Heart failure

doi:10.1016/S0140-6736(05)66621-4

The Lancet

Volume 365, Issue 9474, 28 May–3 June 2005, Pages 1877-1889

https://doi.org/10.1016/S0140-6736(05)66621-4 Get rights and content

Summary

Although heart failure is common, disabling, and deadly, there are now many effective treatments, at least for patients with low left-ventricular ejection fraction. For all, angiotensin-converting-enzyme inhibitors and β blockers are the essential disease-modifying treatments, improving symptoms, reducing hospital admissions, and increasing survival. Implantable cardioverter defibrillators also improve survival. For patients with persistent symptoms, angiotensin-receptor blockers and aldosterone antagonists have additional benefits. These treatments are now preferred to digoxin, although this drug can still be useful at an earlier stage in patients with atrial fibrillation. In some patients with persistently severe symptoms and a wide QRS on the electrocardiogram, cardiac resynchronisation therapy also reduces mortality and morbidity. The role of other markers of ventricular dys-synchrony is under investigation. There is growing evidence that left-ventricular assist devices are indicated in some patients with end-stage heart failure. Organised delivery of care also improves outcome. However, there is still no firmly evidence-based treatment for heart failure with preserved ejection fraction. Many new pharmacological, device, and surgical treatments for heart failure are currently under evaluation in clinical trials, and other approaches, including stem-cell treatment, are at an earlier stage of investigation.

Section snippets

Epidemiology

The epidemiology of symptomatic heart failure in more developed countries is well understood (figure 1).1, 2, 3, 4, 5, 6, 7, 8, 9 Between 1% and 2% of the adult population have heart failure, although it mainly affects elderly people; 6–10% of people over the age of 65 years have the disorder.1, 2, 3, 4, 5, 6, 7, 8, 9, 10 The lifetime risk of developing heart failure is roughly one in five for a person aged 40 years.11, 12 The age-adjusted incidence of heart failure has remained stable over the

Aetiology and pathophysiology

The syndrome of heart failure arises as a consequence of an abnormality in cardiac structure, function, rhythm, or conduction. In more developed countries, ventricular dysfunction is the commonest underlying problem. It results mainly from myocardial infarction (systolic dysfunction), hypertension (diastolic and systolic dysfunction), or in many cases both. Degenerative valve disease is becoming more common. Other common causes include “idiopathic” dilated cardiomyopathy, some cases of which

Comorbidity

Heart failure does not occur in isolation. It is caused by an underlying cardiac defect, generally in elderly individuals, many of whom are being treated for other medical problems. Consequently, many patients with heart failure have comorbidity related to the underlying cardiac problem or its cause (eg, angina, hypertension, diabetes, smoking-related lung disease) and age (eg, osteoarthritis), as well as a consequence of heart failure (eg, arrhythmias) and its treatment (eg, gout from

Diagnosis

Heart failure can present suddenly, as the consequence of an acute cardiac event such as myocardial infarction, chronically, in most cases in the community to a primary-care physician, or in an acute-on-chronic fashion, when a period of worsening symptoms and signs is followed by an emergency presentation with decompensation. Most of the cardinal symptoms (dyspnoea and fatigue) and signs (peripheral oedema) of heart failure are non-specific, especially in elderly patients, and could be due to

Treatment

An understanding of the pathophysiology and natural history of heart failure underpins the therapeutic approaches used to achieve the goals of treatment, which are to relieve symptoms, to avoid hospital admission, and to prolong life. On the basis of a large number of randomised controlled trials (table 1), drugs are the mainstay of treatment of all patients with heart failure and reduced left-ventricular systolic function. How care is organised and delivered can also influence outcome,⁹¹ and

Further challenges and directions

Despite the impressive number of effective treatments available, patients with heart failure continue to experience progressively worsening symptoms, frequent admission to hospital, and premature death. Better treatments are needed, although additional drugs will exacerbate the problem of polypharmacy; there is increasing interest in finding better options rather than in simply adding extra treatments. Comorbidity seems to be an increasing problem, which in many cases limits the use of proven

Search strategy and selection criteria

This Seminar is based on a PubMed search for articles with “heart failure” or “cardiac failure” in their titles, as well as reading of other review articles, major guidelines, and book chapters. We prioritised more recently published papers and those published in journals with high impact factors. Owing to space constraints, we could not cite all articles that support statements made. There was no restriction on language or date of publication.

