Angulation of the inflow cannula >7° from the apical axis (axis connecting mitral valve and ventricular apex) leads to markedly unfavorable hemodynamics as determined by computational fluid dynamics. Computational hemodynamic simulations incorporating Lagrangian and Eulerian metrics are a powerful tool for studying optimization of LVAD implantation strategies, with the long-term potential of improving outcomes.
This study quantifies thrombogenic potential of a wide range of LVAD outflow graft anastomosis angles through. This study aims at clarifying the influence of a single parameter (outflow graft angle) on the thrombogenesis associated with flow patterns in the aortic root after LVAD implantation. This is an important and poorly-understood aspect of LVAD therapy, because several studies have shown strong inter-and intra-patient thrombogenic variability and current LVAD implantation strategies do not incorporate outflow graft angle optimization. Accurate platelet-level investigation, enabled by statistical treatment of outliers in Lagrangian particle tracking, demonstrate a strong influence of outflow graft anastomoses angle on thrombogenicity (platelet residence times and activation state characterized by shear stress accumulation) with significantly reduced thrombogenic potential for acutely-angled anastomosed outflow grafts. The methodology presented in this study provides a device-neutral platform for conducting comprehensive thrombogenicity evaluation of LVAD surgical configurations, empowering optimal patient-focused surgical strategies for long-term treatment and care for advanced heart failure patients.
Background-Whether individuals with peripheral artery disease (PAD) identified by screening ankle-brachial index (ABI) benefit from preventative therapies to reduce cardiovascular risk is unknown. We aimed to determine the number of US adults with PAD not receiving preventative therapies and whether treatment is associated with reduced mortality in PAD subjects without known cardiovascular disease (CVD).Methods and Results-We analyzed data from the National Health and Nutrition Examination Survey (NHANES) 1999-2004 with mortality follow-up through December 31, 2006. PAD was defined as ABI ≤ 0.90. Of 7458 eligible participants ≥ 40 years, weighted PAD prevalence was 5.9% ± SE 0.3%, corresponding to approximately 7.1 million US adults with PAD. Statin use was reported in only 30.5% ± 2.5%, angiotensin converting enzyme inhibitor/angiotensin receptor blocker (ACEI/ARB) use in 24.9% ± 1.9%, and aspirin use in 35.8% ± 2.9%, corresponding to 5.0 million adults with PAD not taking statins, 5.4 million not taking ACEI/ARBs, and 4.5 million not receiving aspirin. Adjusting for age, gender, and race/ethnicity, PAD was associated with all-cause mortality (HR 2.4 [1.9-2.9], p<0.0001). Even after excluding individuals with known CVD, subjects with PAD had higher mortality rates (16.1% ± 2.1%) than subjects without PAD or CVD (4.1% ± 0.3%) with adjusted HR 1.9 [1.3-2.8], p=0.001. Among PAD subjects without CVD, use of multiple preventative therapies was associated with 65% lower all-cause mortality ], p=0.02).Conclusions-Millions of US adults with PAD are not receiving secondary prevention therapies. Treatment with multiple therapies is associated with reduced all-cause mortality.
The prevalence of ventricular assist device (VAD) therapy has continued to increase due to a stagnant donor supply and growing advanced heart failure (HF) population. We hypothesize that left ventricular (LV) size strongly influences biocompatibility and risk of thrombosis. Unsteady computational fluid dynamics (CFD) was used in conjunction with patient-derived computational modeling and virtual surgery with a standard, apically implanted inflow cannula. A dual-focus approach of evaluating thrombogenicity was employed: platelet-based metrics to characterize the platelet environment and flow-based metrics to investigate hemodynamics. Left ventricular end-diastolic dimensions (LVEDds) ranging from 4.5 to 6.5 cm were studied and ranked according to relative thrombogenic potential. Over 150,000 platelets were individually tracked in each LV model over 15 cardiac cycles. As LV size decreased, platelets experienced markedly increased shear stress histories (SHs), whereas platelet residence time (RT) in the LV increased with size. The complex interplay between increased SH and longer RT has profound implications on thrombogenicity, with a significantly higher proportion of platelets in small LVs having long RT times and being subjected to high SH, contributing to thrombus formation. Our data suggest that small LV size, rather than decreased VAD speed, is the primary pathologic mechanism responsible for the increased incidence of thrombosis observed in VAD patients with small LVs.
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