Inflammatory responses in small vessels play an important role in the development of cardiovascular diseases, including hypertension, stroke, and small vessel disease. This involves various complex molecular processes including oxidative stress, inflammasome activation, immune-mediated responses, and protein misfolding, which together contribute to microvascular damage. In addition, epigenetic factors, including DNA methylation, histone modifications, and microRNAs influence vascular inflammation and injury. These phenomena may be acquired during the aging process or due to environmental factors. Activation of proinflammatory signaling pathways and molecular events induce low-grade and chronic inflammation with consequent cardiovascular damage. Identifying mechanism-specific targets might provide opportunities in the development of novel therapeutic approaches. Monoclonal antibodies targeting inflammatory cytokines and epigenetic drugs, show promise in reducing microvascular inflammation and associated cardiovascular diseases. In this article, we provide a comprehensive discussion of the complex mechanisms underlying microvascular inflammation and offer insights into innovative therapeutic strategies that may ameliorate vascular injury in cardiovascular disease.
Background: Risk prediction scores have received much attention the past years in the primary prevention of cardiovascular disease (CVD). Based on easily assessed characteristics, like age, sex, smoking habits, blood pressure and lipids’ levels, the risk for a future CVD event is calculated; and public health professionals may identify people at high risk. Objectives: Although diet has been independently associated with CVD risk, its role in the accuracy of the developed scores has rarely been studied. Thus, in this review, the role of dietary patterns’ assessment on the predictive ability of CVD risk scores was critically discussed. Methods: A computer-assisted literature search in relevant databases (Pubmed, Scopus) retrieved 13 studies that were published in English from 1994 until January 2013, and evaluated dietary patterns in relation to CVD risk. Results: Only one out of the 13 studies evaluated the role of dietary patterns’ on the accuracy of the developed CVD risk scores. The inclusion of dietary habits improved the accuracy of risk prediction by 37%. Conclusions: There is a need for separately evaluating the role of diet in the accuracy of CVD risk prediction scores, in order to better understand its role in correctly identifying the potential candidate for CVD event, and in the eventual case of favorable results, for developing more accurate CVD risk scores through the addition of an inexpensive predictor, that of dietary habits. Τα σκορ eκτίμησης κινδύνου αποτeλούν αντικeίμeνο eντατικής μeλέτης τα τeλeυταία χρόνια, ιδιαίτeρα όσον αφορά στην πρωτογeνή πρόληψη της καρδιαγγeιακής νόσου (ΚΝ). Παρόλο που η δίαιτα έχeι συσχeτισθeί ανeξάρτητα μe τον καρδιαγγeιακό κίνδυνο, ο ρόλος της στην ακρίβeια των χρησιμοποιούμeνων σκορ eκτίμησης καρδιαγγeιακού κινδύνου έχeι eλάχιστα μeλeτηθeί. Συνeπώς, σκοπός της παρούσας ανασκόπησης eίναι η διeρeύνηση του ρόλου της αποτίμησης των διατροφικών συνηθeιών στην προσαρμογή των υποδeιγμάτων και των σκορ eκτίμησης καρδιαγγeιακού κινδύνου. Για το σκοπό αυτό, διeνeργήθηκe ανασκόπηση της βιβλιογραφίας, η οποία ανέδeιξe 13 σχeτικές μeλέτeς, όμως, μόνο δύο από αυτές eίχαν αξιολογήσeι το ρόλο της δίαιτας στην ακρίβeια των διαθέσιμων υποδeιγμάτων. Η προσθήκη της απότίμησης της δίαιτας βeλτίωσe σημαντικά την ακρίβeια του υποδeίγματος. Οι υπόλοιπeς μeλέτeς πρότeιναν μία ανeξάρτητη και προστατeυτική eπίδραση eνός υγιeινού διατροφικού προτύπου στον καρδιαγγeιακό κίνδυνο. Η προσθήκη του διατροφικού παράγοντα στα σκορ eκτίμησης καρδιαγγeιακού κινδύνου θα μπορούσe να αυξήσeι την ακρίβeιά τους και να συμβάλλeι στην ορθότeρη αναγνώριση των ατόμων που διατρέχουν αυξημένο κίνδυνο για την eμφάνιση της νόσου.