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Cited by (735)

Profile of serum microRNAs in heart failure with reduced and preserved ejection fraction: Correlation with myocardial remodeling
2024, Heliyon
Cardiomyocyte hypertrophy and interstitial fibrosis are key components of myocardial remodeling in Heart Failure (HF) with preserved (HFpEF) or reduced ejection fraction (HFrEF). MicroRNAs (miRNAs) are non-coding, evolutionarily conserved RNA molecules that may offer novel insights into myocardial remodeling. This study aimed to characterize miRNA expression in HFpEF (LVEF $\geq$ 45%) and HFrEF (LVEF < 45%) and its association with myocardial remodeling.
Prospectively enrolled symptomatic HF patients (HFpEF:n = 36; HFrEF:n = 31) and controls (n = 23) underwent cardiac magnetic resonance imaging with T1-mapping and circulating miRNA expression (OpenArray system).
13 of 188 miRNAs were differentially expressed between HF groups (11 downregulated in HFpEF). Myocardial extracellular volume (ECV) was increased in both HF groups (HFpEF 30 ± 5%; HFrEF 30 ± 3%; controls 26 ± 2%, p < 0.001). miR-128a-3p, linked to cardiac hypertrophy, fibrosis, and dysfunction, correlated positively with ECV in HFpEF (r = 0.60, p = 0.01) and negatively in HFrEF (r = $-$ 0.51, p = 0.04). miR-423-5p overexpression, previously associated HF mortality, was inversely associated with LVEF (r = $-$ 0.29, p = 0.04) and intracellular water lifetime ( $τ$ _ic) (r = $-$ 0.45, p < 0.05) in both HF groups, and with NT-proBNP in HFpEF (r = $-$ 0.63, p < 0.01).
miRNA expression profiles differed between HF phenotypes. The differential expression and association of miR-128a-3p with ECV may reflect the distinct vascular, interstitial, and cellular etiologies of HF phenotypes.
Structure-based design of non-hypertrophic apelin receptor modulator
2024, Cell
Apelin is a key hormone in cardiovascular homeostasis that activates the apelin receptor (APLNR), which is regarded as a promising therapeutic target for cardiovascular disease. However, adverse effects through the β-arrestin pathway limit its pharmacological use. Here, we report cryoelectron microscopy (cryo-EM) structures of APLNR-G_i1 complexes bound to three agonists with divergent signaling profiles. Combined with functional assays, we have identified “twin hotspots” in APLNR as key determinants for signaling bias, guiding the rational design of two exclusive G-protein-biased agonists WN353 and WN561. Cryo-EM structures of WN353- and WN561-stimulated APLNR-G protein complexes further confirm that the designed ligands adopt the desired poses. Pathophysiological experiments have provided evidence that WN561 demonstrates superior therapeutic effects against cardiac hypertrophy and reduced adverse effects compared with the established APLNR agonists. In summary, our designed APLNR modulator may facilitate the development of next-generation cardiovascular medications.
Pterostilbene attenuates heart failure by inhibiting myocardial ferroptosis through SIRT1/GSK-3β/GPX4 signaling pathway
2024, Heliyon
Sustained myocardial injury due to hypertension and diabetes mellitus leads to production of endogenous reactive oxygen species (ROS) and insufficient myocardial antioxidant capacity, increasing the risk of cardiomyocyte ferroptosis. Ferroptosis is a nonapoptotic form of cell death driven by unrestricted lipid peroxidation. Dysfunction of the glutathione peroxidase 4 (GPX4) antioxidant system also plays an important role in ferroptosis. Cardiomyocyte ferroptosis ultimately leads to myocardial deterioration, such as inflammation, fibrosis, and cardiac remodeling, resulting in structural and functional changes. Pterostilbene (PTS), a demethylated derivative of resveratrol, exhibits strong anti-inflammatory and antioxidative activities. In this study, we used in vitro experiments to explore ferroptosis induced by angiotensin II (Ang II) of primary cardiac myocytes (CMs) and in vivo experiments to prepare a transverse aortic constriction (TAC)-induced cardiac dysfunction mouse model. PTS can significantly ameliorate Ang II-induced cardiomyocyte ferroptosis in vitro and reduce cardiac remodeling, while improving cardiac function in mice after TAC in vivo. Further mechanistic investigations revealed that PTS exerts its protective effect through the SIRT1/GSK-3β/GPX4 pathway. After siRNA-mediated knockdown of SIRT1 or GPX4 in CMs, the protective effects of PTS on cardiomyocytes were abolished. This study provides important theoretical support for the potential of PTS to attenuate pathological cardiac remodeling and heart failure and provides a preliminary exploration of the molecular pathways involved in its protective mechanism.
