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Objective: To assess whether women with atrial fibrillation (AF) have a higher risk of adverse events than men during long-term follow-up since controversial data have been published.Methods: In the context of two very similar observational multicentre cohort studies, we prospectively followed 3894 patients (28% women) with previously documented AF for a median of 4.02 (3.00-5.83) years. The primary outcome was a composite of ischaemic stroke, myocardial infarction and cardiovascular death. Secondary outcomes included the individual components of the composite outcome, hospitalisation for heart failure, major and clinically relevant non-major bleeding, stroke or systemic embolism and non-cardiovascular death.Results: Mean age was 73.1 years in women vs 70.8 years in men. The incidence of the primary endpoint in women versus men was 2.46 vs 3.24 per 100 patient-years, respectively (adjusted HR (aHR) 0.74, 95% CI 0.58 to 0.94; p=0.01). Women died less frequently from cardiovascular (aHR 0.57, 95% CI 0.41 to 0.78; p<0.001) and non-cardiovascular causes (aHR 0.68, 95% CI 0.47 to 0.98; p=0.04). There were no significant sex-specific differences in stroke (incidence 1.05 vs 1.00; aHR 1.02, 95% CI 0.70 to 1.49, p=0.93), myocardial infarction (incidence 0.67 vs 0.72; aHR 0.98, 95% CI 0.61 to 1.57, p=0.94), major and clinically relevant non-major bleeding (incidence 4.51 vs 4.34; aHR 0.95, 95% CI 0.79 to 1.15, p=0.63) or heart failure hospitalisation (incidence 3.28 vs 3.07; aHR 1.06, 95% CI 0.85 to 1.32, p=0.60).Conclusion: In this large study of patients with established AF, women had a lower risk of death than men, but there were no sex-specific differences in other adverse outcomes. [ABSTRACT FROM AUTHOR]

Objective: The prognostic value of left atrial (LA) dimensions may differ between patients with and without atrial fibrillation (AF).Methods: MEDLINE and EMBASE were searched for studies that investigated the association between LA echocardiographic parameters measured by transthoracic echocardiography and cardiovascular outcomes in patients with or without AF. Data were independently abstracted by two reviewers and pooled using random-effects meta-analysis. The primary outcome was incident stroke or thromboembolic events. Secondary outcomes were heart failure, all-cause mortality and major adverse cardiac events (MACE).Results: Twenty-three studies of patients with AF (14 939 patients) and 68 studies of patients without AF (50 720 patients) in this systematic review. Increasing LA diameter was significantly associated with stroke and thromboembolic events in patients without AF (risk ratio (RR) 1.38, 95% CI 1.02 to 1.87; p=0.03), but not in patients with AF (RR 1.02, 95% CI 0.98 to 1.07; p=0.27; p for difference=0.05). Increasing LA diameter index was significantly associated with MACE in patients with AF (RR 1.13, 95% CI 1.09 to 1.17; p<0.001) and in patients without AF (RR 2.98, 95% CI 1.90 to 4.66; p<0.001), with stronger effects in non-AF populations (p for difference <0.001). Greater LA volume index was significantly associated with the risk of MACE in patients with AF (RR 1.01, 95% CI 1.00 to 1.02; p=0.03) and in non-AF populations (RR 1.08, 95% CI 1.05 to 1.10; p<0.001), the association being stronger in individuals without AF (p for difference <0.001).Conclusions: Larger LA parameters were associated with various adverse cardiovascular events. Many of these associations were stronger in individuals without AF, highlighting the potential importance of LA myopathy. [ABSTRACT FROM AUTHOR]

Objective: It is not clear whether patients who received an implantable cardioverter-defibrillator (ICD) for primary prevention should undergo device replacement if they never experienced an appropriate ICD therapy during the first generator longevity. This study evaluated the incidence and predictors of appropriate ICD therapy after device replacement in this specific population. Methods: From two large prospective ICD registries, we identified all primary prevention patients who had a first ICD replacement without previous appropriate ICD therapy. Cox regression analysis was used to identify predictors of appropriate ICD therapy. Results: Of 403 primary prevention patients needing first ICD replacement, 275 patients (68%) had not received previous appropriate ICD therapy. Patients without previous appropriate ICD therapy before first ICD replacement (mean age at replacement 62±12 years, 75% male) had a mean follow-up of 86±24 months after the initial implantation and 30±24 months