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Lipid lowering, with the use of statins after an acute coronary syndrome (ACS), is a cornerstone, well-established strategy for the secondary prevention of ischemic events in this high-risk cohort. In addition to the positive effect on lipid levels, statins have also been linked to improved atherosclerotic plaque characteristics, such as plaque regression and inflammation reduction, associated with the extent of reduction in LDL-C. The recent emergence of PCSK9 inhibitors for the management of dyslipidemia and the more extensive lipid lowering provided by these agents may provide better prevention for ACS patients when initiated after the ACS event. Several trials have evaluated the immediate post-ACS initiation of PCSK9 inhibitors, which has shown, to date, beneficial results. Furthermore, PCSK9 inhibitors have been linked with positive plaque remodeling and associated mortality benefits, which makes their use in the initial management strategy of such patients appealing. Therefore, in this review, we will analyze the rationale behind immediate lipid lowering after an ACS, report the evidence of PCSK9 inhibition immediately after the ACS event and the available data on plaque stabilization, and discuss treatment algorithms and clinical perspectives for the use of these agents in this clinical setting. [ABSTRACT FROM AUTHOR]

Mitral regurgitation (MR) is one of the most common valvular pathologies worldwide, contributing to the morbidity and mortality of several cardiovascular pathologies, including heart failure (HF). Novel transcatheter treatment for MR has given the opportunity for a safe and feasible alternative, to surgery, in order to repair the valve and improve patient outcomes. However, after the results of early transcatheter edge-to-edge repair (TEER) trials, it has become evident that subcategorizing the mitral regurgitation etiology and the left ventricular function, in patients due to undergo TEER, is of the essence, in order to predict responsiveness to treatment and select the most appropriate patient phenotype. Thus, a novel MR phenotype, atrial functional MR (AFMR), has been recently recognized as a distinct pathophysiological entity, where the etiology of the regurgitation is secondary to annular dilatation, in a diseased left atrium, with preserved left ventricular function. Recent studies have evaluated and compared the outcomes of TEER in AFMR with ventricular functional MR (VFMR), with the results favoring the AFMR. In specific, TEER in this patient substrate has better echocardiographic and long-term outcomes. Thus, our review will provide a comprehensive pathogenesis and mechanistic overview of AFMR, insights into the echocardiographic approach of such patients and pre-procedural planning, discuss the most recent clinical trials and their implications for future treatment directions, as well as highlight future frontiers of research in the setting of TEER and transcatheter mitral valve replacement (TMVR) in AFMR patients. [ABSTRACT FROM AUTHOR]

CT angiography has become, in recent years, a main evaluating modality for patients with coronary artery disease (CAD). Recent advancements in the field have allowed us to identity not only the presence of obstructive disease but also the characteristics of identified lesions. High-risk coronary atherosclerotic plaques are identified in CT angiographies via a number of specific characteristics and may provide prognostic and therapeutic implications, aiming to prevent future ischemic events via optimizing medical treatment or providing coronary interventions. In light of new evidence evaluating the safety and efficacy of intervening in high-risk plaques, even in non-flow-limiting disease, we aim to provide a comprehensive review of the diagnostic algorithms and implications of plaque vulnerability in CT angiography, identify any differences with invasive imaging, analyze prognostic factors and potential future therapeutic options in such patients, as well as discuss new frontiers, including intervening in non-flow-limiting stenoses and the role of CT angiography in patient stratification. [ABSTRACT FROM AUTHOR]

Structural heart disease is increasingly prevalent in the general population, especially in patients of increased age. Recent advances in transcatheter structural heart interventions have gained a significant following and are now considered a mainstay option for managing stable valvular disease. However, the concept of transcatheter interventions has also been tested in acute settings by several investigators, especially in cases where valvular disease comes as a result of acute ischemia or in the context of acute decompensated heart failure. Tested interventions include both the mitral and aortic valve, mostly evaluating mitral transcatheter edge-to-edge repair and transcatheter aortic valve implantation, respectively. This review is going to focus on the use of acute structural heart interventions in the emergent setting, and it will delineate the available data and provide a meaningful discussion on the optimal patient phenotype and future directions of the field. [ABSTRACT FROM AUTHOR]

