Therapeutic inertia in rhythm control strategies in hospitalized patients with fibrillation: Insights from Hellenic Cardiorenal Morbidity Snapshot (HECMOS) study.

BACKGROUND: Current guidelines recommend a rhythm control strategy in patients with symptomatic atrial fibrillation (AF) while catheter ablation has been shown to be a safer and more efficacious approach than antiarrhythmic medications. METHODS: HECMOS was a nationwide snapshot survey of cardiorenal morbidity in hospitalized cardiology patients. In this sub-study, we included 276 cases who had a history of AF, particularly on the rhythm strategy, and catheter ablation procedures had been performed before the index admission. RESULTS: Among 276 AF patients (mean age: 76.4 ±â€¯11.5 years, 58 % male), 60.9 % (N = 168) had persistent AF and 39.1 % (N = 108) had paroxysmal AF. Heart failure was the main cause of admission in 54.3 % (N = 145) of the patients, while 14.1 % (N = 39) were admitted due to paroxysmal AF, 7.3 % (N = 20) due to bradyarrhythmic reasons, and 6.5 % (N = 18) suffered from acute coronary syndrome. Most importantly, heart failure with reduced ejection fraction was present in 76 (27 %) patients. Only 10 patients out of the total (3 %, mean age 59.7 years) had undergone AF ablation while electrical cardioversion had been attempted in 37 (13.4 %) patients. Interestingly, in this AF population with heart failure, 3.6 % (N = 10) had a defibrillator implanted (4 single-chamber), and only 1.5 % (N = 4) had a cardiac resynchronization therapy defibrillator (CRT-D). CONCLUSION: High prevalence of persistent AF was detected in hospitalized patients, with heart failure being the leading cause of admission and main co-morbidity. Rhythm control strategies are notably underused, along with CRT-D implantation in patients with AF and heart failure.

Inflammasomes in Atherosclerosis-From Pathophysiology to Treatment.

Atherosclerosis, a chronic inflammatory disease characterized by arterial plaque accumulation, remains a significant global health challenge. In recent years, inflammasomes, the intracellular multiprotein complexes crucial for initiating innate immune responses, have emerged as key players in atherosclerosis pathophysiology. This review article aims to provide a comprehensive overview of the current understanding of inflammasome activation and its impact on atherosclerosis development and progression. We explore the intricate interplay between traditional cardiovascular risk factors and inflammasome activation, leading to the perpetuation of inflammatory cascades that drive plaque formation and instability. The review focuses on the molecular mechanisms underlying inflammasome activation, including the role of pattern recognition receptors and cytokines in this process. Moreover, we discuss the contribution of inflammasomes to endothelial dysfunction, foam cell formation, and vascular inflammation. Additionally, recent advances in therapeutic strategies targeting inflammasomes are examined, including pharmacological agents and potential immunomodulatory approaches. By collating and analyzing the current evidence, this review provides valuable insights into the potential of inflammasome-targeted therapies for atherosclerosis management and treatment. Understanding the pivotal role of inflammasomes in atherosclerosis pathophysiology offers promising prospects for developing effective and personalized therapeutic interventions that can mitigate the burden of this prevalent cardiovascular disorder and improve patient outcomes.

Novel Anti-Inflammatory Therapies in Coronary Artery Disease and Acute Coronary Syndromes.

Evidence suggests that inflammation plays an important role in atherosclerosis and the consequent clinical presentation, including stable coronary artery disease (CAD) and acute coronary syndromes (ACS). The most essential elements are cytokines, proteins with hormone-like properties that are produced by the immune cells, endothelial cells, platelets, fibroblasts, and some stromal cells. Interleukins (IL-1ß and IL-6), chemokines, interferon-γ (IFN-γ), and tumor necrosis factor-alpha (TNF-α) are the cytokines commonly associated with endothelial dysfunction, vascular inflammation, and atherosclerosis. These molecules can be targeted by commonly used therapeutic substances or selective molecules that exert targeted anti-inflammatory actions. The most significant anti-inflammatory therapies are aspirin, statins, colchicine, IL-1ß inhibitors, and IL-6 inhibitors, along with novel therapies such as TNF-α inhibitors and IL-1 receptor antagonists. Aspirin and statins are well-established therapies for atherosclerosis and CAD and their pleiotropic and anti-inflammatory actions contribute to their efficacy and favorable profile. Colchicine may also be considered in high-risk patients if recurrent ACS episodes occur when on optimal medical therapy according to the most recent guidelines. Recent randomized studies have also shown that therapies specifically targeting inflammatory interleukins and inflammation can reduce the risk for cardiovascular events, but these therapies are yet to be fully implemented in clinical practice. Preclinical research is also intense, targeting various inflammatory mediators that are believed to be implicated in CAD, namely repeated transfers of the soluble mutant of IFN-γ receptors, NLRP3 inflammasome inhibitors, IL-10 delivery by nanocarriers, chemokine modulatory treatments, and reacting oxygen species (ROS) targeting nanoparticles. Such approaches, although intriguing and promising, ought to be tested in clinical settings before safe conclusions can be drawn. Although the link between inflammation and atherosclerosis is significant, further studies are needed in order to elucidate this association and improve outcomes in patients with CAD.

