Abstract Introduction Coronary Artery Bypass Grafting (CABG) surgery is the preferred method in Coronary Artery Disease, particularly in patients with multi-vessel disease and impaired left ventricular function. Besides the success of surgical intervention, achieving a good level of Health-Related Quality of Life (HRQoL) is the primary goal of the entire process. Objective The aim of our study is to evaluate HRQoL before and after CABG surgery and to assess the adherence to pharmacotherapy and the frequency of arrhythmias postoperatively during a 6- month follow-up period. Methods The study design involves a descriptive longitudinal study. The study was conducted in one public hospital and two private hospitals of Cyprus. The follow-up period for participants was determined at 6 months post-CABG surgery. HRQoL assessment was conducted using the MacNew questionnaire, and the evaluation of arrhythmias and other clinical data was performed using a Clinical Data Evaluation Form created for the study purposes. Results Our study included 103 people who had undergone CABG surgery. HRQoL decreased at 3 months post-CABG surgery compared to the preoperative period (Mean: 5.03, SD: ±1.02 vs Mean: 4.75, SD: ±1.00) but improved at 6 months post-surgery (Mean: 6.19, SD: ±0.67). Among the total of patients, 21 (20.6%) developed Atrial Fibrillation (AF) postoperatively. All patients with AF received immediate treatment, and sinus rhythm was restored. Additionally, 6 patients developed other types of arrhythmias, among whom 1 patient experienced cardiac arrest with an initial asystole rhythm and eventually passed away. Conclusion CABG significantly affects HRQoL, showing a temporary decline postoperatively followed by improvement. Arrhythmias and compliance with pharmacotherapy are crucial aspects of postoperative care.

Background: Despite the increasing use of transcatheter aortic valve procedures, many patients still require surgical aortic valve replacement (SAVR). Assessing arterial properties in patients undergoing SAVR for aortic valve stenosis can be challenging, and the existing evidence is inconclusive. Our study aimed to investigate the impact of SAVR on vascular stiffness and the quality of life, as well as the different effects of valve type on arterial properties. Methods: We included 60 patients (mean age 70.25 ± 8.76 years, 65% men) with severe symptomatic aortic stenosis who underwent SAVR. Arterial stiffness (cfPWV, baPWV) and vascular parameters (AIx@75, central pressures, SEVR) were measured at baseline, pre-discharge, and 1-year post-operation. The QOL was assessed using the generic questionnaire—short-form health survey 36 (SF-36) pre-operatively and at 1 year. Results: Post-SAVR, cfPWV increased immediately (7.67 ± 1.70 m/s vs. 8.27 ± 1.92 m/s, p = 0.009) and persisted at 1 year (8.27 ± 1.92 m/s vs. 9.29 ± 2.59 m/s, p ≤ 0.001). Similarly, baPWV (n = 55) increased acutely (1633 ± 429 cm/s vs. 2014 ± 606 cm/s, p < 0.001) and remained elevated at 1 year (1633 ± 429 cm/s vs. 1867 ± 408 cm/s, p < 0.001). Acute decrease in Alx@75 (31.16 ± 10% vs. 22.48 ± 13%, p < 0.001) reversed at 1 year (31.16 ± 10% vs. 30.98 ± 9%, p = 0.71). SEVR improved (136.1 ± 30.4% vs. 149.2 ± 32.7%, p = 0.01) and persisted at 1 year (136.1 ± 30.4% vs. 147.5 ± 30.4%, p = 0.01). SV had a greater cfPWV increase at 1 year (p = 0.049). The QOL improved irrespective of arterial stiffness changes. Conclusions: After SAVR, arterial stiffness demonstrates a persistent increase at 1-year, with valve type having a slight influence on the outcomes. These findings remain consistent despite the perceived QOL.

OBJECTIVE:Monocyte count and red cell distribution width (RDW) have shown prognostic potential in patients with fibrotic lung diseases. Their kinetics and prognostic usefulness of peripheral blood indices in patients with interstitial lung diseases (ILDs) undergoing surgical lung biopsy for diagnostic reasons have not been studied. PATIENTS AND METHODS:We retrospectively included consecutive patients with ILD who underwent surgical lung biopsy for diagnostic purposes Between 07/11/2019 and 11/10/2022. RESULTS:Fifty-five (n=55) patients were included in the study. Median age was 65.0 years (95% CI: 63.0 to 66.0). Postoperative peripheral blood monocyte count on Day 1 was significantly higher compared to preoperative, perioperative, and postoperative values on Day 90 (repeated measures ANOVA, p<0.0001). Patients in the high postoperative monocyte count group had significantly increased length of postoperative hospital stay [Mann-Whitney test, p=0.007] and significantly lower Forced Vital Capacity (FVC)% predicted 3 months after surgery [Mann-Whitney test, p=0.029] compared to patients in the low postoperative monocyte count group. Postoperative RDW on Day 90 was significantly higher compared to preoperative, perioperative and postoperative-Day 1 RDW (repeated measures ANOVA, p=0.008, p=0.006, p<0.0001, respectively). Patients in the high postoperative RDW group did not have increased hospital stay (Mann-Whitney test, p=0.49) or decreased FVC% predicted at 3 months compared to patients in the low postoperative RDW group (Mann-Whitney test, p=0.91). CONCLUSIONS:Peripheral blood monocyte count could be a prognostic biomarker for patients with ILDs undergoing diagnostic surgical lung biopsies. RDW does not seem to represent an acute phase biomarker but seems to increase over time following disease progression. Larger studies are urgently required.

