Safety of outpatient commencement of sotalol.

Background: Inpatient monitoring is recommended for sotalol initiation. Objective: The purpose of this study was to assess the safety of outpatient sotalol commencement. Methods: This is a multicenter, retrospective, observational study of patients initiated on sotalol in an outpatient setting. Serial electrocardiogram monitoring at day 3, day 7, 1 month, and subsequently as clinically indicated was performed. Corrected QT (QTc) interval and clinical events were evaluated. Results: Between 2008 and 2023, 880 consecutive patients who were commenced on sotalol were evaluated. Indications were atrial fibrillation/flutter in 87.3% (n = 768), ventricular arrhythmias in 9.9% (n = 87), and other arrhythmias in 2.8% (n = 25). The daily dosage at initiation was 131.0 ± 53.2 mg/d. The QTc interval increased from baseline (431 ± 32 ms) to 444 ± 37 ms (day 3) and 440 ± 33 ms (day 7) after sotalol initiation (P < .001). Within the first week, QTc prolongation led to the discontinuation of sotalol in 4 and dose reduction in 1. No ventricular arrhythmia, syncope, or death was observed during the first week. Dose reduction due to asymptomatic bradycardia occurred in 3 and discontinuation due to dyspnea in 3 within the first week. Overall, 1.1% developed QTc prolongation (>500 ms/>25% from baseline); 4 within 3 days, 1 within 1 week, 4 within 60 days, and 1 after >3 years. Discontinuation of sotalol due to other adverse effects occurred in 41 patients within the first month of therapy. Conclusion: Sotalol initiation in an outpatient setting with protocolized follow-up is safe, with no recorded sotalol-related mortality, ventricular arrhythmias, or syncope. There was a low incidence of significant QTc prolongation necessitating discontinuation within the first month of treatment. Importantly, we observed a small incidence of late QT prolongation, highlighting the need for vigilant outpatient surveillance of individuals on sotalol.

Echocardiography and strain analysis in Malaysian elite athletes versus young healthy adults.

Background: Athletes have changes that can mimic pathological cardiomyopathy. Methods: Echocardiographic study of 50 male, female athletes (MA, FA) and non-athletes (MNA, FNA) age 18 to 30 years. These athletes participate in sports with predominantly endurance component. All participants exhibit no known medical illnesses or symptoms. Results: MA have thicker wall (IVSd) than MNA. No MA have IVSd > 1.2 cm and no FA have IVSd > 1.0 cm. Left ventricle internal dimension (LVIDd), left ventricle end diastolic volume index (LVEDVi) is bigger in athletes. None have LVIDd > 5.8 cm. Right ventricle fractional area change (FAC) is lower in athletes. (MA vs MNA, p = 0.013, FA vs FNA, p = 0.025). Athletes have higher septal and lateral e' (Septal e'; MA 13.57 ± 2.66 cm/s vs MNA 11.46 ± 2.93 cm/s, p < 0.001, Lateral e'; MA 17.17 ± 3.07 cm/s vs MNA 14.82 ± 3.14 cm/s, p < 0.001), (Septal e'; FA 13.46 ± 2.32 cm/s vs FNA 12.16 ± 2.05 cm/s, p = 0.04, Lateral e'; FA 16.92 ± 2.97 cm/s vs FNA 15.44 ± 2.29 cm/s, p = 0.006).No difference in Global longitudinal (GLS), Right ventricle free wall (RVFWS) and Global circumferential strain (GCS). Left atrial reservoir (LArS) and left atrial booster strain (LAbS) is smaller in athletes. (LArS, MA 44.12 ± 9.55% vs MNA 52.95 ± 11.17%, p < 0.001 LArS, FA 48.07 ± 10.06% vs FNA 53.64 ± 8.99%, p = 0.004), (LAbS, MA 11.59 ± 5.13% vs MNA 17.35 ± 5.27%, p < 0.001 LAbS FA 11.77 ± 4.65% vs FNA 15.30 ± 4.19%, p < 0.001). Conclusion: Malaysian athletes have thicker wall and bigger left ventricle than controls. No athletes have IVSd > 1.2 cm and/or LVIDd > 5.8 cm. There is no difference in GLS, RVFWS and GCS but athletes have smaller LArS and LAbS.

Obesity and atrial fibrillation: Prevalence, pathogenesis, and prognosis.

The prevalence of atrial fibrillation (AF) and obesity are rising significantly. There is a shared association between these conditions with obesity predisposing individuals to a number of shared risk factors. In addition, obesity in itself has been shown to cause changes to the structure, function and hemodynamics of the heart. There is evidence to show that weight-loss has significant impact on AF symptoms, burden and more recently the potential to reverse the type of AF. Through risk factor management and in the case of morbid obesity, bariatric surgery, there is an improved prognosis for patients with AF and obesity. In this paper we provide a review of the current data on obesity and AF prevalence, pathogenesis and prognosis.

Hypertension and atrial fibrillation.

Hypertension is the most prevalent cardiovascular risk factor underlying atrial fibrillation and is present in up to 40% of patients with atrial fibrillation. Furthermore, attributable risk studies have shown that a history of hypertension contributes to up to 24% of incident atrial fibrillation. New data suggest that even early forms of hypertension (prehypertension and aortic stiffness) are associated with an increased risk of atrial fibrillation development. Hypertension and prehypertension are therefore critical mediators for the development of atrial fibrillation. Mechanisms for the association between hypertension and atrial fibrillation include diffuse electro-structural changes to the left atrium, driven by the haemodynamic and neurohormonal influences of hypertension and other, frequently coexisting, cardiovascular risk factors. Management of hypertension in atrial fibrillation should focus not only on blood pressure reduction but also on a comprehensive risk factor modification strategy. Such strategies have been shown to be associated with significant improvements in atrial fibrillation symptom burden as well as improved arrhythmia-free survival and reversal of the progression of atrial fibrillation. These strategies should focus on dietary modifications as well as prescribed exercise programmes involving a multidisciplinary team and patient-centred atrial fibrillation care. Risk factor management, supplemented by antihypertensive medications as needed, provides the optimum strategy for improving outcomes and even reversing the natural progression of atrial fibrillation in patients with hypertension.