Pathophysiology of Acute Coronary Syndromes-Diagnostic and Treatment Considerations.

Coronary artery disease and acute coronary syndromes are accountable for significant morbidity and mortality, despite the preventive measures and technological advancements in their management. Thus, it is mandatory to further explore the pathophysiology in order to provide tailored and more effective therapies, since acute coronary syndrome pathogenesis is more varied than previously assumed. It consists of plaque rupture, plaque erosion, and calcified nodules. The advancement of vascular imaging tools has been critical in this regard, redefining the epidemiology of each mechanism. When it comes to acute coronary syndrome management, the presence of ruptured plaques almost always necessitates emergent reperfusion, whereas the presence of plaque erosions may indicate the possibility of conservative management with potent antiplatelet and anti-atherosclerotic medications. Calcified nodules, on the other hand, are an uncommon phenomenon that has largely gone unexplored in terms of the best management plan. Future studies should further establish the importance of detecting the underlying mechanism and the role of various treatment plans in each of these distinct entities.

Biventricular myocardial function in Covid-19 recovered patients assessed by speckle tracking echocardiography: a prospective cohort echocardiography study.

Although severe acute respiratory syndrome coronavirus 2 causes respiratory disease, it may also lead to cardiovascular involvement with unknown long-term consequences. The aim of our study was to evaluate prospectively cardiac involvement in patients after the recovery from Covid-19, using two-dimensional speckle tracking echocardiography. 100 Covid-19 recovered patients with preserved left ventricular ejection fraction, were included, divided based upon clinical manifestation into two groups, those who were treated ambulant and those who were hospitalized. All patients underwent echocardiographic evaluation after their recovery. Although overall LV systolic function expressed by EF was normal, left ventricular global longitudinal strain (LVGLS) was significantly lower in Covid-19 recovered patients (33.28 ± 9.4 days after diagnosis) compared to controls (- 18.47 ± - 2.4 vs. - 21.07 ± - 1.76% respectively, p < 0.0001). Εspecially the lateral wall longitudinal strain (LATLS) and posterior wall longitudinal strain (POSTLS) were significantly reduced in all patients compared to controls (- 17.77 ± - 3.48 vs. - 20.97 ± - 2.86%, p < 0.0001 and - 19.52 ± - 5.3 vs. - 22.23 ± - 2.65%, p = 0.01). right ventricular global longitudinal strain (RVGLS) was significantly diminished only in the hospitalized group of Covid-19 recovered patients, compared to controls (- 18.17 ± - 3.32 vs. - 26.03 ± - 4.55% respectively, p < 0.0001). LVGLS is affected in almost all individuals after Covid-19 infection independently of the infection severity, with LATLS being the most sensitive marker of LV impairment and with POSTLS to follow. RV shows impaired GLS in severely ill patients highlighting RVGLS as a helpful tool of prognosis. Recovered patients from Covid-19 infection have to be monitored for a long time, since the term "long Covid disease" might also include the cardiac function.

The association of air pollutants exposure with subclinical inflammation and carotid atherosclerosis.

