Evolving trends in the epidemiologic factors of heart failure: Rationale for preventive strategies and comprehensive disease management☆,☆☆,★,★★

The objective of this study was to describe the prevalence of patients with forgone/delayed care for heart failure (HF) and examine the associated demographic characteristics, health care utilization, and costs.

HF is a leading cause of morbidity and mortality, with health care expenditures projected to increase 3-fold from 2012 to 2030. The proportion of HF patients with forgone/delayed medical care and the association with health care expenditures and utilization remain unknown.

Data on patients with HF were obtained from the Medical Expenditure Panel Survey to assess expenditures and health care utilization in the United States from 2004 to 2015. Patients with HF who reported forgone/delayed care, any missed or delayed medical treatment, were compared with those without care lapses.

Overall, 16% of patients with HF reported forgone/delayed care, including 10% among the elderly (aged ≥65 years) and 27% among the nonelderly (aged <65 years). Patients with HF who reported forgone/delayed care had annual health care expenses $8,027 (95% CI: $1,181-$14,872) higher than those who did not. Among the elderly, those reporting forgone/delayed care had more emergency department visits (43% vs 58%; P < 0.05), and had higher annual inpatient costs (+$7,548; 95% CI: $1,109-$13,988) and total health care costs (+$10,581; 95% CI: $1,754-$19,409). Sixty percent of nonelderly and 46% of elderly patients with HF reported deferring care due to financial barriers.

Nearly 1 in 6 patients with HF in the United States reported forgone/delayed medical care, with one-half attributing it to financial reasons, and this was associated with higher overall health care spending.

Increased carotid intima-media thickness (cIMT) is associated with heart failure (HF) in previous studies, but it is not known whether the association of cIMT differs between HF with reduced (HFrEF) versus preserved ejection fraction (HFpEF). We studied 6699 participants (mean age 62 ± 10 years, 47% male, and 38% white) from the Multi-Ethnic Study of Atherosclerosis (MESA) with baseline cIMT measurements. We classified HF events as HFrEF (EF <50%) or HFpEF (EF ≥ 50%) at the time of diagnosis. Cox proportional hazard regression was used to compute hazard ratios (HR), and 95% confidence intervals (CI) for the association between the IMT Z-score (measured maximum IMT of Internal Carotid (IC) and Common Carotid (CC) sites as the mean of the maximum IMT of the near and far walls of right and left sides), and incident HFrEF or HFpEF. Models were adjusted for covariates and interim coronary artery disease (CAD) events. A total of 191 HFrEF and 167 HFpEF events occurred during follow-up. In multivariable analysis, each 1 standard deviation increase in the measured maximum IMT (Z-score) was associated with both HFrEF and HFpEF in the unadjusted and demographically adjusted models [HR, 95% CI 1.57 (1.43 to 1.73)] and [HR, 95% CI 1.61 (1.47 to 1.77)] but not in the fully adjusted models [HR, 95% CI 1.11 (0.96 to 1.28)] and [HR, 95% CI 1.13 (0.98 to 1.30)]. In conclusion, cIMT was significantly associated with incident HF, but the association is partially attenuated with adjustment for demographic factors and becomes non-significant after adjustment for other traditional heart failure risk factors and interim CAD events. There was no difference in the association of IMT measures with HFrEF versus HFpEF.

Myocardial fibrosis (MF) plays a key role in the development and progression of heart failure (HF) with limited effective therapies. Galectin-3 (Gal-3) is a biomarker associated with fibrosis and inflammation in patients with HF. The Gal-3 inhibitor modified citrus pectin (MCP) protects against cardiac dysfunction, though the underlying mechanism remains unclear. The aim of this study was to investigate the effect and mechanism of MCP on MF using an isoproterenol (ISO)-induced rat model of HF. Cardiac function was analyzed by echocardiography and electrocardiography. Histopathological changes in the heart tissue were assessed by hematoxylin-eosin and Masson trichrome staining. The mRNA and protein expression levels of signaling molecules and pro-inflammatory cytokines were monitored by immunohistochemistry, western blot, qRT-PCR and ELISA analyses. The results demonstrated that MCP ameliorated cardiac dysfunction, decreased myocardial injury and reduced collagen deposition. Furthermore, MCP downregulated the expression of Gal-3, TLR4 and MyD88, thereby inhibiting NF-κB-p65 activation. MCP also decreased the expression of IL-1β, IL-18 and TNF-α, which have been implicated in the pathogenesis of HF. These inhibitory effects were observed on day 15 and continued until day 22. Taken together, these results suggest that MCP ameliorates cardiac dysfunction through inhibiting inflammation and MF. These effects may be through downregulating Gal-3 expression and suppressing activation of the TLR4/MyD88/NF-κB signaling pathway. The present study supports the use of Gal-3 as a therapeutic target for the treatment of MF after myocardial infarction.

Congestive Heart Failure (CHF) is a severe pathophysiological condition associated with high prevalence, high mortality rates, and sustained healthcare costs, therefore demanding efficient methods for its detection. Despite recent research has provided methods focused on advanced signal processing and machine learning, the potential of applying Convolutional Neural Network (CNN) approaches to the automatic detection of CHF has been largely overlooked thus far. This study addresses this important gap by presenting a CNN model that accurately identifies CHF on the basis of one raw electrocardiogram (ECG) heartbeat only, also juxtaposing existing methods typically grounded on Heart Rate Variability. We trained and tested the model on publicly available ECG datasets, comprising a total of 490,505 heartbeats, to achieve 100% CHF detection accuracy. Importantly, the model also identifies those heartbeat sequences and ECG’s morphological characteristics which are class-discriminative and thus prominent for CHF detection. Overall, our contribution substantially advances the current methodology for detecting CHF and caters to clinical practitioners’ needs by providing an accurate and fully transparent tool to support decisions concerning CHF detection.

