Current Heart Failure Reports最新文献

Transthyretin cardiac amyloidosis (ATTR-CA) is characterised by the deposition of transthyretin amyloid fibrils in the heart. ATTR-CA affects both men and women although there is evidence of sex differences in prevalence and clinical presentation. PURPOSE OF REVIEW: This review paper aims to comprehensively examine and synthesise the existing literature on sex differences in ATTR-CA. RECENT FINDINGS: The prevalence of ATTR-CA is higher in males although the male predominance is more apparent in older patients in the wild type form and in TTR genetic variants that predominantly result in a cardiac phenotype in the hereditary variant. Women tend to have less left ventricular hypertrophy (LVH) and a higher ejection fraction at clinical presentation which may contribute to a later diagnosis although the prognosis appears to be similar in both sexes. Female sex is a predictor of a good response to tafamidis 20 mg in TTR polyneuropathy but otherwise there are no data on sex differences in the efficacy of other treatments for ATTR-CA. It is crucial to define specific sex differences in ATTR-CA. A lower cut-off value for LVH in women may be needed to improve diagnosis. It is necessary to increase female representation in clinical trials to better understand possible sex differences in therapeutic management.

Purpose of review: We summarise the physiological changes and risk factors for hypertension in females, potential sex-specific management approaches, and long-term prognosis.

Key findings: Pregnancy and menopause are two key phases of the life cycle where females undergo significant biological and physical changes, making them more prone to developing hypertension. Gestational hypertension occurs from changes in maternal cardiac output, kidney function, metabolism, or placental vasculature, with one in ten experiencing pregnancy complications such as intrauterine growth restriction and delivery complications such as premature birth. Post-menopausal hypertension occurs as the protective effects of oestrogen are reduced and the sympathetic nervous system becomes over-activated with ageing. Increasing evidence suggests that post-menopausal females with high blood pressure (BP) experience greater risk of cardiovascular events at lower BP thresholds, and greater vulnerability to treatment-related adverse effects. Hypertension is a key risk factor for cardiovascular disease in females. Current BP treatment guidelines and recommendations are similar for both sexes, without addressing sex-specific factors. Future investigations into ideal diagnostic thresholds, BP control targets and treatment regimens in females are needed.

Purpose of review: People with HIV have an elevated risk of developing heart failure even with optimally controlled disease. In this review, we outline the various mechanisms through which HIV infection may directly and indirectly contribute to heart failure pathology and highlight the emerging relationship between HIV, chronic inflammation, and cardiometabolic disease.

Recent findings: HIV infection leads to chronic inflammation, immune dysregulation, and metabolic imbalances even in those with well controlled disease. These dysregulations occur through several diverse mechanisms which may lead to manifestations of different phenotypes of heart failure in people with HIV. While it has long been known that people with HIV are at risk of developing heart failure, recent studies have suggested numerous complex mechanisms involving chronic inflammation, immune dysregulation, and metabolic derangement through which this may be mediated. Further comprehensive studies are needed to elucidate the precise relationship between these mechanisms and the development of different subtypes of heart failure in people with HIV.

Purpose of review: Limited research has been conducted on sex disparities in heart transplant (HT). The aim of this review is to analyse the available evidence on the influence of sex and gender-related determinants in the entire HT process, as well as to identify areas for further investigation.

Recent findings: Although women make up half of the population affected by heart failure and related mortality, they account for less than a third of HT recipients. Reasons for this inequality include differences in disease course, psychosocial factors, concerns about allosensitisation, and selection or referral bias in female patients. Women are more often listed for HT due to non-ischaemic cardiomyopathy and have a lower burden of cardiovascular risk factors. Although long-term prognosis appears to be similar for both sexes, there are significant disparities in post-HT morbidity and causes of mortality (noting a higher incidence of rejection in women and of malignancy and cardiac allograft vasculopathy in men). Additional research is required to gain a better understanding of the reasons behind gender disparities in eligibility and outcomes following HT. This would enable the fair allocation of resources and enhance patient care.

Purpose of review: Hypertrophic cardiomyopathy (HCM) is a common inherited cardiac condition with potential for severe complications including sudden cardiac death. Early diagnosis allows appropriate risk stratification and prompt intervention to minimise the potential for adverse outcomes. The implications of poorly coordinated screening are significant, either missing relatives at high-risk or burdening low-risk individuals with a diagnosis associated with reduced life expectancy. We aim to guide clinicians through the diagnostic pathway through to novel treatment options. Several conditions mimic the condition, and we discuss the phenocopies and how to differentiate from HCM.

Recent findings: We summarise the latest developments informing clinical decision making in the modern era of myosin inhibitors and future gene editing therapies. Early identification will enable prompt referral to specialist centres. A diagnostic flowchart is included, to guide the general cardiology and heart failure clinician in important decision making regarding the care of the HCM patient and importantly their relatives at risk. We have highlighted the importance of screening because genotype-positive/phenotype-negative patients are likely to have the most to gain from novel therapies.

