BACKGROUND:Utilization of right ventricular mechanical circulatory support (RV-MCS) devices has been limited by a lack of recognition of RV failure as well as a lack of availability and experience with RV-MCS. AIMS:We report a single-center experience with the use of percutaneous RV-MCS and report predictors of adverse outcomes. METHODS:This was a single-center retrospective cohort study. Data from consecutive patients who received RV-MCS for any indication between June 2015 and January 2022 were included. Data on baseline comorbidities, hemodynamics, and laboratory values were collected. The primary outcome was in-hospital mortality analyzed as a logistic outcome in a multivariable model. These variables were further ranked by their predictive value. RESULTS:Among 58 consecutive patients enrolled, the median age was 66 years, 31% were female and 53% were white. The majority of the patients (48%) were hospitalized for acute on chronic heart failure. The majority of the patients were SCAI SHOCK Stage D (67%) and 34 (64%) patients had MCS placed within 24 h of the onset of shock. Before placement of RV-MCS, median central venous pressure (CVP) and RV stroke work index were 20 mmHg and 8.9 g m/m2, respectively. Median serum lactate was 3.5 (1.6, 6.2) mmol/L. Impella RP was implanted in 50% and ProtekDuo in the remaining 50%. Left ventricular MCS was concomitantly used in 66% of patients. Twenty-eight patients (48.3%) died. In these patients, median serum lactate was significantly higher (4.1 [2.3, 13.0] vs. 2.2 [1.4, 4.0]  mmol/L, p = 0.007) and a trend toward higher median CVP (24 [18, 31] vs. 19 [14, 24] mmHg, p = 0.052). In the multivariable logistic model, both serum lactate and CVP before RV-MCS placement were independent predictors of in-hospital mortality. Serum lactate had the highest predictive value. CONCLUSION:In our real-world cohort, 52% of patients treated with RV-MCS survived their index hospitalization. Serum lactate at presentation and CVP were the strongest predictors of in-hospital mortality.

High-sensitivity cardiac troponin-T (hs-cTnT) is a cardiac biomarker primarily utilized in the diagnosis and risk-stratification of patients with acute coronary syndrome. Its role in patients undergoing TAVR is less well studied. This is a single-center prospective study of 173 patients with severe AS (AVA<1.0 cm2) undergoing TAVR at a large medical center between January 1, 2020 and January 1, 2022. The primary endpoint was mortality at 1-year. Secondary endpoints were change in quality of life as assessed by change in Kansas City Questionnaire (KCCQ) scores and change in functional status as assessed by change in distance traveled on a 6-minute walk test (6MWD), from baseline to 30-days and 1-year after TAVR. Blood samples for the assessment of hs-cTnT levels were obtained at baseline, 30-days, and one- year after TAVR. Mortality was observed in 13/173 (7.5%) patients within 1-year of TAVR. The mean age of the cohort was 75.6±12.2 years and 53.8% were male. The baseline hs-cTnT was 25.46±22.93 ng/L. Following TAVR, there was a significant reduction of hs-cTnT by 2.9±10.6 ng/L at 30-days (p=0.007). Pre-TAVR baseline levels of hs-cTnT were significantly higher among those who died vs were alive at 1-year (44.3±29.0 ng/L vs. 23.9±21.7 ng/L, p=0.007). Patients in the highest hs-cTnT tertile (hs-cTnT 24.6-140 ng/L) at baseline had a higher mortality rate (14.3%) compared to those in the middle (hs-cTnT 14.1-24.5 ng/L; 5.5% mortality) and lowest (hs-cTnT 6.0-14.0 ng/L; 3.6% mortality) tertiles (p = 0.05).Δhs-cTnT (30-day hs-cTnT–baseline hs-cTnT) was not associated with 1-year mortality. While TAVR was associated with an improvement in 30-day KCCQ (13.7±20.6), there was no association between baseline orΔhs-cTnT withΔKCCQ orΔ6MWD. Baseline hs-cTnT was significantly associated with all-cause 1-year mortality after TAVR, with the highest tertile patients having a 4-fold greater mortality than the lowest tertile. Baseline andΔhs-cTnT was not associated with changes in quality of life or functional status. These findings suggest baseline hs-cTnT may be a valuable component of a multi-parameter tool to enhance risk stratification and prognostication in patients undergoing TAVR.

Hypertension is a major risk factor for heart disease, heart failure and stroke. Lifestyle changes are recommended as first-line treatment for management of high blood pressure for young adults, when 10-year atherosclerotic cardiovascular disease risk score is < 10 https://www.ClinicalTrials.gov Identifier: NCT03158051, registered 5-15-2017. IRB approval obtained: IRB # 2017 − 0372.

Models to predict patient-specific risk and benefit after TAVR are lacking. Baseline and post-TAVR N-terminal pro-brain natriuretic peptide (NT-pro-BNP) levels have been associated with outcomes after TAVR, though study results have been heterogeneous. This is a single-center prospective study of 173 patients with severe AS (AVA<1.0 cm2) undergoing TAVR at a large medical center between January 1, 2020, and January 1, 2022. The primary endpoint was mortality at 1 year. Secondary endpoints were change in quality of life as assessed by change in Kansas City Questionnaire (KCCQ) scores and change in functional status as assessed by change in distance traveled on a 6-minute walk test (6MWD), from baseline to 30-days and 1-year after TAVR. Blood samples for the assessment of NT-pro-BNP levels were obtained at baseline, 30 days and one year after TAVR. Death occurred in 13/173 (7.5%) patients within 1 year of TAVR. The mean age of the cohort was 75.6±12.2 years and 53.8% were male. The baseline NT-pro-BNP was 2051.55 ± 4869.56 pg/mL. Following TAVR, there was a significant reduction of NT-pro-BNP by 712.7 ± 3451.9 pg/mL at 30-days (p=0.041). Pre-TAVR baseline levels of NT-pro-BNP were significantly higher among those who died vs were alive at 1 year (4163.9 ± 6706.4 pg/mL vs. 1873.2 ± 4667.8 pg/mL, p = 0.004). Patients in the highest NT-pro-BNP tertile (NT-pro-BNP 1233-33875 pg/mL at baseline had a higher mortality rate (14.0%) compared to those in the middle (357-1232 pg/mL; 7.4% mortality) and lowest (11.0-356 pg/mL; 1.8% mortality) tertiles (p = 0.021). ΔNT-pro-BNP at 30 days was not associated with 1-yr mortality. TAVR was associated with an improvement in 30-day KCCQ (13.7±20.6). There was no association between baseline NT-pro-BNP and ΔKCCQ or Δ6MWD. Baseline NT-pro-BNP was significantly associated with all-cause 1-year mortality after TAVR, with the highest tertile patients having a 7.5-fold greater mortality than the lowest tertile. Baseline NT-pro-BNP may be a valuable component of a multi-parameter tool to enhance risk stratification and prognostication in patients undergoing TAVR.