Aims: Revascularization guided by functional severity has presented improved outcomes compared with visual angiographic guidance. Quantitative flow ratio (QFR) is a reliable angiography-based method for functional assessment. We sought to investigate the prognostic value of discordance between QFR and visual estimation in coronary revascularization guidance. Methods and results: We performed offline QFR analysis on all-comers undergoing coronary angiography. Vessels with calculated QFR were divided into four groups based on the decision to perform or defer percutaneous coronary intervention (PCI) and on the QFR result, i.e.: Group A (PCI−, QFR > 0.8); Group B (PCI+, QFR ≤ 0.8); Group C (PCI+, QFR > 0.8); Group D (PCI−, QFR ≤ 0.8). Patients with at least one vessel falling within the disagreement groups formed the discordance group, whereas the remaining patients formed the concordance group. The primary endpoint was the composite endpoint of cardiovascular death, myocardial infarction, and ischaemia-driven revascularization. Overall, 546 patients were included in the study. Discordance between QFR and visual estimation was found in 26.2% of patients. After a median follow-up period of 2.5 years, the discordance group had a significantly higher rate of the composite outcome (hazard ratio: 3.34, 95% confidence interval 1.99–5.60, P < 0.001). Both disagreement vessel Groups C and D were associated with increased cardiovascular risk compared with agreement Groups A and B. Conclusion: Discordance between QFR and visual estimation in revascularization guidance was associated with a worse long-term prognosis. Our results highlight the importance of proper patient selection for intervention and the need to avoid improper stent implantations when not dictated by a comprehensive functional assessment. Graphical Abstract [ABSTRACT FROM AUTHOR]

Ultra-low contrast percutaneous coronary interventions (ULPCIs) are a novel field of interventional cardiology, aiming to reduce the risk of contrast-induced nephropathy (CIN), which is a well-described adverse event after angiography. CIN is a well-described adverse event following PCI, especially in high-risk patients, i.e., patients with an already deteriorating renal function or chronic kidney disease, as well as patients of advanced age or requiring an increased amount of contrast during their intervention. Among the techniques described for ULPCI procedures, intravascular imaging guidance seems a promising option, as it allows lesion recognition and characterization, stent implantation, and PCI optimization. Intravascular ultrasound (IVUS) is the modality most commonly used, as it does not require contrast injection, contrary to optical coherence tomography (OCT). Several clinical trials, assessing IVUS in the context of ULPCI, have shown that it can be safely used in this setting while offering a substantial reduction in contrast media volume, as well as renal adverse outcomes. This review aims to describe the need for ULPCI and technical considerations regarding the use of intravascular imaging in this setting, as well as analyze the available evidence from clinical trials regarding the safety and efficacy of IVUS-ULPCI, in order to provide a comprehensive summary for practicing physicians. [ABSTRACT FROM AUTHOR]

The post-percutaneous coronary intervention (post-PCI) fractional flow reserve (FFR) can detect suboptimal PCI or residual ischemia and potentially lead to fewer adverse clinical outcomes. We sought to investigate the predictive value of the angiography-derived FFR for adverse cardiovascular events in patients after PCI. We conducted a comprehensive search of electronic databases, MEDLINE, EMBASE, and the Cochrane Library, for studies published until March 2023 that investigated the prognostic role of angiography-derived fractional flow reserve values after PCI. We investigated the best predictive ability of the post-PCI angiography-derived FFR and relative risk (RR) estimates with 95% confidence intervals (CIs) between post-PCI angiography-derived FFR values and adverse events. Thirteen cohort studies involving 6961 patients (9719 vascular lesions; mean follow-up: 2.2 years) were included in this meta-analysis. The pooled HR of the studies using specific cut-off points for post-PCI angiography-derived FFR was 4.13 (95% CI, 2.92–5.82) for total cardiovascular events, while the pooled HRs for target vessel revascularization, cardiac death, target vessel myocardial infarction, and target lesion revascularization were 6.87 (95% CI, 4.93–9.56), 6.17 (95% CI, 3.52–10.80), 3.98 (95% CI, 2.37–6.66) and 6.27 (95% CI, 3.08–12.79), respectively. In a sensitivity analysis of three studies with 1789 patients assessing the predictive role of the post-PCI angiography-derived FFR as a continuous variable, we found a 58% risk reduction for future adverse events per 0.1 increase in the post-PCI angiography-derived FFR value. In conclusion, post-PCI angiography-derived FFR is an effective tool for predicting adverse cardiovascular events and could be potentially used in decision making, both during PCI and in the long-term follow-up. [ABSTRACT FROM AUTHOR]

Tricuspid regurgitation (TR) is a common valvular pathology, estimated to affect 1.6 million people in the United States alone. Even though guidelines recommend either medical therapy or surgical treatment for TR, the misconception of TR as a benign disease along with the high mortality rates of surgical intervention led to undertreating this disease and commonly describing it as a "forgotten" valve. Recently, the development of transcatheter interventions for TR show promising potential for use in the clinical setting. There are currently few approved and numerous tested percutaneously delivered devices, which can be categorized, based on their mechanism of action, to either valve repair or valve replacement procedures. Both procedures were tested in clinical trials and show an echocardiographic reduction in TR sustained for at least 1 year after the procedure, as well as symptom relief and functional improvement of the patients. Device selection should be personalized, taking into consideration the anatomy of each valve and the available options at each heart center. Moreover, appropriate patient selection and timing of the procedure are also crucial for the success of the procedure. In this review, we analyze the clinical trials available for all devices currently approved or tested, aiming to provide a comprehensive summary of the most recent evidence in the field of transcatheter TR interventions. [ABSTRACT FROM AUTHOR]

