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Abstract Aims In people at risk of heart failure (HF) enrolled in the Heart ‘OMics’ in AGEing (HOMAGE) trial, spironolactone reduced circulating markers of collagen synthesis, natriuretic peptides, and blood pressure and improved cardiac structure and function. In the present report, we explored factors associated with dyskalaemia. Methods and results The HOMAGE trial was an open‐label study comparing spironolactone (up to 50 mg/day) versus standard care in people at risk for HF. After randomization, serum potassium was assessed at 1 and 9 months and was defined as low when ≤3.5 mmol/L (hypokalaemia) and high when ≥5.5 mmol/L (hyperkalaemia). Multivariable logistic regression models were constructed to identify clinical predictors of dyskalaemia. A total of 513 participants (median age 74 years, 75% men, median estimated glomerular filtration rate 71 mL/min/1.73 m2) had serum potassium available and were included in this analysis. At randomization, 88 had potassium 5.0 mmol/L. During follow‐up, on at least one occasion, a serum potassium 5.0 mmol/L was observed in 38 (8%) and >5.5 mmol/L in 5 (1.0%) participants. The median (percentile25−75) increase in serum potassium with spironolactone during the study was 0.23 (0.16; 0.29) mmol/L. Because of the low incidence of dyskalaemia, for regression analysis, hypokalaemia and hyperkalaemia thresholds were set at 5.0 mmol/L, respectively. The occurrence of a serum potassium > 5.0 mmol/L during follow‐up was positively associated with the presence of diabetes mellitus {odds ratio [OR]: 1.21 [95% confidence interval (CI) 2.14; 3.79]} and randomization to spironolactone (OR: 2.83 [95% CI 1.49; 5.37]). Conversely, the occurrence of a potassium concentration

Aims: In people at risk of heart failure (HF) enrolled in the Heart 'OMics' in AGEing (HOMAGE) trial, spironolactone reduced circulating markers of collagen synthesis, natriuretic peptides, and blood pressure and improved cardiac structure and function. In the present report, we explored factors associated with dyskalaemia. Methods and results: The HOMAGE trial was an open‐label study comparing spironolactone (up to 50 mg/day) versus standard care in people at risk for HF. After randomization, serum potassium was assessed at 1 and 9 months and was defined as low when ≤3.5 mmol/L (hypokalaemia) and high when ≥5.5 mmol/L (hyperkalaemia). Multivariable logistic regression models were constructed to identify clinical predictors of dyskalaemia. A total of 513 participants (median age 74 years, 75% men, median estimated glomerular filtration rate 71 mL/min/1.73 m2) had serum potassium available and were included in this analysis. At randomization, 88 had potassium < 4.0 mmol/L, 367 had potassium 4.0–5.0 mmol/L, and 58 had potassium > 5.0 mmol/L. During follow‐up, on at least one occasion, a serum potassium < 3.5 mmol/L was observed in 6 (1.2%) and <4.0 mmol/L in 46 (9%) participants, while a potassium > 5.0 mmol/L was observed in 38 (8%) and >5.5 mmol/L in 5 (1.0%) participants. The median (percentile25−75) increase in serum potassium with spironolactone during the study was 0.23 (0.16; 0.29) mmol/L. Because of the low incidence of dyskalaemia, for regression analysis, hypokalaemia and hyperkalaemia thresholds were set at <4.0 and >5.0 mmol/L, respectively. The occurrence of a serum potassium > 5.0 mmol/L during follow‐up was positively associated with the presence of diabetes mellitus {odds ratio [OR]: 1.21 [95% confidence interval (CI) 2.14; 3.79]} and randomization to spironolactone (OR: 2.83 [95% CI 1.49; 5.37]). Conversely, the occurrence of a potassium concentration < 4.0 mmol/L was positively associated with the use of thiazides (OR: 2.39 [95% CI 1.32; 4.34]), blood urea concentration (OR: 2.15 [95% CI 1.34; 3.39] per 10 mg/dL), and history of hypertension (OR: 2.32 [95% CI 1.02; 5.29]) and negatively associated with randomization to spironolactone (OR: 0.30 [95% CI 0.18; 0.52]). Conclusions: In people at risk for developing HF and with relatively normal renal function, spironolactone reduced the risk of hypokalaemia and, at the doses used, was not associated with the occurrence of clinically meaningful hyperkalaemia. [ABSTRACT FROM AUTHOR]

