents, stent length, CTO length, the presence of proximal cap ambiguity, moderate to severe calcification, moderate to severe tortuosity, and J-CTO score were higher in the BUs group than in the non-BUs group (p < 0.05). The technical success rate and the procedural success rate were lower in the BUs group than in the non-BUs group (p < 0.05). Multivariable logistic regression analysis showed that ostial stents (OR: 2.011, 95% CI: 1.112-3.921, p = 0.031), the presence of moderate to severe calcification (OR: 3.383, 95% CI: 1.628-5.921, p = 0.024) and moderate to severe tortuosity (OR: 4.816, 95% CI: 2.038-7.772, p = 0.033) were independent predictors of BUs. Conclusion: The initial rate of BUs in ISR-CTO was 23.9%. Ostial stents, presence of moderate to severe calcification, and moderate to severe tortuosity were independent predictors of BUs.

Association of soluble suppression of tumorigenicity 2 protein with new-onset atrial fibrillation in patients with acute ST-segment elevation myocardial infarction undergoing primary PCI.

Background: Previous studies have indicated that the soluble suppression of tumorigenicity 2 protein (sST2) is associated with new-onset atrial fibrillation (NOAF) in patients diagnosed with coronary artery disease (CAD). However, the predictive value of sST2 in patients with acute ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI) has not been well studied. Methods: A total of 580 patients with STEMI undergoing primary PCI were consecutively recruited between January 2021 and January 2023. These patients were then categorized into two groups: the NOAF group and the no NOAF groups based on the presence of NOAF during admission. The concentration of sST2 in blood samples was measured in all patients. The clinical data from the two groups were prospectively analyzed to investigate the predictive factors of NOAF in patients with STEMI undergoing primary PCI. Results: A total of 41 (7.1%) patients developed NOAF. The presence of NOAF has been found to be associated with various factors, including age, diabetes mellitus, hypertension, the left atrial (LA) diameter, N-terminal pro-brain natriuretic peptide, C-reactive protein (CRP), sST2, a Killip class of ≥2, and a final TIMI flow grade of <3. After including multiple factors, it was observed that LA diameter, CRP, sST2, a Killip class of ≥2, and a final TIMI flow grade of <3 remained significant risk factors for developing NOAF. The receiver operating characteristic (ROC) curve showed the following findings: (1) when the LA diameter exceeded 38.5 mm, the sensitivity and specificity values were observed to be 67.2% and 68.2%, respectively, and the area under the ROC curve (AUC) was 0.683 [95% confidence interval (CI): 0.545-0.732; p = 0.003]; (2) when the CRP level exceeded 8.59, the sensitivity and specificity values were observed to be 68.6% and 69.2%, respectively, and the AUC was 0.713 (95% CI: 0.621-0.778; p < 0.001); and (3) when the sST2 value exceeded 53.3, the sensitivity and specificity values were 79.2% and 68.7%, respectively, and the AUC was 0.799 (95% CI: 0.675-0.865; p < 0.001). Conclusion: sST2 has been identified as an independent predictor of NOAF in patients with STEMI undergoing PCI.

[Effects of C-type natriuretic peptide gene transduction on neointimal hyperplasia and endothelial function after angioplasty].

OBJECTIVE: To investigate the effects of C-type natriuretic peptide (CNP) gene transduction on neointimal hyperplasia and endothelial function after angioplasty. METHODS: Eighty-four rabbits were divided into 3 equal groups, namely normal control group, alkaline phosphatase gene transduction group and CNP gene transduction group. The rabbits in the latter two groups were given high-cholesterol diet 7 d before the experiment, followed by establishment of restenosis models by injuring the iliac artery and the specified gene transfer via retroviral vectors. Those in the normal control group were fed with normal diet. Before high-cholesterol diet and killing respectively, 2 ml venous blood samples were taken for testing blood lipid and serum CNP concentration. In the two groups with gene transduction, the injured rabbit iliac arteries were harvested for ex vivo vascular ring tension test, histological and pathological examinations, as well as immunohistochemistry analysis of CNP. The lumen area, neointimal thickness, neointimal area, ratio of intimal to medial area were measured by image analysis system. RESULTS: There were no significant differences in blood lipid and serum CNP concentration between the two gene transduction groups at the same time points both before and after operation. In CNP gene transduction group, endothelium-dependent relaxation of the vascular rings was significantly improved in comparison with the other two groups (P<0.01), irrespective of L-Arg pretreatment, whereas endothelium-independent relaxation function varied little between the 3 groups (P>0.05). Poor relaxation function to Ach of the vascular rings was resulted after pretreatment with LMMA. CNP gene expression at the site of gene transfer was detected in the CNP gene transduction group and in 2 weeks after balloon injury, the neointimal thickness, neointimal area and ratio of the neointimal to tunica media area were markedly increased in the two gene transduction groups, but the measurements were significantly lower in CNP group (P<0.01). CONCLUSION: CNP gene can be successfully transferred and effectively expressed at the injured site in the blood vessels to decrease the hyperplasia and significantly improve endothelial function after angioplasty.