Sparse evidence of the prognostic benefit of the anti-inflammatory drug colchicine in chronic and acute coronary syndromes (CCS/ACS) exists.We performed a systematic search of studies on CCS or ACS comparing colchicine vs. placebo and reporting data on cardiovascular outcomes (primary end points of each study) and/or changes in hs-CRP.Ten studies were selected: three on CCS (LoDoCo, LoDoCo2 and the CCS subgroup of COLCHICINE-PCI; total patient number = 6256), three on ACS (COLCOT, COPS, ACS subgroup of COLCHICINE-PCI; n = 5,654) and five (n = 532) on hs-CRP changes from 1 week to 12 months, in CCS and/or ACS. In patients with CCS, colchicine reduced by 49% risk of a composite end point (hazard ratio [HR] 0.51, 95% confidence interval [CI] 0.32 to 0.81, P = .005). The favourable effect of colchicine on the risk of cardiovascular events did not change when excluding COLCHICINE-PCI from analysis (HR 0.51, 95% CI 0.25 to 1.03, P = .061). In patients with ACS, the use of colchicine tended to decrease the occurrence of the combined end point compared with placebo (HR = 0.77, 95% CI 0.56 to 1.05, P = .100), and colchicine became significantly protective when removing COLCHICINE-PCI from analysis (HR = 0.72, 95% CI 0.56 to 0.92, P = .009). Furthermore, colchicine tended to reduce the hs-CRP increase (standardized mean difference=-0.31, 95% CI -0.72 to 0.1, P = .133) compared with placebo.Colchicine therapy near halves the risk of cardiovascular events in CCS compared with placebo and is associated with a nonsignificant 23% risk reduction in ACS, together with a trend towards a greater reduction of hs-CRP.
Objective: To evaluate the association between a personal history of lactation and indices of subclinical atherosclerosis in postmenopausal women.Methods: We evaluated the association between a history of breastfeeding and indices of subclinical atherosclerosis (pulse wave velocity, PWV; intima-media thickness [IMT]; atherosclerotic plaque presence) in 197 parous postmenopausal women with history of breastfeeding.Results: Women who reported breastfeeding ≥6 months when compared with women who reported breastfeeding for 1–5 months exhibited significantly lower values of common carotid artery IMT (Model R2=15.7%, b-coefficient = −0.170, 95% CI: −0.208—0.001, p-value = .019) and lower odds of subclinical atherosclerosis (Model X2=28.127, OR = 0.491, 95% CI 0.318–0.999, p-value = .049), adjusting for traditional cardiovascular risk factors.Conclusions: Postmenopausal women with a history of breastfeeding for at least 6 months have a lower prevalence of subclinical atherosclerosis, independently of traditional cardiovascular risk factors. A longer duration of breastfeeding may have a beneficial effect on subclinical atherosclerosis later in life.
Leptin is an adipokine, known to be associated with oxidative stress, inflammation, and atherogenesis. Leptin plays an essential role in atheromatosis-associated inflammatory cascade through stimulation of inflammatory mediators such as soluble intracellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1). However, little is known about this association in patients with atherosclerosis and severe internal carotid artery (ICA) stenosis undergoing carotid endarterectomy (CEA). Our objective was to evaluate the variations of serum leptin levels, as well as sICAM-1 and sVCAM-1 levels in these patients during the process of CEA and 24 hours postoperatively.The study group enrolled 50 patients undergoing CEA for ICA stenosis (> 70%). Serum leptin, sICAM-1 and sVCAM-1 plasma concentration measurements were performed at 4 distinct time points: before clamping of the ICA, 30 minutes after clamping of the ICA, 60 minutes after declamping of ICA and 24 hours postoperatively.Leptin was significantly decreased during CEA, but an overshooting in its levels was observed at 24 hours after the operation. Both sICAM-1 and sVCAM-1 initially followed the pattern of leptin changes but after completing CEA and up to 24 hours postoperatively a steep increase in their levels was not established. sVCAM-1 and sICAM-1 correlated with indices of oxidative stress at peak inflammatory burden.Leptin is a circulating marker of carotid atherosclerosis. Oxidative stress and expression of sVCAM-1 and sICAM-1 on vascular endothelial cells are key features in the pathophysiological process of atherosclerosis.
