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Background and aims Worldwide, air pollution is the fourth leading cause of death. Both brief and long-term exposures to air pollution have been associated with marked increases in cardiovascular-related morbidity and mortality. Previous studies have focused on the short-term influence of particulate pollutants on ventricular arrhythmia (VA) development, primarily expressed as 24-hour Holter ECG monitoring arrhythmic burden or as presentation as life-threatening ventricular arrhythmias. The aim of our study was to investigate the association between air pollutant exposure and VA burden in remotely-monitored patients. Methods We enrolled retrospectively 86 patients carriers of implantable cardioverter-defibrillators (ICD), loop recorders (ILR) or pacemaker devices with remote monitoring via CarelinkTM Medtronic or Merlin.netTM PCN Abbott softwares. Intracavitary and ILR tracings were reviewed by EP personnel at our centre to define VA burden and the number of appropriate shocks and ATPs occurred in 2021. Demographic and clinical characteristics (e.g. cardiovascular history, ejection fraction, smoking, antiarrhythmic drugs (AADs)) were collected through telephone interviews. Each patient's residential and working address were used to obtain information on pollutant exposure in the years 2017-2021 in terms of annual mean concentrations of PM10, PM2.5, ozone, sulfur dioxide, carbon dioxide, carbon monoxide and benzene, as determined by European Environmental Agency air quality reports. The primary endpoint was a composite of ventricular fibrillation, sustained and nonsustained ventricular tachycardia, appropriate ATP or shocks in patients with various levels of air pollutants exposure. Results Of 86 patients (58 male, mean age 63.2±18.7 years) enrolled in this study, 44 (51.6%) had received an ICD, 32 of whom (37.2%) with a primary prevention indication. 31 patients (36.1%) had been receiving at least one AAD. History of coronary artery disease (CAD) was present in one third of the study population and baseline mean EF was 49.8±13.8%. VA events occurred in 17 patients (19.8%), all with a significantly lower baseline EF (40.3±12.2% vs 51.5±13.5% p=0.005). Average mean values of benzene concentration in the previous 4 years were significantly higher in patients suffering from a VA event (1.64±0.82 μg/m3 vs 1.12±0.48 μg/m3, p=0.001), as were PM2.5 values (11.64±1.98 vs 10.74±1.28 μg/m3, p=0.023). A weak but positive correlation was found between median PM2.5 concentration, benzene and VAs (p=0.023, p=0.001 respectively). A multivariate regression model was built, including long-term exposure to benzene and PM2.5 and baseline EF, and it would explain 29.8% of the variance in VAs, correctly classifying 78.1% of cases. Conclusions This study was the first to evaluate the relationship between long-term exposure to a wide array of air pollutants and VAs in a European population. In our sample, we found a weak but significant correlation between a higher chronic exposure to benzene and recorded VA events. Possible mechanisms may include oxidative stress and a direct, nonspecific membrane action due to benzene lipophilic properties. Hence, we highlighted the possible role of outdoor benzene exposure in ventricular arrhythmogenesis for the first time, a finding that requires validation through subsequent studies aimed at elucidating the role of air pollution as a ubiquitous, potentially modifiable, population-based risk factor.

Background and aims: Transvenous lead extraction (TLE) has become a pivotal part of a comprehensive lead management strategy, dealing with a continuously increasing demand. Nonetheless, literature about the long-term impact of TLE on survivals still lacking. Given these knowledge gaps, the aim of our study was to analyse very long-term mortality in patients undergoing TLE in public health perspective. Methods: This prospective, single-centre, observational study enrolled consecutive patients with cardiac implantable electronic device (CIED) who underwent TLE, from January 2005 to January 2021. The main goal was to establish the independent predictors of very long-term mortality after TLE. We also aimed at assessing procedural and hospitalization related costs. Results: We enrolled 435 patients (mean age 70 ± 12 years, with mean lead dwelling time 6.8 ± 16.7 years), with prevalent infective indication to TLE (92%). Initial success of TLE was achieved in 98% of population. After a median follow-up of 4.5 years (range 1 month- 15.5 years),150 of the 435enrolled patients (34%) died. At multivariate analysis, death was predicted by: age (≥ 77 years, OR: 2.55, CI: 1.8-3.6, pConclusions: Our study identified three predictors of long-term mortality in a high-risk cohort of patients with a cardiac device infection, undergoing successful TLE. The future development of a mortality risk score before might impact on public health strategy.

