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Hypertrophic cardiomyopathy (HCM) is a common cause of sudden cardiac death in athletes. Cardiac Magnetic Resonance (CMR) imaging is considered an excellent tool to differentiate between HCM and athlete's heart. The aim of this systematic review was to highlight the novel CMR-derived parameters with significant discriminative capacity between the two conditions. A systematic search in the MEDLINE, EMBASE and Cochrane Reviews databases was performed. Eligible studies were considered the ones comparing novel CMR-derived parameters on athletes and HCM patients. Therefore, studies that only examined Cine-derived volumetric parameters were excluded. Particular attention was given to binary classification results from multi-variate regression models and ROC curve analyses. Bias assessment was performed with the Quality Assessment on Diagnostic Accuracy Studies. Five (5) studies were included in the systematic review, with a total of 284 athletes and 373 HCM patients. Several novel indices displayed discriminatory potential, such as native T1 mapping and T2 values, LV global longitudinal strain, late gadolinium enhancement and whole-LV fractal dimension. Diffusion tensor imaging enabled quantification of the secondary eigenvalue angle and fractional anisotropy in one study, which also proved capable of reliably detecting HCM in a mixed athlete/patient sample. Several novel CMR-derived parameters, most of which are currently under development, show promising results in discerning between athlete's heart and HCM. Prospective studies examining the discriminatory capacity of all promising modalities side-by-side will yield definitive answers on their relative importance; diagnostic models can incorporate the best performing variables for optimal results.

Essential hypertension is an important cause of cardiovascular morbidity and mortality worldwide with significant clinical and economic implications. The field of antihypertensive treatment already numbers numerous agents and classes of drugs. However, patients are still developing uncontrolled hypertension. Hence there is a continuous need for novel agents with good tolerability. Advances in this field are focusing both on pharmacotherapy, with the developments in traditional and non-traditional targets, as well as interventional techniques such as renal denervation and baroreflex activation therapy. It is likely that future strategies may involve a tailored approach to the individual patient, with genetic modulation playing a key role.

Aims Eosinophilic heart disease (EHD) is a rare cardiac condition with a wide spectrum of phenotypes. The diagnostic and prognostic value of cardiac magnetic resonance (CMR) in EHD remains unknown. Methods and results This was a retrospective analysis of 250 patients with eosinophilia referred for a CMR scan (period 2000–2020). CMR data sets and clinical/laboratory data were collected. Patients were followed up for a mean of 24 months (range 1–224) for the composite endpoint of death, acute coronary syndrome, hospitalization for acute heart failure, malignant ventricular arrhythmias, or the need for implantable cardiac defibrillator/pacemaker. The main objectives were to explore the diagnostic value of CMR in EHD; relationships between cardiac function, late gadolinium enhancement (LGE), and EHD phenotypes; and the prognostic value of fibrosis and oedema by CMR. The prevalence of findings compatible with EHD was 39% (patients with cardiac symptoms: 57% vs. screening: 20%, P Conclusion The diagnostic yield of CMR screening in patients with persistent eosinophilia, even if asymptomatic, is high. The extent of subendocardial fibrosis correlates with LV remodelling and independently predicts clinical outcomes in patients with eosinophilia.

In the past decade, catheter ablation (CA) has become a rapidly expanding treatment option for ventricular tachycardia (VT); however it is not commonly utilised for patients with post-myocarditis VT. We aimed to systematically review up-to-date evidence regarding feasibility, effectiveness, and safety of CA, with a specific focus on long-term relapse rate and procedural complications.A structured electronic database search (PubMed, Embase, Cochrane) of the scientific literature was performed according to PRISMA guidelines for studies describing outcomes at up to 7.3 years after CA. The primary outcome measured was VT recurrence post-ablation. Procedural success was defined as freedom of ventricular arrhythmias (at the end of follow-up after an ablation procedure). The secondary outcome was significant procedural complications which included procedural death, stroke, cardiac tamponade, acute myocardial infarction, major vascular complications, and major bleeding, assessed on a study-by-study basis.A total of 186 patients were included in analysis with most patients (88%) being male. Over the follow-up period, there was a 18% relapse rate (CA is an effective and durable long-term therapeutic strategy for post-myocarditis VT patients with limited relapse rate and very low complication rates based on these non-randomised data. Larger randomised-controlled trials with standardised treatment and long follow-up are required to compare CA versus conventional treatment in the post-acute myocardial phase.The online version contains supplementary material available at 10.1007/s42399-022-01137-w.

