The Effects of Coenzyme Q10 on Contrast-Induced Acute Kidney Injury in Type 2 Diabetes: A Randomized Clinical Trial.

Contrast-induced acute kidney injury (CI-AKI) is a frequent challenge following the injection of contrast media and its subsequent oxidative stress. The aim of the present study was to evaluate the preventive effects of coenzyme Q10 (Q10), as a mitochondrial-targeted antioxidant in CI-AKI in diabetic patients, who account for a large proportion of angiographic cases. A total of 118 diabetic patients were randomly assigned to receive 120 mg of oral coenzyme Q10 (Q10 group) or placebo (Placebo group) for four days, starting 24 hours before contrast media injection. Blood urea nitrogen (BUN), serum and urinary creatinine, estimated glomerular filtration rate (eGFR), urinary malondialdehyde (UMDA), urinary total antioxidant capacity (UTAC), and urinary mitochondrial to nuclearDNA ratios (mtDNA/nDNA ratio) were evaluated before and after the treatment period. Urine sediments were also evaluated to report the urine microscopy score (UMS).The levels of BUN, serum and urine creatinine, and UMS were similar in the Q10 and placebo groups. EGFR was lower in the Q10 group before the treatment (p=0.013) but not after. The urinary mtDNA/nDNA ratio was 3.05±1.68 and 3.69±2.58 in placebo and Q10 groups, but UTAC was found to be lower in Q10 both before (p=0.006) and after the treatment (p<0.001). The incidence of CI-AKI was 14.40% and the mtDNA/nNDA ratio was similar between CI-AKI and non-CI-AKI patients. In conclusion, Q10 treatment shows no favorable effect on prevention of CI-AKI or a urinary mtDNA/nDNA ratio among diabetic patients.

Very Early Discharge of Patients with ST-Segment-Elevation Myocardial Infarction after Primary Percutaneous Coronary Intervention.

Background: The discharge of uncomplicated patients with ST-segment-elevation myocardial infarction (STEMI) within 48 to 72 hours has been proven safe and feasible. The safety and feasibility of the very early discharge (≤48 h) of such patients, especially during the COVID-19 pandemic with limited bed availability and infection risk, have yet to be evaluated. Methods: In this cohort study on 108 patients with STEMI who presented to Farshchian Heart Center between February and May 2020, 30 patients received fibrinolysis and 78 were scheduled for emergent coronary angiography. One patient had no coronary obstruction, 3 underwent emergent surgery, and 3 had high-risk features mandating a prolonged stay. The remaining patients were assigned to either Group A (≤48 h) or Group B (>48 h) regarding hospital discharge. Demographic, angiographic, procedural, and outcome data were compared between the 2 groups. Results: Group A consisted of 51 patients, including 7 women (13.7%), at a mean age of 62.74±12.35 years, and Group B comprised 20 patients, including 4 women (20.0%), at a mean age of 65.20±12.82 years. The mean hospital length of stay was 38.02±9.15 hours in Group A and 88.20±23.31 hours in Group B (P<0.001). The mean stent diameter was smaller in Group B (3.19±0.34 mm vs 2.96±0.29 mm; P=0.008). Demographic, angiographic, procedural, and outcome data, including the rates of in-hospital, 1-week, and 1-month mortality, were similar between the 2 groups. Conclusion: This study shows that a hospital discharge in less than 48 hours in low-risk patients with STEMI is safe and feasible. The potential advantages of this approach in the COVID-19 pandemic should be balanced against its risks.

Higher circulating levels of ANGPTL8 are associated with body mass index, triglycerides, and endothelial dysfunction in patients with coronary artery disease.

Bac Coronary artery disease (CAD) is the leading cause of death worldwide and most commonly develops as a result of atherosclerosis. ANGPTL8 is a secreted adipokine that regulates lipid metabolism and is associated with cardiometabolic diseases, including type 2 diabetes and CAD. However, the association between circulating ANGPTL8 levels and CAD is inconsistent among studies and the mechanism by which ANGPTL8 contributes to CAD development remains poorly understood. Here we sought to evaluate the relationship between ANGPTL8 levels and endothelial dysfunction and adipose tissue inflammation in CAD patients. Concentrations of ANGPTL8, adiponectin, TNF-α, IL6, hsCRP, ICAM-1, and VCAM-1 were measured by ELISA in serum samples from 192 CAD patients diagnosed with stenosis > 50% in at least one coronary artery by angiography and 71 individuals with normal heart function. Serum ANGPTL8 levels were significantly higher in CAD patients compared to controls (83.84 ± 23.25 ng/mL vs. 50.45 ± 17.73; p < 0.001), independent of adjustment for age, sex, BMI, smoking and statin use. ANGPTL8 could also differentiate CAD patients from controls with 82.3% specificity and 81.4% sensitivity (p < 0.001). Adiponectin levels were lower in CAD patients, while ICAM-1, VCAM-1, TNF-α, IL6, and hsCRP levels were higher compared to non-CAD controls (all p < 0.001). ANGPTL8 levels were associated with BMI in controls and with BMI, TG, and ICAM-1 in CAD patients. The presence of elevated ANGPTL8 levels in CAD patients and independent association with TG and ICAM-1 suggest a possible role related to endothelial dysfunction in the pathogenesis of atherosclerosis.