The association between thrombosis, cancer and inflammation is well-established. Platelets play a major role in atherosclerosis, inflammation and immune response. Furthermore, growing evidence suggests that they are also significantly involved in tumor development and progression so that anti-platelet agents may prevent cancer and improve outcomes in oncological patients. In this review, we aimed at analyzing the relationship between platelets, cardiovascular diseases and cancer. A comprehensive study in the main educational platforms was performed and high-quality original articles and reviews were included.This review will focus on the role of platelets in cardiovascular disease and in cancer genesis and progression, analyzing their function as immune cells that link inflammation to thrombosis. Finally, it will examine the recent controversies on the use of anti-platelet agents as cancer medications, in particular the already known anti-tumor properties of aspirin, as well as the new perspectives regarding P2Y12 inhibitors.Platelet-cancer crosstalk generates a vicious feed-back loop involving tumor cells and secreting molecules that activate platelets, which in turn promote cancer-associated inflammation, proliferation, spreading and immune system evasion. Therefore, platelets inhibition may represent an innovative therapeutical strategy offered to cancer patients, in the perspective of personalized medicine.

Aims Randomized trials support the safety and efficacy of direct oral anticoagulants (DOACs) vs. vitamin K antagonists (VKA) in patients with nonvalvular atrial fibrillation (AF), leading to increased use of these compounds. Crushed forms of DOACs have shown to be reliable, but evidence supporting percutaneous endoscopic gastrostomy (PEG) delivery is lacking. PEG is a long-term option for enteral food and drug delivery in patients unable to maintain oral intake, bypassing the risks and disadvantages of parenteral nutrition. We investigate the safety and efficacy of Edoxaban administered via PEG in patients with atrial fibrillation and a clinical indication for a long-term anticoagulation. Methods and results In this prospective, single centre observational study, 12 PEG-treated patients with indication to anticoagulation will receive edoxaban via PEG and will be followed-up to 6 months. Plasma anti-Factor Xa activity and edoxaban concentrations will be assessed. Thromboembolic (ischaemic stroke, systemic embolism, venous thromboembolism) and bleeding events (Bleeding Academic Research Consortium and Thrombolysis in Myocardial Infarction) will be recorded at 1 and 6 months. A retrospective analysis of 5 AF cases undergoing PEG-implantation at our Institution, who received edoxaban via PEG, showed plasma anti-FXa levels at steady state of 146 ± 15 ng/ml, without major adverse event at a mean follow-up of 6 months. Conclusion We prospectively investigate PEG-administration of edoxaban in PEG-treated patients requiring long term anticoagulation. Our preliminary retrospective data support this route of DOAC administration.

Heart failure is the cardiovascular epidemic of the twenty-first century, with poor prognosis and quality of life despite optimized medical treatment. Despite over the last decade significant improvements, with a major impact on morbidity and mortality, have been made in therapy for heart failure with reduced ejection fraction, little progress was made in the development of devices, with the implantable defibrillator indicated for patients with left ventricle ejection fraction ≤ 35% and cardiac resynchronization therapy for those with QRS ≥ 130 ms and evidence of left bundle branch block. Nevertheless, only a third of patients meet these criteria and a high percentage of patients are non-responders in terms of improving symptoms. Nowadays, in patients with symptomatic heart failure with ejection fraction between 25% and 45% and QRS

Extensive data support the superior safety without any trade-off in efficacy of direct oral anticoagulants (DOACs) compared to vitamin K antagonists (VKA) in patients with nonvalvular atrial fibrillation, deep venous thrombosis or pulmonary embolism. Whether DOACs may be successfully used to treat complex and fragile patients with percutaneous endoscopic gastrostomy (PEG) remains to be proven. The purpose of this pilot study was to evaluate the feasibility, anticoagulant effect, and preliminary safety/efficacy profile of edoxaban administered via PEG in patients with an indication for long-term oral anticoagulation.In this prospective, single-arm, pilot study, 12 patients with PEG and guideline-recommended indication for anticoagulation for nonvalvular atrial fibrillation were prospectively enrolled. Crushed edoxaban at approved doses was administered via PEG. Quantitative measures of edoxaban's anti-factor Xa activity were performed at steady state. Thromboembolic and bleeding events were assessed at one-month follow-up.Steady state edoxaban plasma levels were at therapeutic range in all patients; mean plasma concentration was 208.5 (±78.6) ng/ml. At one month follow-up, none had suffered a thromboembolic event; one developed minor bleeding, and one died from non-cardiovascular death, owing to sudden worsening of a pre-existing underlying severe condition.In this pilot investigation, we report for the first time that crushed edoxaban, administered at approved doses through PEG in fragile and complex patients, is feasible, results in therapeutic edoxaban concentrations, and is apparently effective and safe.

