UNASSIGNED: Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are a class of widely used hypoglycemic agents for the treatment of type 2 diabetes mellitus (T2DM). In addition to lowering blood glucose, SGLT2i protects the heart and kidney, significantly reduces cardiovascular events, and delays the progression of heart failure and chronic kidney disease. However, previous studies have not exhaustively discussed the association between SGLT2i and the risk of developing cardiac arrhythmias. The purpose of this study is to assess the association of SGLT2i with cardiac arrhythmias in patients with T2DM and without T2DM in cardiovascular outcome trials (CVOTs).
UNASSIGNED: We performed a meta-analysis and systematic review of CVOTs that compared SGLT2i with placebo. MEDLINE, Web of Science, The Cochrane Library and Embase were systematically searched from inception to December 2022. We included CVOTs reporting cardiovascular or renal outcomes with a follow-up duration of at least 6 months.
UNASSIGNED: A total of 12 CVOTs with 77,470 participants were included in this meta-analysis (42,016 SGLT2i vs 35,454 control), including patients with T2DM, heart failure (HF), or chronic kidney disease (CKD). Follow-up duration ranged from 9 months to 5.65 years. Medications included empagliflozin, canagliflozin, dapagliflozin and ertugliflozin. SGLT2i were associated with a lower risk of tachycardia (risk ratio (RR) 0.86; 95% confidence interval (CI) 0.79-0.95), supraventricular tachycardia (SVT; RR 0.84; 95% CI 0.75-0.94), atrial fibrillation (AF; RR 0.86; 95% CI 0.75-0.97) and atrial flutter (AFL; RR 0.75; 95% CI 0.57-0.99) in patients with T2DM, HF and CKD. SGLT2i could also reduce the risk of cardiac arrest in CKD patients (RR 0.50; 95% CI 0.26-0.95). Besides, SGLT2i therapy was not associated with a lower risk of ventricular arrhythmia and bradycardia.
UNASSIGNED: SGLT2i therapy is associated with significantly reduced the risk of tachycardia, SVT, AF, and AFL in patients with T2DM, HF, and CKD. In addition, SGLT2i could also reduce the risk of cardiac arrest in CKD patients. Further researches are needed to fully elucidate the antiarrhythmic mechanism of SGLT2i.

The intricate relationship between sports participation and cardiac arrhythmias is a key focus of cardiovascular research. Physical activity, integral to preventing atherosclerotic cardiovascular disease, induces structural, functional, and electrical changes in the heart, potentially triggering arrhythmias, particularly atrial fibrillation (AF). Despite the cardiovascular benefits, the optimal exercise amount remains unclear, revealing a J-shaped association between AF and exercise. Endurance athletes, particularly males, face elevated AF risks, influenced by age. Risk factors vary among sports modalities, with unique physiological responses in swim training potentially elevating AF risk. Clinical management of AF in athletes necessitates a delicate balance between rhythm control, rate control, and anticoagulation therapy. Sport-induced bradyarrhythmias, including sinus bradycardia and conduction disturbances, are prevalent among athletes. Managing bradycardia in athletes proves challenging due to its complex and not fully understood pathophysiology. Careful consideration is required, particularly in symptomatic cases, where pacemaker implantation may be necessary for sinus node dysfunction. Although pacing is recommended for specific atrioventricular (AV) blocks, milder forms often prevail without restricting sports participation. This review explores the nuanced relationship between exercise and tachy- and bradyarrhythmia in athletes, addressing the challenges clinicians face when optimizing patient care in this distinctive population.

A description of an acute hospital presentation with severe tachyarrhythmia requiring multiple direct current cardioversions in a 45-year-old male bodybuilder with underlying cardiomyopathy possibly caused by long-term anabolic steroid abuse and more recent thyroxine misuse is described. A review of the literature regarding the above associations was also done. This case report further adds to the literature regarding the harmful effect of androgenic anabolic steroid misuse (with the added effect of thyroxine misuse in this case) on the heart.