Importance:Uncontrolled hypertension (ie, a 24-hour ambulatory systolic blood pressure of ≥130 mm Hg and diastolic blood pressure of ≥80 mm Hg or clinic systolic blood pressure of ≥140 mm Hg and diastolic blood pressure of ≥90 mm Hg) in young adults is a US public health burden. Objective:To evaluate the effect of a telephone coaching and blood pressure self-monitoring intervention compared with usual care on changes in systolic and diastolic blood pressures and behaviors at 6 and 12 months. Design, Setting, and Participants:This randomized clinical trial included male and female participants aged 18 to 39 years with uncontrolled hypertension confirmed by 24-hour ambulatory blood pressure testing. This was a geographically diverse, multicentered study within 2 large, Midwestern health care systems. Data were collected from October 2017 to February 2022 and analyzed from February to June 2022. Interventions:The My Hypertension Education and Reaching Target (MyHEART) intervention consisted of telephone coaching every 2 weeks for 6 months, with home blood pressure monitoring. Control participants received routine hypertension care. Main Outcomes and Measures:The co-primary clinical outcomes were changes in 24-hour ambulatory and clinic systolic and diastolic blood pressure at 6 and 12 months. The secondary outcomes were hypertension control (defined as ambulatory systolic blood pressure <130 mm Hg and diastolic blood pressure <80 mm Hg or clinic systolic blood pressure <140 mm Hg and diastolic blood pressure <90 mm Hg) and changes in hypertension self-management behavior. Results:A total of 316 participants were randomized (159 to the control group and 157 to the intervention group) from October 2017 to December 2020. The median (IQR) age was 35 (31-37) years, 145 of 311 participants (46.6%) were female, and 166 (53.4%) were male; 72 (22.8%) were Black, and 222 (70.3%) were White. There were no differences in baseline characteristics between groups. There was no significant difference between control and intervention groups for mean 24-hour ambulatory systolic or diastolic blood pressure or clinic systolic or diastolic blood pressure at 6 or 12 months. However, there was appreciable clinical reduction in blood pressures in both study groups (eg, mean [SD] change in systolic blood pressure in intervention group at 6 months, -4.19 [9.77] mm Hg; P < .001). Hypertension control did not differ between study groups. Participants in the intervention group demonstrated a significant increase in home blood pressure monitoring at 6 and 12 months (eg, 13 of 152 participants [8.6%] checked blood pressure at home at least once a week at baseline vs 30 of 86 [34.9%] at 12 months; P < .001). There was a significant increase in physical activity, defined as active by the Godin-Shephard Leisure-Time Physical Activity Questionnaire, in the intervention group at 6 months (69 of 100 [69.0%] vs 51 of 104 [49.0%]; P = .004) but not at 12 months (49 of 86 [57.0%] vs 49 of 90 [54.4%]; P = .76). There was a significant reduction in mean (SD) sodium intake among intervention participants at 6 months (3968.20 [1725.17] mg vs 3354.72 [1365.75] mg; P = .003) but not 12 months. There were no significant differences in other dietary measures. Conclusions and Relevance:The MyHEART intervention did not demonstrate a significant change in systolic or diastolic blood pressures at 6 or 12 months between study groups; however, both study groups had an appreciable reduction in blood pressure. Intervention participants had a significant reduction in dietary sodium intake, increased physical activity, and increased home blood pressure monitoring compared with control participants. These findings suggest that the MyHEART intervention could support behavioral changes in young adults with uncontrolled hypertension. Trial Registration:ClinicalTrials.gov Identifier: NCT03158051.

OBJECTIVE:Smoking increases cardiopulmonary and rheumatic disease risk, yet tobacco cessation intervention is rare in rheumatology clinics. This study aimed to implement a rheumatology staff-driven protocol, Quit Connect, to increase the rate of electronic referrals (e-referrals) to free, state-run tobacco quit lines.METHODS:We conducted a quasi-experimental cohort study of Quit Connect at 3 rheumatology clinics comparing tobacco quit line referrals from 4 baseline years to referrals during a 6-month intervention period. Nurses and medical assistants were trained to use 2 standardized electronic health record (EHR) prompts to check readiness to quit smoking within 30 days, advise cessation, and connect patients using tobacco quit line e-referral orders. Our objective was to use EHR data to examine the primary outcome of tobacco quit line referrals using pre/post design.RESULTS:Across 54,090 pre- and post-protocol rheumatology clinic visits, 4,601 were with current smokers. We compared outcomes between 4,078 eligible pre-implementation visits and 523 intervention period visits. Post-implementation, the odds of tobacco quit line referral were 26-fold higher compared to our pre-implementation rate (unadjusted odds ratio [OR] 26 [95% confidence interval (95% CI) 6-106]). Adjusted odds of checking readiness to quit in the next 30 days increased over 100-fold compared to pre-implementation (adjusted OR 132 [95% CI 99-177]). Intervention led to e-referrals for 71% of quit-ready patients in <90 seconds; 24% of referred patients reported a quit attempt.CONCLUSION:Implementing Quit Connect in rheumatology clinics was feasible and improved referrals to a state-run tobacco quit line. Given the importance of smoking cessation to reduce cardiopulmonary and rheumatic disease risk, future studies should investigate disseminating cessation protocols like Quit Connect that leverage tobacco quit lines.

