Cardiac Failure Review最新文献

Heart failure (HF) and cardiac amyloidosis (CA) are significant clinical challenges, with evolving epidemiological patterns reshaping the understanding of these conditions. Traditionally linked with HF with preserved ejection fraction, CA is increasingly recognised for its specific characteristics, including a considerable subset of patients presenting with reduced left ventricular ejection fraction. This review explores how the neurohormonal activation observed in CA impacts on disease progression and management strategies. Historically, neurohormonal antagonists were considered contraindicated in CA owing to concerns about autonomic dysfunction and chronotropic incompetence. However, recent evidence suggests a paradigm shift, indicating that such agents may offer therapeutic benefits even in these patients. By examining these developments, this review provides a comprehensive overview of current therapeutic approaches, the role of neurohormonal modulation and the need for personalised care strategies to address the complexities of HF in the context of CA.

Recent advances in the pharmacological therapy of heart failure with reduced ejection fraction (HFrEF) have significantly impacted the overall survival, heart failure hospitalisations and rates of sudden cardiac death (SCD). In this context, the relevant timing of placing ICDs as primary prevention is a matter of on-going debate. This manuscript provides evidence for an updated view regarding the timing of implanting ICD in eligible patients with HFrEF receiving optimal guideline-directed medical therapy, accounting for the timing to reverse cardiac remodelling (RCR) occurrence and residual SCD risks over time. Clinically significant RCR occurs beyond 3 months of optimal guideline-directed medical therapy, while the residual risks of SCDs remain low for certain HFrEF populations. However, when deciding on ICD implantation, one should always consider individual modulators of RCR and SCD risks, as well as the non-competing risks of death that can affect patients' overall outcomes. Risk stratification algorithms need to be developed and validated in future pragmatic clinical trials to further define better timing for the use of ICDs in primary prevention.

Background: Weaning and tracheal extubation of patients after vascular surgery is a stressful procedure that triggers the sympathetic nervous system, potentially leading to deterioration of cardiac performance in patients with left ventricular dysfunction. This study compared the efficacy and safety of landiolol, a novel ultra-short-acting β₁-adrenoceptor antagonist, with that of esmolol in terms of the cardiovascular response during the extubation of patients with reduced ejection fraction (EF) admitted to the intensive care unit after major vascular surgery.

Methods: This single-centre, prospective, randomised, open-label study included postoperative patients with cardiac dysfunction. Patients were randomly assigned to either landiolol or esmolol. Landiolol and esmolol infusions began as soon as the respiratory weaning procedure started, and were initiated at doses of 1 and 50 µg/kg/min, respectively (up to 10 and 200 µg/kg/min, respectively). Heart rate, systolic arterial pressure, diastolic arterial pressure, mean arterial pressure (MAP) and cardiac rhythm were recorded every minute up to 30 minutes after extubation.

Results: Thirty-nine patients with cardiac dysfunction (mean [±SD] left ventricular EF 36.6 ± 7.6%; New York Heart Association Class II/III, 32/9) were infused with either landiolol (n=19; mean rate 2.0 ± 2.1 μg/kg/min) or esmolol (n=20; mean rate 150 ± 50 μg/kg/min). Mean age, left ventricular EF, New York Heart Association class and Acute Physiology and Chronic Health Evaluation II and Sequential Organ Failure Assessment scores were similar between the two groups. Landiolol produced a more rapid and substantial decrease in heart rate than esmolol (-40 ± 20 BPM versus -30 ± 16 BPM) without haemodynamic deterioration. A significant reduction in MAP was recorded in the esmolol group.

Conclusion: Landiolol produced a more rapid and potent reduction in heart rate than esmolol. A significant reduction in MAP was only seen in the esmolol group.

Background: For patients eligible for both mechanical and bioprosthetic valves, postoperative quality of life (QOL) is a key factor in determining the type of prosthetic valve used.

Methods: We reviewed patients aged 60-65 years who underwent isolated aortic valve replacement at our centre. Postoperative QOL was assessed through a telephone follow-up using the 36-item Short Form Health Survey questionnaire.

