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Frontiers in Cardiovascular Medicine 2021Evaluate the evidence on the abnormalities of the aortic root and heart valves, risk and prognostic factors for heart valve disease and valve replacement surgery in...
Evaluate the evidence on the abnormalities of the aortic root and heart valves, risk and prognostic factors for heart valve disease and valve replacement surgery in spondyloarthritis. A systematic literature review was performed using Medline, EMBASE and Cochrane databases until July 2021. Prevalence, incidence, risk and prognostic factors for heart valve disease; dimension, morphology, and pathological abnormalities of the valves were analyzed. Patient characteristics (younger age, history of cardiac disease or longer disease duration) and period of realization were considered for the analysis. The SIGN Approach was used for rating the quality of the evidence of the studies. In total, 37 out of 555 studies were included. Overall, the level of evidence was low. The incidence of aortic insufficiency was 2.5-3.9‰. Hazard Ratio for aortic insufficiency was 1.8-2.0. Relative risk for aortic valve replacement surgery in ankylosing spondylitis patients was 1.22-1.46. Odds ratio for aortic insufficiency was 1.07 for age and 1.05 for disease duration. Mitral valve abnormalities described were mitral valve prolapse, calcification, and thickening. Aortic valve abnormalities described were calcification, thickening and an echocardiographic "subaortic bump." Abnormalities of the aorta described were thickening of the wall and aortic root dilatation. The most common microscopic findings were scarring of the adventitia, lymphocytic infiltration, and intimal proliferation. A higher prevalence and risk of aortic valve disease is observed in patients with ankylosing spondylitis. Studies were heterogeneous and analysis was not adjusted by potential confounders. Most studies did not define accurate outcomes and may have detected small effects as being statistically significant.
PubMed: 34631824
DOI: 10.3389/fcvm.2021.719523 -
Journal of Vascular Surgery Jun 2021Restenosis after carotid endarterectomy (CEA) limits its long-term efficacy for stroke prevention. Thus, it is of utmost importance to identify the factors that...
OBJECTIVE
Restenosis after carotid endarterectomy (CEA) limits its long-term efficacy for stroke prevention. Thus, it is of utmost importance to identify the factors that predispose a patient to restenosis after CEA. This systemic review aims to survey the current literature regarding restenosis after CEA and discuss the predictive value of carotid plaque features.
METHODS
A systemic review of studies on the predictive value of carotid plaque features for restenosis after CEA was conducted according to the PRISMA guidelines. PubMed/MEDLINE and Embase databases were searched up to March 20, 2020. Two authors independently extracted the data and assessed the risk of bias with the Quality in Prognosis Studies tool. Given the heterogeneity in the measurement of prognostic factors, types of CEA, and clinical outcomes, a qualitative synthesis was performed.
RESULTS
Twenty-one articles with a sample size that ranged from 11 to 1203 were included in this systematic review. Based on the presence of calcification in original carotid plaques, two progression patterns of restenosis were hypothesized: patients with calcified plaques may experience a temporary increase in the intima-media thickness (IMT) followed by a decrease in IMT after CEA, whereas patients with noncalcified plaques may experience a gradual increase in IMT after CEA. Accordingly, patients with a high calcium score may have a high restenosis rate within 6 months after CEA and a low restenosis rate thereafter. Thus, the late restenosis rate in patients with uniformly echogenic plaques was lower than that in patients with uniformly echolucent plaques. Pathologically, a lipid-rich, inflammatory carotid plaque is associated with a decreased risk of restenosis within 1 year after CEA, mainly owing to the relatively mild reactive intimal hyperplasia at the surgical site and active inflammation in the remaining media and adventitia. Molecular predictors for restenosis included a Mannose-binding lectin 2 genotype, preoperative C-reactive protein, serum homocysteine, apolipoprotein J, vitamin C, and telomere length of carotid plaques.
CONCLUSIONS
This review demonstrated that carotid plaque features, including imaging features, cellular composition, and molecular features, are correlated with the risk of restenosis after CEA. A comprehensive evaluation of plaque characteristics may help to stratify the risk of restenosis after CEA.
Topics: Adult; Aged; Aged, 80 and over; Biomarkers; Carotid Stenosis; Endarterectomy, Carotid; Female; Humans; Male; Middle Aged; Neointima; Plaque, Atherosclerotic; Recurrence; Risk Assessment; Risk Factors; Time Factors; Treatment Outcome; Vascular Calcification
PubMed: 33253876
DOI: 10.1016/j.jvs.2020.10.084 -
Biomedicines Oct 2021The aim of this systematic review was to pool evidence from studies testing if pentagalloyl glucose (PGG) limited aortic expansion in animal models of abdominal aortic...
BACKGROUND
The aim of this systematic review was to pool evidence from studies testing if pentagalloyl glucose (PGG) limited aortic expansion in animal models of abdominal aortic aneurysm (AAA).
METHODS
The review was conducted according to the PRISMA guidelines and registered with PROSPERO. The primary outcome was aortic expansion assessed by direct measurement. Secondary outcomes included aortic expansion measured by ultrasound and aortic diameter at study completion. Sub analyses examined the effect of PGG delivery in specific forms (nanoparticles, periadventitial or intraluminal), and at different times (from the start of AAA induction or when AAA was established), and tested in different animals (pigs, rats and mice) and AAA models (calcium chloride, periadventitial, intraluminal elastase or angiotensin II). Meta-analyses were performed using Mantel-Haenszel's methods with random effect models and reported as mean difference (MD) and 95% confidence intervals (CIs). Risk of bias was assessed with a customized tool.
RESULTS
Eleven studies reported in eight publications involving 214 animals were included. PGG significantly reduced aortic expansion measured by direct observation (MD: -66.35%; 95% CI: -108.44, -24.27; = 0.002) but not ultrasound (MD: -32.91%; 95% CI: -75.16, 9.33; = 0.127). PGG delivered intravenously within nanoparticles significantly reduced aortic expansion, measured by both direct observation (MD: -116.41%; 95% CI: -132.20, -100.62; < 0.001) and ultrasound (MD: -98.40%; 95% CI: -113.99, -82.81; < 0.001). In studies measuring aortic expansion by direct observation, PGG administered topically to the adventitia of the aorta (MD: -28.41%; 95% CI -46.57, -10.25; = 0.002), studied in rats (MD: -56.61%; 95% CI: -101.76, -11.46; = 0.014), within the calcium chloride model (MD: -56.61%; 95% CI: -101.76, -11.46; = 0.014) and tested in established AAAs (MD: -90.36; 95% CI: -135.82, -44.89; < 0.001), significantly reduced aortic expansion. The findings of other analyses were not significant. The risk of bias of all studies was high.
CONCLUSION
There is inconsistent low-quality evidence that PGG inhibits aortic expansion in animal models.
PubMed: 34680560
DOI: 10.3390/biomedicines9101442