BACKGROUND: Air pollution is a well-described environmental factor with evidence suggesting a firm association with cardiovascular diseases. The purpose of this study was to determine the association of exposure to gaseous air pollutants on atherosclerosis burden. METHODS: 1955 inhabitants of the Corinthia region, aged 40 years or older, underwent clinical and biochemical assessment as well as carotid ultrasonography to evaluate carotid intima-media thickness (cIMT) and plaque burden. Analyzers recording time series concentration of CO, NO2, and SO2 were located at 4 different open sites (Regions 1, 2, 3 and 4) based on their proximity to industries, highways or shipyards. RESULTS: A higher concentration of CO, NO2, and SO2 was observed in Region 4 compared to the other regions. Mean cIMT (Region 1: 0.93 ± 0.24 mm; Region 2: 0.96 ± 0.40 mm; Region 3: 0.94 ± 0.39 mm; Region 4: 1.14 ± 0.55 mm, p < 0.001), maximum cIMT (p < 0.001) as well as carotid plaque burden (Region 1: 13.3%; Region 2: 18.8%; Region 3: 22.4%; Region 4: 38.6%, p < 0.001) were significantly higher in individuals of Region 4. Inhabitants of Region 4 had also higher levels of C reactive protein (Region 1: 4.56 ± 4.85 mg/l; Region 2: 3.49 ± 4.46 mg/l; Region 3: 4.03 ± 3.32 mg/l, Region 4: 5.16 ± 8.26 mg/l, p < 0.001). Propensity score analysis revealed higher inter-area differences in mean cIMT of individuals with coronary artery disease (CAD) (high vs low air pollution area: 1.56 ± 0.80 mm; vs. 1.18 ± 0.54 mm, p < 0.001) while there was no difference in cIMT of the matched population without CAD (p = 0.52). CONCLUSIONS: An increased carotid atherosclerotic and inflammatory burden is observed in inhabitants of areas with the highest concentration of air pollutants.

The impact of sleeping duration on atherosclerosis in the community: insights from the Corinthia study.

PURPOSE: Sleep is an essential physiologic process whose disturbances have been regarded as a risk factor in various pathophysiologic processes, including atherosclerosis and cardiovascular disease. Although the negative influence of short sleep duration has been well-established, recent data suggest a possible harmful effect of prolonged sleeping pattern. METHODS: In the setting of the Corinthia cross-sectional study, self-reported night sleep duration was recorded in 1752 apparently healthy individuals and was classified as normal sleep duration (NSD, 7-8 h), short sleep duration (SSD, 6-7 h), very short sleep duration (VSSD, < 6 h), and long sleep duration (LSD, > 8 h). Carotid duplex ultrasonography was performed in order to measure the mean and maximum carotid intima-media thickness (cIMT) as a non-invasive marker of atherosclerosis. RESULTS: Subjects with LSD and VSSD had significantly higher mean cIMT (VSSD: 1.02 ± 0.45 mm, SSD: 0.95 ± 0.35, NSD: 0.96 ± 0.38 mm, LSD: 1.07 ± 0.52 mm; p < 0.001) and maximum cIMT (VSSD: 1.39 ± 0.9 mm, SSD: 1.25 ± 0.71 mm, NSD: 1.23 ± 0.76 mm, LSD: 1.41 ± 0.93 mm). Following a regression analysis adjusting for known cardiovascular risk factors, individuals with LSD and VSSD had higher mean cIMT by 0.054 mm and 0.067 mm respectively compared to those with NSD. CONCLUSION: A balanced sleeping duration of 6-8 h is associated with decreased mean and maximum IMT while both very short sleep duration and long sleep duration are associated with increased carotid intima-media thickness, a marker of subclinical atherosclerosis.

Breakfast association with arterial stiffness and carotid atherosclerotic burden. Insights from the 'Corinthia' study.

BACKGROUND AND AIMS: The role of dietary patterns, in cardiovascular diseases has been challenged. The role of breakfast as an element of balance energy intake has gained research interest. However, the effects of dietary patterns related to breakfast consumption on vascular function are unknown. We explored the association of breakfast consumption habits with arterial wall elastic properties and carotid atherosclerosis. METHODS AND RESULTS: In this cross-sectional study we enrolled 2043 inhabitants of the Corinthia region in Greece. Carotid-femoral pulse wave velocity (cf-PWV) was used to assess arterial stiffness. Carotid intima-media thickness (cIMT) was measured and the mean and the maximum cIMT were calculated. According to food frequency questionnaires, breakfast contribution in total daily energy intake (>20%; 5-20% and <5%) was estimated. Subjects were categorized as high-energy breakfast consumers (HeBC), low-energy breakfast consumers (LeBC) and those skipping breakfast (SBf) respectively. From the study population 240 subjects were categorized as HeBC, 897 as LeBC, and 681 as SBf. The mean cf-PWV was significantly higher in subjects SBf compared to LeBC and HeBC (9.35 ± 2.82 m/s vs. 9.09 ± 2.77 m/s vs. 8.76 ± 2.69 m/s, p = 0.02). The mean cIMT was significantly higher in subjects SBf compared to LeBC and HeBC (1.04 ± 0.46 mm vs. 0.99 ± 0.43 mm vs. 0.92 ± 0.39 mm, p = 0.01). Even after adjustment for potential confounders and cardiovascular risk factors SBf subjects have significantly increased mean cIMT and cf-PWV. CONCLUSION: Skipping breakfast has an adverse effect on arterial stiffness and carotid atheromatic burden. Increased breakfast total energy intake may act protectively against atherosclerosis, a finding worth of further pathophysiologic exploration with potential clinical implications.

