A propensity score matched valuation on feasibility of low frame rate fluoroscopy during primary percutaneous coronary intervention for patients with STEMI.

The present study aimed to evaluate the feasibility of low frame rate fluoroscopy during primary percutaneous coronary intervention (PPCI) for patients with acute ST elevation myocardial infarction (STEMI). From January 2016 to December 2017, 165 consecutive patients with STEMI who underwent PPCI were retrospectively divided into two groups: the 7.5-frame group (fluoroscopy at 7.5 frames/s) and the 15-frame group (fluoroscopy at 15 frames/s), according to the frame rate of fluoroscopy used in their treatment. Reduction of radiation and safety of fluoroscopy at 7.5 frames/s were compared by a method of propensity score matching (PSM) with fluoroscopy at 15 frames/s. After PSM, there were 56 patients in each group. There were no differences in patients' baseline characteristics between two groups. The 7.5-frame protocol resulted in 48.9% reduction of DAP (9917 ± 5543 cGycm2 vs. 14766 ± 7272 cGycm2, P < 0.001) and 61.1% reduction of AK (1209 ± 562 mGy vs. 1948 ± 1105 mGy, P < 0.001) with comparable procedural time (38.1 ± 15.3 min vs. 38.8 ± 17.2 min, P = 0.830), fluoroscopy time (13.0 ± 7.2 min vs. 13.5 ± 8.1 min, P = 0.703) and contrast volume (122.3 ± 39.4 ml vs. 119.3 ± 49.4 ml, P = 0.725) to the 15-frame group. Meanwhile, this new protocol didn't increase the incidence of contrast-induced nephropathy (23.2% vs. 25.0%, OR = 0.907, 95% CI 0.381-2.157, P = 0.825) and peri-PPCI cumulative adverse events (30.4% vs. 28.6%, OR = 1.090, 95% CI 0.483-2.456, P = 0.836). In conclusion, low frame rate fluoroscopy at 7.5 frames/s is a safe and feasible strategy for reducing radiation during PPCI.

Elevated Human Endothelial Cell-Specific Molecule-1 Level and Its Association With Coronary Artery Disease in Patients With Hypertension.

BACKGROUND: Endothelial dysfunction plays an important role in the pathophysiology of coronary artery disease (CAD). Previous studies suggested that human endothelial cell-specific molecule-1 (endocan) may be a novel endothelial dysfunction marker. This study aims to investigate the relationship between serum endocan level and the presence and severity of CAD in patients with hypertension. METHODS: A total of 190 eligible hypertension patients were enrolled in this study. Serum endocan level was measured by enzyme-linked immunosorbent assay. The presence and severity of CAD were evaluated by coronary angiography. RESULTS: Hypertensive patients with CAD had significantly higher serum endocan level than those without CAD (1.63 ± 0.51 ng/mL vs 1.31 ± 0.65 ng/mL, P < 0.05). Multivariate logistic regression revealed that serum endocan level was independently associated with the presence of CAD (odds ratio, 2.662; 95% confidence interval, 1.560-4.544; P < 0.001). Spearman rank correlation analysis demonstrated that serum endocan level was associated with SYNergy between PCI with TAXUS and Cardiac Surgery score (r = 0.349, P = 0.001). CONCLUSIONS: Serum endocan level is independently correlated with the presence and severity of CAD in hypertension patients, and those with high endocan level may have an increased risk of developing atherosclerosis.

Low serum adropin is associated with coronary atherosclerosis in type 2 diabetic and non-diabetic patients.

BACKGROUND: Diabetes increases the risk and severity of atherosclerosis. Adropin, a metabolic homeostasis-related protein, has been implicated in the maintenance of metabolic homeostasis. We examined the relationship between serum adropin level and angiographic severity of coronary atherosclerosis in diabetic and non-diabetic patients. METHODS: A total of 392 patients with suspected coronary artery disease, who underwent coronary angiography, were assigned into the type 2 diabetic and non-diabetic groups and also classified into four groups according to the quartiles of adropin level. Venous serum samples were collected for adropin measurement by enzyme-linked immunosorbent assay and for biochemistry assay. The angiographic severity of coronary atherosclerosis was assessed by Gensini, Friesinger, and SYNTAX scores. RESULTS: Compared with non-diabetic patients, diabetic patients had lower serum adropin level and higher Gensini, Friesinger and SYNTAX scores (all p<0.001). Serum adropin level was inversely correlated with the Gensini, Friesinger and SYNTAX scores (rs=-0.389, -0.390 and -0.386, respectively, all p<0.001) among all patients. Low adropin level was an independent predictor of clinically relevant coronary atherosclerosis (SYNTAX score >11), both in diabetic patients [odds ratio (OR) 0.66, 95% confidence interval (CI) 0.53-0.83; p<0.001] and in non-diabetic patients (OR 0.51, 95% CI 0.35-0.74; p<0.001). CONCLUSIONS: Serum adropin level was significantly lower in type 2 diabetic patients than in non-diabetic patients and was inversely and independently associated with angiographic severity of coronary atherosclerosis, suggesting that serum adropin serves as a novel predictor of coronary atherosclerosis.

