scholarly journals SARS-CoV-2 and Atherosclerosis: Should COVID-19 Be Recognized as a New Predisposing Cardiovascular Risk Factor?

2021 ◽  
Vol 8 (10) ◽  
pp. 130
Author(s):  
Mattia Vinciguerra ◽  
Silvia Romiti ◽  
Giuseppe Massimo Sangiorgi ◽  
David Rose ◽  
Fabio Miraldi ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Adverse Outcomes ◽  
Trigger Factor ◽  
Main Target ◽  
Surgical Device ◽  
Thrombotic Complications ◽  
Artery Disease ◽  
Atherosclerotic Process ◽  
New Evidence

At the beginning of the COVID-19 pandemic, the lung was recognized as the main target organ; now, new evidence suggests that SARS-CoV-2 infection leads to vascular disease. In a previous review, we supposed a bidirectional link between endothelial dysfunction and COVID-19, identifying atherosclerosis as having a crucial role in its pathogenesis. Atherosclerosis with an existing endothelial dysfunction may worsen COVID-19 manifestations, leading to adverse outcomes, as largely reported. However, COVID-19 may be the trigger factor in the progression of the atherosclerotic process up to making it clinically manifest. The thrombotic complications can involve not only the atherosclerotic plaque, but also the durability of the surgical device implanted to treat a pre-existing coronary artery disease as recently reported. The burden of the disease makes necessary a long-term stratification of patients, revising drastically targeted therapy among others.

scholarly journals State-of-the-Art Review: Endothelial Dysfunction in the Pathogenesis of Atherosclerosis

2001 ◽  
Vol 7 (4) ◽  
pp. 276-280 ◽  
Author(s):  
Pavel Poredoš
Keyword(s):  
Risk Factors ◽  
Endothelial Dysfunction ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Common Denominator ◽  
Atherosclerotic Lesions ◽  
Circulating Markers ◽  
Thrombotic Complications ◽  
Atherosclerotic Process ◽  
Von Willebrand

Healthy endothelium plays a central role in cardiovascular control. Therefore, endothelial dysfunction (ED), which is characterized by an imbalance between relaxing and contracting factors, procoagulant and anticoagulant substances, and between proinflammatory and antiinflammatory mediators, may play a particularly significant role in the pathogenesis of atherosclerosis. Endothelial dysfunction is closely related to different risk factors of atherosclerosis, and to their intensity and duration. The involvement of risk factors in ED is also supported by results of interventions studies that showed regression of ED with treatment of risk factors. Because risk factors are commonly accompanied by decreased bioavailability of nitric oxide, the common denominator whereby different risk factors cause ED is most probably increased oxidative stress. Endothelial dysfunction may promote atherogenesis through different mechanisms such as increased adherence of monocytes, macrophages, and enhanced permeability of the endothelial layer. Further, ED probably plays an important role in the growth of atherosclerotic lesions and in the development of thrombotic complications in late stages of the disease. Because ED is a key underlying factor in the atherosclerotic process, markers of endothelial abnormalities have been sought. Detection of ED is based on tests of endothelium-dependent vasomotion (dilation capability of peripheral and coronary arteries) and on circulating markers of endothelial function (endothelin-1, von Willebrand factor, tissue plasminogen activator, plasminogen activator inhibitor, and adhesion molecules). Using these tests it is possible to follow the dose response of harmful effects of risk factors, and the effects of preventive procedures on vessel wall function.

scholarly journals Long-term adverse outcomes associated with drug-eluting stents and bare-metal stent in patients with small coronary artery disease: a systematic review and meta-analysis

2018 ◽  
Vol 15 (1) ◽  
pp. 1-7
Author(s):  
Nabin Chaudhary ◽  
Pravesh Kumar Bundhun ◽  
Sujan Shrestha ◽  
He Yan
Keyword(s):  
Coronary Artery Disease ◽  
Meta Analysis ◽  
Bare Metal Stent ◽  
Adverse Outcomes ◽  
Drug Eluting Stents ◽  
Bare Metal ◽  
Metal Stent ◽  
Drug Eluting ◽  
Artery Disease

Objective: The main purpose of this meta-analysis was to compare the long-term adverse outcomes associated with drug-eluting stents (DES) and bare-metal stent (BMS) in patients with small coronary artery disease (CAD).Method: Randomized Controlled Trials (RCTs) and observational studies comparing the adverse outcomes such as mortality, major adverse cardiovascular events (MACE), myocardial infarction (MI), stent thrombosis (ST), target lesion revascularization (TLR), target vessel revascularization (TVR), and restenosis in small CAD patients receiving DES and BMS were searched from Embase, PubMed, and Cochrane Library databases. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated and the pooled analyses were performed with RevMan 5.3.Result: A total number of 4,106 patients with small CAD (2,123 patients received DES and 1,983 patients received BMS) have been included in this meta-analysis. Pool-analysis demonstrated that the risk of mortality, MACE, MI, ST, TLR, TVR, and restenosis were significantly lower in DES group, with OR 0.77(95%CI 0.59-0.99, P=0.04), 0.48(95%CI 0.41-0.56, P<0.00001), 0.74(95%CI 0.55-0.98, P=0.04), 0.51(95%CI: 0.26-0.98, P=0.04), 0.24(95%CI: 0.16-0.37, P<0.00001), 0.47(95%CI: 0.38-0.59, P<0.00001), and 0.24 (95%CI 0.14-0.43, P<0.00001), respectively.Conclusion: Compared with BMS, DES had lower rates of adverse clinical outcomes, and restenosis during long-term follow-up.Nepalese Heart Journal 2018; 15(1): 1-7