Alcohol Consumption and Aortic Root Dilatation: Insights from the Corinthia Study.

Aortic diameter and progression to thoracic aortic aneurysm are influenced by several factors. In this study, we investigated the association of alcohol consumption with aortic root and ascending aorta dilatation. In the context of the Corinthia study, we examined 1751 patients with echocardiography. Several demographic and clinical characteristics were recorded. Alcohol consumption was assessed based on a questionnaire of frequency, type, and quantity. Accordingly, patients were categorized as everyday alcohol consumers (EDACs) and as social drinkers (SoD). Everyday alcohol consumers were further categorized to group 1: 0 to 1 drink/d; group 2: 1 to 2 drinks/d; and group 3: ≥3 drinks/d. From the study population, 40% were categorized as EDAC and had an increased aortic root diameter (AoRD) and an elevated AoRD index compared with SoD. Interestingly, there was a stepwise increase in aortic root and ascending aorta diameter according to daily alcohol consumption. Specifically, patients consuming ≥3 drinks of alcohol/d had increased indexed aortic by 1.4 mm/m2 compared with SoD even after adjustment for possible confounders. Daily alcohol consumption is associated with increased aortic root diameter. These findings may have important clinical implications, especially in patients with borderline or dilated aortic root, and merit further investigation.

The influence of resting heart rate on pulse wave velocity measurement is mediated by blood pressure and depends on aortic stiffness levels: insights from the Corinthia study.

OBJECTIVE: Increased resting heart rate as well as increased arterial stiffness are both independent predictors of cardiovascular events and mortality. Results of previous studies have failed to converge concerning the association between heart rate and arterial stiffness, regardless of other potential confounders, such as age, gender and particularly blood pressure (BP). We aimed to investigate: (a) the degree of association (if any) between resting heart rate and carotid-to-femoral pulse wave velocity (PWV), the gold standard index of arterial stiffness, (b) if the relationship between heart rate and PWV is mediated by BP levels and (c) whether their association is affected by the levels of aortic stiffening. APPROACH: Demographic, hemodynamic, laboratory and clinical data of 1566 subjects from the cross-sectional observational 'Corinthia' study were analyzed using univariate and multivariate regression models. Mediation analysis was performed to test whether mean arterial pressure (MAP) is a significant mediator in the heart rate-PWV relationship. The total population was divided in two groups of low and high arterial stiffness according to the median PWV value (8.6 m s-1). MAIN RESULTS: We found that (i) there is a significant association between heart rate and PWV, regardless of other confounding factors. An increase in heart rate by 20 b.p.m. can increase PWV by 0.5 m s-1. However, this association was significant only for subjects with increased aortic stiffness (PWV > 8.6 m s-1) and not for those with PWV ⩽ 8.6 m s-1. Further, (ii) heart rate-PWV association was partially mediated by MAP. SIGNIFICANCE: Increased resting heart rate is related to increased aortic stiffness, only in subjects with stiffer aortas, regardless of BP and other risk factors and subjects' characteristics. The synergistic prognostic effect of increased arterial stiffness and elevated heart rate on target organ damage, cardiovascular events and mortality should be explored in future studies.

The impact of sedentary behavior patterns on carotid atherosclerotic burden: Implications from the Corinthia epidemiological study.

