Fatty acids and aortic valve stenosis

Plunde, Oscar; Bäck, Magnus

doi:10.33963/kp.a2021.0003

Cited by 9 publications

(8 citation statements)

References 74 publications

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“…This case extends the recently reported significantly decreased pulse upstroke time after surgical AVR 2 by illustrating the change in pulse wave morphology and systolic time intervals, obtained with concomitant CAVI measurement. This case is of particular interest since the patient lacked several hallmark risk factors for AVS, such as hypertension, 3 obesity, 4 diabetes 5 and CKD. 6 This might be a partial explanation to the remarkably low CAVI before surgery but also signifies that patients with concomitant co-morbidities and risk factors for arterial stiffness are likely to present with falsely low CAVI in patients with severe AVS, as suggested previously.…”

Section: Discussionmentioning

confidence: 99%

Pulse Wave Morphology Changes in Aortic Valve Stenosis Detected with Cardio-Ankle Vascular Index

Plunde¹,

Franco‐Cereceda²,

Bäck³

2023

VHRM

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Background Cardio-ankle vascular index (CAV) is a measure of systemic arterial stiffness and has been shown to increase after aortic valve surgery. However, change in CAVI-derived pulse wave morphology has not previously been addressed. Case Study A 72-year-old female was transferred to a large center for heart valve interventions for evaluation of her aortic stenosis. Few co-morbidities were detected on medical history, other than previous radiation treatment for breast cancer, and no signs of other concomitant cardiovascular disease. The patient was accepted for surgical aortic valve replacement due to severe aortic valve stenosis and arterial stiffness was assessed with CAVI, as part of an ongoing clinical study. The pre-operative CAVI was 4.7 which after surgery increased almost 100% to 9.35. In tandem, the slope of systolic upstroke pulse morphology captured from brachial cuffs was changed from a prolonged flattened pattern to a steeper. Conclusion After aortic valve replacement surgery due to aortic valve stenosis, in addition to increased CAVI-derived measures of arterial stiffness, the slope of the CAVI-derived upstroke pulse wave morphology changes to a steeper slope. This finding could have implications in the future of aortic valve stenosis screening and utilization of CAVI.

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Section: Discussionmentioning

confidence: 99%

Pulse Wave Morphology Changes in Aortic Valve Stenosis Detected with Cardio-Ankle Vascular Index

Plunde¹,

Franco‐Cereceda²,

Bäck³

2023

VHRM

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“…Apart from being present from the onset of CAVD, inflammation orchestrates all subsequent events that lead to aortic valve remodeling [ 78 ]. In summary, as part of the initial innate immune response, activated VICs from prior exposure to mechanical stress and cytotoxic oxLDL prompt the recruitment and infiltration of macrophages, T cells, and mast cells via toll-like receptors 2, 4 (TLRs-2,4) and the NF-kB pathway [ 6 , 14 , 15 , 17 , 21 , 37 ].…”

Section: Immunopathogenesis Behind Aortic Diseasementioning

confidence: 99%

Contribution of Oxidative Stress (OS) in Calcific Aortic Valve Disease (CAVD): From Pathophysiology to Therapeutic Targets

Valasciuc

Gosav

Floria

et al. 2022

Cells

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Calcific aortic valve disease (CAVD) is a major cause of cardiovascular mortality and morbidity, with increased prevalence and incidence. The underlying mechanisms behind CAVD are complex, and are mainly illustrated by inflammation, mechanical stress (which induces prolonged aortic valve endothelial dysfunction), increased oxidative stress (OS) (which trigger fibrosis), and calcification of valve leaflets. To date, besides aortic valve replacement, there are no specific pharmacological treatments for CAVD. In this review, we describe the mechanisms behind aortic valvular disease, the involvement of OS as a fundamental element in disease progression with predilection in AS, and its two most frequent etiologies (calcific aortic valve disease and bicuspid aortic valve); moreover, we highlight the potential of OS as a future therapeutic target.

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“…The latter induces over-production of leukotrienes, which may further amplify the inflammatory response in DAS [ 14 ]. More recent studies indicate a role of novel soluble biomarkers in the calcification process, including Galectin-3, fatty acids concentration on aortic leaflets, and non-coding RNAs involved in calcifications [ 15 , 16 , 17 ].…”

Section: Introductionmentioning

confidence: 99%

Serum and Vascular Stiffness Biomarkers Associated with the Severity of Degenerative Aortic Valve Stenosis and Cardiovascular Outcomes

Baran

Niewiara

Podolec

et al. 2022

JCDD

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Background: Although degenerative aortic valve stenosis (DAS) is the most prevalent growth-up congestive heart valve disease, still little known about relationships between DAS severity, vascular stiffness (VS), echocardiographic parameters, and serum biomarkers in patients undergoing transcatheter (TAVR) or surgical aortic valve replacement (SAVR). The objective of this study was to identify biomarkers associated with DAS severity, and those that are associated with cardiovascular death (CVD) and episodes of chronic heart failure (CHF) exacerbation. Methods: A total of 137 patients with initially moderate-to-severe DAS were prospectively evaluated for the relationship between DAS severity, baseline VS, and serum biomarkers (uPAR, GDF-15, Gal-3, IL-6Rα, ET-1, PCSK9, RANTES/CCL5, NT-proBNP, and hs-TnT), and were followed-up for 48 months. The prognostic significance of each variable for CVD and CHF risk was measured by hazard ratio of risk (HR), which was calculated by Cox’s proportional hazard model. Results: DAS severity showed correlations with IL-6Rα (r = 0.306, p < 0.001), uPAR (r = 0.184, p = 0.032), and NT-proBNP (r = −0.389, p < 0.001). Levels of ET-1 and Gal-3 were strongly correlated with VS parameters (r = 0.674, p < 0.001; r = 0.724, p < 0.001). Out of 137 patients, 20 were referred to TAVR, 88 to SAVR, and 29 to OMT. In TAVR patients, the highest levels of ET-1, Gal-3, and VS were found as compared to other patients. The highest incidence of CVD was observed in patients who underwent TAVR (35%), compared to SAVR (8%) and OMT (10.3%) (p = 0.004). In a multivariate analysis, ET-1 occurred predictive of CVD risk (HR 25.1, p = 0.047), while Gal-3 > 11.5 ng/mL increased the risk of CHF exacerbation episodes requiring hospital admission by 12%. Conclusions: Our study indicated that ET-1 and Gal-3 levels may be associated with the outcomes in patients with DAS.

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Fatty acids and aortic valve stenosis

Cited by 9 publications

References 74 publications

Pulse Wave Morphology Changes in Aortic Valve Stenosis Detected with Cardio-Ankle Vascular Index

Pulse Wave Morphology Changes in Aortic Valve Stenosis Detected with Cardio-Ankle Vascular Index

Contribution of Oxidative Stress (OS) in Calcific Aortic Valve Disease (CAVD): From Pathophysiology to Therapeutic Targets

Serum and Vascular Stiffness Biomarkers Associated with the Severity of Degenerative Aortic Valve Stenosis and Cardiovascular Outcomes

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