Results: A total of 628 valid survey responses were collected, comprising 353 patients with mechanical valves and 275 with bioprosthetic valves. The mean age of the patients was 62.5 ± 1.7 years, and 363 (57.8%) were men. The mean follow-up period was 7.3 ± 3.9 years. There were no significant differences in any QOL subscale or the overall 36-item Short Form Health Survey score between patients with mechanical and bioprosthetic valves. BMI (β=-0.109, p=0.014) and postoperative time (β=-0.251, p<0.001) were the independent predictors of QOL, after adjusting for factors, such as age at the time of surgery, sex, ejection fraction, type of prosthesis and prosthesis effective orifice area index. The rates of stroke and cardiovascular reintervention per patient-year were similar between the two groups. However, in those 12 years after aortic valve replacement, mechanical valves seemed to perform better.

Conclusion: In patients aged 60-65 years undergoing isolated aortic valve replacement, there is no significant difference in postoperative QOL between those receiving mechanical or bioprosthetic valves, but mechanical valves seemed to perform better in the late period.

Despite therapeutic and technological advances, the prognosis for patients with heart failure (HF) remains poor. One reason for this poor prognosis lies in the limited usage of disease-modifying therapies, such as β-blockers, renin-angiotensin system inhibitors, mineralocorticoid receptor antagonists and sodium-glucose cotransporter 2 inhibitors, namely guideline-directed medical therapy (GDMT). Concurrently, technological advances have led to the development of numerous strategies for both invasive and non-invasive telemonitoring of HF patients, potentially intercepting a phase of decompensation before its overt clinical manifestation. As clinical guidelines and the healthcare landscape continue to evolve, HF management is increasingly focusing on integrating advanced technologies and empowering patients and care teams. Traditionally, diuretics have been the cornerstone of preventing HF decompensation because of their decongestive effects. However, emerging evidence suggests that the components of GDMT also exert decongestive effects, alongside their broader positive prognostic impact. The synergistic relationship between GDMT and telemonitoring devices offers a promising approach to congestion management. By adopting protocols that leverage both the pharmacological and non-pharmacological mechanisms of GDMT, care teams can maximise patient outcomes while addressing therapeutic inertia. This narrative review explores the potential for a paradigm shift, emphasising the early and consistent implementation of GDMT, supported by digital health solutions, to improve outcomes from the early stages of HF decompensation.

Background: The growing obesity epidemic highlights the need to understand how various obesity phenotypes affect myocardial structure and increase non-ischaemic cardiomyopathy (NICM) incidence. The aim of this study was to investigate the causal effect of eight obesity-related traits on NICM and 16 cardiac MRI parameters. Potential mediators between obesity and NICM were also investigated.

Methods: Two-sample Mendelian randomisation was used to explore the causal relationship between eight obesity-related traits and NICM and assess their impact on cardiac MRI indicators. The study also used validation dataset analysis and multivariable Mendelian randomisation to ensure robustness, and mediation Mendelian randomisation analysis to identify metabolic markers as potential mediators.

Results: All eight obesity-related traits demonstrated a causal relationship with NICM, with the relationship between BMI and NICM persisting after adjustment for LDL cholesterol, urate level and hypertension (HTN). These traits also influenced arterial and cardiac structure and function, especially with regard to left ventricular mass. HTN was identified as a significant mediator, with a mediation effect ratio of 31%.

Conclusion: There is a robust causal association between obesity and NICM, and with abnormalities in myocardial structure and function. HTN emerges as a pivotal mediator in the obesity-NICM pathway, underscoring the critical role of managing obesity and HTN in preventing NICM progression.

Background: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic is still a burden for healthcare systems worldwide. Now, the focus is not only on acute infections, but also on the long-term effects of COVID-19. The present study aimed to evaluate the impact of SARS-CoV-2 infection on the cardiovascular system, and determine the evolution of these changes over 6 months in patients with mild and moderate COVID-19.

Methods: The prospective observational study included 103 patients with mild and moderate COVID-19. The patients underwent an echocardiography and a measurement of the arterial stiffness parameters at baseline and 6 months from the initial assessment.