Introduction: Transvenous lead extraction (TLE) is critical in the long‐term management of patients with cardiac implanted electronic devices (CIEDs). The aim of the study is to evaluate the outcomes of TLE and to investigate the impact of infection. Methods and Results: Data of patients undergoing extraction of permanent pacemaker and defibrillator leads during October 2014–September 2019 were prospectively analyzed. Overall, 242 consecutive patients (aged 71.0 ± 14.0 years, 31.4% female), underwent an equal number of TLE operations for the removal of 516 leads. Infection was the commonest indication (n = 201, 83.1%). Mean implant‐to‐extraction duration was 7.6 ± 5.4 years. Complete procedural success was recorded in 96.1%, and clinical procedural success was achieved in 97.1% of attempted lead extractions. Major complications occurred in two (0.8%) and minor complications in seven (2.9%) patients. Leads were removed exclusively by using locking stylets in 65.7% of the cases. In the subgroup of noninfective patients, advanced extraction tools were more frequently required compared to patients with CIED infections, to extract leads (success only with locking stylet: 55.8% vs. 67.8%, p =.032). In addition, patients without infection demonstrated lower complete procedural success rates (90.7% vs. 97.2%, p =.004), higher major complication rates (2.4% vs. 0.5%, p =.31) and longer procedural times (136 ± 13 vs. 111 ± 15 min, p =.001). Conclusions: Our data demonstrate high procedural efficacy and safety and indicate that in patients with noninfective indications, the procedure is more demanding, thus supporting the hypothesis that leads infection dissolves and/or prohibits the formation of fibrotic adherences. [ABSTRACT FROM AUTHOR]

Introduction: Malignancies are the second leading cause of death worldwide. Treatment Monoclonal Antibody (MAbs)-based treatment of cancer has been established as one of the most successful therapeutic strategies in the last 20 years; however, there is a growing concern about the effects of these agents on patients' cardiovascular profile. Areas Covered: In this manuscript we summarize current evidence regarding MAb effects on arterial stiffness, which is an recognised biomarker of cardiovascular risk. For this purpose, we explored two bibliographic databases [PubMed, Scopus] and one full-text database (Google-Scholar) for all publications published on MAbs' effects on arterial stiffness until December 2019. Only few of the monoclonal antibody agents used in oncology have been investigated as per their effects on arterial properties and this limited evidence suggests that cancer therapy with monoclonal antibodies demonstrates either a temporary or long-term increase in arterial stiffness. Discussion: It seems that by targeting 'checkpoints' in cancer genesis, anticancer MAbs also affects vascular properties causing endothelial dysfunction and arterial stiffness. Furthermore, several MAbs cause hypertension and may as a result increase pulse wave velocity. On the other hand, MAbs that target inflammatory cytokines seem to improve cardiovascular survival however, their effect on arterial stiffness is yet to be investigated. Further research is warranted in order to elucidate the biochemical pathways, clinical implications and potential reversibility of monoclonal antibody chemotherapy-induced vascular dysfunction. [ABSTRACT FROM AUTHOR]

Introduction: Malignancies and cardiovascular disease are the two leading causes of mortality worldwide. There is a growing concern that anti-cancer drugs may lead to increased cardiovascular morbidity among cancer survivors. This may be the result of direct effects of the cancer treatment on heart function, or due to an indirect acceleration of atherosclerosis.Areas covered: We searched two bibliographic databases [PubMed, Scopus] and one full-text database (Google Scholar) for publications on chemotherapy and arterial stiffness since 1970. Anthracyclines, alkylating agents and tyrosine kinase inhibitors seem to affect arterial elastic properties. These effects can be non-reversible and may appear after treatment termination. Monoclonal antibodies may induce either a temporary increase or no change on arterial stiffness of patients with malignancies. Anti-microtubule agents and antimetabolites have not been extensively studied so far.Expert opinion: This literature review suggests that certain anticancer medications may impair arterial stiffness, and that assessment of arterial elastic properties before and after initiation of anti-neoplasmatic therapy may be clinically useful in order to develop protective strategies against chemotherapy-induced vascular effects. Further research is warranted to confirm the effects of anti-cancer agents on arterial stiffness, as well as their potential clinical implications. Future research lies in finding new targeted biomarkers identifying arterial stiffness such as micro RNAs while imaging techniques could also be implemented in assessment of vascular toxicity. [ABSTRACT FROM AUTHOR]

