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Device-detected subclinical atrial fibrillation (AF) refers to infrequent, short-lasting, asymptomatic AF that is detected only with long-term continuous monitoring. Subclinical AF is common and associated with an increased risk of stroke; however, the risk of stroke with subclinical AF is lower than for clinical AF, and very few patients with subclinical AF alone have been included in large AF anticoagulation trials. The net benefit of anticoagulation in patients with subclinical AF is unknown. ARTESiA is a prospective, multicenter, double-blind, randomized controlled trial, recruiting patients with subclinical AF detected by an implanted pacemaker, defibrillator, or cardiac monitor, and who have additional risk factors for stroke. Patients with clinical AF documented by surface electrocardiogram will be excluded from the study. Participants will be randomized to receive either apixaban (according to standard AF dosing) or aspirin 81mg daily. The primary outcome is the composite of stroke, transient ischemic attack with diffusion-weighted magnetic resonance imaging evidence of cerebral infarction, and systemic embolism. Approximately 4,000 patients will be enrolled from around 230 clinical sites, with an anticipated mean follow-up of 36months until 248 adjudicated primary outcome events have occurred. ARTESiA will determine whether oral anticoagulation therapy with apixaban compared with aspirin reduces the risk of stroke or systemic embolism in patients with subclinical AF and additional risk factors.

Background Arterial stiffness, measured using carotid‐femoral pulse wave velocity (c‐f PWV) and heart rate‐corrected augmentation index (Aix75), is associated with cardiovascular disease, and in some studies incident atrial fibrillation (AF). In this cross‐sectional study, we aimed to investigate whether arterial stiffness is associated with markers of atrial myopathy, which refers to structural and electrical changes in the atria that indicate increased AF risk. Methods We included 1050 participants (age 57 ± 4.3 years, 47% males) from the population‐based Swedish CArdioPulmonary bioImage Study with c‐f PWV and Aix75 data. A random subsample (n = 331) underwent echocardiography. The association between arterial stiffness and atrial myopathy markers was studied using multivariable‐adjusted negative binomial regression models for premature atrial complexes (PACs) on 24 h ECG, linear regression for P‐wave duration and left atrial volume index (LAVi), and logistic regression models for abnormal P‐wave terminal force in V1 (PWTFV1) and P‐wave axis. Results Arterial stiffness was associated with fewer PACs: incidence rate ratio (IRR) 0.45 (95% CI: 0.31 to 0.65, p < 0.001) per 1 m/s increase in c‐f PWV and IRR 0.66 (95% CI: 0.49 to 0.89, p = 0.01) per % increase in Aix75. There was no association between arterial stiffness and P‐wave indices, OR 1.09 (95% CI: 0.85 to 1.40), p = 0.50 for abnormal PWTFV1, and β −0.003 (−0.10 to 0.09), p = 0.95 for P‐wave duration, both per 1 m/s increase in c‐f PWV. Conclusions Arterial stiffness, measured as either c‐f PWV or Aix75, was associated with fewer PACs, whereas no association was found with P‐wave indices. The association between arterial stiffness and atrial myopathy is complex and merits further study. Arterial stiffness, measured as either c‐f PWV or Aix75, was associated with fewer PACs, whereas no association was found with P‐wave indices. The association between arterial stiffness and atrial myopathy is complex and merits further study.

