Discrepancies in Heart Failure With Preserved Ejection Fraction Scoring Systems: A Case Series

Diagnosis of Heart Failure With Preserved Ejection Fraction Relies on Detection of Increased Diastolic Filling Pressure, But How?

IntroductionThere is debate about the diagnostic profile of the heart failure population. Diagnostic criteria for heart failure with reduced ejection fraction (HFREF) are variable and many believe that heart failure...

HFpEF vs. HFrEF: can microRNAs advance the diagnosis?

Validating the HFA-PEFF score - or how to define a disease?

Searching for diagnostic biomarkers of heart failure with preserved ejection fraction: methodological issues.

Vascular Dysfunction in Heart Failure with Preserved Ejection Fraction

As described in Part I of this 2-part article,1 diastolic heart failure is common and causes significant alterations in prognosis. In Part II, experimental studies that have provided insight into the mechanisms that cause diastolic heart failure will be described.2–19⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓ In addition, current treatment strategies and the design of future clinical trials of diastolic heart failure will be discussed. The development of truly effective therapy for diastolic heart failure depends on gaining a clear understanding of the basic mechanisms that alter diastolic function and the ability to efficiently target these mechanisms to correct these abnormalities in diastolic function. Conceptually, the mechanisms that cause abnormalities in diastolic function that lead to the development of diastolic heart failure can be divided into factors intrinsic to the myocardium itself (myocardial) and factors that are extrinsic to the myocardium (extramyocardial; Table 1). Myocardial factors can be divided into structures and processes within the cardiac muscle cell (cardiomyocyte), within the extracellular matrix (ECM) that surrounds the cardiac muscle cell, and that activate the autocrine or paracrine production of neurohormones. Each of these mechanisms are active in the major pathological processes that result in diastolic dysfunction and heart failure. Myocardial and extramyocardial mechanisms, cellular and extracellular mechanisms, and neurohumoral activation each play a role in the development of diastolic heart failure caused by ischemia, pressure-overload hypertrophy, and restrictive and hypertrophic cardiomyopathy. View this table: Table 1105290. Diastolic Heart Failure: Mechanisms ### Cardiomyocyte Diastolic dysfunction can be caused by mechanisms that are intrinsic to the cardiac muscle cells themselves. These include changes in calcium homeostasis caused by (1) abnormalities in the sarcolemmal channels responsible for short- and long-term extrusion of calcium from the cytosol, such as the sodium calcium exchanger and the calcium pump; (2) …

Identification of Subclinical Heart Failure With Preserved Ejection Fraction in Patients With Symptomatic Atrial Fibrillation

Do Existing Definitions Identify Subgroup Phenotypes or Reflect the Natural History of Heart Failure With Preserved Ejection Fraction?

AimsNone of the conventional echocardiographic parameters alone predict increased NTproBNP level and symptoms, making diagnosis of heart failure with preserved ejection fraction (HFpEF) very difficult in some cases, in resting condition. We evaluated LA functions by 2D speckle tracking echocardiography (STE) on top of conventional parameters in HFpEF and preHF patients with diastolic dysfunction (DD), in order to establish the added value of the LA deformation parameters in the diagnosis of HFpEF.MethodsWe prospectively enrolled 125 patients, 88 with HFpEF (68±9 yrs), and 37 asymptomatic with similar risk factors with DD (preHF) (61±8 yrs). We evaluated them by NTproBNP, conventional DD parameters, and STE. Global longitudinal strain (GS) was added. LA reservoir (R), conduit (C), and pump function (CT) were assessed both by volumetric and STE. 2 reservoir strain (S) derived indices were also measured, stiffness (SI) and distensibility index (DI).ResultsLA R and CT functions were significantly reduced in HFpEF compared to preHF group (all p<0.001), whereas conduit was similarly in both groups. SI was increased, whereas DI was reduced in HFpEF group (p<0.001). By adding LA strain analysis, from all echocardiographic parameters, SR_CT<-1.66/s and DI<0.57 (AUC = 0.76, p<0.001) demonstrated the highest accuracy to identify HFpEF diagnosis. However, by multivariate logistic regression, the model that best identifies HFpEF included only SR_CT, GS and sPAP (R2 = 0.506, p<0.001). Moreover, SR_CT, DI, and sPAP registered significant correlation with NTproBNP level.ConclusionsBy adding LA functional analysis, we might improve the HFpEF diagnosis accuracy, compared to present guidelines. LA pump function is the only one able to differentiates preHF from HFpEF patients at rest. A value of SR_CT < -1.66/s outperformed conventional parameters from the scoring system, reservoir strain, and LA overload indices in HFpEF diagnosis. We suggest that LA function by STE could be incorporated in the current protocol for HFpEF diagnosis at rest as a major functional criterion, in order to improve diagnostic algorithm, and also in the follow-up of patients with risk factors and DD, as a prognostic marker. Future studies are needed to validate our findings.