Radial artery (RA) occlusion (RAO) remains the Achilles heel of transradial coronary procedures. Although of silent nature, RAO is relatively frequent, results in graft shortage for future coronary artery bypass surgery, and may occur even after short-lasting, 5F coronary angiography (CAG). The most frequent predictors of RAO are RA size, body size, female gender, and periprocedural anticoagulation intensity. Methods to detect RAO are variable, of which the Barbeau test and ultrasonography have similar diagnostic accuracy. Data indicate that late RAO recanalization may occur. Meticulous handling of RA and the use of appropriate hemostatic devices and techniques along with sufficient heparin dose appear important measures to reduce RAO rates. Recent contradictory studies indicate that the decreasing incidence of RAO overtime is not as uniform as previously thought. In 2 metaanalyses, the benefit of higher over lower anticoagulation intensity became evident. As "it may all be appropriate anticoagulation" for a simplified approach against RAO, the results of an ongoing trial comparing 100 with 50 IU/kg body weight in transradial CAG are eagerly awaited. [ABSTRACT FROM AUTHOR]

Cardiogoniometry (CGM) is method of 3-dimensional electrocardiographic assessment which has been shown to identify patients with angiographically defined, stable coronary artery disease (CAD). However, angiographic evidence of CAD, does not always correlate to physiologically significant disease. The aim of our study was to assess the ability of CGM to detect physiologically significant coronary stenosis defined by fractional flow reserve (FFR). In a tertiary cardiology centre, elective patients with single vessel CAD were enrolled into a prospective double blinded observational study. A baseline CGM recording was performed at rest. A second CGM recording was performed during the FFR procedure, at the time of adenosine induced maximal hyperaemia. A significant CGM result was defined as an automatically calculated ischaemia score < 0 and a significant FFR ratio was defined as < 0.80. Measures of diagnostic performance (including sensitivity and specificity) were calculated for CGM at rest and during maximal hyperaemia. Forty-five patients were included (aged 61.1 ± 11.0; 60.0% male), of which eighteen (40%) were found to have significant CAD when assessed by FFR. At rest, CGM yielded a sensitivity of 33.3% and specificity of 63.0%. At maximal hyperaemia the sensitivity and specificity of CGM was 71.4 and 50.0% respectively. The diagnostic performance of CGM to detect physiologically significant stable CAD is poor at rest. Although, the diagnostic performance of CGM improves substantially during maximal hyperaemia, it does not reach sufficient levels of accuracy to be used routinely in clinical practice. [ABSTRACT FROM AUTHOR]

Background: Following cardiac catheterization using radial artery (RA) access, persistent endothelial dysfunction may limit the use of RA as a conduit during coronary artery bypass graft (CABG) surgery. We reviewed published literature to investigate the effects of transradial coronary catheterization on RA endothelial function.Methods: We searched PubMed from inception to April 2017 for published studies assessing RA endothelial function late (≥1 month) after coronary catheterization. A total of 12 eligible published studies (n = 490 patients) were included in the final quantitative synthesis. Statistical heterogeneity among studies was assessed by the I2 . A random effects model was used to calculate the pooled estimate for standardized mean difference (SMD). Meta-regression analysis was used to explore predictors of change in RA endothelial function following catheterization.Results: In all studies, a significant reduction in endothelium dependent response was observed post-catheterization (SMD = -0.53, 95% confidence interval [CI]: -0.93 to -0.13, P = 0.01) and a marginal, non-significant, reduction in endothelium independent response (SMD = -0.38, 95%CI: -0.77, 0.01, P < 0.059). In controlled studies, using the contralateral RA as a control, a significant impairment in endothelial function was confirmed (SMD = -6.26, 95%CI: -9.71 to -2.81, P < 0.0001), while the change in endothelium-independent response was not significant (SMD = -4.46, 95%CI: -13.3 to 4.37, P = 0.32). In meta-regression analysis male gender (z = 2.36, P = 0.018) and increasing time following catheterization (z = 2.62, P = 0.009) were associated with less RA endothelial dysfunction.Conclusions: Transradial catheterization impairs endothelium dependent vasodilatory properties of the cannulated RA, which do not recover even several months post-catheterization. Non-recovery of vasomotor function of cannulated RAs may limit their use as arterial grafts during CABG surgery. [ABSTRACT FROM AUTHOR]

Background: Aortic stiffness and inflammation are predictors of cardiovascular risk. Anti-vascular endothelial growth factor agents (anti-VEGF), injected intravitreally, can reverse the course of exudate age-related macular degeneration (AMD). We investigated the association of changes in aortic stiffness and inflammation with response to anti-VEGF therapy. Methods: 54 patients (mean age: 76 ± 10 years) with AMD received two consecutive monthly intravitreal injections of ranibizumab (0.5 mg). The primary outcome measure was change in carotid-femoral pulse wave velocity (PWV) from baseline to 1 month after the second injection. Results: Ranibizumab caused a decrease in PWV after the first (by 0.36 ± 1.4 m/s) and the second injection (by 0.31 ± 1.4 m/s) and remained decreased 1 month after the second injection (overall P < 0.05). PWV decreased significantly in good responders (according to clinical criteria and fundus findings, P = 0.004), whereas it increased numerically in poor responders (P = 0.21) over the study period. In responders, hsIL-6 decreased after the first injection and remained decreased 1 month after the second injection (by 0.63 ± 0.35 pg/ml, overall P = 0.02). PWV (P = 0.005) and hsIL-6 (P = 0.042) were independent predictors of improvement after adjusting for age, hypertension and diabetes. The decrease in PWV throughout the study period correlated with the reduction in hsIL-6 (r = 0.36, P < 0.01). Conclusions: Intravitreal ranibizumab injections lead to a decrease in PWV and hsIL-6. Both parameters predict clinical improvement and may aid in improving treatment targeting and therapeutic outcome in AMD patients. [ABSTRACT FROM AUTHOR]

