Publications by authors named "Christos A Goudis"

Background And Aims: Vitamin D deficiency is a common disorder and has been linked with atrial fibrillation (AF) in several observational studies, although the causal relationships remain unclear. We conducted a Mendelian randomization (MR) analysis to determine the causal association between serum 25-hydroxyvitamin D [25(OH)D] concentrations and AF.

Methods And Results: The analyses were performed using summary statistics obtained for single-nucleotide polymorphisms (SNPs) identified from large genome-wide association meta-analyses conducted on serum 25(OH)D ( = 79,366) and AF ( = 1,030,836).

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Article Synopsis
  • The study investigates the circadian patterns of acute myocardial infarction (AMI) and atrial fibrillation (AF) in diabetic patients within a Mediterranean country, examining 178 patients aged 67.7 on average.
  • Findings indicate that AMI occurs more frequently during midnight hours (21:00-23:59) and AF peaks around noon (12:00-14:59) among diabetic patients.
  • The results suggest that factors like autonomic nervous system changes, glycemic variations, and treatment timing may influence these patterns, calling for more research to guide potential therapeutic strategies.
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Background: Galectin-3 is an inflammatory marker that is raised in myocardial fibrosis and inflammation. Recent studies have explored its role in predicting atrial fibrillation (AF) outcomes. The aim of this systematic review and meta-analysis is to examine the association between serum concentration of galectin-3 and AF.

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Atrial fibrillation (AF) has different underlying substrates. Atrial remodeling involves electrophysiological and structural abnormalities that promote the development and perpetuation of AF. Experimental and clinical data indicate that inflammation is implicated in the pathophysiology of atrial remodeling.

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Aims: We examined whether the use of a renin-angiotensin-aldosterone system (RAS) inhibitor plays a role in protecting against left atrial appendage thrombus (LAAT) in patients with hypertension complicated by atrial fibrillation (AF).

Methods: Two observational studies were conducted on patients with diagnoses of hypertension and AF, who were categorized into RAS inhibitor user or nonuser groups. Demographic characteristics, clinical characteristics, echocardiographic parameters and hemostatic markers were examined and the occurrence of LAAT during follow-up were recorded.

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Background: Atrial fibrillation (AF) is the most common arrhythmia in clinical practice and is associated with increased cardiovascular morbidity and mortality. Epicardial adipose tissue (EAT) serves as a biologically active organ with important endocrine and inflammatory function. Review An accumulating body of evidence suggests that EAT is associated with the initiation, perpetuation, and recurrence of AF, but the precise role of EAT in AF pathogenesis is not completely elucidated.

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Chronic obstructive pulmonary disease (COPD) is a complex disorder that primarily affects the lungs and is characterized not only by local pulmonary, but also by systemic inflammation which promotes the development of extrapulmonary and cardiovascular co-morbidities. Angiotensin converting enzyme (ACE) inhibitors and ARBs (angiotensin receptor blockers) are widely used drugs in the treatment of cardiovascular diseases, with growing evidence suggesting potential benefits in COPD patients. The purpose of this review is to describe the correlation of renin-angiotensin system (RAS) with COPD pathophysiology and to present the latest data regarding the potential role of RAS blockers in COPD.

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Introduction: Atrial structural remodeling in the form of fibrosis contributes to the arrhythmic substrate in atrial fibrillation (AF). The aim of this study was to investigate the effects of doxycycline on chronic intermittent hypoxia (CIH)-induced atrial fibrosis and the pathophysiological mechanisms underlying such changes.

Methods: A total of 30 Sprague Dawley rats were randomized into three groups: control group, CIH group, and CIH with doxycycline treatment (CIH-D) group.

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Chronic obstructive pulmonary disease (COPD) is independently associated with atrial fibrillation (AF). Decreased oxygenation, hypercapnia, pulmonary hypertension, diastolic dysfunction, oxidative stress, inflammation, changes in atrial size by altered respiratory physiology, increased arrhythmogenicity from nonpulmonary vein foci commonly located in the right atrium, and respiratory drugs have been implicated in the pathogenesis of AF in COPD. The understanding of the relationship between COPD and AF is of particular importance, as the presence of the arrhythmia has significant impact on mortality, especially in COPD exacerbations.

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Atrial fibrillation (AF) is the commonest arrhythmia in clinical practice and is associated with increased cardiovascular morbidity and mortality. Obstructive sleep apnea (OSA), a common breathing disorder, is an independent risk factor for AF. Several pathophysiological mechanisms, including apnea-induced hypoxia, intrathoracic pressure shifts, sympathovagal imbalance, atrial remodeling, oxidative stress, inflammation and neurohumoral activation have been implicated in the occurrence of AF in OSA patients.

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Chronic obstructive pulmonary disease (COPD) is independently associated with an increased burden of cardiovascular disease. Besides coronary artery disease (CAD) and congestive heart failure (CHF), specific electrocardiographic (ECG) abnormalities and cardiac arrhythmias seem to have a significant impact on cardiovascular prognosis of COPD patients. Disturbances of heart rhythm include premature atrial contractions (PACs), premature ventricular contractions (PVCs), atrial fibrillation (AF), atrial flutter (AFL), multifocal atrial tachycardia (MAT), and ventricular tachycardia (VT).

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Background: Atrial fibrillation (AF) is associated with abnormal atrial substrate. We investigated whether patients with persistent lone AF and patients with persistent AF and nonischemic dilated cardiomyopathy (NIDCM) exhibit any differences in electrophysiological and electroanatomical properties of right atrium (RA) and collagen turnover. We also investigated the relationship between mean RA bipolar voltage and collagen turnover.