Aims Atrial and ventricular tachyarrhythmias are common among patients with adult congenital heart disease (ACHD) and can impair quality of life and prognosis. Catheter ablation is often the main treatment option in this population, despite anatomical hurdles. Substrate mapping findings have not been thoroughly investigated as predictors of arrhythmia recurrence success and cardiovascular clinical outcome after ablation. We sought to determine the prognostic value of myocardial scar and chamber enlargement detected at electroanatomical mapping in ACHD patients undergoing catheter ablation of tachyarrhythmias. Methods and results Consecutive ACHD patients undergoing catheter ablation of atrial and ventricular tachycardias using different electroanatomical mapping systems were retrospectively identified from a hospital-based database. Scar extent detected at the electroanatomical mapping, as well as the total mapped area, was calculated. Arrhythmia recurrence, hospitalization for cardiovascular (CV) reasons, and a combined endpoint (arrhythmia recurrence and/or CV hospitalization) were evaluated during the follow-up. The relationship between the aforementioned electroanatomical findings and the patients’ outcome was assessed. Twenty patients (12 male, 60%; mean age 40 ± 11 years) undergoing atrial (n = 14; 70%) or ventricular (n = 6; 30%) tachyarrhythmia were included. Acute procedural success (arrhythmia termination and/or no reinduction) was achieved in all the patients. At a mean follow-up of 171 ± 135 weeks, eight patients (40%) had arrhythmia recurrence (4/6 in the ventricular tachycardia group, 67%, 4/14 in the atrial tachycardia group, 28%). Patients with arrhythmia recurrence had a more extensive bipolar scar (P = 0.029) and a larger total mapped area (P = 0.03) than patients without recurrence, and so did the patients with the composite endpoint (P = 0.029 and P = 0.03, respectively). Patients with subsequent CV hospitalization had a larger total mapped area than patients without CV hospitalization (P = 0.017). The presence of a bipolar scar ≥22.95 cm2 predicted arrhythmia relapse (0.039) at the multivariate analysis. Conclusions Patients with ACHD show a high recurrence rate after catheter ablation, especially for ventricular tachycardias. A large bipolar scar at the electroanatomical mapping and total mapped area predict arrhythmia recurrence, likely due to the presence of more extensive reentry circuits. A large total mapped area, which may reflect a greater disease severity, predicts both arrhythmia recurrence and CV hospitalizations. Early referral of ACHD patients for catheter ablation may be a sound strategy in order to perform the procedure in the setting of less advanced heart disease.

Despite continuous technological developments, transvenous pacemakers (PM) are still associated with significant immediate and long-term complications, mostly lead or pocket-related. Recent technological advances brought to the introduction in clinical practice of leadless PM for selected cohort of patients. These miniaturize devices are implanted through the femoral vein and advanced to the right ventricle, without leaving leads in place. Lack of upper extremity vascular access and/or high infective risk in patients requiring VVI pacing are the most common indications to leadless PM. The recently introduced MICRA AV leadless PM also allows ventricular synchronization through mechanical sensing of atrial contraction waves, thus solving the problem of AV synchronization. This review will discuss and summarize available clinical evidence on leadless PM, their performance compared to transvenous devices, current applications and future perspectives.

Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) recently emerged in Wuhan, Hubei-China, as responsible for the coronavirus disease 2019 (COVID-19) and then spread rapidly worldwide. While most individuals remain asymptomatic or develop only mild symptoms, approximately 5% develop severe forms of COVID-19 characterized by acute respiratory distress syndrome (ARDS) and multiple-organ failure (MOF) that usually require intensive-care support and often yield a poor prognosis. Summary: The pathophysiology of COVID-19 is far from being completely understood, and the lack of effective treatments leads to a sense of urgency to develop new therapeutic strategies based on pathophysiological assumptions. The exaggerated cytokine release in response to viral infection, a condition known as cytokine release syndrome (CRS) or cytokine storm, is emerging as the mechanism leading to ARDS and MOF in COVID-19, thus endorsing the hypothesis that properly timed anti-inflammatory therapeutic strategies could improve patients’ clinical outcomes and prognosis. Key Messages: The objective of this article is to explore and comment on the potential role of the promising immunomodulatory therapies using pharmacological and nonpharmacological approaches to overcome the dysregulated proinflammatory response in COVID-19.