Background: Catheter ablation (CA) for atrial fibrillation (AF) has been proposed as a means of improving outcomes among patients with heart failure and reduced ejection fraction (HFrEF) who are otherwise receiving appropriate treatment. Unlike HFrEF, treatment options are more limited in patients with preserved ejection fraction (HFpEF) and the data pertaining to the management of AF in these patients are controversial. The aim of this systematic review and meta-analysis was to investigate the effects of CA on outcomes of patients with AF and HFpEF, such as functional status, post-procedural complications, hospitalization, morbidity and mortality, based on data from observational studies. Methods: We systematically searched the electronic databases MEDLINE, PUBMED, EMBASE and the Cochrane Library for Central Register of Clinical Trials until May 2020. Results: Overall, the pooling of our data showed that sinus rhythm was achieved long-term in 58.0% (95% CI 0.44–0.71). Long-term AF recurrence was noticed in 22.3% of patients. Admission for HF occurred in 6.2% (95% CI 0.04–0.09) whilst all-cause mortality was identified in 6.3% (95% CI 0.02–0.13). Conclusion: This meta-analysis is the first to focus on determining the benefits of a rhythm control strategy for patients with AF and HFpEF using CA, suggesting it may be worthwhile to investigate the effects of a CA rhythm control strategy as the default treatment of AF in HFpEF patients in randomized trials.

Background: The 2018 United-Network-for-Organ-Sharing (UNOS) allocation-system changes resulted in greater recognition of mechanical circulatory support (MCS), leading to more heart transplantations (HTx) in patients with MCS. We aimed to investigate the effect of the new UNOS allocation system on the need for a permanent pacemaker and associated complications following HTx. Methods: The UNOS Registry was questioned, to identify patients that received HTx in the US between 2000 and 2021. The primary objectives were to identify risk factors for the need for a pacemaker implantation following HTx. Results: 49,529 HTx patients were identified, 1421 (2.9%) requiring a pacemaker post-HTx. Patients who required a pacemaker were older (53.9 ± 11.5 vs. 52.6 ± 12.8 years, p < 0.001), more frequently white (73% vs. 67%; p < 0.001) and less frequently black (18% vs. 20%; p < 0.001). In the pacemaker group, UNOS status 1A (46% vs. 41%; p < 0.001) and 1B (31% vs. 27%; p < 0.001) were more prevalent, and donor age was higher (34.4 ± 12.4 vs. 31.8 ± 11.5 years; p < 0.001). One-year survival was no different between the groups (HR: 1.08; 95% CI: 0.85, 1.37; p = 0.515). An era effect was observed (per year: OR: 0.97; 95% CI: 0.96, 0.98; p = 0.003), while ECMO pre-transplant was associated with lower risk of a pacemaker (OR: 0.41; 95% CI: 0.19, 0.86; p < 0.001). Conclusions: While associated with various patient and transplant characteristics, pacemaker implantation does not seem to impact one-year survival after HTx. The need for pacemaker implantation was lower in the more recent era and in patients who required ECMO pre-transplant, a finding explained by recent advances in perioperative care.

Sports physicians and physiologists have aimed to assess exercise in young and master athletes so as to work out their conditioning levels and design training programs accordingly [...]

Heart failure with preserved ejection fraction (HFpEF) and chronic kidney disease (CKD) are global diseases of increasing prevalence and are frequent co-diagnoses. The two conditions share common risk factors and CKD contributes to HFpEF development by a variety of mechanisms including systemic inflammation and myocardial fibrosis. HFpEF patients with CKD are generally older and have more advanced disease. CKD is a poor prognostic indicator in HFpEF, while the impact of HFpEF on CKD prognosis is not sufficiently investigated. Acute kidney injury (AKI) is common during admission with acute decompensated HFpEF, but short and long-term outcomes are not clear. Pharmacological treatment options for HFpEF are currently minimal, and even more so limited in the presence of CKD with hyperkalaemia being one of the main concerns encountered in clinical practice. Recent data on the role of sodium-glucose cotransporter 2 (SGLT2) inhibitors in the management of HFpEF are encouraging, especially in light of the abundance of evidence supporting improved renal outcomes. Herein, we review the pathophysiological links between HFpEF and CKD, the clinical picture of dual diagnosis, as well as concerns with regards to renal impairment in the context of HFpEF management.