Results: The diastolic dysfunction (the left atrium volume) was statistically significant at baseline and at the 6-month follow-up in men with moderate COVID-19. The ejection fraction presented significant differences globally in mild versus moderate COVID-19 (p=0.043) that disappeared at 6-month follow-up. Global longitudinal strain alterations were also found in both mild and moderate COVID-19 cases. Regarding the aortic pulse wave velocity, the SARS-CoV-2 infection did not influence the arterial stiffness. Ventricular arterial coupling was significantly altered in moderate COVID-19 at the 6-month evaluation (p=0.0218). Male patients presented a lower tricuspid annular plane systolic excursion at baseline. Right ventricular systolic dysfunction was more frequent among men. Systolic pulmonary arterial pressure increased significantly only in men with moderate disease. Additionally, statistically significant changes at baseline and at 6 months were found regarding the intima-media thickness.

Conclusion: This study shows the cardiovascular long-term sequelae associated with COVID-19 in mild and moderate cases, and emphasises the appropriate investigations for their diagnosis and follow-up.

Hypertrophic cardiomyopathy (HCM) is a complex genetic disorder that has garnered significant attention because of its diverse manifestations, including arrhythmias and heightened risk of sudden cardiac death. Advances in precision diagnostics, such as genetic testing and cardiac imaging with late gadolinium enhancement, have refined HCM diagnosis, enabling targeted therapeutic and risk stratification approaches. AF, prevalent in HCM, exacerbates symptoms and stroke risk, while ventricular arrhythmias pose a direct threat to survival. Catheter ablation offers symptom relief in AF patients with HCM, yet recurrence remains high because of unique myocardial changes, highlighting the need for refined patient selection and long-term monitoring. The risk of sudden cardiac death in HCM, particularly in younger individuals, underscores the importance of precise risk stratification tools such as the European Society of Cardiology HCM Risk-SCD model. The expanding role of ICDs and emerging pharmacological agents, including myosin inhibitors, marks a shift toward more individualised management of HCM. This review integrates recent developments in arrhythmia management, targeted therapies and risk assessment, offering a comprehensive perspective on HCM tailored to improve clinical outcomes through a precision-medicine lens.

Congestion is the hallmark and the main therapeutic target in patients with decompensated heart failure (HF). Residual clinical congestion is defined as a high left ventricular diastolic pressure associated with signs and symptoms of HF, such as dyspnoea, rales and oedema, persisting despite guideline-directed medical treatment. Residual congestion in the predischarge and early post-discharge phase is the major risk factor for HF readmission and mortality. Therefore, prompt recognition of congestion and rapid optimisation of medical and device therapy are crucial to induce remission in this malignant process. In this paper we discuss the definitions, prevalence and prognosis of HF decompensation; the significance of assessing residual congestion in HF patients; the results of observational and randomised clinical trials to detect and treat residual congestion; and the current guidelines to prevent recurrent HF decompensation in the context of residual congestion. Strategies to detect and address residual congestion are crucial to stopping readmissions after an acute HF hospitalisation and improving long-term prognosis.

The concept of heart failure (HF) has undergone significant transformation from ancient times to the present, evolving from rudimentary understandings to a complex clinical syndrome. Early descriptions by Egyptian, Greek and Roman physicians laid the groundwork for understanding cardiac dysfunction. The Renaissance period brought crucial insights with Harvey's discovery of blood circulation. In the 20th century, the Framingham Heart Study provided a pivotal shift, formally defining HF as a clinical syndrome with diagnostic criteria. Over the decades, definitions of HF have evolved, integrating advancements in pathophysiology, biomarkers and imaging techniques. Initially focused on symptomatic and clinical presentations, modern definitions emphasise underlying structural and functional cardiac abnormalities. This evolution reflects the growing complexity and precision of diagnosing and managing HF. A historical perspective underscores the progressive refinement in HF definitions, which enhances diagnostic precision and therapeutic strategies, ultimately improving patient outcomes. Understanding this evolution is crucial for appreciating contemporary HF management and anticipating future advances.