Aims Elderly patients with heart failure (HF) are associated with frequent all-cause readmission or death. The present study sought to develop an accurate and easy-to-use model to predict all-cause readmission or death risk in Chinese elderly patients with HF. Methods and resultsThis was a prospective cohort study in patients with HF aged 65 or older. Demographic, comorbidity, laboratory, and medication data were collected. A Cox regression model was used to identify factors for the prediction of readmission or death at 30 days and 1 year. A nomogram was developed with bootstrap validation. Of the included 854 patients, the cumulative all-cause readmission and mortality rates were 10.5% and 11.6% at 30 days and 34.9% and 19.7% at 1 year, respectively. The independent risk factors associated with both 30 day and 1 year readmission or death were older age, stroke, diastolic blood pressure < 60 mmHg, body mass index ≤ 18.5 kg/m 2 , lower estimated glomerular filtration rate, and BNP > 400 pg/mL (all P < 0.05). Anaemia, abnormal neutrophils, and admission without angiotensin-converting enzyme inhibitors/angiotensin receptor blockers were the specific independent risk factors of 30 day all-cause readmission or death (all P < 0.05), whereas serum sodium ≤ 140 mmol/L and admission without beta-blockers were the specific independent risk factors of 1 year all-cause readmission or death (all P < 0.05). The Cindex of the 30 day and 1 year diagnosis prediction model was 0.778 [95% confidence interval (CI) 0.693-0.862] and 0.738 (95% CI 0.640-0.836), respectively. Conclusions We developed accurate and easy-to-use nomograms to predict all-cause readmission or death in Chinese elderly patients with HF. The nomograms will assist in reducing the all-cause readmission and mortality rates.

Heart failure (HF) is a major global healthcare problem accounting for substantial deterioration of prognosis. As a complex clinical syndrome, HF often coexists with multi-comorbidities of which cognitive impairment (CI) is particularly important. CI is increasing in prevalence among patients with HF and is present in around 40%, even up to 60%, of elderly patients with HF. As a potent and independent prognostic factor, CI significantly increases the hospitalization and mortality and decreases quality of life in patients with HF. There has been a growing awareness of the complex bidirectional interaction between HF and CI as it shares a number of common pathophysiological pathways including reduced cerebral blood flow, inflammation, and neurohumoral activations. Research that focus on the precise mechanism for CI in HF is still ever insufficient. As the tremendous adverse consequences of CI in HF, effective early diagnosis of CI in HF and interventions for these patients may halt disease progression and improve prognosis. The current clinical guidelines in HF have begun to emphasize the importance of CI. However, nearly half of CI in HF is underdiagnosed, and few recommendations are available to guide clinicians about how to approach CI in patients with HF. This review aims to synthesize knowledge about the link between HF and cognitive dysfunction, issues pertaining to screening, diagnosis and management of CI in patients with HF, and emerging therapies for prevention. Based on data from current studies, critical gaps in knowledge of CI in HF are identified, and future research directions to guide the field forward are proposed.

Acute myocardial infarction (AMI) is recognized as being a life-threatening event. Both microvascular obstruction (MVO) and intramyocardial hemorrhage (IMH) have been recognized as poor prognostic factors in myocardial infarct (MI) since they adversely affect left ventricular remodeling. MVO refers to small vessels changes that prevent adequate tissue perfusion despite revascularization whereas IMH is a severe form of MVO. A limited number of studies have demonstrated the segmental intervention time and the clinical factors in the presence of MVO and IMH. Therefore, we aimed in this study to determine the correlations of the intervention-associated and clinical indexes with malignant cardiovascular magnetic resonance (CMR) signs in patients with AMI.Sixty-three patients with STEMI who underwent primary percutaneous coronary intervention (PPCI) within 12 hours were included in this study. A 3.0-T CMR scan was prescribed, and the subsequent image analysis was conducted by researchers blinded to the clinical index results. Late-gadolinium enhancement (LGE) and T2∗ sequences were mainly used for MVO and IMH identification and quantification.Patients exhibiting both MVO and IMH had the highest level of LGE (P < .001) and were significantly more frequently assigned to a pre-PPCI thrombolysis in myocardial infarction (TIMI) flow class of 0 (n=25, 89.3%). The MVO size correlated positively with the IMH size (r = 0.81, P < .01). A pre-PPCI TIMI flow class of 0 was found to reliably predict the presence of IMH (P < .001). Patients who received the intervention 4 to 6 hours after MI onset were more likely to exhibit MVO and IMH, although this trend was not statistically significant.We showed in our study that both MVO and IMH correlated with the degree of AMI and the pre-PPCI coronary flow, and both tended to occur more frequently in cases involving an interval of 4 to 6 hours between the onset of MI and the intervention. CMR is a reliable method for assessing MVO and IMH and its imaging features following gadolinium administration are characteristic. These findings stress the importance of using CMR in evaluating and improving the outcome of the medical management.