Objective The goals of the present study were to assess the prevalence of asymptomatic heart failure with preserved ejection fraction (HFpEF) in subjects at high risk of developing HF and to define the diagnostic accuracy of NT-pro BNP assay compared with echocardiography in this setting.Material and methods This cross-sectional study included subjects aged from 35 to 64 years, with high risk of HF, who had no clinical symptoms of HF. Risk factors of HF were detected by clinical examinations. NT-pro BNP determination was performed using immunoassay analyzer (FIA8000, Getein Bio Medical Inc, China),. The cut-off point for NT-pro BNP was 125 pg/ml. Diagnosis of HFpEF was based on criteria recommended by 2016 ESC heart failure guidelines. Diastolic dysfunction was assessed according to the algorithm proposed in the joint recommendations of the ASE/EACVI.Results 602 patients with risk factors of HF were included in the study, of which 256 (42.5 %) were males and 346 (57.5 %) females. The mean age was 51.71±8.07 years. 83 patients (13.8 %) showed elevated NT-pro BNP levels of ≥125 pg / ml. Our study has shown that NT-pro BNP concentration was positively correlating with age, both systolic and diastolic blood pressure, left ventricular mass and E / e' ratio and negatively correlating with waist circumference, body mass index, left ventricular EF and E / A ratio in asymptomatic population. The likelihood of positive NT-pro BNP test was independently (p&lt;0.05) associated with age, hypertension and diabetes. The diagnosis of asymptomatic HFpEF was confirmed in 12.3 % of studied population. A cutoff value of 125 pg / ml for NT-proBNP concentration showed the following diagnostic re-abilities in identifying asymptomatic HFpEF: sensitivity 85.0 %, specificity 88.6 % and area under curve 0.92 (95 % CI 0.86-0.98).Conclusion Subjects with raised NT-pro BNP level (≥125 pg/ml) were more likely to have a confirmed diagnosis of asymptomatic HFpEF after screening. In summary, in at-risk population, natriuretic peptide based screening combined with echocardiography identifies high prevalence of asymptomatic HFpEF.

Introduction: Heart failure with preserved ejection fraction (HFpEF) carries high morbidity and mortality. Compared to heart failure with reduced ejection fraction (HFrEF), HFpEF is more difficult to diagnose and lacks in evidence-based treatments. We assessed the perceptions of CV specialists and primary care physicians (PCP) regarding HFpEF diagnosis and management. Methods: The online survey targeted 200 specialists and 200 (PCPs), offering a token honorarium. A total of 159 cardiologists (C), 59 internists (I), and 200 PCPs completed the survey. Results: All provinces were represented. The perceived prevalence of HFpEF vs HFrEF was similar across physician types (58% HFrEF, 42% HFpEF). Roughly 25% of PCPs did not differentiate between HF types. All physician types ranked symptom and mortality reduction as treatment priorities. The majority of specialists felt that HFpEF is best co-managed by primary and specialty care. One fifth of PCPs felt that HFpEF should be managed by primary care alone. Compared to specialists, PCPs were more likely to underestimate HFpEF mortality vs. HFrEF, less aware of gender differences, and less able to identify clinical findings of HFpEF vs. HFrEF. Fewer PCPs (33%) than specialists (50%) use natriuretic peptide (NP) levels for diagnosis, with PCPs expressing more uncertainty with NP utility. All physician types listed cost and limited availability as restrictions to use of NP testing. For evidence-based treatments in HF (ACEi/ARB, beta blockers, loop diuretics, mineralocorticoid receptor antagonists), &gt;50% of PCPs incorrectly identified all agents as effective for HFpEF, with &lt;10% stating that none improved outcomes. Cardiologists were more likely than internists to identify the lack of evidence-based treatments. Conclusions: This survey reveals substantial knowledge and treatment gaps in the diagnosis and management of HFpEF, specifically amongst PCPs. Given the prevalence of HFpEF in primary care, and its substantial morbidity and mortality, strategies are required to reduce these gaps. All physician types recognized the need for increased availability of NP testing for HFpEF diagnosis.