Σκοπός: Οι πολυμορφισμοί του γονιδίου του αγγειοτασινογόνου (M235T) και της συνθάσηςαλδοστερόνης (C-344T), έχουν συσχετισθεί με αυξημένη επίπτωση της αρτηριακήςυπέρτασης (ΑΥ) και πιθανά σχετίζονται με υποκλινική βλάβη στα όργανα στόχους. Στηνπαρούσα μελέτη διερευνήθηκαν κατά πόσον οι συγκεκριμένοι πολυμορφισμοί μπορούν ναπαρέχουν πληροφορίες σε σχέση με υπερηχοκαρδιογραφικούς δείκτες, με μικρο-και μακρο-αγγειακές αλλοιώσεις και με τη νεφρική λειτουργία στα πλαίσια της νόσου καθώς και τουςπιθανούς υποκείμενους μηχανισμούς που μπορεί να είναι κλινικά σημαντικοί, όπως ηφλεγμονή και η συστατίνη-C.Μέθοδοι: Τον πληθυσμό της μελέτης αποτέλεσαν 319 νεοδιαγνωσθέντες υπερτασικοί μηθεραπευόμενοι ασθενείς και 193 υγιή άτομα. Η προσδιορισμός των πολυμορφισμώνπραγματοποιήθηκε με αλυσιδωτή αντίδραση πολυμεράσης (PCR). Η αρτηριακή σκληρίαεκτιμήθηκε βάσει της ταχύτητας του καρωτιδο-μηριαίου σφυγμικού κύματος (PWV) και ηενδοθηλιακή λειτουργία εκτιμήθηκε στη βραχιονίο από τη ροή μετά από ίσχαιμη περίδεση(FMD). Επίσης αξιολογήθηκαν ο σφυροβραχιόνιος δείκτης (ABI), η πάχυνση του έσω-μέσουχιτώνα (IMT) και η επίπτωση της αμφιβληστροειδοπάθειας με βυθοσκόπηση. Η εκτίμηση τωνκαρδιακών δεικτών, όσον αφορά την αριστερή καρδιακή δομή και λειτουργία, αξιολογήθηκανμε υπερηχοκαρδιογραφία. Μετρήθηκαν τα επίπεδα της κρεατινίνης ορού, και εκτιμήθηκε ορυθμός σπειραματικής διήθησης (GFR) με τον τύπο των Cockcroft-Gault. Τα επίπεδα τηςυψηλής ευαισθησίας C-αντιδρώσας πρωτεΐνης (hsCRP) και ινωδογόνου εκτιμήθηκαν μεανοσονεφελομετρία, ενώ τα επίπεδα της συστατίνης-C και των μορίων προσκόλλησης ICAM-1, VCAM-1 με μέθοδο ELISA. Τέλος, μετρήθηκαν τα επίπεδα της ομοκυστεΐνης με βάση τηντεχνική του ανοσοφθορισμού.Αποτελέσματα: O 235TT γονότυπος συσχετίσθηκε με την ΑΥ (OR 1,11; 95% CI 1,049-1,180; P = 0,0017). Επίσης, οι 235ΤΤ ομοζυγώτες είχαν σημαντικά χαμηλότερη FMD σε σχέση με τους φορείς του Μ-αλληλόμορφου στην ομάδα ελέγχου (p=0,038) και υψηλότερηPWV στους υπερτασικούς ασθενείς (p=0,025). Όσον αφορά το C-344T πολυμορφισμόπαρατηρήθηκαν υψηλότερες τιμές του IMT στην TT ομοζυγωτία, στην ομάδα τωνυπερτασικών (712,5±16,2 έναντι 781,6±33,5 μm, p=0,039). Επίσης, βρέθηκε ότι η ομοζυγωτίατου T-αλληλομόρφου σχετίστηκε σημαντικά με την υψηλότερη επικράτηση τωναθηρωματικών πλακών στο συνολικό πληθυσμό (OR: 0,32, p=0,020), και παρόμοιααποτελέσματα ελήφθησαν για υπερτασικούς, χωρίς όμως να είναι στατιστικά σημαντικά(p=0,057). Επιπλέον, τα επίπεδα της συστατίνης-C συσχετίστηκαν σημαντικά με την PWVτόσο στο σύνολο (r=0,26, p75οτεταρτημόριο)συσχετίστηκαν με υψηλότερες τιμές PWV (p=0,002). Αναφορικά στον C-344Tπολυμορφισμό, οι ΤΤ υπερτασικοί ομοζυγώτες παρουσίασαν σημαντικά υψηλότερες τιμέςLVMI σε σχέση με τους φορείς του C-αλληλομόρφου (88,2±30,2 έναντι 79,9±24,6 g/m2,p=0,020) καθώς και υψηλότερη επίπτωση της συγκεντρικής υπερτροφίας (p

