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Predictors and prognosis for incident in-hospital heart failure in patients with preserved ejection fraction after first acute myocardial infarction: An observational study.

ABSTRACT: Patients with acute myocardial infarction (AMI) complicated by heart failure with preserved ejection fraction (HFpEF) are likely to have more adverse cardiovascular events and higher mortality. The purpose of this study was to examine the predictors and outcomes in AMI patients complicated by HFpEF.We examined the demographics, clinical data, and clinical outcomes in 405 consecutive subjects who firstly presented with AMI after undergoing emergency percutaneous coronary intervention from January 2013 to June 2016.Three hundred twenty patients and eighty-five patients were classified into the nonheart failure (non-HF) group and HFpEF group, respectively. Patients with HFpEF had higher prevalence of prior hypertension, had higher levels of biomarkers, and had a larger left atrial diameter with a nondilated left ventricle were more likely to develop multivessel disease-vessels and had infarction-related artery located in left anterior descending artery than patients without HF. Moreover, patients with HFpEF had a higher probability of developing the in-hospital incident cardiovascular complications and death than non-HF patients.Two routine biomarkers, levels of hypersensitive C-reactive protein and N-terminal-pro brain natriuretic peptide, and number of diseased-vessels were independent predictors for in-hospital HFpEF incidence in AMI patients with preserved LVEF. AMI patients with HFpEF had a higher probability of in-hospital cardiovascular outcomes and mortality.

SUBMITTER: Xu M

PROVIDER: S-EPMC6024188 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature

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Predictors and prognosis for incident in-hospital heart failure in patients with preserved ejection fraction after first acute myocardial infarction: An observational study.

Xu Mingzhu M Yan Lihua L Xu Jialiang J Yang Xiangjun X Jiang Tingbo T

Medicine 20180601 24

Patients with acute myocardial infarction (AMI) complicated by heart failure with preserved ejection fraction (HFpEF) are likely to have more adverse cardiovascular events and higher mortality. The purpose of this study was to examine the predictors and outcomes in AMI patients complicated by HFpEF.We examined the demographics, clinical data, and clinical outcomes in 405 consecutive subjects who firstly presented with AMI after undergoing emergency percutaneous coronary intervention from January ...[more]

PMID: 29901624

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Project description:BACKGROUND:The role of coronary microvascular disease and its impact on functional and energetic reserve in heart failure with preserved ejection fraction (HFpEF) remains unclear. We hypothesized that in response to submaximal pharmacologic stress (dobutamine), patients with HFpEF have impairment in left ventricular (LV) myocardial mechanical (external work [EW]), energetic (myocardial O2 consumption [MVO2]), and myocardial blood flow (MBF) reserve. We further assessed whether coupling of MBF to EW is impaired in HFpEF and associated with compensatory increases or pathological decreases in myocardial O2 extraction. Lastly, we assessed whether coupling of MVO2 to EW (mechanical efficiency) was impaired in HFpEF. METHODS AND RESULTS:In prospectively enrolled patients with HFpEF (n=19) and age/sex-matched healthy controls (n=19), we performed 11C-acetate positron emission tomography assessing MVO2 and MBF at rest and during dobutamine infusion. EW was calculated as stroke volume (echo)×end-systolic pressure×heart rate. At rest, compared with controls, patients with HFpEF had higher LV EW, MVO2, and MBF. With dobutamine, LV EW, MVO2, and MBF increased in both HFpEF and controls; however, the magnitude of increases was significantly smaller in HFpEF. In both groups, MBF increased in relation to EW, but in HFpEF, the slope of the relationship was significantly smaller than in controls. Myocardial O2 extraction was increased in HFpEF. Mechanical efficiency was similar in HFpEF and controls. In a post hoc analysis, HFpEF patients with LV hypertrophy (n=10) had significant reductions in LV mechanical efficiency relative to controls. CONCLUSIONS:In HFpEF during submaximal dobutamine stress, there is myocardial mechanical-, energetic- and flow-reserve dysfunction with impaired coupling of blood flow to demand and slight increases in myocardial O2 extraction. These findings provide evidence that coronary microvascular dysfunction is present in HFpEF, limits O2 supply relative to demand, and is associated with reserve dysfunction.