Left atrial appendage exclusion (LAAE) has been shown in randomized trials to reduce ischemic stroke risk in patients undergoing cardiac surgery with known atrial fibrillation (AF). Many patients undergoing cardiac surgery without pre-existing AF are at risk of stroke and may benefit from LAAE. Left Atrial Appendage Exclusion for Prophylactic Stroke Reduction (LeAAPS) is an international, prospective, randomized, multicenter, blinded trial evaluating the effectiveness of LAAE in preventing ischemic stroke or systemic embolism in patients undergoing cardiac surgery at increased risk of AF and ischemic stroke. The trial will enroll 6500 patients at increased risk of stroke in whom a cardiac surgery is planned at 250 sites worldwide. Eligible patients are ≥18 years old, have no pre-existing AF but are at increased risk for AF and stroke (based on age, CHA2DS2-VASc score, left atrium size or brain natriuretic peptide). Patients are randomized 1:1 to receive either LAAE with AtriClip or no LAAE during cardiac surgery. Healthcare providers outside of the operating room and the patient will be blinded to allocation. The primary effectiveness endpoint is the first occurrence of ischemic stroke, systemic arterial embolism, or surgical or endovascular LAA closure. The powered secondary effectiveness endpoint is ischemic stroke or systemic arterial embolism. The primary safety endpoint is the occurrence of one of the following events (through 30 days): pericardial effusion requiring percutaneous or surgical treatment, peri-operative major bleeding, deep sternal wound infection, or myocardial infarction. Other endpoints include mortality, rehospitalizations, clinically diagnosed AF, transient ischemic attack, and cognitive and quality of life assessments. Follow-up is every 6 months for a minimum of 5 years; primary analysis occurs when 469 patients have had an ischemic stroke or systemic embolism. The results of the LeAAPS trial will demonstrate whether LAAE with AtriClip at the time of other routine cardiac surgery reduces stroke or systemic arterial embolism during long-term follow-up in patients at high risk of stroke without pre-existing AF. ClinicalTrials.gov, Identifier: NCT05478304, https://clinicaltrials.gov/study/NCT05478304?term=%20NCT05478304&rank=1.

BackgroundPremature ventricular complexes (PVCs) predict coronary heart disease, heart failure, atrial fibrillation and death, all of which are also related to sodium intake. We studied estimated sodium intake and PVC frequency in the randomly selected population-based Swedish CArdioPulmonary bioImage Study cohort.MethodsIn our cross-sectional study, we included 5636 individuals with 24-hour ECG registration and fasting morning urine sampling. Sodium intake was estimated using the Kawasaki formula, and the association between sodium intake and PVC frequency was modelled using multivariable negative binomial regression, adjusted for age, sex, body mass index, level of education, height, physical activity and smoking status, across prespecified strata of sodium intake: <2 g/day, 2–2.99 g/day, 3–3.99 g/day (reference category), 4–4.99 g/day and ≥5 g/day.ResultsThe median age was 57.6 years, and 51.9% were female. The median daily PVC count was 8 (IQR 3–41); 5.9% had ≥500 PVCs/24 hours. The mean estimated sodium intake was 3.3 g/day. There was a U-shaped association between sodium intake and PVCs. Compared with the reference of 3–3.99 g/day (28% of participants), sodium intakes <2 g/day (15% of participants) and ≥5 g/day (10% of participants) were associated with 26% (95% CI 6% to 49%) and 52% (95% CI 26% to 84%, p<0.01) increases in PVC frequency, respectively, but intakes of 2–2.99 g/day and 4–4.99 g/day were not (5% (95% CI −8% to 20%) and 4% (95% CI −11% to 22%) increase, respectively).ConclusionThere was a U-shaped association between sodium intake and PVC frequency, with both low and high sodium intake associated with higher PVC frequency.

Splice-site variants in cardiac genes may predispose carriers to potentially lethal arrhythmias. To investigate, we screened 1315 probands and first-degree relatives enrolled in the Canadian Hearts in Rhythm Organization (HiRO) registry. 10% (134/1315) of patients in the HiRO registry carry variants within 10 base-pairs of the intron-exon boundary with 78% (104/134) otherwise genotype negative. These 134 probands were carriers of 57 unique variants. For each variant, American College of Medical Genetics and Genomics (ACMG) classification was revisited based on consensus between nine in silico tools. Due in part to the in silico algorithms, seven variants were reclassified from the original report, with the majority (6/7) downgraded. Our analyses predicted 53% (30/57) of variants to be likely/pathogenic. For the 57 variants, an average of 9 tools were able to score variants within splice sites, while 6.5 tools responded for variants outside these sites. With likely/pathogenic classification considered a positive outcome, the ACMG classification was used to calculate sensitivity/specificity of each tool. Among these, Combined Annotation Dependent Depletion (CADD) had good sensitivity (93%) and the highest response rate (131/134, 98%), dbscSNV was also sensitive (97%), and SpliceAI was the most specific (64%) tool. Splice variants remain an important consideration in gene elusive inherited arrhythmia syndromes. Screening for intronic variants, even when restricted to the ±10 positions as performed here may improve genetic testing yield. We compare 9 freely available in silico tools and provide recommendations regarding their predictive capabilities. Moreover, we highlight several novel cardiomyopathy-associated variants which merit further study.

