Heart Failure 1 Fall 2024 PDF

Heart Failure J E N N I F E R S. B Y R D, P H A R M D, B C AC P, B C - A D M Topic Outline Introduction to heart failure Diagnosis of heart failure Clinical presentation of heart failure Pharmacotherapy of chronic heart failure with reduced ejection fraction (HFrEF) Pharmacotherapy of...

Heart Failure J E N N I F E R S. B Y R D, P H A R M D, B C AC P, B C - A D M Topic Outline Introduction to heart failure Diagnosis of heart failure Clinical presentation of heart failure Pharmacotherapy of chronic heart failure with reduced ejection fraction (HFrEF) Pharmacotherapy of heart failure with preserved ejection fraction (HFpEF) Advanced heart failure and special topics Acute decompensated heart failure basics (covered in-depth Pharmacotherapy 5) Guideline Resources 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines 2023 ACC Expert Consensus Decision Pathway on Management of Heart Failure With Preserved Ejection Fraction: A Report of the American College of Cardiology Solution Set Oversight Committee 2024 ACC Expert Consensus Decision Pathway for Treatment of Heart Failure With Reduced Ejection Fraction: A Report of the American College of Cardiology Solution Set Oversight Committee 2024 ACC Expert Consensus Decision Pathway on Clinical Assessment, Management, Trajectory of Patients Hospitalized with Heart Failure Focused Update 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR Guideline for the Management of Hypertrophic Cardiomyopathy: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines Objectives Define heart failure and distinguish between heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF) Explain the pathophysiological mechanisms leading to heart failure and how these differ between systolic and diastolic dysfunction Describe effects of guideline-directed medical therapy (GDMT) on components of the neurohormonal model Apply signs and symptoms, labs, diagnostic criteria, and staging criteria in patients with HFrEF Identify medications that can exacerbate heart failure Identify appropriate pharmacotherapeutic interventions for a patient with HFrEF, HFmrEF, and HFpEF based on current treatment guideline recommendations Introduction to Heart Failure What is heart failure (HF)? HF is a clinical syndrome with symptoms and/or signs caused by a structural and/or functional cardiac abnormality and corroborated by elevated natriuretic peptide levels and/or objective evidence of pulmonary or systemic congestion Those "at-risk" for heart failure (Stage A and B) are individuals who are asymptomatic with or without structural heart disease or cardiomyopathies; they are not included in the formal definition of heart failure provided above Heart failure is the final common pathway for numerous cardiac disorders including those affecting the pericardium, heart valves, and myocardium https://watchlearnlive.heart.org/index.php?moduleSelect=hrtflr Heart Failure Prevalence Approximately 6.7 million Americans over 20 years of age have HF, and the prevalence is expected to rise to 8.5 million Americans by 2030 Improved survival for comorbidities such as coronary artery disease and hypertension and use of device therapy has likely contributed to the increased incidence and prevalence J Card Fail. 2023; 29 P1412-1451 Heart Failure Lifetime Risk The lifetime risk of HF has increased to 24%, approximately 1 in 4 persons will develop HF in their lifetime J Card Fail. 2023; 29 P1412-1451  HF mortality rates have been increasing since 2012 HF Mortality HF is associated with a loss of 15 years of median survival for adults aged 65–90 years of age compared with the general US population Age-adjusted HF mortality rates are highest for non-Hispanic Black individuals Black, American Indian, and Alaska Native individuals with HF have the highest all-cause age-adjusted mortality compared with other racial and ethnic groups From 2010 to 2020, HF mortality rates have increased for Black women and men at a rate faster than any other racial or ethnic group, particularly for individuals below the age of 65 Age-adjusted mortality rates (AAMRs) for HF have increased in the last decade with similar patterns of increase in women and men A greater relative annual increase in HF-related mortality rates has been noted for younger (35–64 years) compared with older (65–84 years) adults Rural areas demonstrate higher HF mortality rates for both younger and older age groups compared with urban areas  Prognosis remains poor with a 5-year mortality rate of 50% or higher left natriuretic sympto ventricul renal peptide extent of m age ar diabetes function concentratio CAD severity ejection ns fraction Prognosis Sudden cardiac death occurs in about 40% of patients Normal Heart Function Heart Valves HTTPS://WWW.HEARTFOUNDATION.ORG.NZ /YOUR-HEART/HEART-CONDITIONS/HEART- VALVE-DISEASE  “Understanding the anatomy and normal blood flow of the heart will help make both the symptoms of HF and drug therapy make sense.” Kim Jones 15 Types of Chronic Heart Failure Right-ventricle Left-ventricle Reduced cardiac heart failure heart failure output relative to the (RHF) needs of the