Extensive research has been conducted to elucidate and substantiate the crucial role of the Renin-Angiotensin System (RAS) in the pathogenesis of hypertension, cardiovascular disorders, and renal diseases. Furthermore, the role of oxidative stress in maintaining vascular balance has been well established. It has been observed that many of the cellular effects induced by Angiotensin II (Ang II) are facilitated by reactive oxygen species (ROS) produced by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. In this paper, we present a comprehensive overview of the role of ROS in the physiology of human blood vessels, specifically focusing on its interaction with RAS. Moreover, we delve into the mechanisms by which clinical interventions targeting RAS influence redox signaling in the vascular wall.

Little is known about the role of serum and tissue mediators in the progression of ascending aortic aneurysms and dissections. We examined how the tissue expression of microRNAs and matrix metalloproteinases (MMPs), as well as the serum levels of osteoprotegerin, adiponectin, and high sensitivity C-reactive protein (hsCRP) are associated with these entities. We enrolled 21 patients with ascending aortic aneurysm, 11 with acute Stanford type A aortic dissection and 18 controls. The serum levels of osteoprotegerin, adiponectin, and hsCRP, as well as the tissue expression of MMPs 2 and 9 and tissue microRNAs 29 and 195 were compared among groups. There was no difference regarding serum osteoprotegerin, adiponectin, and tissue MMP2 and MMP9 levels. hsCRP was higher in the dissection group (P = .03). Tissue expression of microRNA 29 was 2.11-fold higher in the dissection (P = .001) and 2.99-fold higher in the aneurysm group (P < .001), compared with the control group. Tissue expression of microRNA 195 was 2.72-fold higher in the dissection (P < .001) and 2.00-fold lower in the aneurysm group (P = .08), compared with to the control group. These findings support the contribution of microRNAs in the progression of aneurysm formation and dissection, suggesting a role as potential biomarkers and future therapeutic targets.

Over 20 years of intensified research in the field of stem cells brought about unprecedented possibilities in treating heart diseases. The investigators were initially fascinated by the idea of regenerating the lost myocardium and replacing it with new functional cardiomyocytes, but this was extremely challenging. However, the multifactorial effects of stem cell-based therapies beyond mere cardiomyocyte generation, caused by paracrine signaling, would open up new possibilities in treating cardiovascular diseases. To date, there is a strong body of evidence that the anti-inflammatory, anti-apoptotic, and immunomodulatory effects of stem cell therapy may alleviate atherosclerosis progression. In the present review, our objective is to provide a brief overview of the stem cell-based therapeutic options. We aim to delineate the pathophysiological mechanisms of their beneficial effects in cardiovascular diseases especially in coronary artery disease and to highlight some conclusions from important clinical studies in the field of regenerative medicine in cardiovascular diseases and how we could further move onwards.

Beneki, Eirinia; Dimitriadis, Kyriakosa; Koumallos, Nikolaosb; Tsioufis, Konstantinosa; Aggeli, Konstantinaa Author Information

Abstract Funding Acknowledgements Type of funding sources: None. Background/Introduction The increasing efficacy of transcatheter aortic valve implantation (TAVI) justifies a renewed assessment of quality of life (QOL) after surgical aortic valve replacement (SAVR). Purpose The aim of this study was to evaluate long-term QOL in elderly patients undergoing isolated SAVR. Methodology 60 patients with severe aortic stenosis (AS) enrolled in our study (mean age 70.25±8.76, n=21 women). Clinical and QOL data collected pre surgery and at 1 year. For the assessment of QOL we used the instruments SF-36 (36-Item Short Form Health Survey Questionnaire), Euro-QOL 5 Dimensions (EQ-5D) and the visual analogue scale (VAS). Bivariate and multiple logistic regression analyses were performed. Results QoL is significantly improved 1 year after SAVR according to the three assessment tools. The physical health score (PCS) was 58±10% preoperatively and 80±10% (p<.001) after 1 year. Similarly, mental health score (MCS) improved (55±6% vs 77±9%, p<.001). Multivariate analysis showed that patients with a biological or Perceval valve and a preoperative EF <50% had greater improvement in PCS 1 year after SAVR than patients who received a mechanical valve or had a preoperative EF >50%. Conclusions The perceived QOL of patients with AS improved significantly 1 year after SAVR. The results could be useful in informing future patients and giving them realistic expectations.

