No abstract

Endocan is a soluble proteoglycan, secreted by human vascular endothelial cells. Endocan is a marker for vascular pathologies and an important mediator of angiogenesis, strongly associated with inflammation, vascular endothelial dysfunction, and atherosclerosis. The relationship between coronary artery ectasia (CAE) and endocan has not been evaluated. We aimed to investigate this association. Fifty-four patients with isolated CAE without coronary stenosis and 30 controls with normal coronary angiogram were included in this study. Endocan plasma concentrations were measured using an enzyme-linked immunosorbent assay. Patients with isolated CAE had significantly higher levels of endocan compared to the controls (18.9 ± 7.3 vs 15.6 ± 3.6 ng/mL; P = .007). There was a significant correlation between endocan levels and severity of isolated CAE according to the Markis classification ( r = -.593, P < .001). Plasma endocan levels may reflect the presence and severity of isolated CAE, suggesting that endocan may be involved in pathogenesis of isolated CAE.

Objective: In this study, we aimed to analyze the TURKMI registry to identify the factors associated with delays from symptom onset to treatment that would be the focus of improvement efforts in patients with acute myocardial infarction (AMI) in Turkey. Methods: The TURKMI study is a nation-wide registry that was conducted in 50 centers capable of 24/7 primary percutaneous coronary intervention (PCI). All consecutive patients (n=1930) with AMI admitted to coronary care units within 48 hours of symptom onset were prospectively enrolled during a predefined 2-week period between November 1, 2018, and November 16, 2018. All the patients were examined in detail with regard to the time elapsed at each step from symptom onset to initiation of treatment, including door-to-balloon time (D2B) and total ischemic time (TIT). Results: After excluding patients who suffered an AMI within the hospital (2.6%), the analysis was conducted for 1879 patients. Most of the patients (49.5%) arrived by self-transport, 11.8% by emergency medical service (EMS) ambulance, and 38.6% were transferred from another EMS without PCI capability. The median time delay from symptom-onset to EMS call was 52.5 (15-180) min and from EMS call to EMS arrival 15 (10-20) min. In ST-segment elevation myocardial infarction (STEMI), the median D2B time was 36.5 (25-63) min, and median min. TIT was significantly prolonged from 151 (90-285) min to 250 (165-372) min in patients transferred from non-PCI centers. The major significant factors associated with time delay were patient-related delay and the mode of hospital arrival, both in STEMI and non-STEMI. Conclusion:The baseline evaluation of the TURKMI study revealed that an important proportion of patients presenting with AMI within 48 hours of symptom onset reach the PCI treatment center later than the time proposed in the guidelines, and the use of EMS for admission to hospital is extremely low in Turkey. Patient-related factors and the mode of hospital admission were the major factors associated with the time delay to treatment.

The main aim of the present study was to investigate the association between epicardial adipose tissue (EAT) and arterial function in patients with asymptomatic hypertension. Patients with hypertension (n = 155) were enrolled consecutively. Patients with decreased arterial compliance (AC) and increased cardioankle vascular index (CAVI) had higher EAT values compared with those with normal AC and CAVI (6.23 ± 1.67 vs 4.91 ± 1.40, P < .001 and 6.02 ± 1.61 vs 4.96 ± 1.46, P = .01, respectively). Analysis using the receiver-operating characteristics curve demonstrated that EAT 5.5 mm constitutes the cutoff value for the presence of increased CAVI with 67% sensitivity and 62% specificity (area under the curve [AUC]: 0.702, 95% confidence interval [CI] 0.590-0.814) and decreased AC with 77% sensitivity and 65% specificity (AUC: 0.756, 95% CI 0.645-0.867). Assessment of EAT during echocardiography examination may provide information on arterial function in patients with asymptomatic hypertension. The link between EAT and arterial stiffness deserves further investigation.

Left ventricular thrombus (LVT) is associated with inflammatory response in survivors with anterior ST-elevation myocardial infarction (STEMI). The C-reactive protein to albumin ratio (CAR) has been proposed as a marker of inflammation. However, there is a lack of data with respect to the role of CAR in LVT development. We investigated the relationship between CAR and LVT development in patients with anterior STEMI treated percutaneously; 955 consecutive patients were enrolled and LVT was observed in 126 (13.2%) patients. Clinical, demographic, and laboratory parameters were recorded. The CAR was significantly higher in patients with LVT (12.6 [8.6-16.1] vs 18.1 [11.5-23], P < .001). Other independent predictors for LVT development were lower ejection fraction, the presence of left ventricular apical aneurysm, proximal left anterior descending lesion location, glycoprotein IIb/IIIa inhibitors treatment, >1 diseased arteries, higher total protein level, neutrophil count, and peak creatine kinase myocardial band activity. In conclusion, the CAR may be useful as a simple tool for predicting LVT development among survivors of anterior STEMI.