scholarly journals Long-Term Consequences of Placental Vascular Pathology on the Maternal and Offspring Cardiovascular Systems

Biomolecules ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 1625
Author(s):  
Marisa Benagiano ◽  
Salvatore Mancuso ◽  
Jan J. Brosens ◽  
Giuseppe Benagiano
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Endothelial Dysfunction ◽  
Growth Restriction ◽  
Arterial System ◽  
Vascular Pathology ◽  
Long Term Consequences ◽  
Artery Disease

Over the last thirty years, evidence has been accumulating that Hypertensive Disorders of Pregnancy (HDP) and, specifically, Preeclampsia (PE) produce not only long-term effects on the pregnant woman, but have also lasting consequences for the fetus. At the core of these consequences is the phenomenon known as defective deep placentation, being present in virtually every major obstetrical syndrome. The profound placental vascular lesions characteristic of this pathology can induce long-term adverse consequences for the pregnant woman’s entire arterial system. In addition, placental growth restriction and function can, in turn, cause a decreased blood supply to the fetus, with long-lasting effects. Women with a history of HDP have an increased risk of Cardiovascular Diseases (CVD) compared with women with normal pregnancies. Specifically, these subjects are at a future higher risk of: Hypertension; Coronary artery disease; Heart failure; Peripheral vascular disease; Cerebrovascular accidents (Stroke); CVD-related mortality. Vascular pathology in pregnancy and CVD may share a common etiology and may have common risk factors, which are unmasked by the “stress” of pregnancy. It is also possible that the future occurrence of a CVD may be the consequence of endothelial dysfunction generated by pregnancy-induced hypertension that persists after delivery. Although biochemical and biophysical markers of PE abound, information on markers for a comparative evaluation in the various groups is still lacking. Long-term consequences for the fetus are an integral part of the theory of a fetal origin of a number of adult diseases, known as the Barker hypothesis. Indeed, intrauterine malnutrition and fetal growth restriction represent significant risk factors for the development of chronic hypertension, diabetes, stroke and death from coronary artery disease in adults. Other factors will also influence the development later in life of hypertension, coronary and myocardial disease; they include parental genetic disposition, epigenetic modifications, endothelial dysfunction, concurrent intrauterine exposures, and the lifestyle of the affected individual.

scholarly journals Short- and Long-Term Black Tea Consumption Reverses Endothelial Dysfunction in Patients With Coronary Artery Disease

Circulation ◽  
2001 ◽  
Vol 104 (2) ◽  
pp. 151-156 ◽  
Author(s):  
Stephen J. Duffy ◽  
John F. Keaney Jr ◽  
Monika Holbrook ◽  
Noyan Gokce ◽  
Peter L. Swerdloff ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Endothelial Dysfunction ◽  
Black Tea ◽  
Tea Consumption ◽  
Short And Long Term ◽  
Artery Disease

scholarly journals Alkaline Phosphatase-to-Albumin Ratio as a Novel Predictor of Long-Term Adverse Outcomes in Coronary Artery Disease Patients Who underwent PCI

2021 ◽  
Author(s):  
Xin-Ya Dai ◽  
Ying-Ying Zheng ◽  
Jun-Nan Tang ◽  
Wei Wang ◽  
Qian-Qian Guo ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Alkaline Phosphatase ◽  
Coronary Artery ◽  
Cox Regression ◽  
Independent Predictor ◽  
Adverse Outcomes ◽  
Cardiac Events ◽  
Albumin Ratio ◽  
Artery Disease