Impact of stent type on incidence of major adverse cardiac events in large coronary arteries with tubular and diffuse lesions.

BACKGROUND: The aim of this study was to compare 3 year incidence of major adverse cardiac events (MACE) between bare metal stents (BMS) and drug-eluting stents (DES) in large coronary arteries with tubular and diffuse lesions. METHODS: Seven hundred forty-five consecutive patients (894 lesions) who underwent percutaneous coronary intervention (PCI) on large coronary arteries (3.0, 3.5 and 4 mm) with tubular (10-20 mm length) or diffuse (>20 mm) lesions using BMS or DES at Ekbatan University Hospital, Hamadan, Iran between October 2009 and September 2012 were included. Patients were divided into six groups based on the diameter and length of the stents: 3.0*≤20 mm, 3.0*>20 mm, 3.5*≤20 mm, 3.5*>20 mm, 4.0*≤20 mm and 4.0*>20 mm. Follow-up visits were set at 1, 2, and 3 years after the procedure. Endpoints of the study were MACE including cardiac death, nonfatal MI (due to in-stent thrombosis) and target lesion revascularization (TLR). RESULTS: Cardiac death occurred in 12 patients (1.7%), (1.8% in BMS vs. 1.2% in DES). The incidence of MACE was significantly higher in 3-mm coronary arteries with diffuse lesions (>20 mm) in BMS group; however, there were no statistically significant difference in the incidence of MACE following PCI with BMS and DES in 3, 3.5 and 4 mm coronary arteries with tubular lesions (≤20 mm) and 3.5 and 4 mm coronary arteries with diffuse lesions. CONCLUSIONS: Since the incidence of MACEs did not differ significantly between BMS and DES in most sizes, we suggested that PCI with BMS for coronary arteries in the mentioned sizes can be safe and effective. Further randomized clinical trials focusing simultaneously on diameter and the length of stents are required to corroborate this finding.

Effect of Heparin Administration during Coronary Angiography on Vascular or Peripheral Complications: A Single-Blind Randomized Controlled Clinical Trial.

BACKGROUND: Coronary angiography consists of the selective injection of contrast agents in coronary arteries. Optimal strategy for heparin administration during coronary angiography has yet to be determined. We assessed the effect of heparin administration during coronary angiography on vascular, hemorrhagic, and ischemic complications. METHODS: Five hundred candiates for diagnostic coronary angiography (femoral approach) were randomly divided into case (intravenous Heparin [2000-3000 units]) and control (placebo) groups. Assessment included vascular complications like groin hematoma, retroperitoneal hematoma, pseudoaneurysm, active hemorrhage, cerebral ischemia, and clot formation in the catheter or the sheath during angiography. Information was obtained about the patients' age, sex, and hypertension and diabetes mellitus history. Patients with severe peripheral vascular disease, aortic stenosis, history of coagulopathy, and angiography over 30 minutes were excluded. RESULTS: Nine patients from each group were excluded. The remaining 482 patients included 285 (59.1%) men and 197 (40.9%) women. In the case group (n=241), 7 (2.9%) patients experienced active hemorrhage at the site of angiographic puncture, 2 (0.83%) developed groin hematoma, and 8 (3.32%) experienced clot formation during angiography, while the corresponding figures for the control group (n=241) were 3 (1.24%), 2 (083%), and 13 (5.39%), respectively. No significant differences were found in hemorrhagic, ischemic, and vascular complications between the two groups. CONCLUSION: Heparin administration during coronary angiography had no effect on clot formation as well as hemorrhagic, ischemic, and vascular complications in our patients. TRIAL REGISTRATION NUMBER: IRCT201202199080N1.

Plasma homocysteine level and its genotypes as a risk factor for coronary artery disease in patients undergoing coronary angiography.

BACKGROUND: Hyperhomocysteinemia has recently been identified as a risk factor for coronary artery disease. Some genetic variants (such as C677T polymorphism) are postulated in this regard. We studied the relation between hyperhomocysteinemia and the above genetic variant and risk of coronary artery disease (CAD) and also the number of involved vessels. MATERIALS AND METHODS: From a total of 90 patients, 45 showed angiographically documented CAD and 45 had clinical manifestations of CAD but a negative angiography. Blood homocysteine level and C677T polymorphism were evaluated by Enzyme-linked immunosorbent assay (ELISA) and polymerase chain reaction (PCR) respectively. RESULTS: Homocysteine level was significantly higher in the case group (P < 0.001) but no correlation was found between its level and extent of CAD. More homozygote cases of C677T allele were detected in the case group which was not related to the extent of CAD either. CONCLUSION: Presence of hyperhomocysteinemia increases the risk of CAD but does not predict the extent of it.