Heart failure is associated with high rates of readmission and mortality, and there is a need for measures to improve outcomes. This study aims to assess the impact of the implementation of a protocol-based follow-up program for heart failure patients on readmission and mortality rates and quality of life.

A quasi-experimental study was performed, with a prospective registry of 50 consecutive patients discharged after hospitalization for acute heart failure. The study group was followed by a cardiologist at days 7-10 and the first, third, sixth and 12th month after discharge, with predefined procedures. The control group consisted of patients hospitalized for heart failure prior to implementation of the program and followed on a routine basis.

No significant differences were observed between the two groups regarding mean age (67.1±11.2 vs. 65.8±13.4 years, p=0.5), NYHA functional class (p=0.37), or median left ventricular ejection fraction (27% [19.8-35.3] vs. 29% [23.5-40]; p=0.23) at discharge. Mean follow-up after discharge was similar (11±5.3 vs. 10.9±5.5 months, p=0.81).

The protocol-based follow-up program was associated with a significant reduction in all-cause readmission (26% vs. 60%, p=0.003), heart failure readmission (16% vs. 36%, p=0.032), and mortality (4% vs. 20%, p=0.044). In the study group there was a significant improvement in all quality of life measures (p<0.001).

A protocol-based follow-up program for patients with heart failure led to a significant reduction in readmission and mortality rates, and was associated with better quality of life.

Os doentes com insuficiência cardíaca (IC) apresentam taxas elevadas de reinternamento e mortalidade, tornando necessária a implementação de medidas que conduzam à sua redução. Avaliou-se o impacto da implementação de um programa de seguimento estruturado de doentes com IC nas taxas de reinternamento e mortalidade e na qualidade de vida.

Estudo quasi-experimental, de registo prospetivo, que incluiu 50 doentes consecutivos com alta após internamento por insuficiência cardíaca aguda. Os doentes iniciaram seguimento protocolado após alta, por cardiologista, com consulta aos 7-10 dias, 1, 3, 6 e 12 meses, com procedimentos pré-definidos. O grupo-controlo foi constituído por doentes internados por insuficiência cardíaca previamente à implementação do programa, seguidos após a alta em consultas de rotina.

Não houve diferenças entre ambos os grupos no respeitante à idade média (67,1±11,2 versus 65,8±13,4 anos; p=0,5), classe funcional da NYHA (p=0,37) e mediana da fração de ejeção do ventrículo esquerdo [27% (19,8-35,3) versus 29% (23,5-40); p=0,23] à data da alta; o tempo de seguimento médio foi idêntico (11±5,3 versus 10,9±5,5 meses; p=0,81).

O seguimento protocolado associou-se a redução significativa das taxas de reinternamento por qualquer causa (26% versus 60%, p=0,003), reinternamento por insuficiência cardíaca (16% versus 36%, p=0,032) e mortalidade total (4% versus 20%, p=0,044). No grupo em estudo verificou-se melhoria significativa em todos os parâmetros de qualidade de vida (p<0,001).

Um programa de seguimento protocolado de doentes com insuficiência cardíaca permitiu redução significativa nas taxas de reinternamento e mortalidade e associou-se a melhoria da qualidade de vida.

Chronic myocardial injury, defined as persistent troponin levels >99th percentile values when measured with high-sensitivity assays (hs-cTn), is common. The association between chronic myocardial injury and stroke is unknown. This study aimed to investigate the association between chronic myocardial injury and stroke.

From 2011 to 2014, we included patients with chest pain and high-sensitivity cardiac troponin T levels measured concurrently but without acute conditions associated with elevated high-sensitivity cardiac troponin T levels. Cox regression was used to calculate hazard ratios (HRs) with 95% confidence intervals (CIs) for stroke in patients with stable high-sensitivity cardiac troponin T levels of 5-9, 10-14, 15-29, 30-49, and ≥50 ng/L, using <5 ng/L as reference group. Categories >14 ng/L were defined as chronic myocardial injury.

A total of 19,460 patients were included, among whom 1528 (7.9%) had chronic myocardial injury. During a mean follow-up of 2.1 years, there were 244 (1.2%) strokes. With increasing high-sensitivity cardiac troponin T levels yearly stroke rates increased from 0.24% to 4.0%. Adjusted hazard ratios with 95% confidence intervals for stroke were 1.83 (1.27-2.64) in patients with high-sensitivity cardiac troponin T levels of 5-9 ng/L, increasing to 1.95 (1.21-3.14), 3.38 (1.80-6.35), and 4.32 (1.89-9.91) in patients with high-sensitivity cardiac troponin T levels of 15-29, 30-49, and ≥50 ng/L, respectively.

Patients with chronic myocardial injury have up to a 4-fold increased risk of stroke compared with patients with high-sensitivity cardiac troponin T levels <5 ng/L. Our findings indicate that patients with any detectable high-sensitivity cardiac troponin T level, in particular those with chronic myocardial injury, have an increased risk of stroke and require further attention.