Cardiac Failure Review最新文献

Cardiovascular disease (CVD) represents a significant threat to women's health. Heart failure (HF) is one CVD that still has an increasing incidence and about half of all cases involve women. HF is characterised by strong sex-specific features in aetiology, clinical manifestation and outcomes. Women are more likely to have hypertensive heart disease and HF with preserved ejection fraction, they experience worse quality of life but have a better overall survival rate. Women's hearts also have unique morphological characteristics that should be considered during cardiovascular assessment. It is important to understand and highlight these sex-specific features to be able to provide a tailored diagnostic approach and therapeutic management. The aim of this article is to review these aspects together with the challenges and the unique characteristics of different imaging modalities used for the diagnosis and follow-up of women with HF.

Heart failure (HF) with preserved left ventricular ejection fraction is a common disease with a poor prognosis and rising prevalence in the community. The current paradigm of treatment includes symptomatic therapy, such as diuretics, and risk factor control and treatment of comorbidities. According to European guidelines, there is no effective therapy for patients with HF with left ventricular ejection fraction (LVEF) ≥50%, while drugs normally used in HF with reduced LVEF might also be effective for patients with mildly reduced LVEF (40-50%), with a IIB class of recommendation. The recently published EMPEROR-Preserved trial has challenged current guidelines, demonstrating improved outcomes in patients with HF and LVEF >40% with the sodium-glucose cotransporter 2 inhibitor (SGLT2I) empagliflozin, compared with placebo. This result was consistent in patients with and without diabetes as well as in those with LVEF below and above 50%. The authors describe the rationale for this therapy, presenting the main results of the EMPEROR-Preserved trial, and provide some recommendations for the everyday clinical management of HF with preserved left ventricular ejection with an SGLT2I.

Despite the high prevalence of heart failure among Black and Hispanic populations, patients of colour are frequently under-prescribed guideline-directed medical therapy (GDMT) and American-Indian populations are not well characterised. Clinical inertia, financial toxicity, underrepresentation in trials, non-trustworthy medical systems, bias and structural racism are contributing factors. There is an urgent need to develop evidence-based strategies to increase the uptake of GDMT for heart failure in patients of colour. Postulated strategies include prescribing all GDMT upon first encounter, aggressive outpatient uptitration of GDMT, intervening upon social determinants of health, addressing bias and racism through changing processes or policies that unfairly disadvantage patients of colour, engagement of stakeholders and implementation of national quality improvement programmes.

Heart failure with preserved ejection fraction (HFpEF) currently accounts for approximately half of all new heart failure cases in the community. HFpEF is closely associated with chronic lifestyle-related diseases, such as obesity and type 2 diabetes, and clinical outcomes are worse in those with than without comorbidities. HFpEF is pathophysiologically distinct from heart failure with reduced ejection fraction, which may explain, in part, the disparity of treatment options available between the two heart failure phenotypes. The mechanisms underlying HFpEF are complex, with coronary microvascular dysfunction (MVD) being proposed as a potential key driver in its pathophysiology. In this review, the authors highlight the evidence implicating MVD in HFpEF pathophysiology, the diagnostic approaches for identifying MVD (both invasive and non-invasive) and the prevalence and prognostic significance of MVD.

Effective treatment for heart failure with preserved ejection fraction (HFpEF) is an unmet need in cardiovascular medicine. The pathophysiological drivers of HFpEF are complex, differing depending on phenotype, making a one-size-fits-all treatment approach unlikely. Remarkably, sodium-glucose cotransporter 2 inhibitors (SGLT2is) may be the first drug class to improve cardiovascular outcomes in HFpEF. Randomised controlled trials suggest a benefit in mortality, and demonstrate decreased hospitalisations and improvement in functional status. Limitations in trials exist, either due to small sample sizes, differing results between trials or decreased efficacy at higher ejection fractions. SGLT2is may provide a class effect by targeting various pathophysiological HFpEF mechanisms. Inhibition of SGLT2 and Na⁺/H⁺ exchanger 3 in the kidney promotes glycosuria, osmotic diuresis and natriuresis. The glucose deprivation activates sirtuins - protecting against oxidation and beneficially regulating metabolism. SGLT2is reduce excess epicardial adipose tissue and its deleterious adipokines. Na⁺/H⁺ exchanger 1 inhibition in the heart and lungs reduces sodium-induced calcium overload and pulmonary hypertension, respectively.

Implementation of guideline-directed medical therapy for patients with heart failure is suboptimal. The use of guideline-directed medical therapy improves minimally after heart failure hospitalisation, despite this event clearly indicating increased risk of further hospitalisation and death. In-hospital initiation and titration of guideline-directed medical therapies is one potential strategy to fill these gaps in care, both in the acute vulnerable period after hospital discharge and in the long term. The purpose of this article is to review the knowledge gaps in best practices of in-hospital initiation and up-titration of guideline-directed medical therapies, the benefits and risks of in-hospital initiation and post-discharge focused titration of guideline-directed medical therapies, the recent literature evaluating these practices, and propose strategies to apply these principles to the care of patients with heart failure with reduced ejection fraction.

Heart failure (HF) is a major health burden associated with significant morbidity and mortality. Approximately half of all HF patients have reduced ejection fraction (left ventricular ejection fraction <40%) at rest (HF with reduced ejection fraction). The aetiology of HF is complex, and encompasses a wide range of cardiac conditions, hereditary defects and systemic diseases. Early identification of aetiology is important to allow personalised treatment and prognostication. Cardiac imaging has a major role in the assessment of patients with HF with reduced ejection fraction, and typically incorporates multiple imaging modalities, each with unique but complimentary roles. In this review, the comprehensive role of cardiac imaging in the diagnosis, assessment of aetiology, treatment planning and prognostication of HF with reduced ejection fraction is discussed.

Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous disorder developing from multiple aetiologies with overlapping pathophysiological mechanisms. HFpEF diagnosis may be challenging, as neither cardiac imaging nor physical examination are sensitive in this situation. Here, we review biomarkers of HFpEF, of which the best supported are related to myocardial stretch and injury, including natriuretic peptides and cardiac troponins. An overview of biomarkers of inflammation, extracellular matrix derangements and fibrosis, senescence, vascular dysfunction, anaemia/iron deficiency and obesity is also provided. Finally, novel biomarkers from -omics technologies, including plasma metabolites and circulating microRNAs, are outlined briefly. A cardiac-centred approach to HFpEF diagnosis using natriuretic peptides seems reasonable at present in clinical practice. A holistic approach including biomarkers that provide information on the non-cardiac components of the HFpEF syndrome may enrich our understanding of the disease and may be useful in classifying HFpEF phenotypes or endotypes that may guide patient selection in HFpEF trials.

A 46-year-old man with systolic heart failure, end-stage renal disease on dialysis, ventricular tachycardia and pulmonary sarcoidosis presented with decompensated heart failure and cardiogenic shock of unknown aetiology. The hospital course was complicated by worsening shock requiring inotropic and mechanical circulatory support, as well as eventual dual heart and kidney transplantation. Cardiac imaging was used to assess the aetiology of the patient's non-ischaemic cardiomyopathy, including a PET scan and cardiac MRI. Imaging demonstrated findings consistent with left ventricular non-compaction, but was inconclusive for cardiac sarcoidosis. After eventual heart transplantation, histopathology of the patient's explanted heart showed evidence of both non-compaction and cardiac sarcoidosis. In this case report, the authors review the pathophysiology of both cardiac sarcoidosis and left ventricular non-compaction, and highlight a multimodality approach to the diagnosis of non-ischaemic cardiomyopathy.