Heart最新文献

Background: Significant secondary mitral regurgitation (SMR) is known to be associated with worse prognosis. However, data focusing specifically on moderate SMR and associated risk factors are lacking. In the present study, clinical and echocardiographic parameters associated with outcomes were evaluated in a large cohort of patients with moderate SMR.

Methods: Patients with moderate SMR were retrospectively included and stratified by New York Heart Association (NYHA) class and specific aetiology (atrial SMR (aSMR) or ventricular SMR (vSMR)) with a further classification of vSMR based on left ventricular ejection fraction (LVEF) ≥40% or <40%. The primary endpoint was all-cause mortality and the secondary endpoint was the composite of all-cause mortality and heart failure (HF) events.

Results: Of the total 1061 patients with moderate SMR (age 69±11 years, 59% male) included, 854 (80%) were in NYHA class I-II and 207 (20%) were in NYHA class III-IV. Regarding the aetiology, 352 (33%) had aSMR and 709 (67%) had vSMR, of which 329 (46%) had LVEF ≥40% and 380 (54%) had LVEF <40%. During a median follow-up of 82 (IQR 55-115) months, 397 (37%) died and 539 (51%) patients had HF events or died. On multivariable analysis, NYHA class III-IV (HR 1.578; 95% CI 1.244 to 2.002, p<0.001) and SMR aetiology were independently associated with both endpoints. Specifically, compared to aSMR, vSMR with LVEF ≥40% had a HR of 1.528 (95% CI 1.108 to 2.106, p=0.010) and vSMR with LVEF <40% had a HR of 1.960 (95% CI 1.434 to 2.679, p<0.001). To further support these findings, patients were matched for (1) NYHA class and (2) SMR aetiology by propensity scores including age, sex, diabetes, chronic obstructive pulmonary disease, renal function, left atrial volume index, NYHA class (only for SMR aetiology matching), LVEF, SMR aetiology (only for NYHA class matching), tricuspid regurgitation severity and right ventricular pulmonary artery coupling index. After matching, NYHA class and SMR aetiology remained associated with both outcomes (for both: log rank p<0.050).

Conclusion: In patients with moderate SMR, distinction in SMR aetiology and assessment of symptoms are important independent determinants of outcome.

Background: New-onset postoperative atrial fibrillation (POAF) after coronary artery bypass grafting (CABG) increases ischaemic stroke risk, yet factors influencing this risk remain unclear. We sought to identify factors associated with 1-year ischaemic stroke risk, compare the CHA₂DS₂-VASc (Congestive heart failure, Hypertension, Age ≥75 years, Diabetes, previous Stroke/transient ischaemic attack (TIA), Vascular disease, Age 65-74 years, Sex category) and ATRIA (Anticoagulation and Risk Factors in Atrial Fibrillation) scores' predictive abilities for ischaemic stroke, and assess oral anticoagulation (OAC) dispensing at discharge in patients with POAF.

Methods: This nationwide cohort study used prospectively collected data from four mandatory Swedish national registries. All first-time isolated CABG patients who developed POAF during 2007-2020 were included. Multivariable logistic models were used to identify ischaemic stroke predictors and C-statistics to assess the predictive abilities of the CHA₂DS₂-VASc and ATRIA scores in patients without OAC. OAC dispensing patterns were described based on stroke-associated factors.

Results: In total, 10 435 patients with POAF were identified. Out of those not receiving OAC (n=6903), 3.1% experienced an ischaemic stroke within 1 year. Advancing age (adjusted OR (aOR) 1.86 per 10-year increase, 95% CI 1.45 to 2.38), prior ischaemic stroke (aOR 18.56, 95% CI 10.05 to 34.28 at 60 years, aOR 5.95, 95% CI 3.78 to 9.37 at 80 years, interaction p<0.001), myocardial infarction (aOR 1.55, 95% CI 1.14 to 2.10) and heart failure (aOR 1.53, 95% CI 1.06 to 2.21) were independently associated with ischaemic stroke. The area under the receiver-operating characteristic curve was 0.72 (0.69-0.76) and 0.74 (0.70-0.78) for CHA₂DS₂-VASc and ATRIA, respectively (p=0.021). Altogether, 71.0% of patients with a stroke risk >2%/year, according to the CHA₂DS₂-VASc score, were not discharged on OAC.