Background Rheumatologists face time pressures similar to primary care but have not generally benefitted from optimized team-based rooming during the time from the waiting room until the rheumatologist enters the room. Objective The aim of this study was to assess current capacity for population management in rheumatology clinics; we aimed to measure the tasks performed by rheumatology clinic staff (medical assistants or nurses) during rooming. Methods We performed a cross-sectional time-study and work-system analysis to measure rooming workflows at 3 rheumatology clinics in an academic multispecialty practice during 2014–2015. We calculated descriptive statistics and compared frequencies and durations using Fisher exact test and analysis of variance. Results Observing 190 rheumatology clinic previsit rooming sequences (1419 minutes), we found many significant variations. Total rooming duration varied by clinic (median, 6.75–8.25 minutes; p < 0.001). Vital sign measurement and medication reconciliation accounted for more than half of rooming duration. Among 3 clinics, two of 15 tasks varied significantly in duration, and 9 varied in frequency. Findings led clinic leaders to modify policies and procedures regarding 6 high-variation tasks streamlining assessment of weight, height, pain scores, tobacco use, disease activity, and refill needs. Conclusions Assessing rheumatology rooming tasks identified key opportunities to improve quality and efficiency without burdening providers. This project demonstrated user-friendly methods to identify opportunities to standardize rooming and support data-driven decisions regarding rheumatology clinic practice changes to improve population management in rheumatology.

Young adults (18-39 year-olds) with hypertension have a higher lifetime risk for cardiovascular disease. However, less than 50% of young adults achieve hypertension control in the United States. Hypertension self-management programs are recommended to improve control, but have been targeted to middle-aged and older populations. Young adults need hypertension self-management programs (i.e., home blood pressure monitoring and lifestyle modifications) tailored to their unique needs to lower blood pressure and reduce the risks and medication burden they may face over a lifetime. To address the unmet need in hypertensive care for young adults, we developed MyHEART (My Hypertension Education And Reaching Target), a multi-component, theoretically-based intervention designed to achieve self-management among young adults with uncontrolled hypertension. MyHEART is a patient centered program, based upon the Self-Determination Theory, that uses evidence-based health behavior approaches to lower blood pressure. Therefore, the objective of this study is to evaluate MyHEART's impact on changes in systolic and diastolic blood pressure compared to usual care after 6 and 12 months in 310 geographically and racially/ethnically diverse young adults with uncontrolled hypertension. Secondary outcomes include MyHEART's impact on behavioral outcomes at 6 and 12 months, compared to usual clinical care (increased physical activity, decreased sodium intake) and to examine whether MyHEART's effects on self-management behavior are mediated through variables of perceived competence, autonomy, motivation, and activation (mediation outcomes). MyHEART is one of the first multicenter, randomized controlled hypertension trials tailored to young adults with primary care. The design and methodology will maximize the generalizability of this study.

Objective Recognizing high blood pressure (BP) as the most prevalent cardiovascular risk factor in patients with rheumatic diseases and all adults, experts recommend clinic protocols to improve BP control. The aim of this study was to adapt and implement a specialty clinic protocol, "BP Connect," to improve timely primary care follow-up after high BP measurements in rheumatology clinics. Methods We examined BP Connect in a 6-month preimplementation and postimplementation quasi-experimental design with 24-month follow-up in 3 academic rheumatology clinics. Medical assistants and nurses were trained to 1) check (re-measuring BPs >= 140/90 mm Hg), 2) advise (linking rheumatic and cardiovascular diseases), and 3) connect (timely [EHR] orders). We used EHR data and multivariable logistic regression analysis to examine the primary outcome of timely primary care follow-up for patients with in-network primary care. Staff surveys were used to assess perceptions. Interrupted time series analysis was performed to examine sustainability and BP trends in the clinic populations. Results Across both 4,683 preimplementation and 689 postimplementation rheumatology visits by patients with high BP, 2,789 (57%) encounters were eligible for in-network primary care follow-up. Postimplementation, the odds of timely primary care BP measurement follow-up doubled (odds ratio 2.0, 95% confidence interval 1.4-2.9). Median time to follow-up decreased from 71 days to 38 days. Moreover, rheumatology visits by patients with high BP decreased from 17% to 8% over 24 months, suggesting significant population-level declines (P < 0.01). Conclusion Implementing the BP Connect specialty clinic protocol in rheumatology clinics improved timely follow-up and demonstrated reduced population-level rates of high BP. These findings highlight a timely strategy to improve BP follow-up amid new guidelines and quality measures.

INTRODUCTION:The goal of this study is to describe the state of mental health of Wisconsin medical students.METHODS:Online wellness surveys were distributed to students at the University of Wisconsin School of Medicine and Public Health (UWSMPH) and Medical College of Wisconsin (MCW) during the 2016-2017 school year.RESULTS:Of UWSMPH respondents, 40.0% and 12.5% reported experiencing depression/other mood changes and suicidal ideation during medical school, respectively. Twelve percent of MCW respondents screened positive for depression using the Patient Health Questionnaire-2, and 7.8% reported experiencing suicidal ideation in the last 2 weeks.DISCUSSION:Similar to results shown worldwide, Wisconsin medical students experience diminished mental health relative to nonmedical peers. Changes in medical education are needed to improve student mental well-being.