Project description:AimsThe prevalence of heart failure (HF) after acute myocardial infarction (AMI) is common. Contemporary data are lacking on the prognostic utility of the measurement of biomarker for patients with AMI complicated by HF according to preserved (HFpEF) and reduced ejection fraction (HFrEF). We aim to assess the association between D-dimer levels and all-cause mortality in patients with AMI complicated by different HF subtypes during hospitalization in the context of other risk factors.Methods and resultsWe enrolled 4495 patients with AMI with complete clinical and laboratory variable assessments in this cohort. D-dimer levels were measured on admission immediately at baseline. We used Cox proportional hazards analysis to assess this association accounting for 18 relevant clinical variables. During the index hospitalization, 589 patients with AMI developed HFpEF, 513 patients with AMI developed HFrEF, and 3393 patients with AMI did not develop HF. The patients were divided into HFpEF, HFrEF, and non-HF groups accordingly. The median length of follow-up was 1 year (range: 1 to 24 months). During the whole follow-up, 58 (15.5%), 107 (27.9%), and 96 (4.2%) of the patients experienced death event in HFpEF, HFrEF, and non-HF groups, respectively. In each group, the patients were divided into high or low D-dimer levels according to D-dimer concentration (145 ng/mL). In the fully adjusted model, the risk of all-cause mortality of those patients with high D-dimer levels was 2.09 [95% confidence intervals (CI): 1.08 to 4.02, P = 0.02] times as high as the risk of patients with low D-dimer levels in HFpEF group. When analysing D-dimer as a continuous variable, this associations still existed. But there was no significant association between D-dimer concentration and all-cause mortality in HFrEF [hazard ratio (HR): 1.25, CI: 0.76 to 2.04, P = 0.37] or non-HF (HR: 1.56, CI: 0.98 to 2.47, P = 0.06), respectively, after fully adjustment for other key clinical variables.ConclusionsHigh D-dimer levels on admission were found to be strongly associated with the subsequent cumulative incidence of all-cause mortality in patients with AMI complicated by HFpEF.

Project description:BackgroundHeart failure (HF) with preserved ejection fraction (HFpEF) constitutes half of all HF but lacks effective therapy. Understanding of its myocardial biology remains limited because of a paucity of heart tissue molecular analysis.MethodsWe performed RNA sequencing on right ventricular septal endomyocardial biopsies prospectively obtained from patients meeting consensus criteria for HFpEF (n=41) contrasted with right ventricular septal tissue from patients with HF with reduced ejection fraction (HFrEF, n=30) and donor controls (n=24). Principal component analysis and hierarchical clustering tested for transcriptomic distinctiveness between groups, effect of comorbidities, and differential gene expression with pathway enrichment contrasted HF groups and donor controls. Within HFpEF, non-negative matrix factorization and weighted gene coexpression analysis identified molecular subgroups, and the resulting clusters were correlated with hemodynamic and clinical data.ResultsPatients with HFpEF were more often women (59%), African American (68%), obese (median body mass index 41), and hypertensive (98%), with clinical HF characterized by 65% New York Heart Association Class III or IV, nearly all on a loop diuretic, and 70% with a HF hospitalization in the previous year. Principal component analysis separated HFpEF from HFrEF and donor controls with minimal overlap, and this persisted after adjusting for primary comorbidities: body mass index, sex, age, diabetes, and renal function. Hierarchical clustering confirmed group separation. Nearly half the significantly altered genes in HFpEF versus donor controls (1882 up, 2593 down) changed in the same direction in HFrEF; however, 5745 genes were uniquely altered between HF groups. Compared with controls, uniquely upregulated genes in HFpEF were enriched in mitochondrial adenosine triphosphate synthesis/electron transport, pathways downregulated in HFrEF. HFpEF-specific downregulated genes engaged endoplasmic reticulum stress, autophagy, and angiogenesis. Body mass index differences largely accounted for HFpEF upregulated genes, whereas neither this nor broader comorbidity adjustment altered pathways enriched in downregulated genes. Non-negative matrix factorization identified 3 HFpEF transcriptomic subgroups with distinctive pathways and clinical correlates, including a group closest to HFrEF with higher mortality, and a mostly female group with smaller hearts and proinflammatory signaling. These groupings remained after sex adjustment. Weighted gene coexpression analysis yielded analogous gene clusters and clinical groupings.ConclusionsHFpEF exhibits distinctive broad transcriptomic signatures and molecular subgroupings with particular clinical features and outcomes. The data reveal new signaling targets to consider for precision therapeutics.

