Predictive value of the inconsistency between the residual and post-PCI QFR for prognosis in PCI patients.

Introduction: To investigate the prognostic value of the consistency between the residual quantitative flow ratio (QFR) and postpercutaneous coronary intervention (PCI) QFR in patients undergoing revascularization. Methods: This was a single-center, retrospective, observational study. All enrolled patients were divided into five groups according to the ΔQFR (defined as the value of the post-PCI QFR minus the residual QFR): (1) Overanticipated group; (2) Slightly overanticipated group; (3) Consistent group; (4) Slightly underanticipated group; and (5) Underanticipated group. The primary outcome was the 5-year target vessel failure (TVF). Results: A total of 1373 patients were included in the final analysis. The pre-PCI QFR and post-PCI QFR were significantly different among the five groups. TVF within 5 years occurred in 189 patients in all the groups. The incidence of TVF was significantly greater in the underanticipated group than in the consistent group (P = 0.008), whereas no significant differences were found when comparing the underanticipated group with the other three groups. Restricted cubic spline regression analysis showed that the risk of TVF was nonlinearly related to the ΔQFR. A multivariate Cox regression model revealed that a ΔQFR≤ -0.1 was an independent risk factor for TVF. Conclusions: The consistency between the residual QFR and post-PCI QFR may be associated with the long-term prognosis of patients. Patients whose post-PCI QFR is significantly lower than the residual QFR may be at greater risk of TVF. An aggressive PCI strategy for lesions is anticipated to have less functional benefit and may not result in a better clinical outcome.

Effects of percutaneous coronary intervention and diabetes mellitus on short- and long-term prognosis assessed by the three-vessel quantitative flow ratio.

AIMS: We aimed to investigate the impact of percutaneous coronary intervention (PCI) and diabetes mellitus (DM) on short- and long-term prognosis in patients with coronary artery disease using three-vessel quantitative flow ratio (3 V-QFR) assessment. METHODS: A retrospective analysis of 2440 vessels in 1181 patients who underwent PCI was performed. The patients were categorized according to the presence or absence of DM and the median 3 V-QFR. The primary outcome was the occurrence of major adverse cardiac events (MACE), defined as a combination of cardiovascular death, myocardial infarction, and ischemia-driven revascularization, over a 5-year period. RESULTS: The pre-PCI and post-PCI 3 V-QFR values for the entire population were 2.37 (2.04-2.56) and 2.94 (2.82-3.00), respectively. Landmark analysis showed that the incidence of MACE was comparable among all groups within the first year (log-rank p = 0.088). Over the course of 2 years, the incidence of MACE was higher in both groups with a post-PCI 3 V-QFR < 2.94 (log-rank p < 0.001). However, from 2 to 5 years, patients with DM had higher rates of MACE (log-rank p = 0.013). CONCLUSIONS: In the short term, a low post-PCI 3 V-QFR is a predictor of high risk for MACE. However, in the long term, DM emerges as the dominant risk factor.

Impact of diabetes on coronary physiology evaluated by quantitative flow ratio in patients who underwent percutaneous coronary intervention.

AIMS/INTRODUCTION: There are mixed opinions on the influence of diabetes on the prognosis of patients receiving percutaneous coronary intervention (PCI). Therefore, in this study, the quantitative flow ratio (QFR), an emerging technology of functional evaluation, was used to explore the impact of diabetes on coronary physiology in patients who underwent PCI. MATERIALS AND METHODS: Patients who underwent successful PCI and a 1-year angiographic follow up were retrospectively screened and analyzed by the QFR. Based on the presence or absence of diabetes, 677 enrolled patients (794 vessels) were classified into a diabetes group (211 patients, 261 vessels) and a non-diabetes group (466 patients, 533 vessels). The results of QFR analysis and clinical outcomes were compared between the two groups. RESULTS: The two groups reached a similar level of post-PCI QFR (0.95 ± 0.09 vs 0.96 ± 0.06, P = 0.292). However, at the 1-year follow up, the QFR was lower (0.93 ± 0.11 vs 0.96 ± 0.07, P < 0.001), and the degree of QFR decline was more obvious (-0.024 ± 0.090 vs -0.008 ± 0.070, P = 0.023) in the diabetes group. Additionally, diabetes was independently associated with functional restenosis (odds ratio 2.164, 95% confidence interval 1.210-3.870, P = 0.009) and target vessel failure (odds ratio 2.654, 95% confidence interval 1.405-5.012, P = 0.003). CONCLUSION: As evaluated by the QFR, patients with diabetes received less coronary physiological benefit from PCI, which was consistent with their clinical outcomes.