Background/Objective Given heightened cardiovascular disease (CVD) risk in rheumatoid arthritis (RA) and that higher blood pressure (BP) represents greater CVD risk, we hypothesized that higher BP would predict more BP-related communication in rheumatology visits. We examined predictors of documented BP communication during RA clinic visits. Methods This was a retrospective cohort study of RA patients identified in electronic health record records with uncontrolled hypertension (HTN) receiving both primary and rheumatology care. Trained abstractors reviewed RA visit notes for “BP communication” using a standardized tool to elicit documentation about BP or HTN beyond recording vital signs. We used multivariate logistic regression to examine the impact of BP category (American Heart Association: ideal normotension, pre-HTN, and stages I and II HTN) on odds ratios (95% confidence intervals) of BP communication. Results Among 1267 RA patients, 40% experienced BP elevations meeting the definition of uncontrolled HTN. Of 2677 eligible RA visits, 22% contained any documented BP communication. After adjustment, models predicted only 31% of visits with markedly high BPs 160/100 mm Hg or greater would contain BP communication. Compared with stage I, stage II elevation did not significantly increase communication (odds ratio, 2.0 [95% confidence interval, 1.4–2.8] vs. 1.5 [1.2–2.2]), although both groups' odds exceeded pre-HTN and normotension. Less than 10% of eligible visits resulted in documented action steps recommending follow-up of high BP. Conclusions Regardless of BP magnitude, most RA clinic visits lacked documented communication about BP despite compounded CVD risk. Future work should study how rheumatology clinics can facilitate follow-up of high BPs to address HTN as the most common and reversible CVD risk factor.

HomeCirculationVol. 136, No. 62017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplementary MaterialsFree AccessReview ArticlePDF/EPUB2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America Clyde W. Yancy, MD, MSc, MACC, FAHA, FHFSA, Chair, Mariell Jessup, MD, FACC, FAHA, Vice Chair, Biykem Bozkurt, MD, PhD, FACC, FAHA, Javed Butler, MD, MBA, MPH, FACC, FAHA, Donald E. CaseyJr, MD, MPH, MBA, FACC, Monica M. Colvin, MD, FAHA, Mark H. Drazner, MD, MSc, FACC, FAHA, FHFSA, Gerasimos S. Filippatos, MD, Gregg C. Fonarow, MD, FACC, FAHA, FHFSA, Michael M. Givertz, MD, FACC, FHFSA, Steven M. Hollenberg, MD, FACC, JoAnn Lindenfeld, MD, FACC, FAHA, FHFSA, Frederick A. Masoudi, MD, MSPH, FACC, Patrick E. McBride, MD, MPH, FACC, Pamela N. Peterson, MD, FACC, FAHA, Lynne Warner Stevenson, MD, FACC and Cheryl Westlake, PhD, RN, ACNS-BC, FAHA, FHFSA Clyde W. YancyClyde W. Yancy Search for more papers by this author , Mariell JessupMariell Jessup Search for more papers by this author , Biykem BozkurtBiykem Bozkurt *, †, ‡, §, ‖, ¶, #, **, †† Search for more papers by this author , Javed ButlerJaved Butler *, †, ‡, §, ‖, ¶, #, **, †† Search for more papers by this author , Donald E. CaseyJrDonald E. CaseyJr *, †, ‡, §, ‖, ¶, #, **, †† Search for more papers by this author , Monica M. ColvinMonica M. Colvin *, †, ‡, §, ‖, ¶, #, **, †† Search for more papers by this author , Mark H. DraznerMark H. Drazner *, †, ‡, §, ‖, ¶, #, **, †† Search for more papers by this author , Gerasimos S. FilippatosGerasimos S. Filippatos *, †, ‡, §, ‖, ¶, #, **, †† Search for more papers by this author , Gregg C. FonarowGregg C. Fonarow *, †, ‡, §, ‖, ¶, #, **, †† Search for more papers by this author , Michael M. GivertzMichael M. Givertz *, †, ‡, §, ‖, ¶, #, **, †† Search for more papers by this author , Steven M. HollenbergSteven M. Hollenberg *, †, ‡, §, ‖, ¶, #, **, †† Search for more papers by this author , JoAnn LindenfeldJoAnn Lindenfeld *, †, ‡, §, ‖, ¶, #, **, †† Search for more papers by this author , Frederick A. MasoudiFrederick A. Masoudi *, †, ‡, §, ‖, ¶, #, **, †† Search for more papers by this author , Patrick E. McBridePatrick E. McBride *, †, ‡, §, ‖, ¶, #, **, †† Search for more papers by this author , Pamela N. PetersonPamela N. Peterson *, †, ‡, §, ‖, ¶, #, **, †† Search for more papers by this author , Lynne Warner StevensonLynne Warner Stevenson *, †, ‡, §, ‖, ¶, #, **, †† Search for more papers by this author and Cheryl WestlakeCheryl Westlake *, †, ‡, §, ‖, ¶, #, **, †† Search for more papers by this author Originally published28 Apr 2017https://doi.org/10.1161/CIR.0000000000000509Circulation. 2017;136:e137–e161Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2017: Previous Version 1 Table of ContentsPreamblee e1381. Introduction e1391.1 Methodology and Evidence Reviewe e1401.2. Organization of the Writing Group e1411.3. Document Review and Approval e1416. Initial and Serial Evaluation of the HF Patient e1416.3. Biomarkers e1416.3.1. Biomarkers for Prevention: Recommendation e1426.3.2. Biomarkers for Diagnosis: Recommendation e1426.3.3. Biomarkers for Prognosis or Added Risk Stratification: Recommendations e1427. Treatment of Stages A to D e1447.3. Stage C e1447.3.2. Pharmacological Treatment for Stage C HF With Reduced Ejection Fraction: Recommendations e1447.3.2.10. Renin-Angiotensin System Inhibition With Angiotensin-Converting Enzyme Inhibitor or Angiotensin Receptor Blocker or ARNI: Recommendations e1447.3.2.11. Ivabradine: Recommendation e1457.3.3. Pharmacological Treatment for Stage C HFpEF: Recommendations e1469. Important Comorbidities in HF e1479.2. Anemia: Recommendations e1479.5. Hypertension (New Section) e1499.5.1. Treating Hypertension to Reduce the Incidence of HF: Recommendation e1499.5.2. Treating Hypertension in Stage C HFrEF: Recommendation e1499.5.3. Treating Hypertension in Stage C HFpEF: Recommendation e1499.6. Sleep-Disordered Breathing: Recommendations e149References e151Appendix 1. Author Relationships With Industry and Other Entities (Relevant) e156Appendix 2. Reviewer Relationships With Industry and Other Entities (Comprehensive) e158Appendix 3. Abbreviations e161PreambleSince 1980, the American College of Cardiology (ACC) and American Heart Association (AHA) have translated