Project description:Importance:Nearly half of all patients with heart failure have preserved ejection fraction (HFpEF) as opposed to reduced ejection fraction (HFrEF), yet associations of biomarkers with future heart failure subtype are incompletely understood. Objective:To evaluate the associations of 12 cardiovascular biomarkers with incident HFpEF vs HFrEF among adults from the general population. Design, Setting, and Participants:This study included 4 longitudinal community-based cohorts: the Cardiovascular Health Study (1989-1990; 1992-1993 for supplemental African-American cohort), the Framingham Heart Study (1995-1998), the Multi-Ethnic Study of Atherosclerosis (2000-2002), and the Prevention of Renal and Vascular End-stage Disease study (1997-1998). Each cohort had prospective ascertainment of incident HFpEF and HFrEF. Data analysis was performed from June 25, 2015, to November 9, 2017. Exposures:The following biomarkers were examined: N-terminal pro B-type natriuretic peptide or brain natriuretic peptide, high-sensitivity troponin T or I, C-reactive protein (CRP), urinary albumin to creatinine ratio (UACR), renin to aldosterone ratio, D-dimer, fibrinogen, soluble suppressor of tumorigenicity, galectin-3, cystatin C, plasminogen activator inhibitor 1, and interleukin 6. Main Outcomes and Measures:Development of incident HFpEF and incident HFrEF. Results:Among the 22 756 participants in these 4 cohorts (12 087 women and 10 669 men; mean [SD] age, 60 [13] years) in the study, during a median follow-up of 12 years, 633 participants developed incident HFpEF, and 841 developed HFrEF. In models adjusted for clinical risk factors of heart failure, 2 biomarkers were significantly associated with incident HFpEF: UACR (hazard ratio [HR], 1.33; 95% CI, 1.20-1.48; P < .001) and natriuretic peptides (HR, 1.27; 95% CI, 1.16-1.40; P < .001), with suggestive associations for high-sensitivity troponin (HR, 1.11; 95% CI, 1.03-1.19; P = .008), plasminogen activator inhibitor 1 (HR, 1.22; 95% CI, 1.03-1.45; P = .02), and fibrinogen (HR, 1.12; 95% CI, 1.03-1.22; P = .01). By contrast, 6 biomarkers were associated with incident HFrEF: natriuretic peptides (HR, 1.54; 95% CI, 1.41-1.68; P < .001), UACR (HR, 1.21; 95% CI, 1.11-1.32; P < .001), high-sensitivity troponin (HR, 1.37; 95% CI, 1.29-1.46; P < .001), cystatin C (HR, 1.19; 95% CI, 1.11-1.27; P < .001), D-dimer (HR, 1.22; 95% CI, 1.11-1.35; P < .001), and CRP (HR, 1.19; 95% CI, 1.11-1.28; P < .001). When directly compared, natriuretic peptides, high-sensitivity troponin, and CRP were more strongly associated with HFrEF compared with HFpEF. Conclusions and Relevance:Biomarkers of renal dysfunction, endothelial dysfunction, and inflammation were associated with incident HFrEF. By contrast, only natriuretic peptides and UACR were associated with HFpEF. These findings highlight the need for future studies focused on identifying novel biomarkers of the risk of HFpEF.

Project description:AimsThe diagnostic and treatment of patients with heart failure with preserved ejection fraction (HFpEF) are both hampered by an incomplete understanding of the pathophysiology of the disease. Novel imaging tools to adequately identify these patients from individuals with a normal cardiac function and respectively patients with HF with reduced EF are warranted. Computing multilayer myocardial strain with feature tracking is a fast and accurate method to assess cardiac deformation. Our purpose was to assess the HFpEF diagnostic ability of multilayer strain parameters and compare their sensitivity and specificity with other established parameters.Methods and resultsWe included 20 patients with a diagnosis of HFpEF and, respectively, 20 matched controls. We assessed using feature-tracking cardiac magnetic resonance longitudinal and circumferential myocardial strain at three distinct layers of the myocardium: subendocardial (Endo-), mid-myocardial (Myo-), and subepicardial (Epi-). Comparatively, we additionally assessed various others clinical, imaging, and biochemical parameters with a putative role in HFpEF diagnostic: left ventricular end-diastolic volume (LVEDV), left ventricular mass (LVM), interventricular septum (IVS) wall thickness and free wall thickness, left atrial volume and strain, septal and lateral mitral annular early diastolic velocity (e`), E/e´ ratio, and plasma levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP). Global longitudinal strain (GLS) is significantly impaired at Endo (-20.8 ± 4.0 vs. -23.2 ± 3.4, P = 0.046), Myo- (-18.0 ± 3.0 vs. -21.0 ± 2.5, P = 0.002), and Epi- (-12.2 ± 2.0 vs. -16.2 ± 2.5, P < 0.001) levels. Compared with any other imaging parameter, an Epi-GLS lower than 13% shows the highest ability to detect patients with HFpEF [area under the curve (AUC) = 0.90 (0.81-1), P < 0.001] and in tandem with NT-proBNP can diagnose with maximal sensibility (93%) and specificity (100%), patients with HFpEF from normal, composed variable [AUC = 0.98 (0.95-1), P < 0.001]. In a logistic regression model, a composite predictive variable taking into account both GLS Epi and NT-proBNP values in each individual subject reached a sensitivity of 89% and a specificity of 100% with an AUC of 0.98 (0.95-1), P < 0.001, to detect HFpEF.ConclusionsEpi-GLS is a promising new imaging parameter to be considered in the clinical assessment of HFpEF patients. Given its excellent specificity, in tandem with a highly sensitive parameter such as NT-proBNP, Epi-GLS holds the potential to greatly improve the current diagnostic algorithms.

Dataset Information

Predictors and prognosis for incident in-hospital heart failure in patients with preserved ejection fraction after first acute myocardial infarction: An observational study.

Publications

Predictors and prognosis for incident in-hospital heart failure in patients with preserved ejection fraction after first acute myocardial infarction: An observational study.

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