Heart failure (HF) is a complex clinical syndrome characterised by significant morbidity and mortality worldwide. Evidence-based therapies for the management of HF include several well-established neurohormonal antagonists and antiarrhythmic drug therapy to mitigate the onset of cardiac arrhythmia. However, the degree of rate and rhythm control achieved is often suboptimal and mortality rates continue to remain high. Implantable cardioverter-defibrillators (ICDs), cardiac resynchronization (CRT), and combined (CRT-D) therapies have emerged as integral and rapidly expanding technologies in the management of select patients with heart failure with reduced ejection fraction (HFrEF). ICDs treat ventricular arrhythmia and are used as primary prophylaxis for sudden cardiac death, while CRT resynchronizes ventricular contraction to improve left ventricular systolic function. Left ventricular assist device therapy has also been shown to provide clinically meaningful survival benefits in patients with advanced HF, and His-bundle pacing has more recently emerged as a safe, viable, and promising pacing modality for patients with CRT indication. Catheter ablation is another important and well-established strategy for managing cardiac arrhythmia in HF, demonstrating superior efficacy when compared with antiarrhythmic drug therapy alone. In this article, we provide a comprehensive and in-depth evaluation of the role of implantable devices and catheter ablation in patients with HFrEF, outlining current applications, recent advances, and future directions in practice.

Acute‐onset presentation with breathlessness and calcific pericardial thickening encapsulating the heart. Extremely chylous pericardium, which is by itself rare, in combination with constriction assessed with multiple imaging modalities.

Background: Cardiopulmonary exercise testing (CPET) has been widely used for the functional evaluation of patients with heart failure. Patients with amyloidosis and cardiac involvement typically present with heart failure with preserved or mildly reduced ejection fraction. We sought to evaluate the use of CPET parameters in patients with AL amyloidosis for the assessment of disease severity and prognosis and their association with cardiac imaging findings. Methods: A single-center prospective analysis was conducted, which included 23 consecutive ambulatory patients with AL amyloidosis with cardiac involvement, not requiring hospitalization or intravenous diuretics. Patient evaluation included CPET, laboratory testing, echocardiography and cardiac MRI. The cohort was divided according to the presence of high-risk CPET characteristics (below median peak VO2 and above median VE/VCO2). Results: Patients with AL amyloidosis and cardiac involvement (median age was 60 years (56.5% males) had median peak relative VO2 (VO2/kg) of 17.8 mL/kg/min, VE/VCO2 slope of 39.4 and circulatory power of 2362.5 mmHg⋅mL/kg/min. Peak relative VO2 gradually declined across Mayo stages (p = 0.046) and exhibited a significant inverse correlation with NT-proBNP levels (r = −0.52, p = 0.01). Among imaging parameters, peak VO2 positively correlated with global work efficiency (r = 0.61, p < 0.001), and global work index (r = 0.45, p = 0.04). The group of patients with high-risk CPET findings showed evidence of more advanced disease, such as higher NT-proBNP levels (p = 0.007), increased septal and posterior left ventricular wall thickness (p = 0.043 and p = 0.033 respectively) and decreased global work efficiency (p = 0.027) without substantial differences in cardiac MRI parameters. In this group of patients, peak VO2 and VE/VCO2 were not associated significantly with overall survival and cardiac response at one year. Conclusion: In patients with AL amyloidosis, evaluation of exercise capacity with CPET identified a group of patients with more advanced cardiac involvement. The potential of CPET as a risk stratification tool in AL amyloidosis with cardiac involvement warrants further research.

Diabetes mellitus (DM) and peripheral artery disease (PAD) are two clinical entities closely associated. They share many pathophysiological pathways such as inflammation, endothelial dysfunction, oxidative stress and pro-coagulative unbalance. Emerging data focusing on agents targeting these pathways may be promising. Moreover, due to the increased cardiovascular risk, there is a growing interest in cardiovascular and “pleiotropic” effects of novel glucose lowering drugs. This review summarizes the main clinical features of PAD in patients, the diagnostic process and current medical/interventional approaches, ranging from “classical treatment” to novel agents.

Background: Chronic inflammation and immune system activation underlie a variety of seemingly unrelated cardiac conditions including not only atherosclerosis and the subsequent coronary artery disease but also peripheral artery disease, hypertension with target organ damage and heart failure. The beneficial effects of HMG-CoA reductase inhibitors or statins are mainly attributed to their ability to inhibit hepatic cholesterol biosynthesis. Beyond their lipid lowering activity, ample evidence exists in support of their potent anti-inflammatory properties which initiate from the inhibition of GTPase isoprenylation, activating a cataract of secondary pathways and extend to the inhibition and blocking of immune cell activation and interaction. Objective: To summarize the anti-inflammatory mechanisms of statins in clinical and experimental settings in cardiovascular disease. Methods: A systematic search of PubMed and the Cochrane Database was conducted in order to identify the majority of trials, studies, current guidelines and novel articles related to the subject. Results: In vitro, statins have immuno-modulatory and anti-inflammatory effects, and they can exert antiatherosclerotic effects independently of their hypolipidemic actions. In addition, positive results have emerged from mechanistic and experimental studies on the active role of HMG-CoA reductase inhibitors in HF. By extrapolating those data in clinical setting, we further understand how HMG-CoA reductase inhibitors can beneficially affect not only systolic but also diastolic HF. Conclusion: In this review article, we present the basic pathophysiologic data supporting the anti-inflammatory actions of statins in clinical and experimental settings and we link these mechanisms with confirmatory clinical data on the potent non lipid lowering effects of HMG-CoA reductase inhibitors.