While treatment with low-dose aspirin has been established as a therapeutic tool for secondary prevention, the role of aspirin on primary prevention remains controversial. Aortic stiffness and wave reflections are independent predictors of cardiovascular events. The aim of the present study was to investigate the effect of low-dose aspirin on aortic stiffness and wave reflections in hypertensive patients. We studied 30 patients with grade I hypertension. Fifteen patients were treated with 160 mg of aspirin and 15 patients with placebo. Aortic stiffness and wave reflections were assessed by measuring carotid–femoral pulse wave velocity (PWV) and heart rate-adjusted augmentation index (AIx75), respectively. All measurements were conducted at baseline and 2 weeks after treatment. In the aspirin group, there was a significant reduction in PWV compared to the placebo group (from 8.9±1.5 to 8.5±1.6 m/s for the aspirin group vs from 8.6±1.4 to 8.7±1.6 m/s for the placebo group, net change: –0.5 m/s; p=0.02). AIx75 showed a marginal decrease (from 28.0±5.4 to 26.2±5.0% for the aspirin group vs from 31.2±9.7 to 30.6±9.2% for the placebo group, net change: –1.2%; p=0.06). In conclusion, a 2-week course of aspirin administration has a favorable effect on aortic stiffness and, to a lesser extent, on wave reflections in hypertensive patients. Whether the reduction in arterial stiffness is translated to fewer cardiovascular events needs to be confirmed by future prospective studies. [ABSTRACT FROM AUTHOR]

Despite the remarkable development of the medical industry in the current era, herbal products with therapeutic potentials arise as attractive alternative treatments. Consequently, Chios mastiha, a natural, aromatic resin obtained from the trunk and brunches of the mastic tree, has recently gained increasing scientific interest due to its multiple beneficial actions. Chios mastiha is being exclusively produced on the southern part of Chios, a Greek island situated in the northern Aegean Sea, and its therapeutic properties have been known since Greek antiquity. There is now substantial evidence to suggest that mastiha demonstrates a plethora of favorable effects, mainly attributed to the anti-inflammatory and anti-oxidative properties of its components. The main use of mastiha nowadays, however, is for the production of natural chewing gum, although an approval by the European Medicines Agency for mild dyspeptic disorders and for inflammations of the skin has been given. The aim of this article is to summarize the most important data about the therapeutic actions of Chios mastiha and discuss future fields for its medical application. [ABSTRACT FROM AUTHOR]

BACKGROUND Androgen deficiency confers an independent risk for cardiovascular events and total mortality. Hypertension, a major contributory factor to the development of cardiovascular disease, has also been associated with increased prevalence of low testosterone. We investigated whether low androgen concentration predicts incident major adverse cardiovascular events (MACE) in middle-aged nondiabetic hypertensive patients without clinical atherosclerosis. METHODS MACE in relation to total testosterone (TT) were analyzed with proportional hazards models in 228 male patients (mean age 56 years). RESULTS During a mean follow-up of 44 months, 19 of 228 participants (8.3%) experienced a MACE. Compared to patients who did not experience MACE, hypertensive subjects who developed MACE had lower TT concentration (3.9±0.7ng/ml vs. 4.6±1.5ng/ml, P < 0.01) and a higher prevalence of hypogonadism (36% vs. 16%, P < 0.05). Subjects in the lowest TT tertile (<4.0ng/ml) had a statistically significant higher risk of MACE compared to those in the highest tertile (>4.9ng/ml) in multivariate Cox models adjusted for age, systolic blood pressure, and risk factors (all P < 0.05). A TT plasma level of 5.04ng/ml was associated with a negative predictive value (ability to “rule out” MACE) of 97.2%. Addition of TT to standard risk factors model yielded a net reclassification improvement of 38.8 % (P < 0.05). CONCLUSIONS Our results show that low plasma testosterone is associated with increased risk for a MACE in hypertensive patients. Low endogenous androgen concentration improves risk prediction when added to standard risk factors and may represent a valuable biomarker of prediction of cardiovascular disease risk in these patients. [ABSTRACT FROM PUBLISHER]