BACKGROUND:From a variety of ring types, semirigid ring is more preferred for mitral annuloplasty during mitral valve repair particularly in patients whose native mitral saddle shape annulus is well maintained. During mitral annuloplasty artificial chord implantation with the appropriate neochord length is surgically challenging. We present our experience of using the Memo 3D ReChord, a semirigid ring with additional chordal guiding system for mitral valve repair.PATIENTS AND METHODS:From September 2018 to February 2020, we successfully treated ten patients with severe (4+/4+) degenerative mitral valve regurgitation due to posterior leaflet prolapse with chordal rupture with the implantation Memo 3D ReChord and neo-chords.RESULTS:We implanted from one to three neo-chords and always a ring in our patients. None of the patients had any residual mitral valve regurgitation at the end of the repair and on their discharge evaluated through transesophageal and transthoracic echocardiography respectively. There was no mortality at 30-days or on midterm follow-up. During the 3-month follow-up no regurgitation was noticed either. We included in our study only the patients successfully treated. We also used it in two patients, who underwent valve replacement during the same operation due to mild to moderate mitral valve regurgitation.CONCLUSIONS:This, in our knowledge, is the first Greek series of the implantation of the Memo 3D Rechord. The initial excellent results give us the enthusiasm to continue while long-term results and the durability of this technique are necessary to establish this semirigid annuloplastic ring in our every-day practice.

Interleukin-6 (IL-6) is a cytokine centrally involved in several immune responses and it has been recognized as a driver of enhanced atherothrombotic risk. Immunity and inflammation are intrinsically involved in atherosclerosis progression. This generated 'inflammation hypothesis', which is now validated in large-scale clinical trials. Abundant evidence supports the distinctive role of IL-6 in coronary artery disease. The focus on this cytokine stems from epidemiological studies linking high plasma concentrations of IL-6 with greater risk for adverse cardiovascular events, genetic studies which implicate a causative role of IL-6 in atherosclerosis and murine data which support the involvement of IL-6 in various pathophysiological cascades of atherothrombosis. The fact that high IL-6 levels are equivalent to increased cardiovascular risk created an unmet need to address those who are at 'residual inflammatory risk'. Moreover, the opposing effects of IL-6 underlined the importance of deciphering specific signaling cascades, which may be responsible for different effects. Finally, murine data and some small clinical trials highlighted the possibility of reversing the pro-atherogenic effects of IL-6 by directly targeting it. While IL-1 blockage was proved effective, it is reasonable to examine if moving more downstream in the inflammation cascade could be more selective and effective than other anti-inflammatory therapies. In the present review, we examine the role of IL-6 as a biomarker of 'residual inflammatory risk', its vital role in the pathophysiology of atherosclerosis progression and the possibility of targeting it to stall coronary artery disease progression.

The role of lipoprotein(a) (Lp[a]) as a significant and possibly causal cardiovascular disease (CVD) risk factor has been well established. Many studies, mostly experimental, have supported inflammation as a mediator of Lp(a)-induced increase in CVD risk. Lp(a), mainly through oxidized phospholipids bound to its apolipoprotein(a) part, leads to monocyte activation and endothelial dysfunction. The relationship between Lp(a) and inflammation is bidirectional as Lp(a) levels, besides being associated with inflammatory properties, are regulated by inflammatory stimuli or anti-inflammatory treatment. Reduction of Lp(a) concentration, especially by potent siRNA agents, contributes to partial reversion of the Lp(a) related inflammatory profile. This review aims to present the current pathophysiological and clinical evidence of the relationship between Lp(a) and inflammation.

Cardiac erosion is a rare but life-threatening complication after the interventional closure of an atrial septal defect. We present the case of a patient who developed cardiac erosion 9 years after the placement of an Amplatzer Septal Occluder. The patient presented to our hospital with symptoms of tamponade. Surgical exploration revealed a tear in the roof of the left atrium. To our knowledge, this is one of the most delayed presentations reported. In these cases, diagnosis is difficult and a level of clinical suspicion is demanded.