Effect of Low-Density Lipoprotein Cholesterol Goal Achievement on Vascular Physiology Evaluated by Quantitative Flow Ratio in Patients Who Underwent Percutaneous Coronary Intervention.

Purpose: The change in coronary physiology from lipid-lowering therapy (LLT) lacks an appropriate method of examination. Quantitative flow ratio (QFR) is a novel angiography-based approach allowing rapid assessment of coronary physiology. This study sought to determine the impact of low-density lipoprotein cholesterol (LDL-C) goal achievement on coronary physiology through QFR. Methods: Cases involving percutaneous coronary intervention (PCI) and 1-year angiographic follow-up were screened and assessed by QFR analysis. Patients were divided into two groups according to the LDL-C level at the 1-year follow-up: (1) goal-achievement group (LDL-C < 1.8 mmol/L or reduction of ≥50%, n = 146, lesion = 165) and (2) non-achievement group (n = 286, lesion = 331). All QFR data and major adverse cardiovascular and cerebrovascular events (MACCEs) at 1 year were compared between groups. Results: No differences between the groups in quantitative coronary angiography (QCA) data or QFR post-PCI were found. At the 1-year follow-up, lower percentage diameter stenosis (DS%) and percentage area stenosis (AS%) were recorded in the goal-achievement group (27.89 ± 10.16 vs. 30.93 ± 12.03, p = 0.010, 36.57 ± 16.12 vs. 41.68 ± 17.39, p = 0.003, respectively). Additionally, a better change in QFR was found in the goal-achievement group (0.003 ± 0.068 vs. -0.018 ± 0.086, p = 0.007), with a lower incidence of physiological restenosis and MACCEs (2.1 vs. 8.4%, p = 0.018, 5.4 vs. 12.6%, p = 0.021, respectively). Conclusion: Evaluated by QFR, patients who achieved the LDL-C goal appear to have a better coronary physiological benefit. This group of patients also has a better clinical outcome.

Coronary artery aneurysm combined with myocardial bridge: A case report.

BACKGROUND: Coronary artery aneurysm combined with myocardial bridge is a very rare clinical situation. The prognosis of this clinical situation is not yet clear. CASE SUMMARY: A coronary artery aneurysm and myocardial bridge in the same segment of the coronary artery were found in a 54-year-old female patient who underwent coronary angiography and intravascular ultrasound examination. Through conservative treatment, the patient was discharged from the hospital smoothly, and she was in good condition during 5 mo of follow-up. CONCLUSION: Coronary artery aneurysm combined with myocardial bridge seems to have a good prognosis, but due to the rarity of this clinical situation, further research and follow-up are needed.

Prevention of Contrast-Induced Nephropathy by Inferior Vena Cava Ultrasonography-Guided Hydration in Chronic Heart Failure Patients.

INTRODUCTION: Contrast-induced nephropathy (CIN) is a common complication resulting from the administration of contrast media. This study was designed to determine whether inferior vena cava (IVC) ultrasonography (IVCU)-guided hydration can reduce the risk of CIN in chronic heart failure patients undergoing coronary angiography or coronary angiography with percutaneous coronary intervention compared with standard hydration. METHODS: This prospective clinical trial enrolled 207 chronic heart failure patients from February 2016 to November 2017, who were randomly assigned to either the IVCU-guided hydration group (n = 104) or the routine hydration group (n = 103). In the IVCU-guided group, the hydration infusion rate was set according to the IVC diameter determined by IVCU, while the control group received intravenous infusion of 0.9% saline at 0.5 mL/(kg·h). Serum Cr was measured before and 48-72 h after the procedure. All patients were followed up for 18 months. The incidence of nephropathy and major adverse cardiovascular or cerebrovascular events (MACCEs) was also compared between the 2 groups. RESULTS: Statistically significant difference between the 2 groups regarding the occurrence of CIN was observed (12.5 vs. 29.1%, p = 0.004). The hydration volume of the IVCU-guided group was significantly higher than that of the routine group (p < 0.001). In addition, patients receiving IVCU-guided hydration had significantly lower risk of developing MACCEs than patients in the control group during the 18-month follow-up (14.4 vs. 27.2%, p = 0.027). CONCLUSION: Our findings support that IVCU-guided hydration is superior to standard hydration in prevention of CIN and may substantially reduce longtime composite major adverse events.