Long-term outcomes of device closure of very large secundum atrial septal defects: a comparison of transcatheter vs intraoperative approaches.

BACKGROUND: Transcatheter device closure (TCDC) and intraoperative device closure (IODC) have emerged as minimally invasive methods in the treatment of secundum atrial septal defects (ASDs), but the long-term safety and efficacy remains uncertain for the large ASDs. HYPOTHESIS: TCDC may be as safe and efficacious as IODC for closure of large ASDs in terms of long-term clinical outcomes. METHODS: Ninety-two patients who had ASDs with a defect diameter of ≥30 mm were included in this study. The patients received either TCDC (n = 42) or IODC (n = 50). An Amplatzer septal occluder was used in both groups. The dumbbell-like device deploying technique was introduced in the TCDC group. Physical exams, electrocardiography, and echocardiography were performed preprocedurally and postprocedurally at the index follow-up visits. RESULTS: The procedural immediate success rate was 97.6% for TCDC and 98.0% for IODC (P = 0.328). The rate of periprocedural complications was 9.5% for TCDC and 28.0% for IODC (P = 0.026). The mean hospital stay was 7.5 ± 2.7 days for TCDC and 11.9 ± 3.8 days for IODC (P < 0.001). For the mean follow-up of 5.4 ± 0.5 years, there were no cardiac deaths and late complications in either group. No significant residual shunts were documented, and symptoms were significantly improved in both groups. Right and left ventricular diameter, pulmonary artery diameter, and pulmonary systolic pressure were all significantly decreased in both groups (P < 0.05). CONCLUSIONS: The present study confirmed the long-term safety and efficacy for closing a large ASD either by TCDC or IODC. Either of them could become an effective alternative to the surgery for large ASD closure. The authors have no funding, financial relationships, or conflicts of interest to disclose.

Transplantation with survivin-engineered mesenchymal stem cells results in better prognosis in a rat model of myocardial infarction.

AIMS: To investigate the effect of survivin (SVV)-engineered mesenchymal stem cells (MSCs) on post-infarction cardiac performance and remodelling in rats. METHODS AND RESULTS: Mesenchymal stem cells from male Sprague-Dawley rat bone marrow were infected with the self-inactive lentiviral vector GFP-wre-CMV/LTR and Flap-Ubiqutin promoter (GCFU) carrying green fluorescent protein (GFP) gene and SVV recombinant vector (GCFU-SVV). In vitro, modification with SVV increased the secretion of vascular endothelial growth factor (VEGF) by 1.28-fold under hypoxic conditions. In vivo, after permanent left anterior descending artery occlusion, rats were randomized (n = 18 per group) to receive intra-myocardial injections of 100 microL of phosphate-buffered saline without cells (group vehicle) or containing 2 million MSC(GFP) (group MSC(GFP)) or MSC(SVV) (group MSC(SVV)) cells. Cellular survival assessed by reverse transcriptase-polymerase chain reaction for GFP in the MSC(SVV) group was 2.5-fold higher at 7 days and 4.3-fold higher at 28 days after transplantation than in the MSC(GFP) group. When compared with transplantation with MSC(GFP), transplantation with MSC(SVV) further upregulated VEGF expression at 7 and 28 days after myocardial infarction (MI), increased capillary density by 38%, reduced the infarct size by 12.7%, significantly inhibited collagen deposition, and further improved cardiac function at 28 days after MI. CONCLUSION: Transplantation with SVV-engineered MSCs by lentiviral vector leads to better prognosis for MI by enhancing cellular survival.