Evaluation of short and mid-term clinical outcomes in patients with aortic coarctation treated with self-expandable stents.

The present study aimed to evaluate the outcomes of percutaneous treatment of aortic coarctation using self-expandable uncovered Nitinol stents. We conducted a retrospective clinical data review of all patients with aortic coarctation and treated with self-expandable uncovered Nitinol stents at our institution between 2009 and 2019. The gradient pressure across the coarctation site was measured using aortography. Follow-up echocardiography and computed tomography angiography were performed to assess possible stent complications. A total of 127 stents were successfully implanted in 125 patients (64.8% males) with a mean age of 35.36 ± 11.9 years. The gradient across the coarctation site decreased significantly from 67.48 ± 14.79 to 5.04 ± 3.01 mmHg (P < 0.001) after self-expandable stent implantation. Systolic blood pressure (SBP) decreased significantly from 175.53 ± 15.99 to 147.22 ± 12.83 mmHg (P < 0.001) after self-expandable stenting. There were no major technical or clinical complications, including balloon rupture, aneurysmal formation, infection, secondary stent migration, thrombosis, death during the procedure, and in-hospital mortality. On a mean follow-up of 48 ± 23.6 months (12-120 months), the gradient [from 59.43 ± 15.42 to 3.72 ± 1.38 mmHg (P < 0.001)] and SBP [from 175.53 ± 15.99 to 127.99 ± 7.82 mmHg (P < 0.001)] decreased significantly. There was no mortality, aneurysmal formation in the stent site, dislocation, or aortic re-stenosis requiring intervention during mid-term follow-up. Treatment of aortic coarctation using a self-expandable uncovered nitinol stent is safe and effective with promising mid-term outcomes.

High proviral load of human T cell lymphotropic virus type-1 facilitates coronary artery diseases.

OBJECTIVES: Coronary artery disease (CAD) is known as a life threatening disease, worldwide. In this study the role of HTLV-1 infection was evaluated on cardiac involvement in an endemic region of northeastern Iran. MATERIALS AND METHODS: Serologic and molecular tests for HTLV-1 infection were carried out in subjects who had coronary angiography. A real-time PCR, TaqMan method, to quantify HTLV-1 proviral load (PVL), and routine hematological and biochemical tests were performed for study subjects. RESULTS: Twenty nine patients were HTLV-1+CAD+ and 13 cases were HTLV-1+CAD-. Although, there were no significant differences for risk factors like FBS, HDL, triglyceride, systolic and diastolic blood pressure (Cbp, Dbp), waist circumference (WC), hip circumference (WL), cholesterol (P=0.003), and LDL (P=0.007) levels, and monocyte count (P=0.05) had meaningful differences. The mean HTLV-1 PVL in HTLV-1+CAD+ subjects was 992.62±120 which was higher compared with HTLV-1+CAD- group (406.54±302 copies/104 PBMCs). Moreover, HTLV-1 PVL in males (833±108) was lower compared with females (1218±141 copies/104 PBMCs) (P=0.05). Patients with HTLV-1-PVL of more than 500 copies/104 had more diffused atherosclerosis plaque than patients with less than 500 (OR=6.87, 95% CI=1.34-35.05; P=0.016). Furthermore, patients with diffused coronary atherosclerosis had significantly higher levels of HTLV-1 PVL than patients with middle, proximal, and normal location of coronary sclerotic lesions (P<0.05). CONCLUSION: Taken together, in endemic area, HTLV-1 infection, more likely is a facilitating factor for heart complications and the high HTLV-1 PVL might affect CAD manifestations.

HTLV-1-host interactions facilitate the manifestations of cardiovascular disease.

Atherosclerosis is a multifactorial life-threatening disease which an epidemiologic study in Northeastern Iran showed its association with HTLV-1 infection. Therefore, a cross-sectional study of 39 newly diagnosed subjects with angiography test in three groups including 14 coronary artery disease+HTLV-1+ (CAD+HTLV-1+), 8 CAD-HTLV-1+, and 17 CAD+HTLV-1- patients and 11 healthy subjects (CAD-HTLV-1-) were conducted. In the present study, Tax and proviral load (PVL) as HTLV-1 virulence factors, along with host chemokine receptor 1 (CCR1), and CCR2 were investigated. Real-time PCR TaqMan method was carried out for PVL measurement and HTLV-1-Tax, CCR1, and CCR2 expressions in peripheral blood mononuclear cells (PBMCs). Furthermore, the main risk factors, lipid profile, and complete blood count (CBC) were assessed. Expression of CCR1 in CAD+HTLV-1+ group was higher than CAD-HTLV-1+ (P = 0.01) and healthy subjects (P = 0.02). Expression of CCR1 in CAD+HTLV-1+ was higher in comparison with CAD+HTLV-1-group but did not meet 95% CI (P = 0.02), but meaningful at 91% CI. In addition, expression of CCR2 in CAD+HTLV-1+ subjects was higher than CAD-HTLV-1+ and CAD+HTLV-1- (P = 0.001, P = 0.005, respectively). In CAD+HTLV-1- subjects, CCR2 was higher than CAD-HTLV-1+ (P = 0.03). The mean PVL in CAD+HTLV-1+ group is more than CAD-HTLV-1+ (P = 0.041). In HTLV-1+ patients Tax had a positive correlation with cholesterol (R = 0.59, P = 0.01), LDL (R = 0.79, P = 0.004) and a negative correlation with HDL (R = -0.47, P = 0.04). These correlations were stronger in CAD+HTLV-1+. Findings showed that HTLV-1 could alter the expression of CCR2 and, less effect, on CCR1. Moreover, the strong correlation between CCR2 and HTLV-1-Tax with cholesterol, LDL and HDL showed that Tax as the main HTLV-1 virulence factor in cytokine deregulation might be had indirect effects on cholesterol, LDL, and HDL levels.