scientific evidence into clinical practice guidelines (guidelines) with recommendations to improve cardiovascular health. These guidelines, which are based on systematic methods to evaluate and classify evidence, provide a cornerstone for quality cardiovascular care. The ACC and AHA sponsor the development and publication of guidelines without commercial support, and members of each organization volunteer their time to the writing and review efforts. Guidelines are official policy of the ACC and AHA.Intended UsePractice guidelines provide recommendations applicable to patients with or at risk of developing cardiovascular disease. The focus is on medical practice in the United States, but guidelines developed in collaboration with other organizations may have a global impact. Although guidelines may be used to inform regulatory or payer decisions, their intent is to improve patients’ quality of care and align with patients’ interests. Guidelines are intended to define practices meeting the needs of patients in most, but not all, circumstances and should not replace clinical judgment.Clinical ImplementationGuideline recommended management is effective only when followed by healthcare providers and patients. Adherence to recommendations can be enhanced by shared decision making between healthcare providers and patients, with patient engagement in selecting interventions based on individual values, preferences, and associated conditions and comorbidities.Methodology and ModernizationThe ACC/AHA Task Force on Clinical Practice Guidelines (Task Force) continuously reviews, updates, and modifies guideline methodology on the basis of published standards from organizations including the Institute of Medicine1,2 and on the basis of internal reevaluation. Similarly, the presentation and delivery of guidelines are reevaluated and modified on the basis of evolving technologies and other factors to facilitate optimal dissemination of information at the point of care to healthcare professionals. Given time constraints of busy healthcare providers and the need to limit text, the current guideline format delineates that each recommendation be supported by limited text (ideally, <250 words) and hyperlinks to supportive evidence summary tables. Ongoing efforts to further limit text are underway. Recognizing the importance of cost-value considerations in certain guidelines, when appropriate and feasible, an analysis of the value of a drug, device, or intervention may be performed in accordance with the ACC/AHA methodology.3To ensure that guideline recommendations remain current, new data are reviewed on an ongoing basis, with full guideline revisions commissioned in approximately 6-year cycles. Publication of new, potentially practice-changing study results that are relevant to an existing or new drug, device, or management strategy will prompt evaluation by the Task Force, in consultation with the relevant guideline writing committee, to determine whether a focused update should be commissioned. For additional information and policies regarding guideline development, we encourage readers to consult the ACC/AHA guideline methodology manual4 and other methodology articles.5–8Selection of Writing Committee MembersThe Task Force strives to avoid bias by selecting experts from a broad array of backgrounds. Writing committee members represent different geographic regions, sexes, ethnicities, races, intellectual perspectives/biases, and scopes of clinical practice. The Task Force may also invite organizations and professional societies with related interests and expertise to participate as partners, collaborators, or endorsers.Relationships With Industry and Other EntitiesThe ACC and AHA have rigorous policies and methods to ensure that guidelines are developed without bias or improper influence. The complete relationships with industry and other entities (RWI) policy can be found online. Appendix 1 of the current document lists writing committee members’ relevant RWI. For the purposes of full transparency, writing committee members’ comprehensive disclosure information is available online. Comprehensive disclosure information for the Task Force is also available online.Evidence Review and Evidence Review CommitteesWhen developing recommendations, the writing committee uses evidence-based methodologies that are based on all available data.4–7 Literature searches focus on randomized controlled trials (RCTs) but also include registries, nonrandomized comparative and descriptive studies, case series, cohort studies, systematic reviews, and expert opinion. Only key references are cited.An independent evidence review committee (ERC) is commissioned when there are 1 or more questions deemed of utmost clinical importance that merit formal systematic review. This systematic review will strive to determine which patients are most likely to benefit from a drug, device, or treatment strategy and to what degree. Criteria for commissioning an ERC and formal systematic review include: a) the absence of a current authoritative systematic review, b) the feasibility of defining the benefit and risk in a time frame consistent with the writing of a guideline, c) the relevance to a substantial number of patients, and d) the likelihood that the findings can be translated into actionable recommendations. ERC members may include methodologists, epidemiologists, healthcare providers, and biostatisticians. When a formal systematic review has been commissioned, the recommendations developed by the writing committee on the basis of the systematic review are marked with“SR”.Guideline-Directed Management and TherapyThe term guideline-directed management and therapy (GDMT) encompasses clinical evaluation, diagnostic testing, and pharmacological and procedural treatments. For these and all recommended drug treatment regimens, the reader should confirm the dosage by reviewing product insert material and evaluate the treatment regimen for contraindications and interactions. The recommendations are limited to drugs, devices, and treatments approved for clinical use in the