Background: Low-density lipoprotein cholesterol (LDL), and especially its oxidized form, renders the atherosclerotic plaque vulnerable to rupture in acute coronary syndromes (ACS). On the other hand, high-density lipoprotein (HDL) is considered an anti-atherogenic molecule. The more re-cent HDL-targeted drugs may prove to be superior to those used before. Indeed, delipidated HDL and HDL mimetics are efficient in increasing HDL levels, while the apoA-I upregulation with RVX-208 appears to offer a clinical benefit which is beyond the HDL related effects. HDL treatment however has not shown a significant improvement in the outcomes of patients with ACS so far, studies have therefore focused again on LDL. In addition to statins and ezetimibe, novel drugs such as PSCK9 in-hibitors and apolipoprotein B inhibitors appear to be both effective and safe for patients with hyper-lipidemia. Conclusion: Data suggest these could potentially improve the cardiovascular outcomes of patient with ACS. Yet, there is still research to be done, in order to confirm whether ACS patients would benefit from LDL- or HDL-targeted therapies or a combination of both.

The age of initiation and the rate of progression of atherosclerosis vary markedly among individuals and have been difficult to predict with traditional cardiovascular risk assessment models. Although these risk models provide good discrimination and calibration in certain populations, cardiovascular disease (CVD) risk may not be accurately estimated in low- and intermediate risk individuals. Therefore, imaging techniques such as Ankle-Brachial Index (ABI), Coronary Artery Calcium score (CAC), carotid Intima-Media Thickness (cIMT), flow mediated dilation (FMD) and Positron Emission Tomography (PET) have been developed and used to reclassify these individuals. In the present article we review the role of the most commonly used imaging techniques for CVD risk assessment.

Introduction and objectives We examined whether the rs180070 and rs2070011 polymorphisms of the fibrinogen gene could affect the risk of coronary artery disease in hypertensive patients by modifying the inflammatory process and coagulation. Methods A total of 744 participants underwent coronary angiography due to symptoms of stable angina, while hypertension was present in 332 patients. Results The presence of the A allele (rs180070) was associated with significantly high levels of fibrinogen in hypertensive patients ( P = .05). On multivariate analysis, A homozygosity (rs180070) (β = 0.257 ± 18.6; P P = .29) was an independent predictor of fibrinogen levels. In hypertensive patients, higher fibrinogen levels > 443 mg/dL ( odds ratio = 3.50; 95% confidence interval, 1.14-10.90; P = .029), but not A homozygosity ( odds ratio = 3.00; 95% confidence interval, 0.78-11.90; P = .110) were independent predictors of the presence of coronary artery disease. Moreover, interleukin-6 levels were higher in A homozygotes for the rs180070 polymorphism compared with all other genotypes ( P = .046). Indeed, this genotype was the only adjusted independent predictor of interleukin-6 levels (β = 0.151 ± 0.642; P = .032). It was also associated with higher D-dimer levels in hypertension compared with G allele carriers ( P = .048). Conclusions The presence of A homozygosity (rs180070) is associated with increased levels of inflammatory mediators and a higher incidence of angiographic coronary artery disease. Importantly, fibrinogen is an independent predictor of the angiographic presence of coronary artery disease in hypertensive patients.

Resumen Introduccion y objetivos Se examina si los polimorfismos rs180070 y rs2070011 del gen del fibrinogeno podrian afectar al riesgo de enfermedad coronaria de los pacientes hipertensos al modificar el proceso inflamatorio y la coagulacion. Metodos Se practico una angiografia coronaria a causa de sintomas de angina estable a 744 participantes, de los que 332 tenian hipertension. Resultados La presencia del alelo A (rs180070) se asocio a cifras de fibrinogeno significativamente elevadas en los pacientes hipertensos (p = 0,05). En el analisis multivariable, la homocigosis para A (rs180070) (β = 0,257 ± 18,6; p 443 mg/dl ( odds ratio = 3,50; intervalo de confianza del 95%, 1,14-10,90; p = 0,029), pero no la homocigosis para A ( odds ratio = 3,00; intervalo de confianza del 95%, 0,78-11,90; p = 0,110), fueron un factor independiente predictivo de enfermedad coronaria. Ademas, los valores de interleucina 6 fueron mas altos en los individuos homocigotos para el polimorfismo rs180070 que en todos los demas genotipos (p = 0,046). De hecho, este genotipo fue el unico factor independiente predictivo de la concentracion de interleucina 6 en el analisis ajustado (β = 0,151 ± 0,642; p = 0,032). Tambien se asocio a cifras de dimero D superiores en la hipertension en comparacion con los portadores del alelo G (p = 0,048). Conclusiones La presencia de homocigosis para A (rs180070) se asocia a un aumento de las concentraciones de mediadores inflamatorios y mayor incidencia de enfermedad coronaria angiografica. Tiene importancia que el fibrinogeno es un factor independiente predictivo de la presencia angiografica de enfermedad coronaria en los pacientes hipertensos.