BACKGROUND AND AIMS: Sedentary lifestyle, unlike leisure time physical activity (PA), is associated with atherosclerosis progression. Regarding the interrelationship between television watching, as a sedentary behavior pattern, and cardiovascular disease burden, few data exist. METHODS: In this cross-sectional epidemiological study based on 2043 inhabitants of the Corinthia region, in Greece, ultrasonography was used to measure carotid intima-media thickness (IMT) in both carotid arteries. The average (meanIMT) and maximum thickness (maxIMT) were determined as representative values of subclinical atherosclerosis. We evaluated PA using the self-reported International Physical Activity Questionnaire (IPAQ). Based on specific questions, the average hours per week spent on watching television (TV), videos or DVD was calculated for each participant. RESULTS: According to TV viewing time, subjects were categorized into the low (≤7 h/week), moderate (7˃ TV hours/week ≤21) and high (˃21 h/week) TV viewing time groups. Prevalence of carotid atheromatic plaque was lower in the low TV viewing time group compared to the moderate and high TV viewing time groups (p = 0.02). TV viewing time was associated with increased carotid IMT (p = 0.03) and the prevalence of carotid atheromatic plaque (p = 0.02), even after adjustment for age, body mass index, cardiovascular risk factors or history of cardiovascular disease. Subjects in the high TV viewing time group have 80% increase odds of carotid atheromatic plaque compared to patients categorized in the low TV viewing time group (p = 0.01). CONCLUSIONS: The present findings have important public health implications, providing a better understanding of the components of sedentary behavior that are associated with atherosclerotic progression.

Arterial stiffness and subclinical aortic damage of reclassified subjects as stage 1 hypertension according to the new 2017 ACC/AHA blood pressure guidelines.

Background: The 2017 ACC/AHA blood pressure (BP) guidelines generated controversies due to the new proposed BP cut-off values defining hypertension. We aimed to assess aortic stiffness of subjects who are reclassified as stage 1 hypertensive according to the new guidelines and compare them with the subjects of "elevated BP" category. Patients and methods. Data from the "Corinthia" study, an observational, cross-sectional survey of 2,043 participants were analyzed. Subjects were classified into 4 groups: group A: systolic pressure (SBP) 120-129 and diastolic pressure (DBP) < 80 mmHg, group B: SBP 130-139 or DBP 80-89 mmHg, group B1: SBP 130-139 and DBP < 80 mmHg and group B2: SBP 130-139 and DBP 80-89 mmHg. Aortic stiffness was assessed by carotid-to-femoral pulse wave velocity (PWV). A value of PWV > 10m/s was consider indicative of asymptomatic organ damage while values of PWV exceeded the 90 % percentile for each age group were consider as abnormal. Results: Groups B, B1 and B2 have significantly increased PWV compared to group A, independently from age and other risk factors (PWV: 9.2 ± 2.8 vs 9.4 ± 2.7 vs 8.6 ± 2.5 vs 8.1 ± 2.3 m/s, p < 0.01, respectively). The prevalence of PWV > 10 m/s and abnormal PWV values in group A was significantly lower than the corresponding prevalence in randomly selected, age-matched subjects from group B (13.5 % vs 24.4 %, p = 0.027 and 5.6 % vs 14.2 %, p = 0.022, respectively). Conclusions: The reclassified subjects as stage 1 hypertensive by the new guidelines have a significantly increased aortic stiffness and greater prevalence in asymptomatic aortic damage compared to subjects with elevated BP. This finding may indirectly explain the increased cardiovascular risk of this group.

Environment and cardiovascular disease: rationale of the Corinthia study.

Environmental factors constitute an important but underappreciated risk factor towards the development and progression of cardiovascular disease (CVD). Environmental exposure to variable pollutants is implicated in the derangement or propagation of adverse pathophysiological processes linked with atherosclerosis, including genetic, hemodynamic, metabolic, oxidative and inflammation parameters. However, no data exist on environmental pollution in rural or semi-rural areas. Therefore, the purpose of the "Corinthia" study is to examine the impact of environmental pollution in indices of cardiovascular morbidity and mortality in a cross-sectional and longitudinal design. The Corinthia study began in October 2015 and is planned to recruit 1,500 individuals from different regions of Corinthia country with different environmental exposures to pollutants and different patterns of soil/ground and/or air pollution until December 2016. Baseline measurements will include lifestyle measurements, anthropometric characteristics and a comprehensive cardiovascular examination. The follow-up is planned to extend prospectively up to 10 years and this study is anticipated to provide valuable data on the distinct impact of soil and air pollution on early markers of atherosclerosis and cardiovascular disease and on the overall impact of environment pollution to cardiovascular morbidity and mortality.