Canadian Journal of Cardiology最新文献

Background: Atrial fibrillation (AF) is prevalent in older adults and has been associated with functional decline beyond its cardiovascular complications. However, the interplay between AF, multimorbidity, and functional decline remains poorly understood. In this study we investigated the effect of AF and multimorbidity on longitudinal transitions in functional status among older adults, considering initial self-sufficiency levels.

Methods: This longitudinal analysis included 3083 community-dwelling individuals aged 65 years or older from the Progetto Veneto Anziani (Pro.V.A.) study. Functional status was classified into 3 states-independent, moderately impaired, and severely impaired in activities of daily living-and modelled through continuous-time multistate models. Independent variables included AF, multimorbidity, and covariates such as age, sex, education, living arrangements, smoking status, body mass index, Mini-Mental State Examination and Geriatric Depression Scale scores.

Results: Over a median follow-up of 4.4 years (standard deviation, 0.5), 33.5% of independent individuals experienced functional decline, 13% died, and only 12.2% improved after moderate impairment. AF was significantly associated with transition from independence to severe functional impairment (hazard ratio [HR], 4.12; 95% confidence interval [CI], 1.83-9.24), although this estimate is on the basis of a small number of events and should be interpreted with caution, from moderate to severe impairment (HR, 1.75; 95% CI, 1.01-3.1), and with mortality in moderately impaired individuals (HR, 1.66; 95% CI, 1.16-2.38). Multimorbidity showed no association with worsening transitions but was associated with mortality among independent individuals (HR, 1.15; 95% CI, 1.07-1.24).

Conclusions: AF is a marker of greater risk of severe functional decline in older adults, whereas multimorbidity primarily increases mortality. Routine functional assessments and person-centred interventions are essential to preserve autonomy and prevent disability in older adults with AF.

Lipoprotein(a) [Lp(a)] is a genetically determined and independent risk factor for atherosclerotic cardiovascular disease, including acute coronary syndrome, peripheral arterial disease, and stroke, as well as calcific aortic stenosis. Despite its high prevalence, affecting an estimated 20% of Canadians, Lp(a) remains under-recognized and undermeasured in clinical practice. This report provides guidance on the assessment and management of Lp(a) in primary and secondary prevention in the Canadian context. It outlines when and how to measure Lp(a), with a recommendation for universal, one-time testing in adulthood. The report summarizes the pathophysiologic role of Lp(a) in promoting atherosclerosis, thrombosis, and aortic stenosis, and highlights significant ethnic variability in Lp(a) levels and associated risk. It also addresses the limitations of existing cardiovascular risk calculators that omit Lp(a) and discusses the potential role of emerging imaging and treatment strategies, including novel Lp(a)-lowering therapies. Special attention is given to clinical interpretation of Lp(a) values, the role of cascade screening in families, and recommendations for preventive interventions, with an emphasis on current approaches for managing patients with elevated Lp(a) level while awaiting the availability of targeted therapies. The goal of this report is to support clinicians in identifying at-risk individuals earlier and guiding appropriate risk reduction strategies in primary and secondary prevention settings.

The objective of diagnostic investigations should be to confirm or refute the presence of abnormal coronary function and to identify patients who might benefit from specific therapeutic interventions. In the field of coronary microvascular and vasomotor dysfunction, progress toward this goal is hampered if diagnostic pathways differ among sites, the meaning of the results are unclear, or the potential benefits of current therapies are not well established. In this second companion paper, we define the metrics that can be derived from the invasive assessment of the coronary function assessed in the Canadian Coronary Physiology Registry, discuss the theoretical and practical value and limitations of singular vs multiple combined metrics, and propose a flexible interpretative framework. We also provide early phenomapping analysis of the noninvasive data, which both confirm the complexity and demonstrate the power of machine learning to unravel this problem. The combination of the multiple invasive metrics with the comprehensive clinical assessment will determine the phenotypic and pathophysiological relevance of these metrics that will guide further research efforts.

Background: The long-term efficacy of stent extension in thoracic endovascular aortic repair (TEVAR) for Stanford type B aortic dissection (TBAD) has not been thoroughly evaluated.

Methods: This retrospective multicentre study included patients with TBAD undergoing TEVAR between 2014 and 2021. On the basis of distal descending aorta coverage, patients were stratified into stent extension (SE) and nonstent extension (non-SE) groups. Stent extension was defined as the intentional distal placement of an additional covered stent to lengthen the repair zone within the descending aorta. After 1:1 propensity score matching (PSM) to balance baseline and perioperative characteristics, long-term outcomes were compared. Multivariate regression analysis identified risk factors.

Results: Among 511 enrolled patients with a median age of 56 (51-63) years, 241 patients received stent extension, and the average follow-up time was 69.4 months. After PSM (131 pairs), the groups were comparable. The SE group showed significantly lower rates of aortic-related mortality (3.8% vs 10.7%; P = 0.032), negative aortic remodelling (13.7% vs 23.7%; P = 0.039), follow-up entry flow (8.4% vs 18.3%; P = 0.018), and reoperation (3.8% vs 11.5%; P = 0.020). Stent extension was a protective factor against entry flow (odds ratio [OR], 0.67; P = 0.014) and negative remodelling (OR, 0.73; P = 0.002). Risk factors included smaller true lumen diameter and patent false lumen for entry flow and patent false lumen with multiple distal tears for negative remodelling. Entry flow independently predicted aortic-related mortality (OR, 3.54; P < 0.001) and reoperation (OR, 5.63; P < 0.001).

Conclusions: Stent extension during TEVAR for TBAD is associated with improved long-term outcomes, reducing complications and reinterventions. Prospective trials are warranted for validation.

Clinical trial registration: ▪.

Inherited arrhythmia syndromes predispose to malignant arrhythmic events, including cardiac arrest and sudden cardiac death, which can be particularly catastrophic in young and otherwise healthy individuals. Despite considerable progress in clinical management in recent decades, the therapeutic options for many conditions remain limited and often expose patients to significant side effects that impair quality of life. There is therefore a pressing need for more effective and better-tolerated therapies. Owing to the predominantly monogenic nature of these diseases, and in light of the remarkable advances in molecular biology over the past two decades, gene therapies offer unprecedented potential by directly targeting the molecular determinants of arrhythmogenesis. In this review, we discuss advances in nucleic acid-based therapies for inherited cardiac arrhythmias, highlighting preclinical successes-some already progressing to first-in-class clinical trials-as well as the existing limitations. In light of accumulating preclinical evidence, we also discuss the impact of heterogeneous cardiac transduction/transfection by gene therapy vectors for arrhythmia treatment, a critical yet underexplored concept that carries theoretical concerns for pro-arrhythmia, but may also offer therapeutic opportunities. Finally, we briefly review future directions for the field, including the development of nucleic acid-based therapeutics for more prevalent arrhythmic disorders, such as post-myocardial infarction ventricular tachycardia and atrial fibrillation.