after device replacement. Following replacement, 3-year cumulative incidence of appropriate ICD therapy was 13.7% (95% CI 8.6 to 18.8%). No predictive factors associated with appropriate ICD therapy after replacement could be identified in spite of including seven clinically relevant factors. Conclusions: A considerable number of primary prevention patients without previous appropriate ICD therapy before first ICD replacement received appropriate ICD therapy after replacement. As there were no predictors of appropriate ICD therapy after replacement, replacing an ICD is still recommended in all primary prevention patients despite the lack of appropriate ICD therapy during first battery service life. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The implantable cardioverter defibrillator (ICD) is very effective in the prevention of sudden cardiac death, but its benefit is impaired by competing risks. A simple risk model to predict mortality was designed for patients with primary prevention and ischaemic cardiomyopathy. We aimed to apply this score to a general ICD population. METHODS: This retrospective registry study included all patients in whom an ICD was implanted at a tertiary referral hospital. Risk factors were age >70 years, QRS width >120 ms, atrial fibrillation, New York Heart Association Functional Classification class >2 and glomerular filtration rate <60 mL/min/1.73 m(2). Kaplan-Meier curves were constructed according to the presence of 0, 1, 2 and >2 risk factors. RESULTS: The cohort consists of 1032 patients, 881 (86%) were men, mean age was 61±14 years and mean follow-up 66±46 months. 256 patients (25%) died 58±41 months after implant. The setting was secondary prevention in 498 patients (48%). No risk factors was present in 32% of patients, 1 in 27%, 2 in 20% and >2 in 21%, respectively. There was a significant and comprehensible relation between risk score and mortality. Cumulative survival was 82% in patients with 0 risk factors, 63% in those with 1, 41% in those with 2 and 23% in those with >2 risk factors (p < 0.0001). ICD therapies were documented in 421 patients (41%) without correlation to risk factors. CONCLUSIONS: In a mixed population of primary and secondary preventive ICD carriers, application of a simple risk score predicts long-term mortality but not appropriate use of the ICD. [ABSTRACT FROM AUTHOR]

Objective The early diagnosis of acute myocardial infarction (AMI) can be particularly challenging in patients with known coronary artery disease (CAD) due to pre-existing ECG changes and chronic increases in cardiac troponin (cTn) levels Design Of 1170 consecutive patients presenting with symptoms suggestive of AMI, 433 (37%) with pre-existing CAD were analysed in a prospective multicentre study and the diagnostic and prognostic impact of copeptin in combination with either fourth generation cardiac troponin T (cTnT) or high-sensitivity cTnT (hs-cTnT) was evaluated. Results AMI was the final diagnosis in 78 patients with pre-existing CAD (18%). Copeptin was significantly higher in patients with AMI than in those without (26 pmol/l (IQR 9e71) vs 7 pmol/l (IQR 4e16), p<0.001). The diagnostic accuracy for AMI as quantified by the area under the receiver operating characteristic curve (AUC) was significantly higher for the combination of copeptin and cTnT than for cTnT alone (0.94 vs 0.86, p<0.001). The combination of copeptin and hs-cTnT (0.94) was trending to superiority compared with hs-cTnT alone (0.92, p=0.11). The combination of copeptin and the cTn assays was able to improve the negative predictive value up to 99.5% to rule out AMI. Copeptin was a strong and independent predictor of 1-year mortality (HR 4.18e 4.63). Irrespective of cTn levels, patients with low levels of copeptin had an excellent prognosis compared with patients with raised levels of both copeptin and cTn (360- day mortality 2.8e3.6% vs 23.1e33.8%, p<0.001). Conclusion In patients with pre-existing CAD, copeptin significantly improves the diagnostic accuracy if used in addition to cTnT, but only trended to superiority compared with hs-cTnT alone. Copeptin provides independent prognostic information, largely by overcoming the challenging interpretation of mild increases in hs-cTnT. [ABSTRACT FROM AUTHOR]