Abstract Aims Guidelines support the role of B‐type natriuretic peptide (BNP) and amino‐terminal pro‐BNP (NT‐proBNP) for risk stratification of patients in programmes to prevent heart failure (HF). Although biologically formed in a 1:1 ratio, the ratio of NT‐proBNP to BNP exhibits wide inter‐individual variability. A report on an Asian population suggests that molar NT‐proBNP/BNP ratio is associated with incident HF. This study aims to determine whether routine, simultaneous evaluation of both BNP and NT‐proBNP is warranted in a European, Caucasian population. Methods and Results We determined BNP and NT‐proBNP levels for 782 Stage A/B HF patients in the STOP‐HF programme. The clinical, echocardiographic, and biochemical associates of molar NT‐proBNP/BNP ratio were analysed. The primary endpoint was the adjusted association of baseline molar NT‐proBNP/BNP ratio with new‐onset HF and/or progression of left ventricular dysfunction (LVD). We estimated the C‐statistic, integrated discrimination improvement, and the category‐free net reclassification improvement metric for the addition of molar NT‐proBNP/BNP ratio to adjusted models. The median age was 66.6 years [interquartile range (IQR) 59.5–73.1], 371 (47.4%) were female, and median molar NT‐proBNP/BNP ratio was 1.91 (IQR 1.37–2.93). Estimated glomerular filtration rate, systolic blood pressure, left ventricular mass index, and heart rate were associated with NT‐proBNP/BNP ratio in a linear regression model (all P

Purpose of Review: Over the past few decades, multiple glucose lowering therapies have been developed, but until now, no single drug has proven to both decrease cardiovascular mortality and improve renal outcomes. The purpose of this review is to outline the key findings of the recent major outcome clinical trials on SGLT2 inhibitors, review the indications for their use, and improve adoption of these medications in patients with type 2 diabetes mellitus (T2DM). Recent Findings: Recent studies have shown a benefit for SGLT2 inhibitors in patients with heart failure (HF) and kidney disease both in the presence and absence of T2DM. Additional benefits also include improvements in fluid status, blood pressure, serum uric acid levels, and weight loss. Summary: Available data suggests that SGLT2 inhibitors should be used in all eligible patients with HFrEF and/or CKD with albuminuria to decrease progression of CKD, hospitalizations for heart failure, major atherosclerotic cardiovascular events, and cardiovascular death, with and without T2DM [ABSTRACT FROM AUTHOR]

Aims: Guidelines support the role of B‐type natriuretic peptide (BNP) and amino‐terminal pro‐BNP (NT‐proBNP) for risk stratification of patients in programmes to prevent heart failure (HF). Although biologically formed in a 1:1 ratio, the ratio of NT‐proBNP to BNP exhibits wide inter‐individual variability. A report on an Asian population suggests that molar NT‐proBNP/BNP ratio is associated with incident HF. This study aims to determine whether routine, simultaneous evaluation of both BNP and NT‐proBNP is warranted in a European, Caucasian population. Methods and Results: We determined BNP and NT‐proBNP levels for 782 Stage A/B HF patients in the STOP‐HF programme. The clinical, echocardiographic, and biochemical associates of molar NT‐proBNP/BNP ratio were analysed. The primary endpoint was the adjusted association of baseline molar NT‐proBNP/BNP ratio with new‐onset HF and/or progression of left ventricular dysfunction (LVD). We estimated the C‐statistic, integrated discrimination improvement, and the category‐free net reclassification improvement metric for the addition of molar NT‐proBNP/BNP ratio to adjusted models. The median age was 66.6 years [interquartile range (IQR) 59.5–73.1], 371 (47.4%) were female, and median molar NT‐proBNP/BNP ratio was 1.91 (IQR 1.37–2.93). Estimated glomerular filtration rate, systolic blood pressure, left ventricular mass index, and heart rate were associated with NT‐proBNP/BNP ratio in a linear regression model (all P < 0.05). Over a median follow‐up period of 5 years (IQR 3.4–6.8), 247 (31.5%) patients developed HF or progression of LVD. Log‐transformed NT‐proBNP/BNP ratio is inversely associated with HF and LVD risk when adjusted for age, gender, diabetes, hypertension, vascular disease, obesity, heart rate, number of years of follow‐up, estimated glomerular filtration rate, and baseline NT‐proBNP (odds ratio 0.71, 95% confidence interval 0.55–0.91; P = 0.008). However, molar NT‐proBNP/BNP ratio did not increase the C‐statistic (Δ −0.01) and net reclassification improvement (0.0035) for prediction of HF and LVD compared with NT‐proBNP or BNP alone. Substitution of NT‐proBNP for BNP in the multivariable model eliminated the association with HF and LVD risk. Conclusions: This study characterized, for the first time in a Caucasian Stage A/B HF population, the relationship between NT‐proBNP/BNP ratio and biological factors and demonstrated an inverse relationship with the future development of HF and LVD. However, this study does not support routine simultaneous BNP and NT‐proBNP measurement in HF prevention programmes amongst European, Caucasian patients. [ABSTRACT FROM AUTHOR]