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Obesity is a worldwide health problem with epidemic proportions that has been associated with atrial fibrillation (AF). Even though the underlying pathophysiological mechanisms have not been completely elucidated, several experimental and clinical studies implicate obesity in the initiation and perpetuation of AF. Of note, hypertension, diabetes mellitus, metabolic syndrome, coronary artery disease, and obstructive sleep apnea, represent clinical correlates between obesity and AF.

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Diabetes mellitus (DM) represents one of the most important risk factors for atrial fibrillation (AF) while AF is a strong and independent marker of overall mortality and cardiovascular morbidity in diabetic patients. Autonomic, electrical, electromechanical, and structural remodeling, including oxidative stress, connexin remodeling and glycemic fluctuations seem to be implicated in AF pathophysiology in the setting of DM. The present review highlights the association between DM and AF, provides a comprehensive overview of the responsible pathophysiological mechanisms and briefly discusses potential upstream therapies for DM-related atrial remodeling.

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Atrial fibrillation is the most common arrhythmia in athletes and may be associated with endurance sport practice. Atrial ectopic beats, chronic systemic inflammation, autonomic system alterations, anatomic adaptation, myocardial injury and illicit drugs seem to be implicated in the increased prevalence of atrial fibrillation in athletes, but clear evidence is lacking. Treatment of the arrhythmia is a challenging issue, as atrial fibrillation may impair athletic performances and deteriorate athletes' quality of life.

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Aims: Collagen turnover and atrial fibrosis have been implicated in the generation and perpetuation of atrial fibrillation (AF). We evaluated the importance of serum markers of collagen turnover in predicting the outcome of electrical cardioversion (CV) of persistent AF and the relationship between AF and fibrosis.

Methods And Results: Serum C-terminal pro-peptide of collagen type-I (CICP) and C-terminal telopeptide of collagen type-I (CITP) were measured in 164 patients with AF before and 2 months after CV.

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Atrial fibrillation is a complex arrhythmia with multiple possible mechanisms. A lot of experimental and clinical studies have shed light on the pathophysiological mechanisms of arrhythmia, especially on molecular basis. Electrical, contractile and structural remodeling, calcium handling abnormalities, autonomic imbalance and genetic factors seem to play a crucial role in atrial fibrillation initiation and maintenance.

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Long QT syndrome is characterized by prolongation of the corrected QT (QTc) interval on the surface electrocardiogram and is associated with precipitation of torsade de pointes (TdP), a polymorphic ventricular tachycardia that may cause sudden death. Acquired long QT syndrome describes pathologic excessive prolongation of the QT interval, upon exposure to an environmental stressor, with reversion back to normal following removal of the stressor. The most common environmental stressor in acquired long QT syndrome is drug therapy.

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Atrial fibrillation is the most common arrhythmia in clinical practice and is associated with increased cardiovascular morbidity and mortality. Atrial fibrosis, a detrimental process that causes imbalance in extracellular matrix deposition and degradation, has been implicated as a substrate for atrial fibrillation, but the precise mechanisms of structural remodelling and the relationship between atrial fibrosis and atrial fibrillation are not completely understood. A large number of experimental and clinical studies have shed light on the mechanisms of atrial fibrosis at the molecular and cellular level, including interactions between matrix metalloproteinases and their endogenous tissue inhibitors, and profibrotic signals through specific molecules and mediators such as angiotensin II, transforming growth factor-β1, connective tissue growth factor, and platelet-derived growth factor.

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Objectives: Supraventricular tachycardias (SVT) often lead to emergency room and primary care visits. Not only cardiologists, but also general practitioners (GPs) and internists are involved to an increasing extent in the acute and long-term management of SVT. We aimed to explore the differences between practice patterns of cardiologists and noncardiologists with regard to SVT management in Greece.

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Objectives: We investigated prospectively whether serum markers of collagen turnover could be used as predictors for the occurrence of malignant ventricular arrhythmias in patients with nonischemic dilated cardiomyopathy (NIDC) who had received an implantable cardioverter-defibrillator (ICD) for primary prevention.

Background: Extracellular matrix alterations in NIDC might provide electrical heterogeneity, thus potentially contributing to the occurrence of ventricular arrhythmia and subsequent sudden cardiac death (SCD).

Methods: Serum C-terminal propeptide of collagen type-I, C-terminal telopeptide of collagen type-I, matrix metalloproteinase (MMP)-1, and tissue inhibitor of MMP-1 were measured as markers of collagen synthesis and degradation in 70 patients with mild to moderate symptomatic heart failure due to NIDC with left ventricular ejection fraction <35%, who received an ICD for primary prevention of SCD.

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Introduction: We aimed to assess trends in the management of atrial fibrillation (AF) at various levels of medical care in Greece and to compare the treatment practices of cardiologists to those of non-cardiologists.

Methods: From January to May 2007, 500 questionnaires were mailed to cardiologists, internists and general practitioners, randomly selected from regional medical associations. Questions assessed management practices for paroxysmal, persistent and permanent AF.

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Because humoral alterations have been implicated in the generation and perpetuation of atrial fibrillation (AF), we aimed to elucidate possible abnormalities in atrial endocrine function in the setting of lone AF. Levels of plasma apelin and amino terminal fragment of the brain natriuretic peptide prohormone (NT-pro-BNP) were measured in 40 patients with persistent AF, before and 1 month after electrical cardioversion, and in 15 controls in sinus rhythm (SR). All patients were successfully cardioverted to SR, although in 9 of them AF recurred.

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