Studies of cardiac resynchronization therapy in addition to an implantable cardioverter defibrillator in patients with mild to moderate congestive heart failure had not been shown to reduce mortality until the recent RAFT trial (Resynchronization/Defibrillation for Ambulatory Heart Failure Trial). We performed a meta-analysis including the RAFT trial to determine the effect of cardiac resynchronization therapy with or without an implantable defibrillator on mortality. We searched electronic databases and other sources for reports of randomized trials using a parallel or crossover design. We included studies involving patients with heart failure receiving optimal medical therapy that compared cardiac resynchronization therapy with optimal medical therapy alone, or cardiac resynchronization therapy plus an implantable defibrillator with a standard implantable defibrillator. The primary outcome was mortality. The optimum information size was considered to assess the minimum amount of information required in the literature to reach reliable conclusions about cardiac resynchronization therapy. Of 3071 reports identified, 12 studies (n = 7538) were included in our meta-analysis. Compared with optimal medical therapy alone, cardiac resynchronization therapy plus optimal medical therapy significantly reduced mortality (relative risk [RR] 0.73, 95% confidence interval [CI] 0.62–0.85). Compared with an implantable defibrillator alone, cardiac resynchronization therapy plus an implantable defibrillator significantly reduced mortality (RR 0.83, 95% CI 0.72–0.96). This last finding remained significant among patients with New York Heart Association (NYHA) class I or II disease (RR 0.80, 95% CI 0.67–0.96) but not among those with class III or IV disease (RR 0.84, 95% CI 0.69–1.07). Analysis of the optimum information size showed that the sequential monitoring boundary was crossed, which suggests no need for further clinical trials. The cumulative evidence is now conclusive that the addition of cardiac resynchronization to optimal medical therapy or defibrillator therapy significantly reduces mortality among patients with heart failure.

In this trial, patients with mild-to-moderate heart failure were randomly assigned to receive an implantable cardioverter–defibrillator (ICD) alone or an ICD plus cardiac-resynchronization therapy. Patients in the latter group had lower rates of death and hospitalization for heart failure. The use of implantable cardioverter–defibrillators (ICDs) improves survival among patients who have New York Heart Association (NYHA) class II or III heart failure with left ventricular systolic dysfunction despite optimal medical therapy. 1 Cardiac-resynchronization therapy (CRT) improves symptoms of heart failure, quality of life, exercise capacity, 2 – 6 and left ventricular function 7 when used in patients with NYHA functional class III or ambulatory class IV heart failure with a wide QRS complex. CRT has also been shown to reduce mortality among patients not receiving an ICD. 8 However, studies have not shown a survival benefit of CRT in patients with NYHA class II . . .

Cardiovascular disease is the leading cause of death in developed countries. In Canada, in 1999, cardiovascular disease was responsible for 36% of all deaths. Ischemic heart disease accounts for the greatest percentage of these deaths (20% of all deaths), half of which are due to the acute effects of myocardial infarction. The other half are related to the late manifestations and complications of myocardial infarction. Once coronary arteriosclerosis has reached the point where it results in myocardial infarction, two main complications can ensue, loss of myocardial function and disturbance of cardiac rhythm. Progressive loss of myocardial pump function results in the syndrome of congestive heart failure. Abnormalities of the heart rhythm result in ventricular fibrillation, which is the direct cause of sudden death. Congestive heart failure rates have been easy to track because of the frequent need for hospitalization and we know from analysis of administrative databases that the annual rate of death from heart failure is about 2.5% in Canada. Sudden death, however most often occurs at home and without warning, making it much more difficult to quantitate its impact. However, the most conservative estimates suggest that no less than 25% of deaths in patients with a diagnosis of ischemic heart disease are due to ventricular fibrillation.