United States.Class of Recommendation and Level of EvidenceThe Class of Recommendation (COR) indicates the strength of the recommendation, encompassing the estimated magnitude and certainty of benefit in proportion to risk. The Level of Evidence (LOE) rates the quality of scientific evidence that supports the intervention on the basis of the type, quantity, and consistency of data from clinical trials and other sources (Table 1).4–6Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care* (Updated August 2015)Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care* (Updated August 2015)Glenn N. Levine, MD, FACC, FAHAChair, ACC/AHA Task Force on Clinical Practice Guidelines1. IntroductionThe purpose of this focused update is to update the “2013 ACCF/AHA Guideline for the Management of Heart Failure”9 (2013 HF guideline) in areas in which new evidence has emerged since its publication. For this update and future heart failure (HF) guidelines, the Heart Failure Society of America (HFSA) has partnered with the ACC and AHA to provide coordinated guidance on the management of HF.The scope of the focused update includes revision to the sections on biomarkers; new therapies indicated for stage C HF with reduced ejection fraction (HFrEF); updates on HF with preserved ejection fraction (HFpEF); new data on important comorbidities, including sleep apnea, anemia, and hypertension; and new insights into the prevention of HF.This focused update represents the second part of a 2-stage publication; with the first part having been published as the “2016 ACC/AHA/HFSA Focused Update on New Pharmacological Therapy for Heart Failure,”10 which introduced guidance on new therapies, specifically for the use of an angiotensin receptor–neprilysin inhibitor (ARNI) (valsartan/sacubitril) and a sinoatrial node modulator (ivabradine). That focused update was published concurrently with the European Society of Cardiology’s complete guideline, “2016 ESC Guidelines for the Diagnosis and Treatment of Acute and Chronic Heart Failure.”111.1. Methodology and Evidence ReviewTo identify key data that influence guideline recommendations, the Task Force and members of the 2013 HF guideline writing committee reviewed clinical trials that were presented at the annual scientific meetings of the ACC, AHA, and European Society of Cardiology and other scientific meetings and that were published in peer-reviewed format from April 2013 through November 2016. The evidence is summarized in tables in the Online Data Supplement. All recommendations (new, modified, and unchanged) for each clinical section are included to provide a comprehensive assessment. The text explains new and modified recommendations, whereas recommendations from the previous guideline that have been deleted or superseded no longer appear. Please consult the full-text version of the 2013 HF guideline9 for text and evidence tables supporting the unchanged recommendations and for clinical areas not addressed in this focused update. Individual recommendations in this focused update will be incorporated into the full-text guideline in the future. Recommendations from the prior guideline that remain current have been included for completeness, but the LOE reflects the COR/LOE system used when the recommendations were initially developed. New and modified recommendations in this focused update reflect the latest COR/LOE system, in which LOE B and C are subcategorized for greater specificity.4–6 The section numbers correspond to the full-text guideline sections.1.2. Organization of the Writing GroupFor this focused update, representative members of the 2013 HF guideline writing committee were invited to participate. They were joined by additional invited members to form a new writing group, which is referred to as the 2017 HF focused update writing group. Members were required to disclose all RWI relevant to the data under consideration. The group was composed of experts representing general cardiologists, HF and transplantation specialists, electrophysiologists, pharmacists, and general internists. The 2017 HF focused update writing group included representatives from the ACC, AHA, and HFSA, as well as the American Academy of Family Physicians, American College of Chest Physicians, American College of Physicians, and International Society for Heart and Lung Transplantation.1.3. Document Review and ApprovalThe focused update was reviewed by 2 official reviewers each nominated by the ACC, AHA, and HFSA; 1 reviewer each from the American Academy of Family Physicians, American College of Chest Physicians, and International Society for Heart and Lung Transplantation; and 19 individual content reviewers. Reviewers’ RWI information is published in this document (Appendix 2).This document was approved for publication by the governing bodies of the ACC, AHA, and HFSA.6. Initial and Serial Evaluation of the HF Patient6.3. BiomarkersAssays for BNP (B-type natriuretic peptide) and NT-proBNP (N-terminal pro-B-type natriuretic peptide), which are both natriuretic peptide biomarkers, have been used increasingly to establish the presence and severity of HF. In general, both natriuretic peptide biomarker values track similarly, and either can be used in patient care settings as long as their respective absolute values and cutpoints are not used interchangeably. Notably, BNP, but not NT-proBNP, is a substrate for neprilysin. Therefore, ARNI increases BNP levels12 but not NT-proBNP levels.13 Note that the type of natriuretic peptide assay that has been performed must be considered during interpretation of natriuretic peptide biomarker levels in patients on ARNI. In 2 studies with ARNI, NT-proBNP levels were reduced,12,14 with the reduction in 1 study being associated with improved clinical outcomes.12A substantial evidence base exists that supports the use of natriuretic peptide biomarkers to assist in the diagnosis or exclusion of HF as a cause of symptoms (eg, dyspnea, weight gain) in the setting of chronic ambulatory HF15–21 or in the setting of acute care with decompensated HF,22–30 especially when the cause of dyspnea