Aims  To investigate the effects of spironolactone on fibrosis and cardiac function in people at increased risk of developing heart failure. Methods and results  Randomized, open-label, blinded-endpoint trial comparing spironolactone (50 mg/day) or control for up to 9 months in people with, or at high risk of, coronary disease and raised plasma B-type natriuretic peptides. The primary endpoint was the interaction between baseline serum galectin-3 and changes in serum procollagen type-III N-terminal pro-peptide (PIIINP) in participants assigned to spironolactone or control. Procollagen type-I C-terminal pro-peptide (PICP) and collagen type-1 C-terminal telopeptide (CITP), reflecting synthesis and degradation of type-I collagen, were also measured. In 527 participants (median age 73 years, 26% women), changes in PIIINP were similar for spironolactone and control [mean difference (mdiff): −0.15; 95% confidence interval (CI) −0.44 to 0.15 μg/L; P  = 0.32] but those receiving spironolactone had greater reductions in PICP (mdiff: −8.1; 95% CI −11.9 to −4.3 μg/L; P  < 0.0001) and PICP/CITP ratio (mdiff: −2.9; 95% CI −4.3 to −1.5; <0.0001). No interactions with serum galectin were observed. Systolic blood pressure (mdiff: −10; 95% CI −13 to −7 mmHg; P  < 0.0001), left atrial volume (mdiff: −1; 95% CI −2 to 0 mL/m2; P  = 0.010), and NT-proBNP (mdiff: −57; 95% CI −81 to −33 ng/L; P  < 0.0001) were reduced in those assigned spironolactone. Conclusions  Galectin-3 did not identify greater reductions in serum concentrations of collagen biomarkers in response to spironolactone. However, spironolactone may influence type-I collagen metabolism. Whether spironolactone can delay or prevent progression to symptomatic heart failure should be investigated. Open in new tab Download slide Open in new tab Download slide [ABSTRACT FROM AUTHOR]