Heart failure with preserved ejection fraction (HFpEF), the most prevalent type of heart failure (HF), is associated with significant morbidity and mortality and a high rate of hospitalizations. HFpEF incidence is projected to continue to rise over the coming decades, primarily due to the increasing prevalence of multiple risk factors that contribute to the development of this syndrome. Obesity, low cardiorespiratory fitness, hypertension, and chronic kidney disease (CKD) have emerged as crucial elements in the pathogenesis of the syndrome. Obesity, in particular, can trigger and potentiate the systemic inflammatory state that is now recognized as central to the pathogenesis of HFpEF. In HFpEF, a range of cardiovascular changes are observed at the cellular and molecular level, including endothelial dysfunction, cardiomyocyte hypertrophy, abnormal calcium handling, microvascular rarefaction, interstitial fibrosis, and excessive collagen deposition (1). A biomarker to assist in diagnosis and risk stratification of HFpEF would improve patient evaluation and management and enable clinical and preclinical research to impact the course of this syndrome. The ideal biomarker would reliably aid in the diagnosis of HFpEF at early stages, guide medical management, and predict disease complications. However, the quest to identify a biomarker with these characteristics has proven elusive as most previous biomarker candidates have fallen short of reaching the clinical stage. Of the biomarkers currently used in the clinic, B-type natriuretic peptide and N-terminal pro-B-type natriuretic peptide (NT-proBNP) support the diagnosis of HFpEF in symptomatic individuals and predict adverse outcomes but cannot distinguish HFpEF from heart failure with reduced ejection fraction (HFrEF). Moreover, levels can be normal in up to 30% of patients with HFpEF; are commonly suppressed in patients with high body mass; and are increased substantially in the setting of CKD, pulmonary hypertension, and atrial fibrillation (1). In asymptomatic individuals, small elevations in NT-proBNP and high sensitivity troponin T and I identify individuals at risk for HF but cannot accurately differentiate future risk of HFpEF from HFrEF.

Sodium-glucose co-transporter 2 inhibitors in heart failure with preserved ejection fraction: reasons for optimism.

Heart failure with preserved ejection fraction (HFpEF) is a multi-organ systemic syndrome that involves cardiac and extra-cardiac pathophysiological abnormalities. Its growing prevalence causes a major public concern worldwide. HFpEF is usually associated with multiple comorbidities, and non-cardiovascular death is common in patients with HFpEF. In Asia, patients with HFpEF has a younger age, higher prevalence of diabetes and chronic kidney disease than Western countries. A 2-step diagnostic algorithm is recommended in this guideline. In the first step, the diagnosis of HFpEF can be made if patients have symptoms and/or signs of heart failure, left ventricular ejection fraction ≥ 50%, increased natriuretic peptide, and objective evidence of left atrial or left ventricular abnormalities or raised left ventricular filling pressure. If diagnosis is still uncertain, invasive or noninvasive stress test can be performed in the second step. Comorbidities need to be controlled in HFpEF. Weight reduction for obesity and supervised exercise training are recommended for HFpEF. For pharmacological therapy, diuretic is used to relieve congestion and sodium-glucose cotransporter 2 inhibitor, empagliflozin or dapagliflozin, is recommended to improve prognosis of HFpEF. The research on HFpEF is advancing at a rapid pace. It is expected that newer modalities for diagnosis and management of HFpEF could appear in the near future.