Vascular injury mobilizes bone marrow–derived proangiogenic cells into the circulation, where these cells can facilitate vascular repair and new vessel formation. We sought to determine the relationship between a new biomarker of circulating bone marrow–derived proangiogenic cell activity, the presence of atherosclerotic cardiovascular disease (CVD) and its risk factors, and clinical outcomes. Circulating proangiogenic cell activity was estimated using a reproducible angiogenic colony-forming unit (CFU-A) assay in 532 clinically stable subjects aged 20 to 90 years and ranging in the CVD risk spectrum from those who are healthy without risk factors to those with active CVD. CFU-A counts increased with the burden of CVD risk factors (p < 0.001). CFU-A counts were higher in subjects with symptomatic CVD than in those without (p < 0.001). During follow-up of 232 subjects with CVD, CFU-A counts were higher in those with death, myocardial infarction, or stroke than in those without (110 [70–173] vs 84 [51–136], p = 0.01). Therefore, we conclude that circulating proangiogenic cell activity, as estimated by CFU-A counts, increases with CVD risk factor burden and in the presence of established CVD. Furthermore, higher circulating proangiogenic cell activity is associated with worse clinical outcome in those with CVD. [ABSTRACT FROM PUBLISHER]

BackgroundSerum uric acid (UA) plays a key role in the development and progression of hypertension. We investigated the association of UA levels and indices of arterial function in a cohort of newly diagnosed, never-treated hypertensive subjects.MethodsOne thousand two hundred and twenty-five patients with a new diagnosis of mild to moderate arterial hypertension for which they had never received treatment were enrolled in the study (mean age 52.9 years, 728 men). Serum UA, carotid-femoral pulse-wave velocity (cfPWV), an index of aortic stiffness and augmentation index (AIx), a composite marker of wave reflections and arterial stiffness were measured.ResultsIn univariable analysis, UA levels correlated with cfPWV (r = 0.23, P < 0.001) and AIx (r = −0.24, P < 0.001). In multiple linear regression analysis, an independent positive association of cfPWV with UA levels was observed after adjusting for confounders (standardized regression coefficient β = 0.169, P < 0.001, adjusted R2 = 0.402), indicating an increase in aortic stiffness with higher values of UA. In contrast, an independent negative association of AIx with UA levels was observed after adjusting for confounders (standardized regression coefficient β = −0.064, P = 0.011, adjusted R2 = 0.557), indicating a decrease in wave reflections with higher values of UA. In gender-specific analyses, UA positively correlated with cfPWV in both genders, whereas a negative correlation with AIx existed only in females.ConclusionsSerum UA levels are independently associated with aortic stiffening and wave reflections in never-treated hypertensives. Future studies are warranted in order to explore its exact role on arterial function in the hypertensive setting.American Journal of Hypertension (2011) doi:10.1038/ajh.2010.111 [ABSTRACT FROM AUTHOR]

BackgroundNonalcoholic fatty liver disease (NAFLD) is the most common liver disease both in the general and pediatric population and has been associated with increased cardiovascular risk. Arterial function and early atherosclerotic changes are markers of cardiovascular disease and independent predictors of the corresponding risk. Through a global approach, we investigated the relationships between NAFLD and functional arterial changes and early atherosclerosis.MethodsA total of 23 consecutive patients (mean age 55 ± 14 years, 11 males) with biopsy evidence of NAFLD and 28 control subjects matched for age, gender, body mass index, and other cardiovascular risk factors participated in the study.ResultsCompared to controls, NAFLD subjects had significantly higher carotid-femoral pulse wave velocity (PWV; 8.2 ± 1.3 m/s vs. 6.9 ± 1.3 m/s, P = 0.001), higher carotid intima-media thickness (IMT; 0.79 ± 0.18 mm vs. 0.67 ± 0.13 mm, P = 0.01), and reduced flow-mediated dilatation (FMD; 1.92 ± 2.11% vs. 4.8 ± 2.43%, P < 0.001). In multivariable analysis, presence of NAFLD was an independent determinant of both PWV and FMD, whereas leptin was an independent determinant of PWV (B = 0.036, P < 0.05), and adiponectin was independently associated with FMD (B = 0.104, P < 0.05). In addition, histological activity of liver disease expressed by the global Brunt Grade was associated independently with FMD (B = -1.054, P < 0.05).ConclusionsNAFLD is associated with arterial stiffness and endothelial dysfunction. Given the important independent prognostic role of these arterial indexes, these findings have important implications for increased cardiovascular risk in patients with NAFLD.American Journal of Hypertension (2010). doi:10.1038/ajh.2010.144 [ABSTRACT FROM AUTHOR]

Aims: To calculate robust quantitative estimates on the predictive value of central pressures and derived central haemodynamic indices for cardiovascular (CV) outcomes and all-cause mortality by meta-analysis of longitudinal studies. [ABSTRACT FROM PUBLISHER]