Conclusions: Prior ischaemic stroke, advancing age, history of heart failure and myocardial infarction were associated with 1-year ischaemic stroke risk in patients with POAF after CABG. CHA₂DS₂-VASc and ATRIA scores predicted stroke risk with similar accuracy as in non-surgical atrial fibrillation cohorts. OAC dispense at discharge does not seem to reflect individual stroke risk.

Background: Hypertrophic cardiomyopathy is a common cause of non-ischaemic sudden cardiac death (SCD). Left ventricular hypertrophy (LVH) without cardiomyopathy-related myocardial disarray is a common autopsy finding and is often associated with prior hypertension in SCD subjects. Our aim was to investigate novel rare gene variants among SCD subjects with presumably hypertension-related LVH and myocardial fibrosis at autopsy.

Methods: Whole exome sequencing was used to study rare variants (minor allele frequency<0.005) estimated to be deleterious in 96 non-ischaemic SCD subjects with presumably hypertension-related LVH and myocardial fibrosis. Associations of the identified variants with cardiac disease endpoints were replicated in the Finnish national genetic study (FinnGen) dataset.

Results: 18 variants were estimated likely to affect protein function and 14 of these were associated with cardiomyopathies, heart failure, conduction abnormalities, hypertension and/or cardiac arrest in Finnish population (FinnGen). Three of the variants were classified as pathogenic or likely pathogenic. These include the splice site variant NM_000449.3:c.234-1G>A in regulatory factor X5 and frameshift variants NM_000449.3:c.234-1G>A in dehydrogenase/reductase 7C and NM_015873.3:c.1164del in villin like.

Conclusions: We identified rare deleterious variants associated with LVH in SCD subjects. Several of the identified rare variants associated with cardiovascular endpoints including heart failure, cardiomyopathies, cardiac arrest and hypertension in general population.

Background: Limited empirical evidence informs driving restrictions after implantable cardioverter-defibrillator (ICD) implantation. We sought to evaluate real-world motor vehicle crash risks after ICD implantation.

Methods: We performed a retrospective cohort study using 22 years of population-based health and driving data from British Columbia, Canada (2019 population: 5 million). Individuals with a first ICD implantation between 1997 and 2019 were age and sex matched to three controls. The primary outcome was involvement as a driver in a crash that was attended by police or that resulted in an insurance claim. We used survival analysis to compare crash risk in the first 6 months after ICD implantation to crash risk during a corresponding 6-month interval among controls.

Results: A crash occurred prior to a censoring event for 296 of 9373 individuals with ICDs and for 1077 of 28 119 controls, suggesting ICD implantation was associated with a reduced risk of subsequent crash (crude incidence rate, 8.5 vs 10.5 crashes per 100 person-years; adjusted HR (aHR), 0.71; 95% CI 0.61 to 0.83; p<0.001). Results were similar after stratification by primary versus secondary prevention ICD. Relative to controls, ICD patients had more traffic contraventions in the 3 years prior to ICD implantation but fewer contraventions in the 6 months after implantation, suggesting individuals reduced their road exposure (hours or miles driven per week) or drove more conservatively after ICD implantation.

Conclusions: Crash risk is lower in the 6 months after ICD implantation than among matched controls, likely because individuals reduced their road exposure in order to comply with contemporary postimplantation driving restrictions. Policymakers might consider liberalisation of postimplantation driving restrictions while monitoring crash rates.

Congenital heart defects are the most common type of birth defect, affecting 1% of live births. The underlying cause of congenital heart disease is frequently unknown. However, advances in human genetics and genome technologies have helped expand congenital heart disease pathogenesis knowledge during the last few decades. When the cardiac defects are part of a genetic syndrome, they are associated with extracardiac conditions and require multidisciplinary care and surveillance. Some genetic syndromes can have subtle clinical findings and remain undiagnosed well into adulthood. Each syndrome is associated with specific congenital and acquired comorbidities and a particular clinical risk profile. A timely diagnosis is essential for risk stratification, surveillance of associated conditions and counselling, particularly during family planning. However, genetic testing and counselling indications can be challenging to identify in clinical practice. This document intends to provide an overview of the most clinically relevant syndromes to consider, focusing on the phenotype and genotype diagnosis, outcome data, clinical guidelines and implications for care.