Underuse of heart failure medications and poor long-term prognosis in chronic heart failure patients with polypharmacy – A report from the CHART-2 study
2024, IJC Heart and Vasculature
In patients with chronic heart failure (CHF), comorbidities are often managed with multiple medications, characterized by polypharmacy, leading to increased risk of potentially inappropriate medication and adverse effects.
We studied 4,876 consecutive patients with CHF (Stage C/D, age 69.0 ± 12.3 years) in the CHART-2 study to evaluate the association among polypharmacy, underuse of HF medications, and all-cause death. Polypharmacy was defined as the daily use of ≥ 8 medications for the survival classification and regression tree analysis.
The average number of medications was 10 in the polypharmacy group and 5 in the non-polypharmacy group, respectively. Over a median of 8.3 (4.1–11.7) years, the incidence rate of all-cause death was significantly higher in the polypharmacy group (n = 2,108) than in the non-polypharmacy group (57.3 % vs. 40.6 %; adjusted hazard ratio [aHR] 1.34 (95 %CI, 1.22–1.48), P < 0.001), even in age < 55 years (26.6 % vs. 14.3 %; adjusted hazard ratio [aHR] 1.61 (95 %CI, 1.04–2.50), P = 0.033). In patients with polypharmacy, those without renin-angiotensin system inhibitors (RAS-I) and/or beta-blockers (N = 1,023) were associated with increased incidence of all-cause death as compared with those with both medications (aHR 1.18; 95 %CI 1.04–1.35, P = 0.012).
Polypharmacy was associated with poor long-term prognosis, even in younger patients with CHF. Among 4,876 patients with CHF, 1023 (20.9%) with polypharmacy and underuse of RAS-I and/or beta-blocker were associated with increased risk of all-cause death.
Association between estimated pulse wave velocity and all-cause death in patients with heart failure
2024, Revista Clinica Espanola
La arteriosclerosis ha demostrado ser un factor de riesgo para el desarrollo de insuficiencia cardiaca y readmisión. ePWV es un indicador novedoso, no invasivo y simple de la rigidez arterial, y este estudio tiene como objetivo investigar su relación con la tasa de mortalidad por todas las causas en pacientes con insuficiencia cardiaca.
Este estudio es un estudio de cohorte que incluyó a 1.272 pacientes con insuficiencia cardiaca de los datos de NHANES de 1999 a 2018. El ePWV se dividió en tres grupos y se calculó la tasa de mortalidad acumulada de pacientes con insuficiencia cardiaca utilizando curvas de supervivencia de KM. La relación entre ePWV y la tasa de mortalidad por todas las causas en pacientes con insuficiencia cardiaca se representó mediante un ajuste de curva suavizado. Se utilizó análisis de regresión de COX para evaluar la asociación entre ePWV y la tasa de mortalidad por todas las causas en pacientes con insuficiencia cardiaca.
La edad promedio de la población del estudio fue de 67,8 ± 12,6 años, con 862 hombres y 650 mujeres. Durante el período de seguimiento de 12 meses, hubo 790 casos de mortalidad por todas las causas. Se utilizó un análisis de regresión de Cox para validar la relación entre ePWV y la tasa de mortalidad por todas las causas en pacientes con insuficiencia cardiaca. Los pacientes con niveles más altos de ePWV tendían a tener una tasa de mortalidad por todas las causas más alta. Después del ajuste de múltiples factores, un aumento en ePWV se asoció positivamente con la tasa de mortalidad por todas las causas (HR = 1,17, intervalo de confianza [IC] del 95%: 1,12-1,22). En comparación con el tercil más bajo, la HR ajustada por múltiples variables y el IC del 95% para el tercil más alto de ePWV fueron 1,81 (IC del 95%: 1,45-2,27). Además, se utilizó un ajuste de curva suavizado para observar la relación entre ePWV y la tasa de mortalidad, donde la curva demostró una correlación positiva entre ePWV y la tasa de mortalidad por todas las causas. Además, las curvas de supervivencia de KM indicaron que la tasa de mortalidad por todas las causas aumentó con el aumento de ePWV. El análisis de subgrupos sugirió una correlación entre ePWV y la tasa de mortalidad.