Heart failure is the cardiovascular epidemic of the 21st century, with poor prognosis and quality of life despite optimized medical treatment. In the past two decades, only two new drugs have been added to therapeutic strategies for patients with symptomatic heart failure and even less progresses have been made on devices, with the implantable defibrillator indicated for patients with ejection fraction ≤35% and cardiac resynchronization therapy for those with QRS130 ms and evidence of left bundle branch block. Nevertheless, only a third of patients meet these criteria and a high percentage of patients are non-responders in terms of improving symptoms. Nowadays, in patients with symptomatic heart failure with ejection fraction between 25% and 45% and QRS130 ms, not eligible for cardiac resynchronization therapy, cardiac contractility modulation represents a concrete treatment option, having proved to be safe and effective in reducing hospitalizations for heart failure and improving symptoms, functional capacity and quality of life.The aim of this review is therefore to summarize the pathophysiological mechanisms, the current indications and the recent developments regarding the new applications of cardiac contractility modulation for patients with chronic heart failure.

Amiodarone is a drug commonly used to treat and prevent cardiac arrhythmias, but it is often associated with several adverse effects, the most serious of which is pulmonary toxicity. A 79-year-old man presented with respiratory failure due to interstitial pneumonia during coronavirus disease 2019 (COVID-19) pandemic. The viral etiology was nevertheless excluded by repeated nasopharyngeal swabs and serological tests and the final diagnosis was amiodarone induced organizing pneumonia. The clinical and computed tomography findings improved after amiodarone interruption and steroid therapy. Even during a pandemic, differential diagnosis should always be considered and pulmonary toxicity has to be taken into account in any patient taking amiodarone and who has new respiratory symptoms., Lay abstract Amiodarone is a drug used to treat and prevent heart rhythm alterations (cardiac arrhythmias). Although it is effective, it is associated with some side effects, including pulmonary toxicity (in 2–18% of patients), which is a serious side effect impacting the lungs of the patient. A 79-year-old man presented with a dry cough and shortness of breath during the coronavirus disease 2019 (COVID-19) pandemic, but repeatedly tested negative for the virus. The diagnosis was determined to be amiodarone induced pneumonia, a condition that inflames the air sacs in the lungs. The patient stopped taking amiodarone and steroid therapy was started, leading to an improvement in the patient's condition. Even if the diagnosis initially seemed to be of COVID-19, amiodarone toxicity should always be considered in patients taking this drug and with respiratory symptoms.

Heart failure is the cardiovascular epidemic of the twenty-first century, with poor prognosis and quality of life despite optimized medical treatment. Despite over the last decade significant improvements, with a major impact on morbidity and mortality, have been made in therapy for heart failure with reduced ejection fraction, little progress was made in the development of devices, with the implantable defibrillator indicated for patients with left ventricle ejection fraction ≤ 35% and cardiac resynchronization therapy for those with QRS ≥ 130 ms and evidence of left bundle branch block. Nevertheless, only a third of patients meet these criteria and a high percentage of patients are non-responders in terms of improving symptoms. Nowadays, in patients with symptomatic heart failure with ejection fraction between 25% and 45% and QRS 130 ms, not eligible for cardiac resynchronization, the cardiac contractility modulation (CCM) represents a concrete therapeutic option, having proved to be safe and effective in reducing hospitalizations for heart failure and improving symptoms, functional capacity, and quality of life. The aim of this review is therefore to summarize the pathophysiological mechanisms, the current indications, and the recent developments regarding the new applications of the CCM for patients with chronic heart failure.

From first cases reported on December 31, 2019, in Wuhan, Hubei-China, SARS-CoV2 has spread worldwide and finally the World Health Organization declared the pandemic status. We summarize what makes SARS-CoV2 different from previous highly pathogenic coronaviruses and why it is so contagious, with focus on its clinical presentation and diagnosis, which is mandatory to start the appropriate management and reduce the transmission. As far as infection pathophysiology is still not completely clarified, this review focuses also on the cardiovascular (CV) implication of COVID-19 and the capability of this virus to cause direct myocardial injury, myocarditis and other CV manifestations. Furthermore, we highlight the relationship between the virus, enzyme ACE2 and ACE inhibitors. Clinical management involves the intensive care approach with intubation and mechanical ventilation in the most serious cases and drug therapy with several apparently promising old and new molecules. Aim of this review is then to summarize what is actually known about the SARS-CoV2 and its cardiovascular implications.