Low Serum Calcitonin Gene-Related Peptide Level is Associated with Severity of Coronary Stenosis.

PURPOSE: To evaluate the relationship between the serum calcitonin gene-related peptide (CGRP) level and severity of coronary stenosis. METHODS: A total of 233 eligible patients who underwent coronary angiography were divided into two groups: a control and a coronary heart disease (CHD) group. The angiographic severity of coronary stenosis was evaluated by SYNTAX and Gensini scores. The incidence of major adverse cardiovascular events within two years was collected. RESULTS: A negative correlation between serum CGRP levels and Gensini scores was observed in all patients (r=-0.352, p<0.001), the control group (r=-0.422, p<0.001) and the CHD group (r=-0.393, p<0.001). Serum CGRP levels were negatively associated with SYNTAX scores in the CHD group (r=-0.522, p<0.001). The area under the curve of CGRP for identifying high SYNTAX scores (>22) was 0.772 [95% confidence interval (CI): 0.673-0.870, p<0.001], and for identifying high Gensini scores was 0.744 (95% CI: 0.646-0.842, p<0.001). A CGRP concentration of 25.05 pg/ml was selected as the cutoff point. A low CGRP level (<25.05 pg/ml) was an independent predictor of severe coronary stenosis, a SYNTAX score >22 [odds ratio (OR) =5.819, 95% CI: 2.240-15.116; p<0.001] and a high Gensini score (>64) (OR=4.943, 95% CI: 2.020-12.095; p<0.001). The low CGRP group had a higher incidence of major adverse cardiovascular events within two years (11.1 vs. 3.1%, p=0.031). CONCLUSION: In coronary atherosclerosis patients without acute myocardial injury, serum CGRP levels were negatively associated with the severity of coronary stenosis.

Physiological benefits evaluated by quantitative flow ratio in patients with reduced left ventricular ejection fraction who underwent percutaneous coronary intervention.

BACKGROUND: To explore the clinical benefits of revascularization in patients with different levels of left ventricular ejection fraction (LVEF) from the perspective of quantitative flow ratio (QFR). METHODS: Patients who underwent successful percutaneous coronary intervention (PCI) and one-year angiographic follow-up were retrospectively screened and computed by QFR analysis. Based on their LVEF, 301 eligible patients were classified into reduced LVEF (≤ 50%, n = 48) and normal LVEF (> 50%, n = 253) groups. Pre-PCI QFR, post-PCI QFR, follow-up QFR, late lumen loss (LLL), LVEF and major adverse cardiovascular and cerebrovascular events (MACCEs) at one year were compared between groups. RESULTS: The reduced LVEF group had a lower mean pre-PCI QFR than the normal LVEF group (0.67 ± 0.16 vs. 0.73 ± 0.15, p = 0.004), but no significant difference was found in the post-PCI or one-year follow-up QFR. No association was found between LVEF and QFR at pre-PCI or follow-up. The reduced LVEF group had greater increases in QFR (0.27 ± 0.18 vs. 0.22 ± 0.15, p = 0.043) and LVEF (6.05 ± 9.45% vs. - 0.37 ± 8.11%, p < 0.001) than the normal LVEF group. The LLL results showed no difference between the two groups, indicating a similar degree of restenosis. The reduced LVEF group had a higher incidence of MACCEs (14.6% vs. 4.3%, p = 0.016), which was mainly due to the higher risk of heart failure (6.3% vs. 0%, p = 0.004). CONCLUSION: Compared to the corresponding normal LVEF patients, patients with reduced LVEF who underwent successful PCI were reported to have greater increases in QFR and LVEF, a similar degree of restenosis, and a higher incidence of MACCEs due to a higher risk of heart failure. It seems that patients with reduced LVEF gain more coronary benefits from successful revascularization from the perspective of flow physiology evaluations.

Punicalagin protects H9c2 cardiomyocytes from doxorubicin-induced toxicity through activation of Nrf2/HO-1 signaling.