The vascular endothelium comprises a continuous single cell layer of endothelial cells which line the entire cardiovascular system. Impaired endothelial function underlies the pathogenesis and contributes to the progression of atherosclerosis. Oxidative stress, vasoconstriction, inflammation, proliferation and thrombosis occur in dysfunctional endothelium while the latter, is primarily mediated by platelet activation and adherence to vascular wall. Despite the primary action of antiplatelet agents including aspirin, P2Y12 ADP receptor antagonists and glycoprotein IIb/IIIa inhibitors, a growing body of literature suggests that an important mechanism of their action involves complex modulation of endothelial function via platelet-endothelial interactions, modification of the inflammatory cytokine cascade and nitric oxide mediated effects. These agents represent the mainstay in pharmacological treatment of all aspects of cardiovascular disease both in primary and secondary prevention. However beyond these properties, it is important to note that pharmacological modification of endothelial dysfunction has been postulated as a therapeutic target for reduction of cardiovascular events.

The purpose of this study was to assess the effects of renin‐angiotensin system (RAS) inhibitors vs other antihypertensive agents on cardiovascular outcomes in hypertensive black patients. The authors performed a systematic review and meta‐analysis of studies that compared the effects of angiotensin‐converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) with calcium channel blockers (CCBs), diuretics, and β‐blockers in hypertensive black patients on cardiovascular outcomes. A total of 38,983 patients with a mean age of 60 years and mean follow‐up of 4 years were included in our meta‐analysis. No significant differences were found in all‐cause mortality, myocardial infarction, heart failure, and cardiovascular mortality rates among patients treated with RAS inhibitors compared with CCBs, diuretics, and β‐blockers. The incidence of stroke was significantly increased in patients treated with RAS inhibitors compared with CCBs (odds ratio, 1.56; 95% confidence interval, 1.31–1.87 [P

Patients with ST-elevation myocardial infarction (STEMI) constitute a vulnerable group that demands the careful assessment and application of all the up-to-date clinical and experimental knowledge, with final aim, the improvement of their prognosis. Statins are an indispensable part of the primary and secondary prevention of coronary artery disease (CAD), not only due to their strong hypolipidemic effect, but also due to their numerous pleiotropic properties that play an important role in the treatment of CAD, especially when the more vulnerable group of STEMI patients is addressed. Nevertheless, there are still issues that require further discussion and clarification, such as the type of statin, the dose of the regimen, the administration time, and the treatment duration.

Background:White-coat hypertension (WCH) is a frequent condition particularly in children and elderly individuals. The prognostic significance of WCH is still a matter of debate.Methods:The present study was designed to systematically review cohort studies and assess the effects of WCH compared with

Purpose of review Cardiovascular magnetic resonance (CMR) is frequently used in the investigation of suspected cardiac disease in athletes. In this review, we discuss how CMR can be used in athletes with suspected cardiomyopathy with particular reference to volumetric analysis and tissue characterization. We also discuss the finding of non-ischaemic fibrosis in athletes describing its prevalence, distribution and clinical importance. Recent findings The strengths of CMR include high spatial resolution, unrestricted imaging planes and lack of ionizing radiation. Regular physical exercise leads to cardiac remodeling that in certain situations can be clinically challenging to differentiate from various cardiomyopathies. Thorough morphological assessment by CMR is fundamental to ensuring accurate diagnosis. Developments in tissue characterization by late gadolinium enhancement and T1 mapping have the potential to be powerful additional tools in this challenging clinical situation. Using late gadolinium enhancement, it is also possible to detect non-ischaemic fibrosis in athletes who do not have overt cardiomyopathy. The mechanisms of this fibrosis are unclear; however, it does appear to be clinically important. We also review data on the prevalence of non-ischaemic fibrosis in athletes. Summary CMR is a powerful tool to aid in the diagnosis of cardiomyopathy in athletes. It may also have a future role in assessing fibrosis related to long-term participation in sport.

