International Journal of Heart Failure最新文献

Background and objectives: We sought to assess incidence, cause of death, and survival for amyloidosis. We acquired amyloidosis data from the National Health Insurance Service in Korea from 2006 through 2017 (n=2,233; male 53.5%).

Methods: We calculated the age-standardized incidence rate, analyzed the survival rate (SR) using the Kaplan-Meier method, and analyzed the death risk using Cox proportional hazards methods.

Results: The mean age was 57.0±16.7 years in males and 56.8±15.6 years in females (p=0.795). The proportion of death was 34.7%. The causes of death were endocrine, nutritional, and metabolic diseases (33.9%), malignant neoplasm (20.8%), and diseases of the circulatory system (9.68%). The overall age-standardized incidence rate was 0.47 persons per 100,000 persons in 2017. Overall, the 10-year SR for amyloidosis was 57.7%. Adjusted hazard ratios were 9.16 among 40s', 16.1 among 50s', 30.3 among 60s', 48.7 among 70s', 80.1 among people 80 years or older, and 1.21 in the medium-level socioeconomic position group.

Conclusions: The age-standardized incidence rate of amyloidosis was about 0.5 persons per 100,000 persons in 2017. The 10-year SR of amyloidosis was about 58%. The most common cause of death was endocrine, nutritional, and metabolic diseases. The risk of death from amyloidosis increased with age and medium socioeconomic position.

Background and objectives: Persistent atrial fibrillation (PeAF) with heart failure (HF) arguably constitutes the sickest subset of atrial fibrillation (AF) patients.

Methods: A systematic search was made in PubMed, Embase, and Scopus databases. Network meta-analysis (NMA) of PeAF patients with systolic HF comparing all-cause mortality, change in HF-related quality of life (QoL) and hospitalization due to heart failure (HHF) were performed among catheter ablation (CA) of AF, rate-controlling drugs (RCDs), anti-arrhythmic drugs (AADs), and atrio-ventricular nodal ablation (AVNA) using Bayesian random effect model.

Results: Ablation strategies resulted significantly lower mortality than medical therapies (odds ratio [OR], 0.51; 95% confidence interval [CI], 0.35 to 0.76). CA of AF was associated with lower trend of mortality (OR, 0.78; 95% credible interval [CrI], 0.08 to 7.63) in comparison to AVNA in the Bayesian NMA. Rhythm control strategies resulted significantly higher improvement of QoL than rate control strategies (mean difference [MD], -12.78; 95% CI, -21.26 to -4.31). Bayesian NMA showed that CA of AF was better than AAD (MD, -7.98; 95% CrI, -27.68 to 8.27), however ranked AVNA to be lowest. Ablation strategies provided significantly lower HHF than medical therapies (OR, 0.42; 95% CI, 0.30 to 0.58). Bayesian NMA showed that CA of AF performed not only better than AAD (OR, 0.33; 95% CrI, 0.09 to 1.3) to reduce HHF, but also than AVNA (OR, 0.20; 95% CrI, 0.00 to 4.76). Of note, RCD ranked lowest with regard to mortality and HHF.

Conclusions: CA of AF remains the best strategy even for the sickest group of PeAF patients with systolic HF in regards to all-cause mortality, HF-related QoL and HHF.

Over the past three decades, pharmacological treatment of heart failure (HF) with reduced ejection fraction (HFrEF) has witnessed a significant progress with the introduction of multiple disease-modifying therapies with a proven benefit on morbidity, mortality and quality of life. Recently, several novel medications (sacubitril/valsartan, sodium-glucose contransporter-2 [SGLT2] inhibitors, vericiguat and omecamtiv mecarbil) have shown to provide further improvement in outcomes in patients already receiving standard therapy for HFrEF. Available evidence suggests that sacubitril/valsartan and SGLT2 inhibitors (dapagliflozin and empagliflozin) are beneficial and well-tolerated in the majority inpatients and could be the mainstay treatment of HFrEF. Another group of medications (vericiguat and omecamtiv mecarbil) has shown promising results in reducing the risk of the composite of HF hospitalisation or cardiovascular mortality in patients with the more severe or advanced HF requiring recent hospitalisation. Therefore, these medications may be considered for the treatment of select group of patients with HFrEF with persisting or worsening symptoms despite optimal treatment. In addition, advances in pharmacological management of comorbidities frequently seen in HFrEF patients (diabetes, iron deficiency/anaemia, hyperkalaemia) provide further opportunities to improve outcomes. Given the increasing complexity of evidence-based therapies for HFrEF, there is a growing need to provide a practical perspective to their use. The purpose of this review is to summarise scientific evidence on the efficacy and safety of new and emerging medical therapies in HFrEF, with a focus on the clinical perspective of their use.

Pulmonary hypertension (PH) is traditionally defined as a mean pulmonary arterial pressure (mPAP) ≥25 mmHg. Although various factors cause PH, the most common etiology is PH due to left heart disease (PH-LHD). The underlying LHD is characterized by heart failure (HF) with reduced ejection fraction (HFrEF), HF with preserved ejection fraction (HFpEF), valvular heart disease, cardiomyopathies, or arrhythmic diseases. Regardless of its underlying cause, elevated left atrial (LA) filling pressure is a manifestation of advanced heart disease. High LA pressure then causes persistent backflow to the pulmonary veins, which increases mPAP. PH-LHD at this stage is named isolated postcapillary PH (IpcPH). Further progression of IpcPH is associated with pulmonary vasculature remodeling and hypertrophy, which consists of adding the precapillary component of PH to the pre-existing postcapillary PH. This form of PH-LHD is called combined precapillary and postcapillary PH (CpcPH). To date, therapeutic strategies for PH-LHD have been investigated in the context of HFrEF or HFpEF. Pulmonary arterial hypertension (PAH)-specific drugs have been tested in HFrEF and HFpEF populations, although encouraging results have not been demonstrated. As PAH-specific drugs target the precapillary component of PH-LHD, future studies utilizing such therapeutics in PH-LHD patients with CpcPH appear to have a more robust pathobiological basis. This article reviews the diagnosis, pathophysiology, treatment, and future direction of PH in HF.