ArticleThe Annals of thoracic surgery2019
A Novel Toroidal-Flow Left Ventricular Assist Device Minimizes Blood Trauma: Implications of Improved Ventricular Assist Device Hemocompatibility.
Article in The Annals of thoracic surgery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 29 citations in OpenAlex.
- Hemocompatibility of Mechanical Circulatory Support Devices: An Integrated Review of Platelet Function Assessment in In-Vitro Blood Experiments.Annals of biomedical engineering · 2026Review
- Recent Developments in Ventricular Assist Device Therapy.Reviews in cardiovascular medicine · 2025Review
- Current status and future directions in pediatric ventricular assist device.Heart failure reviews · 2024Review
- Review
- Preservation of von Willebrand Factor Activity With the ModulHeart Device.JACC. Basic to translational science · 2024Article
- Advances in Extracorporeal Support Technologies in Critically Ill Children.Indian journal of pediatrics · 2023Review
- Review
- Effect of pulsatility on shear-induced extensional behavior of Von Willebrand factor.Artificial organs · 2022Article
- Pathologic von Willebrand factor degradation is a major contributor to left ventricular assist device-associated bleeding: pathophysiology and evolving clinical management.Annals of cardiothoracic surgery · 2021Article
- Reinventing the displacement left ventricular assist device in the continuous-flow era: TORVAD, the first toroidal-flow left ventricular assist device.Annals of cardiothoracic surgery · 2021Article
- Longitudinal assessment of the platelet transcriptome in advanced heart failure patients following mechanical unloading.Platelets · 2020Article
- Cardiac prostheses-related hemolytic anemia.Clinical cardiology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundContinuous-flow left ventricular assist devices (LVADs) cause blood trauma that includes von Willebrand factor degradation, platelet activation, and subclinical hemolysis. Blood trauma contributes to bleeding, thrombosis, and stroke, which cause significant morbidity and mortality. The TORVAD (Windmill Cardiovascular Systems, Inc, Austin, TX) is a first-of-its kind, toroidal-flow LVAD designed to minimize blood trauma. We tested the hypothesis that the TORVAD causes less blood trauma than the HeartMate II (Abbott Laboratories, Pleasanton, CA) LVAD.
methodsWhole human blood was circulated for 6 hours in ex vivo circulatory loops with a HeartMate II (n = 8; 10,000 rpm, 70 ± 6 mm Hg, 4.0 ± 0.1 L/min) or TORVAD (n = 6; 144 rpm, 72 ± 0.0 mm Hg, 4.3 ± 0.0 L/min). von Willebrand factor degradation was quantified with electrophoresis and immunoblotting. Platelet activation was quantified by cluster of differentiation (CD) 41/61 enzyme-linked immunosorbent assay (ELISA). Hemolysis was quantified by plasma free hemoglobin ELISA.
resultsThe TORVAD caused significantly less degradation of high-molecular-weight von Willebrand factor multimers (-10% ± 1% vs -21% ± 1%, p < 0.0001), accumulation of low-molecular-weight von Willebrand factor multimers (22% ± 2% vs 45% ± 2%, p < 0.0001), and accumulation of von Willebrand factor degradation fragments (7% ± 1% vs 25% ± 6%, p < 0.05) than the HeartMate II. The TORVAD did not activate platelets, whereas the HeartMate II caused significant platelet activation (CD 41/61: 645 ± 20 ng/mL vs 1,581 ± 150 ng/mL, p < 0.001; normal human CD 41/61, 593 ng/mL; range, 400 to 800 ng/mL). Similarly, the TORVAD caused minimal hemolysis, whereas the HeartMate II caused significant hemolysis (plasma free hemoglobin: 11 ± 2 vs 109 ± 10 mg/dL, p < 0.0001; normal human plasma free hemoglobin <4 mg/dL).
conclusionsThe TORVAD design, with markedly lower shear stress and pulsatile flow, caused significantly less blood trauma than the HeartMate II. LVADs with reduced blood trauma are likely to improve clinical outcomes and expand LVAD therapy into patients with less advanced heart failure.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.