Introduction: Emerging evidence suggests that the role of high density lipoprotein (HDL) in the atherosclerotic process is not as clear as previously thought, since atheroprotective HDL becomes atherogenic in states of increased inflammatory processes. Areas covered: In this review we aim to elucidate the role of HDL as a prognostic biomarker and we discuss therapeutic approaches that aim to increase HDL and their possible clinical benefit. Expert opinion: Given the structural variability and biological complexity of the HDL particle, its role in the atherosclerotic process is far from clear. According to current evidence, the atheroprotective role of HDL turns atherogenic in states of increased inflammatory processes, while even minor alterations in systemic inflammation are likely to hinder the endothelial protective effects of HDL. In accordance, significant data have revealed that HDL-related drugs may be effective in reducing cardiovascular mortality; however they are not as encouraging or unanimous as expected. Possible future goals could be to quantify either HDL subclasses or functions in an attempt to reach safer conclusions as to the prognostic importance of HDL in coronary atherosclerosis. Having achieved that, a more targeted therapy that would aim to raise either HDL functionality or to remodel HDL structure would be more easily designed.

It is well known that the endothelium maintains the vascular homeostasis. Importantly, endothelial dysfunction is regarded as a key early step in the development of atherosclerosis. Back in the early 1990s, it was found that asymmetric dimethylarginine (ADMA), an arginine metabolite derived from L-arginine (Arg) residues in proteins by asymmetric dimethylation on its guanidine group, is an endogenous inhibitor of nitric oxide (NO) synthase (NOS) isoforms. Inhibition of NO synthesis from Arg by the endothelial NOS isoform (eNOS) leads to endothelial dysfunction. Due to this action, ADMA participates in the pathophysiology of atherosclerosis and potentially contributes to cardiovascular events. Nowadays, homoarginine (hArg) is considered as a new key player in atherogenesis. hArg is a non-essential, non-proteinogenic amino acid which is synthesized from Arg by arginine:glycine amidinotransferase (AGAT). hArg is structurally related to Arg; formally, hArg is by one methylene (CH2) group longer than Arg, and may serve as a substrate for NOS, thus contributing to NO synthesis. For several decades, the pathophysiological role of hArg has been entirely unknown. hArg has been in the shadow of ADMA. Clinical studies have sought to investigate the relationship between circulating hArg levels and human disease states as well as cardiovascular prognosis. Recent studies indicate that hArg is actively involved in the vascular homeostasis, yet the underlying mechanisms are incompletely understood. In this article, we review the available literature regarding the role of ADMA and hArg in endothelial dysfunction and in cardiovascular disease as well as the possible associations between these endogenous Arg derivatives.

Chronic thromboembolic pulmonary hypertension is defined as pulmonary hypertension (PH) caused by single or recurrent pulmonary emboli and is characterized by chronic obstruction of the pulmonary arteries leading to increased vascular resistance and PH. Also, progressive remodeling may occur in occluded and nonoccluded territories. Better understanding of the underlying mechanisms and risk factors could improve diagnosis and allow appropriate interventions. Pulmonary endarterectomy is an established approach and is considered the definitive treatment for chronic PH, resulting from thromboembolic disease. Furthermore, percutaneous transluminal pulmonary angioplasty is technically feasible, especially for those with peripheral-type of the disease. In addition, several agents, including prostanoids, endothelin receptor antagonists and phosphodiesterase type-5 inhibitors, have been tested in selected patients yielding promising results. Several novel agents are under investigation, and extensive research is currently in progress aiming to resolve uncertainties in the understanding and treatment of the disease.

Arrhythmias can cause symptoms ranging from simple dizziness to life-threatening circulatory collapse. Current management includes medical therapy and procedures such as catheter ablation or device implantation. However, these strategies still pose a risk of serious side effects, and some patients remain symptomatic. Advancement in our understanding of how arrhythmias develop on the cellular level has made more targeted approaches possible. In addition, contemporary studies have found that several genes are involved in the pathogenesis of arrhythmias.In the present review, the authors explore the cellular and genetic mechanisms leading to arrhythmias as well as the progress that has been made in using both gene and cell therapy to treat tachy- and bradyarrhythmias. They also consider why gene and cell therapy has resulted into a few clinical trials with promising results, however still not applicable in routine clinical practice.The question currently is whether such biological therapies could replace current established approaches. The contemporary evidence suggests that despite recent advances in this field, it will need more work in experimental models before this is applied into clinical practice. Gene and cell studies targeting conduction and repolarization are promising, but still not ready for use in the clinical setting.