Background: Alkaline phosphatase (ALP) and albumin (ALB) have been shown to be associated with coronary artery disease (CAD), and it has been reported that alkaline phosphatase-to-albumin ratio (AAR) is associated with the liver damage and poorer prognosis of patients with digestive system malignancy. Moreover, several previous studies showed that there was a higher incidence of malignancy in CAD patients. However, to our knowledge, the relationship between AAR and long-term adverse outcomes in CAD patients after undergoing percutaneous coronary intervention (PCI) has not been investigated. Therefore, we aim to access the relation between AAR and long-term adverse outcomes in post-PCI patients with CAD. Methods: 3378 post-PCI patients with CAD were enrolled in the retrospective CORFCHD-ZZ study from January 2013 to December 2017. The median duration of follow-up was 37.59±22.24 months. The primary endpoint was long-term mortality including all-cause mortality (ACM) and cardiac mortality (CM).The secondary endpoints were major adverse cardiac events (MACEs) and major adverse cardiac and cerebrovascular events (MACCEs). Results: Kaplan-Meier analyses showed that an increased AAR was positively correlated with incidences of long-term ACM (log-rank, P=0.014), CM (log-rank, P=0.011), MACEs (log-rank, P=0.013) and MACCEs (log-rank, P=0.006). Multivariate Cox regression analyses showed that the elevated AAR was an independent predictor of long-term ACM (adjusted HR=1.488 [1.031-2.149], P=0.034), CM (adjusted HR=1.837 [1.141-2.959], P=0.012), MACEs (adjusted HR=1.257 [1.018-1.551], P=0.033) and MACCEs (adjusted HR=1.237 [1.029-1.486], P=0.024). Conclusions: An elevated AAR is a novel independent predictor of long-term adverse outcomes in CAD patients following PCI.

scholarly journals Long-Term Follow-Up of Patients With Mild Coronary Artery Disease and Endothelial Dysfunction

Circulation ◽  
2000 ◽  
Vol 101 (9) ◽  
pp. 948-954 ◽  
Author(s):  
Jassim Al Suwaidi ◽  
Shuichi Hamasaki ◽  
Stuart T. Higano ◽  
Rick A. Nishimura ◽  
David R. Holmes ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Endothelial Dysfunction ◽  
Long Term Follow Up ◽  
Artery Disease

scholarly journals Medium-long-term results of carotid stenting in asymptomic stenosis of the carotid arteries

2021 ◽  
Vol 11 (2) ◽  
pp. 18-27
Author(s):  
S. A. Bagin ◽  
Р. Е. Krainyukov ◽  
Z. Kh. Shugushev ◽  
D. A. Maksimkin ◽  
S. S. Saidov ◽  
...  
Keyword(s):  
Carotid Artery Disease ◽  
Carotid Stenting ◽  
Adverse Outcomes ◽  
Long Term Results ◽  
Asymptomatic Carotid ◽  
Optimal Drug ◽  
Artery Disease ◽  
The Moment ◽  
Stroke Death

The article describes the experience of carotid stenting use in asymptomatic cerebral atherosclerosis. The study included 147 patients with unilateral asymptomatic carotid artery disease. The evaluation of mid-longterm results of carotid stenting in patients with asymptomatic stenosis was carried out in comparison with the use of conservative treatment in this category of patients (“optimal drug treatment”). In the course of the work, no significant intergroup difference was revealed in the incidence of adverse outcomes (TIA/stroke, death from stroke,) within a year from the moment of surgical treatment or the beginning of complex correction of risk factors.  

scholarly journals Association of endothelial activation assessed through endothelin-I precursor peptide measurement with mortality in COVID-19 patients: an observational analysis

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Claudia Gregoriano ◽  
Dominik Damm ◽  
Alexander Kutz ◽  
Daniel Koch ◽  
Selina Wolfisberg ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Surrogate Marker ◽  
Endothelial Activation ◽  
Community Acquired Pneumonia ◽  
Prognostic Accuracy ◽  
Precursor Peptide ◽  
Thrombotic Complications ◽  
Prognostic Implications ◽  
Artery Disease ◽  
Median Admission

Abstract Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease (COVID-19) has been linked to thrombotic complications and endothelial dysfunction. We assessed the prognostic implications of endothelial activation through measurement of endothelin-I precursor peptide (proET-1), the stable precursor protein of Endothelin-1, in a well-defined cohort of patients hospitalized with COVID-19. Methods We measured proET-1 in 74 consecutively admitted adult patients with confirmed COVID-19 and compared its prognostic accuracy to that of patients with community-acquired pneumonia (n = 876) and viral bronchitis (n = 371) from a previous study by means of logistic regression analysis. The primary endpoint was all-cause 30-day mortality. Results Overall, median admission proET-1 levels were lower in COVID-19 patients compared to those with pneumonia and exacerbated bronchitis, respectively (57.0 pmol/l vs. 113.0 pmol/l vs. 96.0 pmol/l, p < 0.01). Although COVID-19 non-survivors had 1.5-fold higher admission proET-1 levels compared to survivors (81.8 pmol/l [IQR: 76 to 118] vs. 53.6 [IQR: 37 to 69]), no significant association of proET-1 levels and mortality was found in a regression model adjusted for age, gender, creatinine level, diastolic blood pressure as well as cancer and coronary artery disease (adjusted OR 0.1, 95% CI 0.0009 to 14.7). In patients with pneumonia (adjusted OR 25.4, 95% CI 5.1 to 127.4) and exacerbated bronchitis (adjusted OR 120.1, 95% CI 1.9 to 7499) we found significant associations of proET-1 and mortality. Conclusions Compared to other types of pulmonary infection, COVID-19 shows only a mild activation of the endothelium as assessed through measurement of proET-1. Therefore, the high mortality associated with COVID-19 may not be attributed to endothelial dysfunction by the surrogate marker proET-1.

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