Background Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome with sex-specific pathophysiology. Estrogen deficiency is believed to be responsible for the development of HFpEF in women. However, estrogen deficiency does not seem to be completely responsible for the differences in HFpEF prevalence between sexes. While diabetes mellitus (DM) frequently coexists with HFpEF in women and is associated with worse outcomes, the changes in myocardial contractility among women with HFpEF and the DM phenotype is yet unknown. Therefore, we aimed to investigate sex-related differences in left ventricular (LV) contractility dysfunction in HFpEF comorbid with DM. Methods A total of 224 patients who underwent cardiac cine MRI were included in this study. Sex-specific differences in LV structure and function in the context of DM were determined. LV systolic strains (global longitudinal strain [GLS], circumferential strain [GCS] and radial strain [GRS]) were measured using cine MRI. The determinants of impaired myocardial strain for women and men were assessed. Results The prevalence of DM did not differ between sexes (p > 0.05). Despite a similar LV ejection fraction, women with DM demonstrated a greater LV mass index than women without DM (p = 0.023). The prevalence of LV geometry patterns by sex did not differ in the non-DM subgroup, but there was a trend toward a more abnormal LV geometry in women with DM (p = 0.072). The magnitudes of systolic strains were similar between sexes in the non-DM group (p > 0.05). Nevertheless, in the DM subgroup, there was significant impairment in women in systolic strains compared with men (p < 0.05). In the multivariable analysis, DM was associated with impaired systolic strains in women (GLS [β = 0.26; p = 0.007], GCS [β = 0.31; p < 0.001], and GRS [β = −0.24; p = 0.016]), whereas obesity and coronary artery disease were associated with impaired systolic strains in men (p < 0.05). Conclusions Women with DM demonstrated greater LV contractile dysfunction, which indicates that women with HFpEF comorbid with DM have a high-risk phenotype of cardiac failure that may require more aggressive and personalized medical treatment.

Background Atherosclerotic plaque vulnerability is a key feature of atheroprogression and precipitating acute cardiovascular events. Although the pivotal role of epigenetic regulation in atherosclerotic plaque destabilization is being recognized, the DNA methylation profile and its potential role in driving the progression and destabilization of atherosclerotic cardiovascular disease remains largely unknown. We conducted a genome-wide analysis to identify differentially methylated genes in vulnerable and non-vulnerable atherosclerotic lesions to understand more about pathogenesis. Results We compared genome-wide DNA methylation profiling between carotid artery plaques of patients with clinically symptomatic (recent stroke or transient ischemic attack) and asymptomatic disease (no recent stroke) using Infinium Methylation BeadChip arrays, which revealed 90,368 differentially methylated sites (FDR < 0.05, |delta beta|> 0.03) corresponding to 14,657 annotated genes. Among these genomic sites, 30% were located at the promoter regions and 14% in the CpG islands, according to genomic loci and genomic proximity to the CpG islands, respectively. Moreover, 67% displayed hypomethylation in symptomatic plaques, and the differentially hypomethylated genes were found to be involved in various aspects of inflammation. Subsequently, we focus on CpG islands and revealed 14,596 differentially methylated sites (|delta beta|> 0.1) located at the promoter regions of 7048 genes. Integrated analysis of methylation and gene expression profiles identified that 107 genes were hypomethylated in symptomatic plaques and showed elevated expression levels in both advanced plaques and ruptured plaques. The imprinted gene PLA2G7, which encodes lipoprotein-associated phospholipase A2 (Lp-PLA2), was one of the top hypomethylated genes with an increased expression upon inflammation. Further, the hypomethylated CpG site at the promoter region of PLA2G7 was identified as cg11874627, demethylation of which led to increased binding of Sp3 and expression of Lp-PLA2 through bisulfate sequencing, chromatin immunoprecipitation assay and enzyme-linked immunosorbent assay. These effects were further enhanced by deacetylase. Conclusion Extensive DNA methylation modifications serve as a new and critical layer of biological regulation that contributes to atheroprogression and destabilization via inflammatory processes. Revelation of this hitherto unknown epigenetic regulatory mechanism could rejuvenate the prospects of Lp-PLA2 as a therapeutic target to stabilize the atherosclerotic plaque and reduce clinical sequelae.