Guidelines are important tools to guide the diagnosis and treatment of patients to improve the decision-making process of health professionals. They are periodically updated according to new evidence. Four new Guidelines in 2021, 2022 and 2023 referred to pediatric pacing and defibrillation. There are some relevant changes in permanent pacing. In patients with atrioventricular block, the heart rate limit in which pacemaker implantation is recommended was decreased to reduce too-early device implantation. However, it was underlined that the heart rate criterion is not absolute, as signs or symptoms of hemodynamically not tolerated bradycardia may even occur at higher rates. In sinus node dysfunction, symptomatic bradycardia is the most relevant recommendation for pacing. Physiological pacing is increasingly used and recommended when the amount of ventricular pacing is presumed to be high. New recommendations suggest that loop recorders may guide the management of inherited arrhythmia syndromes and may be useful for severe but not frequent palpitations. Regarding defibrillator implantation, the main changes are in primary prevention recommendations. In hypertrophic cardiomyopathy, pediatric risk calculators have been included in the Guidelines. In dilated cardiomyopathy, due to the rarity of sudden cardiac death in pediatric age, low ejection fraction criteria were demoted to class II. In long QT syndrome, new criteria included severely prolonged QTc with different limits according to genotype, and some specific mutations. In arrhythmogenic cardiomyopathy, hemodynamically tolerated ventricular tachycardia and arrhythmic syncope were downgraded to class II recommendation. In conclusion, these new Guidelines aim to assess all aspects of cardiac implantable electronic devices and improve treatment strategies.

BACKGROUND: The role of β-blockers in the critically ill has been studied, and data on the protective effects of these drugs on critically ill patients have been repeatedly reported in the literature over the last two decades. However, consensus and guidelines by scientific societies on the use of β-blockers in critically ill patients are still lacking. The purpose of this document is to support the clinical decision-making process regarding the use of β-blockers in critically ill patients. The recipients of this document are physicians, nurses, healthcare personnel, and other professionals involved in the patient\'s care process.
METHODS: The Italian Society of Anesthesia, Analgesia, Resuscitation and Intensive Care (SIAARTI) selected a panel of experts and asked them to define key aspects underlying the use of β-blockers in critically ill adult patients. The methodology followed by the experts during this process was in line with principles of modified Delphi and RAND-UCLA methods. The experts developed statements and supportive rationales in the form of informative text. The overall list of statements was subjected to blind votes for consensus.
RESULTS: The literature search suggests that adrenergic stress and increased heart rate in critically ill patients are associated with organ dysfunction and increased mortality. Heart rate control thus seems to be critical in the management of the critically ill patient, requiring careful clinical evaluation aimed at both the differential diagnosis to treat secondary tachycardia and the treatment of rhythm disturbance. In addition, the use of β-blockers for the treatment of persistent tachycardia may be considered in patients with septic shock once hypovolemia has been ruled out. Intravenous application should be the preferred route of administration.
CONCLUSIONS: β-blockers protective effects in critically ill patients have been repeatedly reported in the literature. Their use in the acute treatment of increased heart rate requires understanding of the pathophysiology and careful differential diagnosis, as all causes of tachycardia should be ruled out and addressed first.