is unclear. The role of natriuretic peptide biomarkers in population screening to detect incident HF is emerging.31–37 Elevated plasma levels of natriuretic peptide biomarkers are associated with a wide variety of cardiac and noncardiac causes (Table 2).38–42 Obesity may be associated with lower natriuretic peptide concentrations, and this may modestly reduce diagnostic sensitivity in morbidly obese patients.42Table 2. Selected Potential Causes of Elevated Natriuretic Peptide Levels38–41Cardiac HF, including RV syndromes Acute coronary syndromes Heart muscle disease, including LVH Valvular heart disease Pericardial disease Atrial fibrillation Myocarditis Cardiac surgery Cardioversion Toxic-metabolic myocardial insults, including cancer chemotherapyNoncardiac Advancing age Anemia Renal failure Pulmonary: obstructive sleep apnea, severe pneumonia Pulmonary hypertension Critical illness Bacterial sepsis Severe burnsModified from Table 8 of the 2013 HF guideline.9HF, indicates heart failure; LVH, left ventricular hypertrophy; and RV, right ventricular.Because of the absence of clear and consistent evidence for improvement in mortality and cardiovascular outcomes,43–62 there are insufficient data to inform specific guideline recommendations related to natriuretic peptide–guided therapy or serial measurements of BNP or NT-proBNP levels for the purpose of reducing hospitalization or deaths in the present document.Like natriuretic peptides, cardiac troponin levels may be elevated in the setting of chronic or acute decompensated HF, suggesting myocyte injury or necrosis.63 Troponins I and T respond similarly for acute coronary syndromes and acute decompensated HF. Elevations in either troponin I or T levels in the setting of acute HF are of prognostic significance and must be interpreted in the clinical context.64In addition to natriuretic peptides and troponins,65–67 multiple other biomarkers, including those of inflammation, oxidative stress, vascular dysfunction, and myocardial and matrix remodeling, have been implicated in HF.68–71 Biomarkers of myocardial fibrosis, soluble ST2 receptor, and galectin-3 are predictive of hospitalization and death and may provide incremental prognostic value over natriuretic peptide levels in patients with HF.72–74 Strategies that combine multiple biomarkers may ultimately prove beneficial in guiding HF therapy in the future, but multicenter studies with larger derivation and validation cohorts are needed.75,76 Several emerging biomarkers await validation with well-defined outcome measures and prognostic accuracy before they can reach the clinical arena.77–84This section categorizes the role of biomarkers into prevention, diagnosis, prognosis, and added risk stratification to clarify evidence-based objectives of their use in clinical practice.6.3.1 Biomarkers for Prevention: RecommendationBiomarkers: Recommendation for Prevention of HFBiomarkers: Recommendation for Prevention of HF6.3.2 Biomarkers for Diagnosis: RecommendationBiomarkers: Recommendation for DiagnosisBiomarkers: Recommendation for Diagnosis6.3.3 Biomarkers for Prognosis or Added Risk Stratification: RecommendationsBiomarkers: Recommendations for PrognosisBiomarkers: Recommendations for Prognosis7. Treatment of Stages A to D7.3. Stage C7.3.2. Pharmacological Treatment for Stage C HF With Reduced Ejection Fraction: Recommendations(See Figure 2 and Table 3).Download figureDownload PowerPointFigure 1. Biomarkers Indications for Use. Colors correspond to COR in Table 1. *Other biomarkers of injury or fibrosis include soluble ST2 receptor, galectin-3, and high-sensitivity troponin. ACC indicates American College of Cardiology; AHA, American Heart Association; ADHF, acute decompensated heart failure; BNP, B-type natriuretic peptide; COR, Class of Recommendation; ED, emergency department; HF, heart failure; NT-proBNP, N-terminal pro-B-type natriuretic peptide; NYHA, New York Heart Association; and pts, patients.Download figureDownload PowerPointFigure 2. Treatment of HFrEF Stage C and D. Colors correspond to COR in Table 1. For all medical therapies, dosing should be optimized and serial assessment exercised. *See text for important treatment directions. †Hydral-Nitrates green box: The combination of ISDN/HYD with ARNI has not been robustly tested. BP response should be carefully monitored. ‡See 2013 HF guideline.9 §Participation in investigational studies is also appropriate for stage C, NYHA class II and III HF. ACEI indicates angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor-blocker; ARNI, angiotensin receptor-neprilysin inhibitor; BP, blood pressure; bpm, beats per minute; C/I, contraindication; COR, Class of Recommendation; CrCl, creatinine clearance; CRT-D, cardiac resynchronization therapy–device; Dx, diagnosis; GDMT, guideline-directed management and therapy; HF, heart failure; HFrEF, heart failure with reduced ejection fraction; ICD, implantable cardioverter-defibrillator; ISDN/HYD, isosorbide dinitrate hydral-nitrates; K+, potassium; LBBB, left bundle-branch block; LVAD, left ventricular assist device; LVEF, left ventricular ejection fraction; MI, myocardial infarction; NSR, normal sinus rhythm; and NYHA, New York Heart Association.Table 3. Drugs Commonly Used for HFrEF (Stage C HF)DrugInitial Daily Dose(s)Maximum Doses(s)Mean Doses Achieved in Clinical TrialsReferencesACE inhibitors Captopril6.25 mg TID50 mg TID122.7 mg QD158 Enalapril2.5 mg BID10–20 mg BID16.6 mg QD129 Fosinopril5–10 mg QD40 mg QDN/A— Lisinopril2.5–5 mg QD20–40 mg QD32.5–35.0 mg QD130 Perindopril2 mg QD8–16 mg QDN/A— Quinapril5 mg BID20 mg BIDN/A— Ramipril1.25–2.5 mg QD10 mg QDN/A— Trandolapril1 mg QD4 mg QDN/A—ARBs Candesartan4–8 mg QD32 mg QD24 mg QD137 Losartan25–50 mg QD50–150 mg QD129 mg QD136 Valsartan20–40 mg BID160 mg BID254 mg QD134ARNI Sacubitril/valsartan49/51 mg BID (sacubitril/valsartan) (therapy may be initiated at 24/26 mg BID)97/103 mg BID (sacubitril/valsartan)375 mg QD; target dose: 24/26 mg, 49/51 mg OR 97/103 mg BID138If channel inhibitor Ivabradine5 mg BID7.5 mg BID6.4 mg BID (at 28 d) 6.5 mg BID (at 1 y)155–157Aldosterone