Nuestro estudio muestra que ePWV se asocia positivamente con la mortalidad por todas las causas en pacientes con insuficiencia cardiaca.
Arteriosclerosis has been proven to be a risk factor for the development of heart failure and readmission. ePWV is a novel non-invasive and simple indicator of arterial stiffness, and this study aims to investigate its relationship with all-cause mortality rate in patients with heart failure.
This study is a cohort study that included 1272 patients with heart failure from NHANES data from 1999 to 2018. The ePWV was divided into three groups, and the cumulative mortality rate of heart failure patients was calculated using KM survival curves. The relationship between ePWV and all-cause mortality rate in heart failure patients was represented by a smoothed curve fitting. COX regression analysis was used to assess the association between ePWV and all-cause mortality rate in heart failure patients.
The average age of the study population was 67.8 ± 12.6 years, with 862 males and 650 females. During the 12-month follow-up period, there were 790 cases of all-cause mortality. Cox regression analysis was used to validate the relationship between ePWV and all-cause mortality rate in patients with heart failure. Patients with higher levels of ePWV tended to have a higher all-cause mortality rate. After adjustment for multiple factors, an increase in ePWV was positively associated with all-cause mortality rate (HR = 1.17, 95% confidence interval [CI]: 1.12-1.22). Compared to the lowest tertile, the multivariable-adjusted HR and 95% CI for the highest tertile of ePWV were 1.81 (95% CI: 1.45-2.27). Additionally, a smoothed curve fitting was used to observe the relationship between ePWV and mortality rate, where the curve demonstrated a positive correlation between ePWV and all-cause mortality rate. Furthermore, KM survival curves indicated that all-cause mortality rate increased with the increase in ePWV. Subgroup analysis suggested a correlation between ePWV and mortality rate.
Our study shows that ePWV is positively associated with all-cause mortality in patients with heart failure.
Systolic heart failure induced by butylparaben in zebrafish is caused through oxidative stress and immunosuppression
2023, Ecotoxicology and Environmental Safety
Due to Butylparaben (BuP) widespread application in cosmetics, food, pharmaceuticals, and its presence as an environmental residue, human and animal exposure to BuP is common, potentially posing hazards to both human and animal health. Congenital heart disease is already a serious problem. However, the effects of BuP on the developing heart and its underlying mechanisms remain unclear. Here, zebrafish embryos were exposed to environmentally and human-relevant concentrations of BuP (0.6 mg/L, 1.2 mg/L, and 1.8 mg/L, calculated but not measured) at 6 h post-fertilization (hpf) and were treated until 72 hpf. Exposure to BuP led to cardiac morphological defects and cardiac dysfunction in zebrafish embryos, manifesting symptoms similar to systolic heart failure. The etiology of BuP-induced systolic heart failure in zebrafish embryos is multifactorial, including cardiomyocyte apoptosis, endocardial and atrioventricular valve damage, insufficient myocardial energy, impaired Ca²⁺ homeostasis, depletion of cardiac-resident macrophages, cardiac immune non-responsiveness, and cardiac oxidative stress. However, excessive accumulation of reactive oxygen species (ROS) in the cardiac region and cardiac immunosuppression (depletion of cardiac-resident macrophages and cardiac immune non-responsiveness) may be the predominant factors. In conclusion, this study indicates that BuP is a potential hazardous substance that can cause adverse effects on the developing heart and provides evidence and insights into the pathological mechanisms by which BuP leads to cardiac dysfunction. It may help to prevent the BuP-based congenital heart disease heart failure in human through ameliorating strategies and BuP discharge policies, while raising awareness to prevent the misuse of preservatives.