Thyroid storm (TS) is a rare and fatal endocrine emergency that occurs due to undiagnosed and inadequately treated hyperthyroidism after stressful conditions in patients with thyroid disorders. The objective of this systematic scoping review was to better understand the pathophysiology of TS and its complications, in terms of myocardial affection, tachyarrhythmia, and cardiogenic shock. In addition, we explored the pharmacological, mechanical, and surgical treatments for TS. We also evaluated the outcomes of TS according to sex and cardiac involvement. Additionally, analytical analysis was performed on the selected data. A literature review of peer-reviewed journals was carried out thoroughly using medical terms, MeSH on PubMed, Google Scholar, and combinations such as thyrotoxicosis-induced cardiomyopathy, thyroid storm, cardiogenic shock, myocardial infarction, endocrine emergency, Burch-Wartofsky score, extracorporeal circulatory support, and thyroidectomy. A total of 231 papers were eligible (2 retrospective studies, 5 case series, and 224 case reports) with a total of 256 TS patients with cardiac involvement between April 2003 and August 2023. All age groups, sexes, patients with TS-induced cardiomyopathy, non-atherosclerotic myocardial infarction, tachyarrhythmia, heart failure, shock, and different forms of treatment were discussed. Non-English language articles, cases without cardiac involvement, and cases in which treatment modalities were not specified were excluded. Female sex was predominant, with 154 female and 102 male patients. Approximately 82% of patients received beta-blockers (BBs), 16.3% were placed on extracorporeal membrane oxygenation (ECMO) support, 16.3% received therapeutic plasma exchange (TPE), and 13.8% underwent continuous renal replacement therapy (CRRT), continuous venovenous hemofiltration (CVVHD), or dialysis. Overall, 18 females and 16 males died. BB-induced circulatory collapse, acute renal failure, CRRT, and ventricular fibrillation were significantly associated with mortality. Awareness of TS and not only thyrotoxicosis is vital for timely and appropriate treatment. The early diagnosis and management of TS in cardiac settings, including pharmacological, mechanical, and surgical modalities, can save high-risk patients. Sex matters in the presentation, treatment, and mortality of this population. However, further large-scale, and well-designed studies are required.

BACKGROUND: Holter electrocardiographic monitoring is a cornerstone of diagnostic testing for arrhythmogenic cardiomyopathy (ACM) in Boxer dogs, but physical activity during monitoring is not controlled. In humans, exercise testing (ExT) can identify latent tachyarrhythmias associated with cardiomyopathy, and exercise increases serum cardiac troponin-I concentrations ([hs-cTnI]). These effects have not yet been investigated in Boxer dogs.
OBJECTIVE: Subjecting Boxer dogs to brief, moderate-intensity ExT can identify changes in Holter recordings and [hs-cTnI] compared to baseline results.
METHODS: Thirty overtly healthy, client-owned Boxer dogs.
METHODS: Prospective interventional study. Dogs underwent baseline diagnostic testing including 24-hour Holter monitoring and [hs-cTnI], followed by brief ExT (accompanied, brisk stair-climbing and -descending for <5 minutes).
RESULTS: Eleven dogs (37%) had >100 premature ventricular complexes (PVCs)/24 hours at baseline (3), ExT (3), or both (5). After ExT, these dogs had more PVCs/24 hours and greater increases in [hs-cTnI] compared to those with ≤100 PVCs/24 hours. Dogs with the striatin mutation had more PVCs/24 hours and a greater increase in [hs-cTnI] after ExT than did dogs without the striatin mutation.
CONCLUSIONS: Exercise testing may improve the binary classification of Boxer dogs with or without ACM by increasing the number of PVCs and [hs-cTnI] in affected dogs to a greater degree than in unaffected dogs. This effect also is associated with presence or absence of the striatin mutation. Exercise should be a controlled variable when screening Boxer dogs for ACM.

Currently, ivabradine is not approved for the treatment of sinus tachycardia secondary to hyperthyroidism. We aimed to increase the recognition of ivabradine as an effective alternative to, or combination with, beta-blockers in controlling sinus tachycardia secondary to hyperthyroidism. Elevated thyroid hormone levels enhance cardiac performance through a positive chronotropic effect, resulting in an increased heart rate (HR), an effect brought on by increasing the If funny current at sinoatrial node (SAN). Ivabradine is a novel, dose-dependent selective inhibitor of If channels. By decreasing SAN pacemaker activity, ivabradine allows for selective reduction of HR with a resultant increase in ventricular filling time. This mechanism sets ivabradine apart from the typical rate-reducing medications, namely beta-blockers and calcium channel blockers, which simultaneously decrease HR and myocardial contractility. We describe a case of hyperthyroidism-induced sinus tachycardia, resistant to maximal doses of beta-blocker, which was successfully managed by ivabradine. After excluding other causes of tachycardia, such as anemia, hypovolemic states, structural heart disease, drug abuse, and infection, ivabradine was given off-label for symptomatic relief of hyperthyroidism-induced sinus tachycardia. Within 24 h, HR steadily decreased to the low 80s. Our patient had a unique presentation in which he presented with hyperthyroidism-induced sinus tachycardia with no relief after administration of maximal dose of beta-blocker. Ivabradine was then given, with resolution of sinus tachycardia within 24 h.