Doxorubicin (DOX) is a wide-spectrum antitumor agent, but its clinical application is largely limited by its cardiotoxicity. Therefore, identification of effective agents against DOX-induced cardiotoxicity is of critical importance. The present study aimed to determine the beneficial role of punicalagin (PUN), a polyphenol isolated from pomegranate, in DOX-induced cardiotoxicity in vitro and explored the underlying mechanisms. H9c2 cardiomyocytes were pretreated with different concentrations (50, 100 and 200 µM) of PUN prior to DOX exposure. The results showed that PUN pretreatment significantly increased cell viability, inhibited lactate dehydrogenase (LDH) release and suppressed cell apoptosis induced by DOX. Additionally, PUN pretreatment attenuated the loss of mitochondrial membrane potential and cytochrome c release. Besides, PUN further enhanced the expression of nuclear Nrf2 and HO-1 in DOX-treated H9c2 cells, and the aforementioned beneficial effects of PUN were partially abolished by small interfering RNA (siRNA)-mediated Nrf2 knockdown. Hence, our findings clearly revealed that PUN might be a promising agent for alleviating the cardiotoxicity of DOX, and Nrf2/HO-1 signaling might serve a critical role during this process.

Elevated endocan concentration is associated with coronary slow flow.

We sought to assess whether serum endocan concentration is correlated with coronary slow flow (CSF). We measured serum endocan concentration in 93 patients with CSF and in 206 controls. Serum endocan concentration was measured by enzyme-linked immunosorbent assay (ELISA). The presence of CSF was assessed by thrombolysis in myocardial infarction (TIMI) frame count (TFC) method. We demonstrated that serum endocan concentration is significantly higher in CSF patients (n = 93) than that in controls (n = 206) (1.03 [range 0.63-1.33] vs. 0.80 [range 0.52-1.09] ng/mL, p = 0.002). Multivariate logistic regression analysis revealed that serum endocan concentration was independently associated with the presence of CSF (odds ratio 1.774, 95% confidence interval 1.064-2.958; p = 0.028). Serum endocan concentration was positively correlated with mean-TFC in CSF patients (r = 0.289, p = 0.005). These results revealed that endocan might be a useful biomarker for predicting the presence and severity of CSF. Therapeutic interventions by down-regulating endocan to delay the progressive process of CSF warrants further investigations.

N,N-dimethylsphingosine attenuates myocardial ischemia-reperfusion injury by recruiting regulatory T cells through PI3K/Akt pathway in mice.

N,N-dimethylsphingosine (DMS) has been documented to be in vitro protective against myocardial ischemia-reperfusion injury (IRI) and can recruit CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs), which may participate in the cardioprotection. We hypothesized that when in vivo applied after a myocardial ischemia, DMS may be cardioprotective by recruiting Tregs. Myocardial IRI was induced in C57BL/6 mice by occluding the left main coronary arteries followed by relaxation, and DMS (0.43 mg/kg) was intravenously injected 5 min after the onset of ischemia. We found that in wild-type (WT) mice, compared with the ischemia-reperfusion group, DMS reduced the infarct size (47.1 ± 8.9 vs. 33.1 ± 3.4 %, p < 0.01), and neutrophil infiltration at 24 h reperfusion (R) evaluated by TTC and immunohistochemical staining, respectively, and increased the aggregation of Tregs [(6 ± 1)/mm(2) vs. (30 ± 4)/mm(2), p < 0.01], peaking at 1 h R by immunofluorescence staining, with reduced gene expression of inflammatory factors at 4 h R in the reperfused myocardium by real-time PCR. This protection was abolished by phosphatidylinositol 3-kinase (PI3K)/Akt inhibitor or Tregs-depleting antibody. Relative to WT mice, the cardioprotection conferred by T cell- and B cell- deficient Rag2 knockout (KO) mice was not strengthened by DMS or by DMS and the adoptive transfer of Tregs from WT mice, but was abolished by DMS and WT non-Tregs and was recaptured by the cotransfer with WT Tregs but not with Akt1(+/-) mice-derived Tregs. In conclusion, applied at an early stage of ischemia, DMS may be in vivo protective against myocardial IRI by recruiting Tregs via PI3K/Akt pathway.