BackgroundIncreased levels of interleukin-18 (IL-18) have been related to plaque progression and vulnerability and cardiovascular outcomes. Arterial functional and structural characteristics and endothelial/inflammatory activation are important determinants of cardiovascular performance and predictors of risk. We investigated whether IL-18 is a determinant of global arterial function and early structural changes in men.MethodsWe evaluated arterial structural and functional characteristics (carotid-femoral pulse wave velocity (PWV), central aortic pressures, wave reflection indexes, flow-mediated dilation of the brachial artery, and common carotid intima–media thickness (IMT)) and we measured systemic inflammatory markers in 97 men (mean age 57.8 ± 8.6 years) without manifest cardiovascular/atherosclerotic disease.ResultsMultivariable analysis adjusting for age, mean pressure, other risk factors, high-sensitivity C-reactive protein (hsCRP), and treatment showed independent associations between IL-18 level and carotid-femoral PWV (P < 0.01) and IMT (P = 0.03). On the other hand, no relationship between IL-18 and flow-mediated dilation, central pressures or augmentation index (AIx) was found. The combination of higher IL-18 level with higher carotid-femoral PWV and carotid IMT values showed greater effect on 10-year risk of a cardiovascular event.ConclusionsIL-18 level is independently associated with aortic stiffening and carotid early atherosclerosis. This finding underlines the important role of IL-18 as a marker of arterial damage, and implies a contribution of this compound to the pathophysiology of cardiovascular disease.American Journal of Hypertension 2010; doi:10.1038/ajh.2009.256 [ABSTRACT FROM AUTHOR]

Abstract: Introduction: Inflammatory state is activated in metabolic syndrome and may explain part of the adverse prognosis of this entity. Arterial stiffness, central blood pressures and wave reflections are independent predictors of cardiovascular risk. This study investigates the relation between low-grade inflammation and arterial stiffness and central hemodynamics in patients with metabolic syndrome. Methods: We studied 106 consecutive hypertensive patients with metabolic syndrome. Arterial stiffness was assessed by carotid-femoral (c-f) and carotid-radial (c-r) pulse wave velocity (PWV). Central blood pressures were evaluated by pulse wave analysis and heart rate corrected augmentation index (AIx75) was used as a measure of wave reflections. White blood cell count (WBC), high sensitivity C-reactive protein (hsCRP) and fibrinogen were measured as inflammatory markers. Results: In univariable analysis, PWVc-f correlated with both hsCRP (p <0.01) and fibrinogen (p <0.01), while PWVc-r correlated with hsCRP (p =0.05). Regarding central blood pressures, aortic SBP correlated positively with hsCRP (p <0.05) and marginally with fibrinogen (p =0.06) and WBC (p =0.08). Interestingly, no correlation was found between AIx75 and any of these biomarkers. After adjustment for age, gender, smoking, mean arterial pressure, heart rate, waist circumference, glucose, total and HDL cholesterol, PWVc-f was independently related to hsCRP (p <0.001) and fibrinogen (p <0.01), while a marginal independent correlation was also found between PWVc-r and hsCRP (p =0.06). Furthermore, aortic PP independently associated with fibrinogen (p <0.05) whereas marginal associations demonstrated between aortic SBP and hsCRP and fibrinogen (p =0.06 for both). Conclusion: Inflammatory status is related to arterial stiffness and central blood pressures (but not to augmentation index) in hypertensives with metabolic syndrome. These findings may have implications for increased cardiovascular risk in these patients. [Copyright &y& Elsevier]

Abstract: Background: Human immunodeficiency virus (HIV) infection is associated with subclinical inflammation and increased cardiovascular risk. Arterial stiffness and enhanced wave reflections are markers of cardiovascular disease and independent predictors of cardiovascular risk. The effect of HIV infection, per se, on aortic stiffness and wave reflections has not been clearly defined. Methods: We studied 51 adults with a recent HIV infection, free of antiretroviral treatment and AIDS diagnosis, as well as 35 controls matched for age, sex and smoking status. Carotid-femoral pulse wave velocity (PWV) and timing of the reflected wave (Tr) were measured as indices of aortic stiffness, while aortic augmentation index (AIx) and augmented pressure (AP) were measured as indices of wave reflections. Results: While PWV was similar in the two populations, Tr was significantly lower in HIV-infected subjects compared to controls (by 16.5ms, p =0.002). In addition, AIx and AP were decreased (by 6.4%, p =0.048 and by 3.3mmHg, p =0.010, respectively) in subjects with HIV infection. Moreover, HIV-infected patients compared with controls had increased values of hs-CRP [1.37 (0.85–2.53) vs. 0.75 (0.41–1.90) mg/l, p =0.007] and interleukin-6 [1.90 (0.91–3.9) vs. 1.28 (0.80–2.65) pg/ml, p=0.048]. Tr was negatively correlated with hs-CRP (r =−0.283, p =0.010) and interleukin-6 (r =−0.278, p =0.018). Conclusions: Our study provides evidence of decreased wave reflections and similar aortic stiffness, as assessed by PWV, in the early stages of HIV infection in treatment-naive patients compared to controls. Subclinical inflammation and resultant peripheral vasodilatation constitute potential mediators of the whole pathophysiological process. [Copyright &y& Elsevier]

