Canadian Journal of Cardiology最新文献

Background: Postoperative myocardial injury is correlated with long-term prognosis after coronary artery bypass grafting (CABG) and is diagnosed according to troponin levels, which vary substantially upon surgical strategies. We aimed to explore the troponin I cutoff values for prognostically significant myocardial injury separately in on-pump and off-pump procedures with the use of a high-sensitivity assay (hs-cTnI).

Methods: Patients who underwent isolated CABG from 2018 to 2020 with available perioperative hs-cTnI measurements were included in this study. We explored the relationships between hs-cTnI levels and different outcomes. To identify hs-cTnI threshold levels indicative of higher risks, restrictive spline regressions were performed for on-pump and off-pump procedures.

Results: A total of 7813 patients were included with a median follow-up of 2.7 years (interquartile range 1.7-3.3 years), 218 (2.8%) of whom died. Adjusting for clinical variables, the study found a significant association between peak hs-cTnI levels within the first 48 hours after surgery and all end points. The spline regressions demonstrated that the hs-cTnI levels measured within 48 hours after surgery that were associated with a hazard ratio of more than 1.00 for all-cause death were 1446 ng/L (55.6 × upper reference limit [URL], 95% confidence interval [CI] 45.0-106.5 × URL) for on-pump and 564 ng/L (21.7 × URL, 95% CI 21.0-30.2 × URL) for off-pump.

Conclusions: Elevated hs-cTnI levels after CABG were associated with poorer longer-term outcomes. A prognosis-relevant hs-cTnI cutoff value within 48 hours after CABG for on-pump is significantly higher than that for off-pump.

Background: Congenital heart disease (CHD) affects 1% of live births and is a risk factors for cardiovascular disease and reduced life expectancy. Previous studies have suggested CHD is associated with impaired vascular health, but this has not been established. Therefore, the objective of this study was to examine the impact of congenital heart disease (CHD) on vascular health.

Methods: Eight electronic databases were searched through April 12, 2024. Studies of all designs (except case studies and reviews) which reported on the population (individuals with CHD of any age), comparator (individuals without CHD), and outcomes of interest: endothelial dependent (flow-mediated vasodilation [FMD%], reactive hyperemia index [RHI]) and independent (nitroglycerine mediated dilation [NMD%]) vascular function, arterial stiffness (pulse-wave velocity [PWV], stiffness index [SI], augmentation index [AIx], distensibility and compliance), and carotid intima-media thickness (cIMT) were included. Results are presented as standardized mean differences and 95% confidence intervals and by effect size.

Results: 138 studies (N=16,115) were included in the meta-analysis. Individuals with CHD exhibited decreased vascular function compared to those without including decreased FMD% -0.96, 95% CI: -1.22, -0.70, I²= 85%, large effect size), RHI by ultrasound -2.88, 95% CI: -4.85, -0.90, I² =96%, large effect size), and NMD% -0.98; 95% CI: -1.35, -0.61, I²= 87%, large effect size). Various CHD subtypes including, coarctation of the aorta, transposition of the great arteries, tetralogy of Fallot, post-Fontan showed significant vascular dysfunction. Shunt lesions did not show significant vascular dysfunction.

Conclusion: CHD is associated with vascular dysfunction, increased arterial stiffness and greater cIMT in both pediatric and adult patients. PROSPERO registration number: CRD42022369180.

In cardiomyocytes, transverse tubules (T-tubules) are sarcolemmal invaginations that facilitate excitation-contraction coupling and diastolic function. The clinical significance of T-tubules has become evident in that their remodelling is recognised as a hallmark feature of heart failure (HF) and a key contributor to disrupted Ca²⁺ homeostasis, compromised cardiac function, and arrhythmogenesis. Further investigations have revealed that T-tubule remodelling is particularly pronounced in HF with reduced ejection fraction (HFrEF), but not in HF with preserved ejection fraction, implying that T-tubule remodelling may play a crucial pathophysiologic role in HFrEF. While research on the functional importance of T-tubules is ongoing, T-tubule remodelling has been found to be reversible. That finding has triggered a surge in studies aimed at identifying specific therapeutic approaches for HFrEF. This review discusses the functional importance of T-tubules and their microdomains, the pathophysiology of T-tubule remodelling, and the potential mechanisms of current HFrEF therapeutic approaches in reversing T-tubule alterations. We also highlight discrepancies regarding the roles of T-tubule proteins in the recovery process across studies to offer valuable insights for future research.

Hypertension represents the major risk factor in the onset of cardiovascular disease worldwide. Preclinically, several mouse models of hypertension have been developed to investigate the pathophysiological link between hypertension and vascular impairment. Specifically, angiotensin-II infusion, transverse aortic constriction, deoxycorticosterone acetate salt, and N(ω)-nitro-L-arginine methyl ester (L-NAME) administration as hypertensive stimuli at the preclinical level permit the unveiling of a proinflammatory response driven by the innate and adaptive immune system and leads to vascular injury in terms of structural and functional alterations. Vascular impairment seems to be particularly critical at the cerebral level wherein arterioles, venules, and capillaries finely tune blood supply across the whole brain leading to the onset of a well known clinical condition named cerebral small vessel disease (cSVD) characterized by extensive brain injury, which culminates in the decline of cognitive functions. Advances in magnetic resonance imaging permit identification and accurate diagnosis of specific cSVD biomarkers including white matter hyperintensities, lacunar strokes, cerebral microbleeds, and enlarged perivascular spaces, each of which proved to be associated with a specific cognitive domain impairment. Such an approach in combination with pharmacological interventions targeted to the lowering of blood pressure and the prevention of vascular thrombosis formation represents a solid strategy in the prevention and the management of cSVD cognitive decay.

Heart failure (HF) is a highly comorbid condition associated with significant mortality, despite advances in current medical management. Patients who suffer from HF represent a high needs disease care population in whom structured, long-term chronic disease care delivery models, such as cardiac rehabilitation (CR), have been shown to be highly cost effective in reducing hospitalizations and improving quality of life. HF with reduced ejection fraction affects a growing number of Canadians and health care costs secondary to this condition are increasing, with further increases over the next decade to be expected. CR is a guideline-directed medical therapy for patients living with HF with reduced ejection fraction, and with increasing numbers of HF patients across the world, there is a prescient need to revisit the benefits, safety, and the prescription of this intervention for the health care professionals who treat this condition. Certainly, there is a clinical need for HF practitioners to better understand the pathophysiological benefits of CR with respect to exercise training, as well as the prudent precautions required to facilitate the safe delivery of this highly cost-effective patient intervention.