See Article Johnson et al

Background: The recent heart failure (HF) guideline recommends the inclusion of cardiac biomarkers in defining Stage B HF., Objectives: The authors evaluated the impact of incorporating cardiac biomarkers to reclassify HF in 5,324 participants (mean age: 75.8 years) without prevalent HF enrolled in the ARIC (Atherosclerosis Risk In Communities) study and assessed prognosis of Stage B using cardiac biomarkers., Methods: Using N-terminal pro-B-type natriuretic peptide (<125 pg/mL or ≥125 pg/mL), high-sensitivity troponin T (<14 ng/L or ≥14 ng/L), and abnormal cardiac structure/function by echocardiography, individuals were classified as Stage A new and Stage B new HF, respectively. Stage B new was further evaluated as elevated biomarker only, abnormal echocardiogram only, and abnormalities in both (echo + biomarker). The authors assessed risk for incident HF and all-cause death using Cox regression., Results: Overall, 4,326 (81.3%) individuals were classified as Stage B new with 1,123 (21.1%) meeting criteria for elevated biomarkers only. Compared with Stage A new , Stage B new was associated with increased risk for incident HF (HR: 3.70 [95% CI: 2.58-5.30]) and death (HR: 1.94 [95% CI: 1.53-2.46]). Stage B biomarkers only and Stage B echo only were associated with increased HF risk, whereas Stage B biomarkers only was also associated with increased death. Stage B echo+biomarker had the highest risk for HF (HR: 6.34 [95% CI: 4.37-9.19]) and death (HR: 2.53 [95% CI: 1.98-3.23])., Conclusions: Incorporating biomarkers based on the new HF guideline reclassified approximately 1 in 5 older adults without prevalent HF to Stage B. The routine measurement of biomarkers can help to identify individuals at higher HF risk who may benefit most from HF prevention efforts., Competing Interests: Funding Support and Author Disclosures The ARIC study has been funded in whole or in part with Federal funds from the National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, under Contract numbers (75N92022D00001, 75N92022D00002, 75N92022D00003, 75N92022D00004, 75N92022D00005). Dr Bozkurt has received consulting fees from Bristol Myers Squibb, scPharmaceuticals, Baxter Healthcare Corporation, Sanofi-Aventis, Relypsa, Amgen; serves on the Clinical Event Committee for GUIDE HF Trial sponsored by Abbott Vascular, and Data Safety Monitoring Committee of ANTHEM trial (Autonomic REGULATION Therapy to Enhance Myocardial Function and Reduce progression of Heart Failure with reduced ejection fraction) sponsored by Liva Nova. Dr Ballantyne has received research support from National Institutes of Health grant R01HL134320 (relevant to study), Abbott Diagnostic, Akcea, Amgen, Arrowhead, Esperion, Ionis, Novartis, Regeneron, Roche Diagnostic, National Institutes of Health, AHA, and ADA; is a consultant for Abbott Diagnostics, Althera, Amarin, Amgen, Arrowhead, AstraZeneca, Denka Seiken, Esperion, Genentech, Gilead, Illumina, Matinas BioPharma Inc, Merck–New Amsterdam, Novartis, Novo Nordisk, Pfizer, Regeneron, Roche Diagnostic, and Sanofi-Synthelabo. Dr Hoogeveen has received research grants from Denka Seiken and serves as a consultant to Denka Seiken. Dr de Lemos has received grant support from Abbott Diagnostics and Roche Diagnostics; and consulting income from Siemen’s Health Care Diagnostics, Quidel, Beckman Coulter, and Ortho Clinical Diagnostics; and is the co-inventor on a patent awarded to University of Maryland using high sensitivity cardiac troponin T and left ventricular hypertrophy as markers of heart failure risk (patent number: 61990386). Dr Nambi has stock ownership in Abbott labs. Dr Shah has received research support from Novartis and Philips Ultrasound; and consulting fees from Philips Ultrasound and Janssen. Dr Selvin has received research funding support from the National Institutes of Health grant R01HL134320 (relevant to study). Dr Virani has received grant support from the U.S. Department of Veterans Affairs, National Institutes of Health, Tahir, and the Jooma Family; and has received honorarium from the American College of Cardiology (Associate Editor for Innovations, acc.org). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Published by Elsevier Inc.)

Background: Heart failure has become one of the major causes of hospitalization worldwide. Hypertension, diabetes mellitus and hyperlipidemia are the major causes of heart failure. In order to effectively prevent heart failure, blood pressure, blood glucose and cholesterol levels shall be closely monitored and controlled as well as medication adherence. This study aimed to investigate the role of pharmacist intervention in prevention of heart failure in high risk elderly patients in the community of Hong Kong.Aim: This study aimed to investigate the role of pharmacist intervention in prevention of heart failure in highrisk elderly patients in the community of Hong Kong.Methods: This prospective uncontrolled study was conducted between July 2012 and April 2013 with two revisits every 3 to 4 months to review elderly patients' medication profiles as well as assess their blood pressure (BP), random capillary blood glucose (RCBG) level, cholesterol levels, signs and symptoms of heart failure and the compliance level. The results collected at the baseline data were analyzed and compared with those collected at the last follow-up visit.Result: A significant increase in number of subjects free of symptoms of heart failure (31.88%, p < 0.001) was found. For chronic disease management, significant reduction in LDL-cholesterol level (-0.86 ± 0.56mmol/L, p = 0.038) and triglyceride level (-1.15 ± 1.09mmol/L, p < 0.001) was observed in overall participants. Yet, no significant reduction in BP level or RCBG level was observed in overall subjects. Significant reduction in mean Morisky Medication Adherence Score (-0.54 ± 1.50, p = 0.005) indicated improvement in medication compliance in participants.Conclusion: The Pharmacy Outreach service has a significant role in prevention of heart failure, by means of minimizing heart failure symptoms, improving medication compliance and enhancing chronic disease management, particularly cholesterol management in community elderly patients. This study provided a reference for further investigation and evaluation of the role of pharmacists in preventing heart failure in the high-risk community elderly patients. [ABSTRACT FROM AUTHOR]