Background Arterial stiffness is an important determinant of cardiovascular morbidity and mortality. The I/D polymorphism of angiotensinconverting enzyme (ACE) gene is associated with cardiovascular disease. However, the relationship between ACE polymorphism, arterial stiffness, and wave reflections in healthy, low-risk population has not been defined yet. Methods The study included 282 apparently healthy, low-risk individuals (mean age 39.7 ± 8.9 years, 178 males). Carotid-femoral pulse wave velocity (PWV) was measured as an index of aortic stiffness, while wave reflections were assessed by augmentation index (AIx) of the central pressure waveform. I/D polymorphism of the ACE gene was determined in all subjects for the prevalence of the DD, ID, and II genotype (39, 44, and 17%, respectively). C-reactive protein (CRP) levels were determined as a marker of chronic, subclinical inflammation. Results After adjustment for potential confounding factors, presence of D allele was associated with lower values of PWV compared to II genotype (P < 0.05), implying lower aortic stiffness for D allele carriers. There was no association between ACE genotype and wave reflections or peripheral and central systolic pressures. Conclusions In apparently healthy individuals, D allele is associated with lower aortic stiffness, whereas there is no association of the ACE polymorphism with wave reflections. This finding provides new insights into the possible links between ACE gene, regulation of large artery stiffness, and has implications for cardiovascular risk. [ABSTRACT FROM AUTHOR]

Summary: During the last decade, several studies have documented the unfavourable effects of inflammation on cardiovascular function and its role in the pathophysiology of atherosclerotic disease. The interplay between inflammation and arterial system is multifaceted. On the one hand, the endothelium contributes to the initiation and the perpetuation of vascular wall inflammation. On the other hand, the inflammatory cascade affects adversely the endothelium-dependent processes and the mechanical properties of the arteries. These effects give rise to impaired vasomotion, arterial stiffening and increased wave reflections and thus result in an unfavourable haemodynamic loading of the heart. Chronic inflammatory diseases (such as rheumatoid arthritis, and others) as well as acute inflammatory stimuli (such as acute infections) may adversely influence the arterial performance. Moreover, systemic subclinical low-grade inflammation, as expressed by high circulating levels of inflammatory markers/mediators, is a common denominator of most cardiovascular risk factors (hypertension, diabetes, etc.) and importantly, it is closely related to impaired arterial elastic properties. In addition, vasculogenic erectile dysfunction, which comprises an alternative phenotype of arterial dysfunction and an emerging cardiovascular risk predictor, is accompanied by low-grade inflammatory activation. Among the several inflammatory markers/mediators, level of C-reactive protein has been consistently associated with indices of arterial function in several populations. However, data regarding a possible direct etiological role of C-reactive protein in arterial dysfunction and atherosclerosis, if any, are yet inconclusive. Current evidence suggests that anti-inflammatory strategies benefit arterial function in several clinical settings. Further research is needed to elucidate whether inflammation may comprise a worthwhile treatment target with regard to the cardiovascular system. [ABSTRACT FROM AUTHOR]

Aims Erectile dysfunction (ED) confers an independent cardiovascular risk. We investigated the role of low-grade inflammation and endothelial dysfunction in ED patients with or without coronary artery disease (CAD). [ABSTRACT FROM PUBLISHER]

Background: Adamantiades-Behcet’s disease (ABD) is a multisystemic inflammatory/autoimmune disease involving both microcirculation and macrocirculation. Aortic stiffness index and aortic augmentation index (AI) are indices for the estimation of arterial stiffness and pressure wave reflections, respectively. The effect of anti-inflammatory and immunosuppressive drugs used in ABD on these indices is unknown. Methods: In this cross-sectional study we examined 74 subjects with ABD (aged 40.1 ± 12.5 years, 24 men) and 24 control subjects by using the noninvasive technique of radial artery applanation tonometry and pulse wave analysis for assessment of aortic AI by application of transfer functions. Echocardiography was used for assessment of aortic stiffness index. Classic cardiovascular (CV) risk factors, left ventricular and endothelial function of the brachial artery, as well as intima-media thickness of carotid artery, were also assessed. Results: Corticosteroids were the only drug having a negative and independent effect on aortic AI, but not on aortic stiffness. Patients taking corticosteroids had lower aortic AI and central systolic blood pressure (BP), but not aortic stiffness and peripheral systolic BP, when compared to those without corticosteroids (21±14% v 12±14%, P < .050). Medication, traditional CV risk factors, and functional or structural CV parameters were all comparable among the two groups. The AI was similar between the control group and patients with ABD taking corticosteroids. Conclusions: The AI, but not aortic stiffness, is lower in patients with ABD taking corticosteroids compared to patients not taking corticosteroids and similar to the control group. These results imply a role of inflammation or immunomodulatory mechanisms in the regulation of pressure wave reflections. [Copyright &y& Elsevier]