antagonists Spironolactone12.5–25 mg QD25 mg QD or BID26 mg QD142 Eplerenone25 mg QD50 mg QD42.6 mg QD159Beta blockers Bisoprolol1.25 mg QD10 mg QD8.6 mg QD160 Carvedilol3.125 mg BID50 mg BID37 mg QD161 Carvedilol CR10 mg QD80 mg QDN/A— Metoprolol succinate extended release (metoprolol CR/XL)12.5–25 mg QD200 mg QD159 mg QD139Isosorbide dinitrate and hydralazine Fixed-dose combination20 mg isosorbide dinitrate/37.5 mg hydralazine TID40 mg isosorbide dinitrate/75 mg hydralazine TID90 mg isosorbide dinitrate/~175 mg hydralazine QD162 Isosorbide dinitrate and hydralazine20–30 mg isosorbide dinitrate/25–50 mg hydralazine TID or QD40 mg isosorbide dinitrate TID with 100 mg hydralazine TIDN/A163Modified (Table 15) from the 2013 HF guideline.9ACE indicates angiotensin-converting enzyme; ARB, angiotensin receptor blocker; ARNI, angiotensin receptor-neprilysin inhibitor; BID, twice daily; CR, controlled release; CR/XL, controlled release/extended release; HF, heart failure; HFrEF, heart failure with reduced ejection fraction; N/A, not applicable; QD, once daily; and TID, 3 times daily.7.3.2.10. Renin-Angiotensin System Inhibition With Angiotensin-Converting Enzyme Inhibitor or Angiotensin Receptor Blocker or ARNI: RecommendationsRecommendations for Renin-Angiotensin System Inhibition With ACE Inhibitor or ARB or ARNIRecommendations for Renin-Angiotensin System Inhibition With ACE Inhibitor or ARB or ARNI7.3.2.11. Ivabradine: RecommendationRecommendation for IvabradineRecommendation for Ivabradine7.3.3. Pharmacological Treatment for Stage C HFpEF: RecommendationsRecommendations for Stage C HFpEFRecommendations for Stage C HFpEF9. Important Comorbidities in HF9.2. Anemia: RecommendationsRecommendations for AnemiaRecommendations for Anemia9.5. Hypertension (New Section)9.5.1. Treating Hypertension to Reduce the Incidence of HF: RecommendationRecommendation for PreventionRecommendation for Prevention9.5.2. Treating Hypertension in Stage C HFrEF: RecommendationRecommendation for Hypertension in Stage C HFrEFRecommendation for Hypertension in Stage C HFrEF9.5.3. Treating Hypertension in Stage C HFpEF: RecommendationRecommendation for Hypertension in Stage C HFpEFRecommendation for Hypertension in Stage C HFpEF9.6. Sleep-Disordered Breathing: Recommendations(Moved from Section 7.3.1.4, Treatment of Sleep Disorders in the 2013 HF guideline.)Recommendations for Treatment of Sleep DisordersRecommendations for Treatment of Sleep DisordersACC/AHA Task Force MembersGlenn N. Levine, MD, FACC, FAHA, Chair; Patrick T. O’Gara, MD, FACC, FAHA, Chair-Elect; Jonathan L. Halperin, MD, FACC, FAHA, Immediate Past Chair*; Sana M. Al-Khatib, MD, MHS, FACC, FAHA; Kim K. Birtcher, PharmD, MS, AACC; Biykem Bozkurt, MD, PhD, FACC, FAHA; Ralph G. Brindis, MD, MPH, MACC*; Joaquin E. Cigarroa, MD, FACC; Lesley H. Curtis, PhD, FAHA; Lee A. Fleisher, MD, FACC, FAHA; Federico Gentile, MD, FACC; Samuel Gidding, MD, FAHA; Mark A. Hlatky, MD, FACC; John Ikonomidis, MD, PhD, FAHA; José Joglar, MD, FACC, FAHA; Susan J. Pressler, PhD, RN, FAHA; Duminda N. Wijeysundera, MD, PhDPresidents and StaffAmerican College of CardiologyMary Norine Walsh, MD, FACC, PresidentShalom Jacobovitz, Chief Executive OfficerWilliam J. Oetgen, MD, MBA, FACC, Executive Vice President, Science, Education, Quality, and PublishingAmelia Scholtz, PhD, Publications Manager, Science, Education, Quality, and PublishingAmerican College of Cardiology/American Heart AssociationKatherine Sheehan, PhD, Director of Guideline Strategy and OperationsLisa Bradfield, CAE, Director, Guideline Methodology and PolicyAbdul R. Abdullah, MD, Science and Medicine AdvisorMorgane Cibotti-Sun, MPH, Project Manager, Clinical Practice GuidelinesSam Shahid, MBBS, MPH, Associate Science and Medicine AdvisorAmerican Heart AssociationSteven R. Houser, PhD, FAHA, PresidentNancy Brown, Chief Executive OfficerRose Marie Robertson, MD, FAHA, Chief Science and Medicine OfficerGayle R. Whitman, PhD, RN, FAHA, FAAN, Senior Vice President, Office of Science OperationsJody Hundley, Production Manager, Scientific Publications, Office of Science Operations* Former Task Force member; current member during the writing effort.FootnotesThe American Heart Association requests that this document be cited as follows: Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE Jr, Colvin MM, Drazner MH, Filippatos GS, Fonarow GC, Givertz MM, Hollenberg SM, Lindenfeld J, Masoudi FA, McBride PE, Peterson PN, Stevenson LW, Westlake C. 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America. Circulation. 2017;136:e137–e161. DOI: 10.1161/CIR.0000000000000509.This document was approved by the American College of Cardiology Clinical Policy Approval Committee, the American Heart Association Science Advisory and Coordinating Committee, the American Heart Association Executive Committee, and the Heart Failure Society of America Executive Committee in April 2017.The Comprehensive RWI Data Supplement table is available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIR.0000000000000509/-/DC1.The Data Supplement is available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIR.0000000000000509/-/DC2.This article has been copublished in the Journal of the American College of Cardiology and the Journal of Cardiac Failure.Copies: This document is available on the World Wide Web sites of the American College of Cardiology (www.acc.org), the American Heart Association (professional.heart.org), and the Heart Failure Society of America (www.hfsa.org). A copy of the document is available at http://professional.heart.org/statements by selecting either the “By Topic” link or the “By Publication Date” link. To purchase additional reprints, call 843-216-2533 or e-mail [email protected].Expert peer review of AHA Scientific Statements is conducted by the AHA Office of Science Operations. For more on AHA statements and guidelines development, visit http://professional.heart.org/statements and select the “Policies and Development” link.Permissions: Multiple copies, modification, alteration, enhancement, and/or di

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