Purpose of review: This article summarizes the role of coagulation factors in the pathophysiology of heart failure including D-dimer, fibrinogen and fibrin, prothrombin, p-selectin, tissue factor, tissue plasminogen activator, von Willebrand factor, β-thromboglobulin, Factor XI, tissue thromboplastin, plasminogen activator inhibitor-1 (PAI-1), thrombomodulin, soluble urokinase-type plasminogen activator receptor (suPAR) and stuart-prower factor.

Recent findings: The D-dimer, P-selectin, prothrombin, von Willebrand factor, tissue plasminogen activator, fibrinogen, suPAR, tissue factor, thrombomodulin and Factor XI play significant roles the pathophysiology of heart failure. However, no associations were found between β-thromboglobulin, tissue thromboplastin, PAI-1 and stuart-prower factor in the context of heart failure. Coagulation factors play significant role in the pathophysiology of heart failure. Consequently, the underlying pathophysiological mechanisms that explain changes in the cascade are closely related to the diagnostic, prognostic and therapeutic roles of coagulation cascade factors, which help physicians identify and treat heart failure.

Purpose of review: This review examines the available evidence concerning the incidence of heart failure in patients with chronic coronary syndrome, with a focus on gender differences.

Recent findings: The incidence of heart failure in the context of chronic coronary syndrome presents conflicting data. Most of the available information stems from studies involving stable patients' post-acute coronary syndrome, revealing a wide range of incidence rates, from less than 3% to over 20%, observed over 5 years of follow-up. Regarding the gender differences in heart failure incidence, there is no consensus about whether women exhibit a higher incidence, particularly in the presence of evidence of obstructive coronary artery disease. However, in cases where obstructive coronary artery disease is absent, women may face a more unfavourable prognosis due to a higher prevalence of microvascular disease and heart failure with preserved ventricular function. The different profile of ischaemic heart disease in women difficult to establish differences in prognosis independently associated with female sex. Targeted investigations are essential to discern the incidence of heart failure in chronic coronary syndrome and explore potential gender-specific associations.

Purpose of review: To provide an overview of (a) protective effects on mitochondria induced by remote ischemic conditioning (RIC) and (b) mitochondrial damage caused by anticancer therapy. We then discuss the available results of studies on mitochondrial protection via RIC in anticancer therapy-induced cardiotoxicity.

Recent findings: In three experimental studies in healthy mice and pigs, there was a RIC-mediated protection against anthracycline-induced cardiotoxicity and there was some evidence of improved mitochondrial function with RIC. The RIC-mediated protection was not confirmed in the two available studies in cancer patients. In adult cancer patients, RIC was associated with an adverse outcome. There are no data on mitochondrial function in cancer patients. Studies in tumor-bearing animals are needed to determine whether RIC does not interfere with the anticancer properties of the drugs and whether RIC actually improves mitochondrial function, ultimately resulting in improved cardiac function.

Purpose of review: Differences in HF biomarker levels by sex may be due to hormonal, genetic, and fat distribution differences. Knowledge of these differences is scarce, and it is not well established whether they may affect their usefulness in the management of HF.

Recent findings: The different biomarker profiles in women and men have been confirmed in recent studies: in women, markers of cardiac stretch and fibrosis (NP and galectin-3) are higher, whereas in men, higher levels of markers of cardiac injury and inflammation (cTn and sST2) are found. The use of new biomarkers, together with growing evidence that a multimarker approach can provide better risk stratification, raises the question of building models that incorporate sex-specific diagnostic criteria. More and more research are being devoted to understanding sex-related differences in HF. The aim of this review is to review the dynamics of HF biomarkers according to sex and in different situations, to learn whether these sex differences may affect their use in the diagnosis and follow-up of HF patients.

Purpose of review: End stage kidney disease can be a slow process and it may be challenging to achieve required follow-up for sufficient events. Therefore, a surrogate kidney endpoint, such as estimated glomerular filtration rate (eGFR) slope maybe attractive to assess the kidney in cardiovascular trials, especially heart failure (HF).

Recent findings: eGFR slope can generate informative results in a shorter follow-up period, has decreased risk of type-2 error, and is less sensitive to eGFR shifts compared with other surrogate kidney endpoints (eGFR decline≥40% or doubling creatinine). However, eGFR slope has its limitations with acute effects, heterogeneity in slope calculation/reporting, and deviations from linearity. eGFR slope is a kidney endpoint which may be well-suited for HF trials. Cross-collaborated guideline recommendations are needed to optimize the use of eGFR slope as a kidney endpoint in patients with HF.