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Left ventricular assist devices (LVADs) mechanically unload the heart and coupled with neurohormonal therapy can promote reverse cardiac remodeling and myocardial recovery. Minimally invasive LVAD decommissioning with the device left in place has been reported to be safe over short-term follow-up. Whether device retention reduces long-term safety, or sustainability of recovery is unknown. This is a dual-center retrospective analysis of patients who had achieved responder status (left ventricular ejection fraction, LVEF ≥40% and left ventricular internal diastolic diameter, LVIDd ≤6.0 cm) and underwent elective LVAD decommissioning for myocardial recovery from May 2010 to January 2020. All patients had outflow graft closure and driveline resection with the LVAD left in place. Emergent LVAD decommissioning for an infection or device thrombosis was excluded. Patients were followed with serial echocardiography for up to 3-years. The primary clinical outcome was survival free of heart failure hospitalization, LVAD reimplantation, or transplant. During the study period 515 patients received an LVAD and 29 (5.6%) achieved myocardial recovery, 12 patients underwent total device explantation or urgent device decommissioning, 17 patients underwent elective LVAD decommissioning, and were included in the analysis. Median age of patients at LVAD implantation was 42 years (interquartile range, IQR: 25-54 years), all had a nonischemic cardiomyopathy, and 5 (29%) were female. At LVAD implantation, median LVEF was 10% (IQR: 5%-15%), and LVIDd 6.6 cm (IQR: 5.8-7.1 cm). There were 11 hydrodynamically levitated centrifugal-flow (65%), and 6 axial-flow LVADs (35%). The median duration of LVAD support before decommissioning was 28.7 months (range 13.5-36.2 months). As compared to the turndown study parameters, 1-month post-decommissioning, median LVEF decreased from 55% to 48% (p = 0.03), and LVIDd increased from 4.8 cm to 5.2 cm (p = 0.10). There was gradual remodeling until 6 months, after which there was no statistical difference on follow-up through 3-years (LVEF 42%, LVIDd 5.6 cm). Recurrent infections affected 41% of patients leading to 3 deaths and 1 complete device explant. Recurrent HF occurred in 1 patient who required a transplant. Probability of survival free of HF, LVAD, or transplant was 94% at 1-year, and 78% at 3-years. LVAD decommissioning for myocardial recovery was associated with excellent long-term survival free from recurrent heart failure and preservation of ventricular size and function up to 3-years. Reducing the risk of recurrent infections, remains an important therapeutic goal for this management strategy. [ABSTRACT FROM AUTHOR]

Background: The contribution of inflammation to the incidence of cardiovascular disease (CVD) has been increasingly recognized in recent years. We investigated the relationship of aortic vascular uptake of 18F-FDG by PET/CT and aortic wall thickness (AWT) by MRI in psoriasis, a chronic inflammatory disease with increased incidence of CVD. One hundred sixty-five patients with plaque psoriasis participated in an ongoing longitudinal cohort study. Subclinical atherosclerosis was assessed as aortic uptake of 18F-FDG by PET/CT reported as target-to-background ratio (TBR) and AWT by MRI reported as maximal thickness. Results: Patients with psoriasis were middle aged, predominantly male, and had mild CV risk by traditional risk factors. Psoriasis severity as measured by PASI score was a notable determinant of AWT (ρ = 0.20, p = 0.01). Moreover, aortic vascular uptake of 18F-FDG associated with AWT by MRI at baseline in unadjusted analysis (β = 0.27 p = 0.001) and following adjustment for traditional cardiovascular risk factors, waist-to-hip ratio, and statin use (β = 0.21 p = 0.01). Finally, following 1 year of psoriasis treatment, a decrease in aortic vascular uptake of 18F-FDG was associated with a reduction in AWT in fully adjusted models (β = 0.33, p = 0.02). Conclusion: In conclusion, we demonstrate that psoriasis severity and aortic vascular uptake of 18F-FDG in the aorta were associated with AWT. Following treatment of psoriasis, a decrease in aortic vascular uptake of 18F-FDG was associated with a reduction in AWT at 1 year. These findings suggest that aortic vascular uptake of 18F-FDG is associated with early evidence of vascular disease assessed by aortic wall thickness. Prospective studies in larger populations including other inflammatory diseases are warranted. [ABSTRACT FROM AUTHOR]

Introduction: Evidence suggests that inflammatory mediators are important in the pathogenesis of atherosclerosis and their inhibition not only reduces cardiovascular (CV) events, but also may favorably modify plaque morphology. Psoriasis (PSO) is a chronic inflammatory disease associated with early myocardial infarction and it was recently shown that it is associated with non-calcified plaque. We hypothesized that anti-inflammatory biologic therapy for psoriasis will favorably modify coronary plaque morphology compared to non-biologic treated patients. Methods: Consecutive patients (n=107) stratified by biologic therapy underwent coronary computed tomography angiography (320 detector row, Toshiba) at baseline and one-year. Coronary plaque indices and attenuation-based plaque sub-components were quantified using dedicated software (QAngio, Medis). Reader was blinded to both time of scan and treatment. Results: PSO patients were middle aged and at low CV risk by traditional risk scores with no significant differences in demographics, laboratory values, or coronary indices between the two groups. At one-year (Table 1) , there was a reduction in non-calcified plaque burden in the biologic treated group only (1.12 ± 0.46 mm2 vs. 1.04 ± 0.40 mm2; p<0.001). While there was a significant reduction in necrotic core (NC) in the biologic group, there was progression of NC in the non-biologic group (ΔNC, Biologic: -0.11 mm2 vs. Non-biologic: 0.005 mm2; p=0.02). Additionally, there was an increase in fibrous burden in both groups; however, the difference between change in fibrous burden (FB) in the biologic group was greater (ΔFB, Biologic: 0.02 mm2 vs. Non-biologic: 0.008 mm2; p=0.02). After adjustment for traditional CV risk factors including age, gender, body mass index, and statin use, biologic therapy was associated with reduction in NC (β=0.13, p=0.02). Conclusions: Biologic therapy had significant effects on coronary plaque morphology, with a reduction in overall non-calcified plaque burden driven by increases in fibrous burden and decrease in necrotic core. These findings suggest that biologic therapies may reduce both coronary plaque burden and high-risk features. Larger, randomized studies are needed to confirm these results. [ABSTRACT FROM AUTHOR]