body Right-ventricle Systolic heart failure dysfunction Reduced cardiac Most common “pumping problem” contractile force cause of RHF is LHF Diastolic Stiffening or other changes in dysfunction the ventricles that prevent "relaxation adequate filling during problem" diastole  Left-ventricle Type of HF According to LVEF Criteria Heart Failure HFrEF (HF with reduced EF) LVEF ≤40% HFimpEF (HF with improved EF) Previous LVEF ≤40% and a follow-up measurement of LVEF >40% HFmrEF (HF with mildly reduced LVEF 41%–49% EF) Evidence of spontaneous or The LVEF is used to classify patients with provokable increased LV filling HF as it identifies specific groups in which pressures (eg, elevated natriuretic guideline-directed medical therapy peptide, noninvasive and invasive (GDMT) improves key clinical outcomes hemodynamic measurement) such as mortality, hospitalization, and symptoms. HFpEF (HF with preserved EF) LVEF ≥50% Evidence of spontaneous or provokable increased LV filling pressures (eg, elevated natriuretic peptide, noninvasive and invasive hemodynamic measurement)  Ejection fraction can be obtained through (least to most accurate): Left Nuclear stress test Cardiac catheterization Ventricular Echocardiogram (ECHO) – most Ejection common Fraction MUGA Scan (Multigated Acquisition Scan) (LVEF) Cardiac MRI Echocardiography Transthoracic The most common A noninvasive test Transesophageal echocardiogram tool to assess involving emission of (TTE): the probe is placed echocardiogram structure and function ultrasound waves, on several locations on the (TEE): the probe is of the heart which travel through chest and upper abdomen advanced through the mouth and into the patient’s tissue and are TTE is imaging modality of esophagus where the reflected back to a ultrasound waves are choice for the assessment transducer probe, transmitted through the of valvular heart disease, posterior aspect of the heart where they are left and right ventricular processed to function, and pericardial TEE commonly used to construct images of effusions evaluate for the presence the heart and related Cornerstone in the of aortic dissections, left structures evaluation of heart atrial appendage 2D and 3D images are failure – LVEF is critical in thrombus prior to therapeutic decision cardioversion, and valvular available making vegetations for suspected endocarditis Two-dimensional apical four-chamber view of the heart. The probe is placed at the left ventricular apex, usually in the fifth intercostal space at the mid- clavicular line. (LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.) Citation: Chapter e29 Evaluation of Cardiovascular Function, DiPiro JT, Yee GC, Haines ST, Nolin TD, Ellingrod VL, Posey L. DiPiro’s Pharmacotherapy: A Pathophysiologic Approach, 12th Edition; 2023. Available at: https://accesspharmacy.mhmedical.com/content.aspx?bookid=3097&sectionid=267225187 Accessed: August 22, 2024 Copyright © 2024 McGraw-Hill Education. All rights reserved ECHO Evaluation *There is limited evidence to guide treatment for patients who improve their LVEF from mildly reduced (41%-49%) to ≥50%. It is unclear whether to treat these patients as HFpEF or HFmrEF. Natriuretic Peptides B-type natriuretic peptide (brain natriuretic peptide; BNP) and its biologically inactive precursor N-terminal pro-BNP (NT-proBNP) are released from ventricular myocytes in response to stretch-related injury Most commonly due to volume overload The natriuretic peptide system serves as a counter-regulatory response to the renin-angiotensin-aldosterone system Natriuretic peptide concentrations can be helpful tools in the diagnosis and evaluation of patients with chronic and acute decompensated heart failure Support diagnosis of HF or exclude HF in the differential diagnosis of patients presenting with dyspnea  BNP and NT-proBNP have different thresholds Factors that influence concentrations: Age (higher with age) Natriuretic Gender (higher in females) Peptides Body weight (lower in overweight or obese patients) Renal function (NT-proBNP undergoes renal elimination) Use of neprilysin inhibitors (increase BNP but not NT- proBNP) HF prognosis and increased long-term morbidity and mortality Can be elevated in other conditions ACS, asymptomatic left ventricular dysfunction, atrial fibrillation, PE, sepsis  Stages Definition and Criteria Stage A: At Risk for HF At risk for HF but without symptoms, structural heart disease, or Stages of Heart Failure cardiac biomarkers of stretch or injury (eg, patients with hypertension, atherosclerotic CVD, diabetes, metabolic syndrome and obesity, exposure to cardiotoxic agents, genetic variant for cardiomyopathy, or positive family history of cardiomyopathy). Stage B: Pre-HF No symptoms or signs of HF and evidence of 1 of the following: ACC/AHA stages of HF emphasize the Structural heart disease: Reduced left or right ventricular systolic function development and progression of disease, Reduced ejection fraction, reduced strain Ventricular hypertrophy and advanced stages and progression are Chamber enlargement associated with reduced survival rates Wall motion abnormalities Valvular heart disease