From December 31th, 2019, a novel highly pathogenic coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has spread worldwide, reaching at present the dimension of a pandemic. In addition to damaging the lungs, SARS-CoV-2 may also damage the heart and this is corroborated by the evidence that cardiovascular comorbidities are associated with a higher mortality and poor clinical outcomes in patient infected by the virus. During the infection myocardial injury, myocarditis and arrhythmias have also been reported, but the pathophysiological mechanisms of these complications are yet to be understood. Great attention is also being posed on the potential beneficial/harmful role of angiotensin converting enzyme (ACE) inhibitors, as far as the virus binds to angiotensin converting enzyme 2 (ACE2) to infect cells, but evidences lack. Furthermore, SARS-CoV-2 can also affect the aspect of acute coronary syndromes, not only because these two distinct pathological entities share pathogenic aspects (such as the systemic inflammatory state and cytokine release), but also and above all for the consequences that the need to contain the infection has on the management of cardiological urgencies. Aim of this review is therefore to summarize the relationship between the virus and the cardiovascular system.

From first cases reported on December 31, 2019, in Wuhan, Hubei-China, SARS-CoV2 has spread worldwide and finally the World Health Organization declared the pandemic status. We summarize what makes SARS-CoV2 different from previous highly pathogenic coronaviruses and why it is so contagious, with focus on its clinical presentation and diagnosis, which is mandatory to start the appropriate management and reduce the transmission. As far as infection pathophysiology is still not completely clarified, this review focuses also on the cardiovascular (CV) implication of COVID-19 and the capability of this virus to cause direct myocardial injury, myocarditis and other CV manifestations. Furthermore, we highlight the relationship between the virus, enzyme ACE2 and ACE inhibitors. Clinical management involves the intensive care approach with intubation and mechanical ventilation in the most serious cases and drug therapy with several apparently promising old and new molecules. Aim of this review is then to summarize what is actually known about the SARS-CoV2 and its cardiovascular implications.

Aims The ORal anticoagulants In fraGile patients with percutAneous endoscopic gastrostoMy and atrIal fibrillation (ORIGAMI) study investigates the safety and efficacy of Edoxaban administered via PEG in patients with atrial fibrillation and a clinical indication for a long-term anticoagulation. Design In this prospective, single-centre observational study, 12 PEG-treated patients with indication to anticoagulation will receive edoxaban via PEG and will be followed up to 6 months. Plasma antifactor Xa activity and edoxaban concentrations will be assessed. Thromboembolic (ischaemic stroke, systemic embolism, venous thromboembolism) and bleeding events (Bleeding Academic Research Consortium and Thrombolysis in Myocardial Infarction) will be recorded at 1 and 6 months. Preliminary results A retrospective analysis of five atrial fibrillation cases undergoing PEG implantation at our Institution who received edoxaban via PEG showed plasma anti-FXa levels at a steady state of 146 ± 15 ng/ml, without major adverse event at a mean follow-up of 6 months. Conclusion ORIGAMI prospectively investigates PEG-administration of edoxaban in PEG-treated patients requiring long-term anticoagulation. Our preliminary retrospective data support this route of DOAC administration. Clinicaltrialsgov identifier NCT04271293.

Over the last several decades, clinicians and clinical scientists have had growing interest in heart failure (HF) diagnosis and treatment. While HF with reduced ejection fraction (EF) is a well-known clinical entity with several therapeutic strategies proven to be successful, HF with preserved ejection fraction is a more heterogenous syndrome with a prevalence that has increased in the last two decades, without effective therapeutic strategies. Great strides have been made in the detection of predisposing risk factors and pathological mechanisms; however, pharmacological therapies have shown to be ineffective in reducing cardiovascular mortality in the HF with preserved EF (HFpEF) population, opening the way to the necessity of developing new precision medicine based approaches. On the other hand, novel therapies and device interventions still require refinements with the ultimate goal of offering new clinically treatments for the HFpEF population. The aim of the present review is to provide insights into the HFpEF pathophysiology, diagnostic pathways and the latest updates on treatment strategies and their potential future application in routine clinical practice.