Background Fibrinogen is a coagulation/inflammatory biomarker strongly associated with atherogenesis. Data have reported that the genetic variability on fibrinogen chains may affect the atherosclerotic process and the risk of coronary artery disease (CAD). We examined the combined effects of the G455A and the G58A fibrinogen genetic polymorphisms on prothrombotic profile, endothelial function and the risk of CAD in a Caucasian population. Methods We recruited 422 patients with angiographically documented CAD and 277 controls matched for age and gender. The two polymorphisms were genotyped by polymerase chain reaction and restriction endonuclease digestion. Fibrinogen and D-Dimers levels, as well as factors' (f) V, X activity were measured by standard coagulometry techniques. Endothelial function was assessed by the flow mediated dilatation (FMD) of the brachial artery. Results The two polymorphisms had no significant effect on the risk for CAD. Although the 58AA subjects had not significantly different levels of fibrinogen compared with the 58GG + GA in both groups (p = NS), we importantly found that the 455AA homozygosity was associated with increased fibrinogen levels not only in the control group (p = 0.035), but also in the CAD group (p < 0.001) compared to the G allele carriers. Moreover, both the 58AA (p = 0.016) and 455AA homozygotes (p = 0.022) presented with higher levels of D-Dimers in the CAD group. Interestingly, the 455AA homozygotes had increased fV activity in the CAD group (p = 0.048). However, no significant effects were observed on fX activity and FMD. Conclusions Both fibrinogen polymorphisms are capable to modify the atherosclerotic process via their effects on the coagulation cascade. © 2013 Elsevier Ireland Ltd.

It is widely accepted that diabetes mellitus (DM) impairs endothelial nitric oxide synthase activity as well as enhances the production of reactive oxygen species, thus resulting in diminished nitric oxide bioavailability and the consequent pro-atherogenetic alterations. Important biomarkers of the vasculature are related to endothelial dysfunction, to inflammatory and coagulation processes, and to oxidative stress in DM. Several therapeutic strategies might exert favorable effects on the vasculature of diabetic patients, such as insulin analogues, antihypertensive agents, statins, and hypoglycemic agents, whereas in spite of the prominent role of oxidative stress in diabetes, antioxidant therapy remains controversial. The use of specific biomarkers related to vascular function could be a useful therapeutic approach in such patients.

Type 2 diabetes mellitus (T2DM) is a metabolic disease affecting an increasing percentage of general population worldwide. Patients with T2DM are frequently characterized by impaired renal function, primarily as a result of diabetic kidney injury, but also by other contributing factors, such as hypertension, atherosclerosis, and medications. Sodium-glucose cotransporter (SGLT)-2 inhibitors have emerged as a new, promising class of antidiabetic agents with actions that seem to extend beyond their hypoglycemic effect.

Stable angina represents the main symptom of established coronary artery disease. In addition atherosclerosis is the common pathological substrate of chronic stable angina as well as acute coronary syndromes. The aim of stable angina management is the symptomatic relief and the secondary prevention. Lifestyle modification and pharmacological therapy are the cornerstones of chronic coronary artery disease management irrespectively of possible surgical or percutaneous revascularization. Optimal medical therapy is a combination of antianginal/antiischemic drugs and disease modifying agents, including nitrates, beta-blockers, calcium channel blockers, antiplatelets, statins and angiotensin converting enzyme inhibitors. Novel classes of treatment with different mechanisms of action have been developed in the last years, including nicorandil, ivabradine, trimetazidine and ranolazine. These drugs, which are currently approved as second-line treatments, have dynamically entered the clinical practice and their long-term effects are still under investigation.

Experimental studies suggest that bone marrow-derived endothelial progenitor cells (EPCs) play an important role in the maintenance of endothelial integrity and hemostasis. The number of circulating EPC has been shown to be inversely correlated with cardiovascular risk factors and vascular function and to predict cardiovascular events independent of both traditional and non-traditional risk factors. Thus, EPCs provide a clinical advantage over the use of other biomarkers as their measurement is directly associated with endothelial function, and available evidence suggests that they are consistently and significantly associated with a spectrum of cardiovascular complications, such as acute coronary syndromes and coronary artery disease. However, many issues in the field of EPC isolation and identification, particularly in regards to the effective and unequivocal molecular characterization of these cells still remain unresolved. In addition, simple EPC counts do not adequately describe cardiovascular disease risk. This limitation is attributable to variation in the definition of EPCs, the number of existing cardiovascular risk factors in different patients as well as a difference in the interaction between EPCs and other hematopoietic progenitor, inflammatory cells or platelets.

The authors investigated the relationship of white-coat hypertension (WCH) with subclinical organ damage and potential relevant mechanisms. A total of 386 untreated patients were enrolled and divided into 204 patients with WCH and 183 with normotension. Flow-mediated dilation (FMD), pulse wave velocity (PWV), intima-media thickness, left ventricular mass index (LVMI), and cystatin C levels were measured. All tests were two-sided, and a P value