Therapeutic interventions in each stage Evidence for increased filling pressures: By invasive hemodynamic measurements aim to: By noninvasive imaging suggesting elevated filling pressures Modify risk factors (stage A) Patients with risk factors and Treat risk and structural heart disease to Increased levels of BNPs or Persistently elevated cardiac troponin in the absence of prevent HF (stage B) competing diagnoses resulting in such biomarker elevations such as acute coronary syndrome, CKD, pulmonary embolus, Reduce symptoms, morbidity and or myopericarditis Stage C: Symptomatic Structural heart disease with current or previous symptoms of HF mortality (stages C and D) HF Stage D: Advanced HF Marked HF symptoms that interfere with daily life and with recurrent hospitalizations despite attempts to optimize GDMT. BNP indicates B-type natriuretic peptide; CKD, chronic kidney disease; CVD, cardiovascular disease; GDMT, guideline-directed medical therapy; and HF, heart failure. HFmrEF, HFrEF, HFpEF HFimpEF Risk Factors for HF Risk factors for HF (Stage A HF) Hypertension – major cause and/or contributor to HFrEF and HFpEF Diabetes ASCVD Obesity Exposure to cardiotoxic agents Genetic variant for cardiomyopathy Hypertrophic cardiomyopathy (HCoM) Amyloid cardiomyopathy Family history of cardiomyopathy Causes of HF H E A R T FA I L U R E W I T H R E D U C E D H E A R T FA I L U R E W I T H P R E S E R V E D EJECTI ON FRACTI ON ( HFREF) EJ ECTI ON FRACTI ON ( HF PEF ) #1 Coronary artery disease (eg, Increased ventricular stiffness myocardial infarction or ischemia) Ventricular hypertrophy (eg, hypertrophic cardiomyopathy, hypertension) Dilated cardiomyopathies (eg, drug- Infiltrative myocardial diseases (eg, induced, viral infections, postpartum) amyloidosis, sarcoidosis, endomyocardial Pressure overload (eg, systemic or fibrosis) pulmonary hypertension, or aortic valve or Myocardial infarction or ischemia pulmonic valve stenosis) Mitral or tricuspid valve stenosis Volume overload (eg, valvular Pericardial disease (eg, pericarditis, regurgitation, shunts, high-output states) pericardial tamponade) Medication- Negative Cardiotoxic induced HF inotropes Chemotherapy Antiarrhythmics, agents (doxorubicin, beta-blockers, non- epirubicin, dihydropyridine daunomycin, calcium channel trastuzumab) blockers, itraconazole Ethanol Amphetamines Sodium and Unknown MOA water retention TNF alpha NSAIDS, TZDs antagonists (pioglitazone), (etanercept, glucocorticoids infliximab, adalimumab) Dronedarone Saxagliptin, alogliptin Heart Valve Disease https://www.heartfoundation.org.nz/your-heart/heart- conditions/heart-valve-disease https://www.heart-valve-surgery.com/heart-surgery-blog/2008/08/29/is-mitral-valve-prolapse-fatal/ Clinical Presentation  Classic Clinical Presentation Primary manifestations of both HFrEF and HFpEF Shortness of breath (dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea) Fatigue Fluid overload Pulmonary edema – crackles/rales on auscultation of lung bases Lower extremity edema Intolerance of daily-life activities Symptom severity LV dysfunction Signs and Symptoms of Heart Failure R I G H T- S I D E D V E N T R I C U L A R F A I L U R E ( R E S T L E F T- S I D E D V E N T R I C U L A R F A I L U R E OF THE BODY): REMEMBER “SWELLING” (LUNGS): REMEMBER “DROWNING” Swelling of legs/hands/liver Dyspnea Weight gain Rales Edema (pitting) Orthopnea Large neck veins (jugular venous Weakness distention - JVD) Nocturnal dyspnea Lethargy Increased heart rate Irregular heart rate Nagging cough Nocturia Gaining weight Girth (increased abdominal size/ascites) New York Heart NYHA Class I Association No limitation during ordinary activity Functional Class NYHA Class II New York Heart Association Class refers Slight limitation by SOB and/or fatigue during to a classification system that categorizes moderate exertion/stress heart failure patients into four classes based on the severity of their symptoms NYHA Class III at rest and with activity, with higher Symptoms with minimal exertion that interfere numbers indicating greater severity. with normal daily activity This system helps physicians in predicting outcomes and monitoring treatment effectiveness in heart failure patients. NYHA Class IV Symptoms at rest  Right-sided heart failure As the right ventricle weakens, it can no longer This causes blood to back up into the systemic veins, resulting in signs of right-sided heart failure, such as pump blood efficiently into the pulmonary peripheral edema, jugular venous distension, circulation hepatomegaly, and ascites Left-sided heart failure This results in increased pressure in the The left ventricle fails to pump blood effectively, pulmonary circulation, leading to fluid causing blood to back up into the left atrium accumulation as well as pulmonary and then into the pulmonary veins hypertension Biventricular heart failure: Left-sided heart failure often leads to increased pulmonary pressures, which place a burden on the right side of the heart, eventually causing it to fail. Thus, patients with advanced left-sided heart failure frequently exhibit signs of right-sided heart failure as well