Abstract: Background: Statins are cholesterol-lowering drugs that have been proved to prevent cardiac events. Their direct effects on cardiac remodeling, when administered in programmed protein restricted animals, still are unknown. Methods and Results: Wistar male 6-month-old offspring from dams fed normal protein (NP, 19% of protein) or low-protein (LP, 5% of protein) during pregnancy and first 10 days after birth were studied. After weaning, male pups were allocated to untreated or treated groups with atorvastatin (low and high doses, 5 or 30 mg·kg·day) in two different periods (from 21 days old to 3 months old and from 3 to 6 months old). The blood pressure (BP) was 30% greater in untreated LP offspring than in treated offspring (from 165 ± 6 mm Hg to 127 ± 3 mm Hg, P < .01). After 1 month of treatment, only untreated LP offspring continued with high BP. Compared with untreated LP offspring, atorvastatin reduced blood glucose (less 30%, P < .05) and cardiomyocyte size (less 24%, P < .05), whereas untreated LP offspring had greater interstitial fibrosis (plus 74%, P < .01), reduction of myocardial vascularization (less 25%, P < .01) and major reduction of cardiomyocyte number (less 38%, P < .01) than treated LP offspring. Conclusion: Atorvastatin from 3 to 6 months olds in both low and high doses (but not from 0 to 3 months) has beneficial effects improving myocardial vascularization by diminishing fibrosis and cardiomyocyte loss. [Copyright &y& Elsevier]

The spontaneously hypertensive rat (SHR) is an animal model of genetic hypertension which develops heart failure with aging, similar to man. The consistent pattern of a long period of stable hypertrophy followed by a transition to failure provides a useful model to study mechanisms of heart failure with aging and test treatments at differing phases of the disease process. The transition from compensated hypertrophy to failure is accompanied by changes in cardiac function which are associated with altered active and passive mechanical properties of myocardial tissue; these events define the physiologic basis for cardiac decompensation. In examining the mechanism for myocardial tissue dysfunction, studies have demonstrated a central role for neurohormonal activation, and specifically the renin-angiotensin-aldosterone system. Pharmacologic attenuation of this system at differing points in the course of the process suggests that prevention but not reversal of myocardial tissue dysfunction is possible. The roles of the extracellular matrix, apoptosis, intracellular calcium, beta-adrenergic stimulation, microtubules, and oxygen supply-demand relationships in ultimately mediating myocardial tissue dysfunction are reviewed. Studies suggest that while considerable progress has been made in understanding and treating the transition to failure, our current state of knowledge is limited in scope and we are not yet able to define specific mechanisms responsible for tissue dysfunction. It will be necessary to integrate information on the roles of newly discovered, and as yet undiscovered, genes and pathways to provide a clearer understanding of maladaptive remodeling seen with heart failure. Understanding the mechanism for tissue dysfunction is likely to result in more effective treatments for the prevention and reversal of heart failure with aging. It is anticipated that the SHR model will assist us in reaching these important goals. [ABSTRACT FROM AUTHOR]

Benefit achieved through use of angiotensin converting enzyme (ACE) inhibitors in patients with reduced left ventricular (LV) systolic function is not confined to those with clinical manifestations of heart failure. Although rates of adverse clinical events are lower in asymptomatic patients, within this population ACE inhibitors have been shown to prevent adverse ventricular remodelling, prevent the development of clinical heart failure, reduce rates of hospitalization for heart failure and, in some studies, reduce mortality. Most of the benefit derived appears to be associated with preventing the progression of L V hypertrophy, dilatation, and dysfunction, resulting in prevention of heart failure. Additionally, the incidence of myocardial infarction is decreased, although the exact physiological basis for this benefit remains uncertain. Given the enormity and growth of heart failure as a public health problem and the potential for influencing the underlying pathophysiology, ACE inhibitor treatment offers substantial benefit for patients with asymptomatic LV systolic dysfunction. [ABSTRACT FROM PUBLISHER]