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SeminarHeart failure

Summary

Section snippets

Epidemiology

Aetiology and pathophysiology

Comorbidity

Diagnosis

Treatment

Further challenges and directions

Search strategy and selection criteria

Am J Med

J Am Coll Cardiol

J Card Fail

Sex, age, and disease affect echocardiographic left ventricular mass and systolic function in the free-living elderly: the Cardiovascular Health Study

Circulation

Congestive heart failure in old age: prevalence, mechanisms and 4-year prognosis in the Helsinki Ageing Study

J Intern Med

Prevalence and clinical characteristics of left ventricular dysfunction among elderly patients in general practice setting: cross sectional survey

BMJ

Left ventricular systolic dysfunction in 75-year old men and women: a population-based study

Eur Heart J

Cross sectional study estimating prevalence of heart failure and left ventricular systolic dysfunction in community patients at risk

Heart

Prevalence of heart failure in Asturias (a region in the north of Spain)

Am J Cardiol

Prevalence of chronic heart failure in South Western Europe: EPICA study

Eur J Heart Fail

Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic

JAMA

Prevalence of heart failure and left ventricular dysfunction in the general population; the Rotterdam Study

Eur Heart J

The epidemiology of heart failure: the Framingham Study

J Am Coll Cardiol

Lifetime risk for developing congestive heart failure: the Framingham Heart Study

Circulation

Quantifying the heart failure epidemic: prevalence, incidence rate, lifetime risk and prognosis of heart failure

Eur Heart J

Long-term trends in the incidence of and survival with heart failure

N Engl J Med

Trends in heart failure incidence and survival in a community-based population

JAMA

Heart failure and the aging population: an increasing burden in the 21st century?

Heart

Trends in hospitalization for heart failure in Scotland, 1990–1996: an epidemic that has reached its peak?

Eur Heart J

Decreasing one-year mortality and hospitalization rates for heart failure in Sweden: data from the Swedish Hospital Discharge Registry 1988 to 2000

Eur Heart J

Angiotensin converting enzyme inhibition and hospitalisation rates for heart failure in the Netherlands, 1980 to 1999: the end of an epidemic?

Heart

Hospitalization of patients with heart failure: a population-based study

Eur Heart J

Prognosis for patients newly admitted to hospital with heart failure: survival trends in 12 220 index admissions in Leicestershire 1993–2001

Heart

Trends in heart failure outcomes and pharmacotherapy: 1992 to 2000

Am J Med

Mortality trends for 23,505 Medicare patients hospitalized with heart failure in Northeast Ohio, 1991 to 1997

Am Heart J

Detecting early clinical deterioration in chronic heart failure patients post-acute hospitalisation: a critical component of multidisciplinary, home-based intervention?

Eur J Heart Fail

The current cost of heart failure to the National Health Service in the UK

Eur J Heart Fail

National survey of the prevalence, incidence, primary care burden, and treatment of heart failure in Scotland

Heart

Impact of heart failure and left ventricular systolic dysfunction on quality of life: a cross-sectional study comparing common chronic cardiac and medical disorders and a representative adult population

Eur Heart J

Survival of patients with a new diagnosis of heart failure: a population based study

Heart

Evidence of improving prognosis in heart failure: trends in case fatality in 66 547 patients hospitalised between 1986 and 1995

Circulation

More ‘malignant’ than cancer? Five-year survival following a first admission for heart failure

Eur J Heart Fail

Heart failure with preserved left ventricular systolic function; epidemiology, clinical characteristics, and prognosis

J Am Coll Cardiol

The epidemiological enigma of heart failure with preserved systolic function

Eur J Heart Fail

Heart failure with preserved systolic function. A different natural history?

J Am Coll Cardiol

Diastolic heart failure: neglected or misdiagnosed?

J Am Coll Cardiol

Outcome of congestive heart failure in elderly persons: influence of left ventricular systolic function: the Cardiovascular Health Study

Seminar
Heart failure

Heart failure and the aging population: an increasing burden in the 21^st century?