The European Society of Cardiology (ESC) EURObservational Research Programme (EORP) Chronic Ischaemic Cardiovascular Disease Long Term (CICD LT) registry aims to study the clinical profile, treatment modalities, and outcomes of patients diagnosed with CICD in a contemporary environment in order to assess whether these patients at high cardiovascular (CV) risk are treated according to ESC guidelines on prevention or on stable coronary disease and to determine mid- and long-term outcomes and their determinants in this population.Nine thousand one hundred and seventy-four patients over 18 years with documented CICD defined by a history acute coronary syndrome with/without ST elevation, previous coronary revascularization, or stable coronary artery disease were enrolled between 1 May 2015 and 31 July 2018. Individual patient data on clinical profile, biology, and treatment modalities were collected across 154 centres from 20 ESC countries. Two years of follow-up is scheduled in order to determine the following clinical outcomes: all-cause and CV death, all-cause and CV hospitalizations, changes in medications, and quality of life using the EuroQol5D-5L score.The CICD LT is an international registry of care and outcomes of patients hospitalized with CICD which will provide insights into the contemporary profile and management of patients with this common disease.
Background and aims Patients with embolic strokes of undetermined source (ESUS) usually present with mild symptoms. We aimed to compare the baseline characteristics between mild and severe ESUS, identify predictors for severe ESUS, and assess outcomes of patients with severe ESUS. Methods In the AF-ESUS (AF-ESUS) dataset, we stratified ESUS severity using the median National Institutes of Health Stroke Scale (NIHSS) score on admission as cut-off. We performed multivariable stepwise regression analyses to identify independent predictors of severe ESUS and to assess the association between ESUS severity and stroke recurrence, death, and new incident atrial fibrillation (AF) on follow-up. The 10-year cumulative probabilities of outcome incidence were estimated by the Kaplan–Meier product limit method. Results In 772 patients (median NIHSS: 6 (interquartile range: 3–12)), 414 (53.6%) patients had severe ESUS (i.e. NIHSS ≥6). Female sex was the only independent predictor for severe ESUS (odds ratio: 1.72 (1.27–2.33)). The rates of recurrence (3.3%/year vs. 3.4%/year, adjusted-hazard ratio: 1.09 (0.73–1.62)) and new incident AF (13.5% vs. 17.0%, adjusted odds ratio: 0.67 (0.44–1.03)) were similar between severe and mild ESUS, but mortality was higher (5.4%/year vs. 3.7%/year, adjusted-hazard ratio: 1.51 (1.05–2.16)) in severe ESUS. The 10-year cumulative probability for stroke recurrence was similar between severe and mild ESUS (38.1% (29.2–48.6) vs. 36.6% (27.8–47.0), log-rank test: 0.01, p = 0.920). The 10-year cumulative probability of death was higher in patients with severe ESUS compared with mild ESUS (40.5% (32.5–50.0) vs. 34.0% (26.0–43.6) respectively; log-rank test: 4.54, p = 0.033). Conclusions Women have more severe ESUS compared with men. Patients with severe ESUS have similar rates of stroke recurrence and new incident AF, but higher mortality compared with mild ESUS.
The presence of a skin-brain connection whereby alterations in the skin can inform on mechanisms underlying neurodegenerative diseases is increasingly recognized. In this study, we used a discovery (n = 321) and replication (n = 147) sample from the Twins UK population to test the association between naevus count and memory function, and its mediation by telomeres. Memory function was assessed in 1999 and 2009 using the paired associates learning test (PAL), while naevus count and leucocyte telomere length (LTL, assessed by the terminal restriction fragment assay) were measured once. Higher baseline naevus count was significantly associated with fewer errors at the baseline and follow-up PAL, as well as with change in PAL score over 10 years. This association was significantly attenuated after adjustment for LTL. The significant association between naevus count and PAL score was reproduced in the replication sample. These findings suggest that melanocytes might be used as model system to study the biological ageing pathways involved in neurodegeneration.
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