Objectives: This study sought to further understand the mechanisms underlying effect of spironolactone and assessed its impact on multiple plasma protein biomarkers and their respective underlying biologic pathways., Background: In addition to their beneficial effects in established heart failure (HF), mineralocorticoid receptor antagonists may act upstream on mechanisms, preventing incident HF. In people at risk for developing HF, the HOMAGE (Heart OMics in AGEing) trial showed that spironolactone treatment could provide antifibrotic and antiremodeling effects, potentially slowing the progression to HF., Methods: Baseline, 1-month, and 9-month (or last visit) plasma samples of HOMAGE participants were measured for protein biomarkers (n = 276) by using Olink Proseek-Multiplex cardiovascular and inflammation panels (Olink, Uppsala, Sweden). The effect of spironolactone on biomarkers was assessed by analysis of covariance and explored by knowledge-based network analysis., Results: A total of 527 participants were enrolled; 265 were randomized to spironolactone (25 to 50 mg/day) and 262 to standard care ("control"). The median (interquartile range) age was 73 years (69 to 79 years), and 26% were female. Spironolactone reduced biomarkers of collagen metabolism (e.g., COL1A1, MMP-2); brain natriuretic peptide; and biomarkers related to metabolic processes (e.g., PAPPA), inflammation, and thrombosis (e.g., IL17A, VEGF, and urokinase). Spironolactone increased biomarkers that reflect the blockade of the mineralocorticoid receptor (e.g., renin) and increased the levels of adipokines involved in the anti-inflammatory response (e.g., RARRES2) and biomarkers of hemostasis maintenance (e.g., tPA, UPAR), myelosuppressive activity (e.g., CCL16), insulin suppression (e.g., RETN), and inflammatory regulation (e.g., IL-12B)., Conclusions: Proteomic analyses suggest that spironolactone exerts pleiotropic effects including reduction in fibrosis, inflammation, thrombosis, congestion, and vascular function improvement, all of which may mediate cardiovascular protective effects, potentially slowing progression toward heart failure. (HOMAGE [Bioprofiling Response to Mineralocorticoid Receptor Antagonists for the Prevention of Heart Failure]; NCT02556450)., Competing Interests: FUNDING SUPPORT AND AUTHOR DISCLOSURES HOMAGE was funded by a grant from the European Union 7th Framework Programme for Research and Technological Development (HEALTH-F7-305507 HOMAGE (EU FP7 305507 http://www.homage-hf.eu). Drs. Ferreira, Rossignol, Girerd, and Zannad are supported by the RHU Fight-HF, a public grant overseen by the French National Research Agency (ANR) as part of the second “Investissements d’Avenir” program (reference: ANR-15-RHUS-0004); the French PIA project “Lorraine Université d’Excellence” (reference: ANR-15-IDEX-04-LUE); Contrat de Plan Etat Lorraine IT2MP; and FEDER Lorraine. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2021 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Heart failure (HF) continues to grow as a cause of morbidity and mortality in our community and presents a significant public health problem, predominantly in individuals ≥65 years of age. Early intervention in asymptomatic HF subjects (Stage A/B) at risk of progression to symptomatic HF (Stage C/D) may provide an opportunity to halt this epidemic. The ability of cardiac imaging to assess cardiac structure and function permits early identification of those at increased risk of developing symptomatic HF. Systolic, diastolic, and structural left ventricular parameters each predict symptomatic HF, but no single parameter has sufficient sensitivity for screening to identify individuals with Stage A/B HF who are at increased risk of disease progression. Transthoracic echocardiography (TTE) has the advantage over other imaging modalities in being able to measure systolic, diastolic, and structural left ventricular parameters, and it identified at least 1 abnormal parameter in >50% of individuals with Stage A/B HF ≥65 years of age. Moreover, identification of at least 1 abnormality according to TTE in individuals with Stage A/B HF ≥65 years of age had 72% to 82% sensitivity for detection of those who subsequently developed symptomatic HF. Therefore, a case can be made for cardiac imaging by using TTE for community-dwelling populations with Stage A/B HF ≥65 years of age to identify those with increased risk of symptomatic HF who can be offered preventative therapies. Further studies are required to determine the best strategy for identifying the risk of symptomatic HF in younger individuals., (Copyright © 2017 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)