Aims: Direct-acting oral anticoagulants (DOACs) have, to a substantial degree, replaced vitamin K antagonists (VKA) as treatments for stroke prevention in atrial fibrillation (AF) patients. However, evidence on the real-world causal effects of switching patients from VKA to DOAC is lacking. We aimed to assess the empirical incremental cost-effectiveness of switching patients to DOAC compared with maintaining VKA treatment., Methods: The target trial approach was applied to the prospective observational Swiss-AF cohort, which enrolled 2415 AF patients from 2014 to 2017. Clinical data, healthcare resource utilisation and EQ-5D-based utilities representing quality of life were collected in yearly follow-ups. Health insurance claims were available for 1024 patients (42.4%). Overall survival, quality-of-life, costs from the Swiss statutory health insurance perspective and cost-effectiveness were estimated by emulating a target trial in which patients were randomly assigned to switch to DOAC or maintain VKA treatment., Results: 228 patients switching from VKA to DOAC compared with 563 patients maintaining VKA treatment had no overall survival advantage over a 5-year observation period (HR 0.99, 95% CI 0.45, 1.55). The estimated gain in quality-adjusted life years (QALYs) was 0.003 over the 5-year period at an incremental costs of CHF 23 033 (€ 20 940). The estimated incremental cost-effectiveness ratio was CHF 425 852 (€ 387 138) per QALY gained., Conclusions: Applying a causal inference method to real-world data, we could not demonstrate switching to DOACs to be cost-effective for AF patients with at least 1 year of VKA treatment. Our estimates align with results from a previous randomised trial., Competing Interests: Competing interests: JHB reports grant support from the Swiss National Foundation of Science, The Swiss Heart Foundation and the Stiftung Kardio; grant support, speakers and consultation fees to the institution from Bayer, Sanofi and Daichii Sankyo. EB reports grants from Swiss Cancer Research Foundation, Amgen, MSD, Novartis, Vifor, all outside the submitted work. MB is supported by grants from the Swiss National Science Foundation and the Swiss Heart Foundation. LB reports personal fees and non-financial support from Amgen, grants from AstraZeneca, personal fees and non-financial support from Bayer, personal fees from Bristol-Myers Squibb, personal fees from Claret Medical, grants from Swiss National Science Foundation, grants from University of Basel, grants from Swiss Heart Foundation, outside the submitted work. DC received consulting fees from Roche Diagnostics, and speaker fees from Servier and BMS/Pfizer, all outside of the current work. MK reports grants from Bayer, grants from Pfizer, grants from Boston Scientific, grants from BMS, grants from Biotronik, grants and personal fees from Daiichi Sankyo. GM has received advisory board and/or speaker’s fees from Astra Zeneca, Bayer, Boehringer Ingelheim, Daiichi Sankyo, Gebro Pharma, Novartis and Vifor, all outside of the submitted study. AM reports fellowship and training support from Biotronik, Boston Scientific, Medtronic, Abbott/St. Jude Medical and Biosense Webster; speaker honoraria from Biosense Webster, Medtronic, Abbott/St Jude Medical, AstraZeneca, Daiichi Sankyo, Biotronik, MicroPort, Novartis, and consultant honoraria for Biosense Webster, Medtronic, Abbott/St. Jude Medcal and Biotronik. SO received research grants from the Swiss National Science Foundation and from the Swiss Heart Foundation, research grants from Foundation for CardioVascular Research Basel, research grants from Roche, educational and speaker office grants from Roche, Bayer, Novartis, Sanofi AstraZeneca, Daiichi-Sankyo and Pfizer. TR has received research grants from the Swiss National Science Foundation, the Swiss Heart Foundation, and the sitem insel support fund, all for work outside the submitted study. Speaker/consulting honoraria or travel support from Abbott/SJM, Astra Zeneca, Brahms, Bayer, Biosense-Webster, Biotronik, Boston-Scientific, Daiichi Sankyo, Medtronic, Pfizer-BMS and Roche, all for work outside the submitted study. Support for his institution’s fellowship programme from Abbott/SJM, Biosense-Webster, Biotronik, Boston-Scientific and Medtronic for work outside the submitted study. MS reports grants from Swiss National Science Foundation, for the conduct of the study; grants from Amgen, grants from MSD, grants from Novartis, grants from Pfizer, grants from Roche, grants and personal fees from BMS and personal fees from Sandoz, all outside the submitted work. MS-B reports grants from the European Commission outside of the present work. CS has received speaker honoraria from Biosense Webster and Medtronic and research grants from Biosense Webster, Daiichi-Sankyo and Medtronic. The remaining authors have nothing to disclose., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)