Abstract Background Assessing arterial properties in patients with aortic valve stenosis undergoing surgical aortic valve replacement (SAVR) is difficult, and the results to date have been inconclusive. Purpose We sought to investigate how SAVR affects vascular stiffness in the short and long term. Methods We included 69 patients (mean age 70.8±8.4 years, 62% men) with severe symptomatic aortic stenosis who underwent SAVR. Arterial stiffness was assessed using the carotid femoral pulse wave velocity (cfPWV) and brachial-ankle pulse wave velocity (baPWV). Measurements in patients with an ankle-brachial index (ABI) <0.9 were excluded from the analysis for baPWV measurments because a low ABI can affect the accuracy of baPWV. Augmentation index corrected for heart rate (Alx@75), central pressures and subendocardial viability ratio (SEVR) were assessed with arterial tonometry. Measurements were conducted at baseline, in the acute phase and 1 year after the operation. Results Immediately after SAVR there was an increase in cfPWV (8.04±1.3 m/s vs 8.54±1.6 m/s, p=0.02) that was sustained at 1 year (8.04±1.3 m/s vs 9.42±2.4 m/s, p≤0.001). Similarly, baPWV (n=55) increased in the acute phase (1633±429 cm/s vs 2014±606 cm/s, p<0.001) and persisted 1 year postoperatively (1633±429 cm/s vs 1867±408 cm/s, p<0.001). Post-SAVR we also observed a decrease in Alx@75 (31.02±10% vs 22.73±12%, p≤0.001) that was attenuated 1 year later (31.02±10% vs 26.65±8%, p≤0.001), and an increase in SEVR (136.1±30.4% vs 149.2±37.7%, p=0.01) which remained improved at 1 year (136.1±30.4% vs 147.5±30.4%, p=0.01). Conclusions After SAVR the arterial system shows an increase of stiffness in response to the acute relief of the obstruction, which is retained in the long term. Funding Acknowledgement Type of funding sources: None.

Objective: Assessing arterial properties in patients with aortic valve stenosis undergoing surgical aortic valve replacement (SAVR) is difficult, and the results to date have been inconclusive. We sought to investigate how SAVR affects vascular stiffness in the short and long term. Design and method: We included 55 patients (mean age 70 ± 8 years, 69% men) with severe symptomatic aortic stenosis who underwent SAVR. Arterial stiffness was assessed using the carotid-femoral pulse wave velocity (cfPWV) and brachial-ankle pulse wave velocity (baPWV). Measurements were conducted at baseline, in the acute phase, and 1 year after the operation. Results: Immediately after SAVR there was an increase in cfPWV (7.66 ± 1.63 m/s vs 8.27 ± 2.06 m/s, p = .010) that was sustained at 1 year (7.66 ± 1.63 m/s vs 8.98 ± 2.31 m/s, p = <.001, figure 1). Similarly, baPWV increased in the acute phase (1597 ± 455 cm/s vs 1954 ± 658 cm/s, p < .001) and persisted 1 year postoperatively (1597 ± 1833 cm/s, p < .001, figure 2). Conclusions: After SAVR the arterial system shows an increase of stiffness in response to the acute relief of the obstruction, which is retained in the long term.

Purpose/Background/Objectives: Acute kidney injury (AKI) is a serious postoperative complication. Increased arterial stiffness has been shown to be an independent risk factor for cardiovascular events. Our aim was to investigate whether arterial stiffness is a predictor of AKI in patients following surgical aortic valve replacement (SAVR). Methods: Eighty-four patients (mean age 72 ± 8 years, 34 females) with moderate to severe aortic stenosis undergoing SAVR were included. As indicators of arterial stiffness aortic hemodynamics, carotid-femoral pulse wave velocity (cfPWV) and brachial-ankle pulse wave velocity (baPWV) were assessed prior to surgery. Renal dysfunction was defined when eGFR was below 60 ml/min (n = 28, 33%). AKI was defined using KDIQO criteria. Results: Twelve patients (14%) developed AKI. There was no significant difference in aortic hemodynamics and cfPWV between the two groups. baPWV significantly correlated with AKI (r = 0.313, p = 0.004). In logistic regression analysis, increase of baPWV per 1 Standard Deviation (Odds Ratio [OR] = 2.76, 95% Confidence intervals [CI]: 1.25–6.11, p = 0.012) and presence of renal dysfunction (OR = 14.93, 95% CI: 2.55–87.32, p = 0.003) were associated with higher risk for AKI even after adjustment for age, gender, systolic blood pressure and diabetes. baPWV was a stronger predictor of AKI than baseline creatinine (Area under the curve [AUC] 0.68, 95% CI: 0.52–0.84, p = 0.05 vs AUC 0.61, 95% CI: 0.46–0.77, p = 0.21; p < 0.05). Conclusion: baPWV could be considered as a useful predictive biomarker for AKI after SAVR, especially in patients with renal dysfunction prior to surgery.