UNASSIGNED: Some patients with cardiac resynchronisation therapy (CRT) experience super-response (LVEF improvements to ≥50%). At generator exchange (GE), downgrading (DG) from CRT-defibrillator (CRT-D) to CRT-pacemaker (CRT-P) could be an option for these patients on primary prevention ICD indication and no required ICD therapies. Long-term data on arrhythmic events in super-responders is scarce.
UNASSIGNED: CRT-D patients with LVEF improvement to ≥50% at GE were identified in four large centres for retrospective analysis. Mortality, significant ventricular tachyarrhythmia and appropriate ICD-therapy were determined, and patient analysis was split into two groups (downgraded to CRT-P or not).
UNASSIGNED: Sixty-six patients (53% male, 26% coronary artery disease) on primary prevention were followed for a median of 129 months [IQR: 101-155] after implantation. 27 (41%) patients were downgraded to CRT-P at GE after a median of 68 [IQR: 58-98] months (LVEF 54% ± 4%). The other 39 (59%) continued with CRT-D therapy (LVEF 52% ± 6%). No cardiac death or significant arrhythmia occurred in the CRT-P group (median follow-up (FU) 38 months [IQR: 29-53]). Three appropriate ICD-therapies occurred in the CRT-D group [median FU 70 months (IQR: 39-97)]. Annualized event-rates after DG/GE were 1.5%/year and 1.0%/year in the CRT-D group and the whole cohort, respectively.
UNASSIGNED: No significant tachyarrhythmia were detected in the patients downgraded to CRT-P during follow-up. However, three events were observed in the CRT-D group. Whilst downgrading CRT-D patients is an option, a small residual risk for arrhythmic events remains and decisions regarding downgrade should be made on a case-by-case basis.

UNASSIGNED: Junctional ectopic tachycardia (JET) is the most common arrhythmia after pediatric open-heart surgeries (OHS), causing high morbidity and mortality. As diagnosis is often missed in patients with minimal hemodynamic instability, its incidence depends on active surveillance. A prospective randomized trial evaluated the efficacy and safety of prophylactic amiodarone and dexmedetomidine to prevent and control postoperative JET.
UNASSIGNED: Consecutive patients aged under 12 years were randomized into amiodarone, dexmedetomidine (initiated during anesthetic induction) and control groups. Outcome measures included incidence of JET, inotropic score, ventilation, and intensive care unit (ICU) duration and hospital stay, as well as adverse drug effects.
UNASSIGNED: Two hundred and twenty-five consecutive patients with a median age of 9 months (range 2 days-144 months) and a median weight of 6.3 kg (range 1.8 kg-38 kg) were randomized with 70 patients each to amiodarone and dexmedetomidine groups, and the rest were controls. Ventricular septal defect and Fallot\'s tetralogy were the common defects. The overall incidence of JET was 16.4%. Syndromic patients, hypokalemia, hypomagnesemia, longer bypass, and cross-clamp duration were the risk factors for JET. Patients with JET had significantly prolonged ventilation (P = 0.043), longer ICU (P = 0.004), and hospital stay (P = 0.034) than those without JET. JET was less frequent in amiodarone (8.5%) and dexmedetomidine (14.2%) groups compared to controls (24.7%) (P = 0.022). Patients receiving amiodarone and dexmedetomidine had significantly lower inotropic requirements, lower ventilation duration (P = 0.008), ICU (P = 0.006), and hospital stay (P = 0.05). Adverse effects such as bradycardia and hypotension after amiodarone and ventricular dysfunction after dexmedetomidine were not significantly different from controls.
UNASSIGNED: Prophylactic amiodarone or dexmedetomidine started before OHS is effective and safe for the prevention of postoperative JET.