Download Free Medical Advanced Therapies in Chronic Heart Failure PowerPoint Presentation

Advanced Therapies in Chronic Heart Failure PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Congestive Heart Failure, which is titled "Advanced Therapies in Chronic Heart Failure", to know about various pharmacologic agents used to manage heart failure (HF), advanced HF, warning signs of advanced HF, inotropes used in chronic HF, indication and contraindication for transplant, and the mechanical circulatory support in the management of chronic HF.

Tags : Congestive Heart Failure, Advanced Therapies, Chronic Heart Failure

Published on : Jul 01, 2021 | Views : 2306 | Downloads : 6

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Advanced Therapies in Chronic Heart Failure By Susan George, DNP, APRN- CNP, CCNS, CCRN, CHFN
Slide 2-

Objectives Briefly review various pharmacologic agents used to manage heart failure (HF) Define advanced HF Identify warning signs of advanced HF Discuss inotropes used in chronic HF Review indication and contraindication for transplant. Describe mechanical circulatory support in the management of chronic HF
Slide 3-

Oklahoma
Slide 4-

Heart Failure More deaths from HF than all forms of cancer combined 10% within 1st year & 50% within 5yrs 300,000 to 800,000 advance HF patients in US 60,000 patients are younger than 65yrs old High morbidity, mortality, and poor quality of life
Slide 5-

Cost In 2012 the estimated was $30.7 billion. $21 billion direct and $10 billion indirect cost Hospitalization accounts for 80% of the direct cost Heidenreich et al. (2013)
Slide 6-

Definition of Systolic HF It is a complex clinical syndrome that can result from any structural or functional cardiac disorders that impairs ability of the left ventricle to ejects blood.
Slide 7-

Classification of Heart Failure Functional classification: NYHA class (I-IV) - Based on clinical signs Staging of HF: ACC/AHA stages (A,B,C,D)
Slide 8-

Management of HF HF tool box Life style modification Medications Electrical Therapy Advanced HF therapy (Transplant/ MCS)
Slide 9-

Goals of HF Management Primary prevention Control of day to day symptoms -Volume management -Congestive symptoms Prevent disease progression -Decrease hospitalization -Decrease mortality -Prevent ventricular remodeling, vascular remodeling, and activation of neurohormones (norepinephrine, angiotensin II, and aldosterone)
Slide 10-

Pharmacotherapy for Heart Failure Diuretics Neurohormonal antagonists (ACEI, ARB, MRA, ARNI) Digoxin Ivabradine Inotropics: (Phosphodiesterase Inhibitors- Milrinone and dobutamine) Vasodilators (Hydralazine, Nitroglycerine & Nesiritide) Yancy et al. 2013 ACC/AHA Guideline for Management of Heart Failure
Slide 11-

Volume Management c Thiazides K Sparing Loop Diuretics Loop of Henle Medulla Cortex Diuretics
Slide 12-

Neurohormonal Antagonist Neurohormonal antagonists (ACEI, ARB, MRA, ARNI) Change the natural history HF disease process by blocking activation of RAAS and SNS. Arrest, prevent, and may even reverse the process of progressive ventricular remodeling. Decrease morbidity and mortality associated with HF
Slide 13-

ACEI/ARB Vasoconstriction Oxidative Stress  Free Radicals Cell Growth Proteinuria LV remodeling Vascular remodeling Angiotensinogen Angiotensin I Angiotensin II AT I receptor Renin Angiotensin Converting Enzyme ACE Inhibitors “prils” (-) Angiotensin Receptor Blockers “Sartans” (-)
Slide 14-

Angiotensin receptor neprilysin inhibitor (ARNI)
Slide 15-

ARNI Entresto (Combintion of Sacubitril and Valsartan) Sacubitril: Prodrug that inhibits neprilysin leading to increased levels of natriuretic peptides Valsartan: Angiotensin II receptor blocker Side Effects Angioedema, hypotension, impaired renal function, and hyperkalemia. Should not be administered concomitantly with ACE inhibitors or within 36 hours of the last dose of an ACEI. 2016 ACC/AHA Update on New Pharmacological therapy for Heart Failure
Slide 16-

Beta-blockers Sympathetic Activation in Heart Failure Packer. Progr Cardiovasc Dis. 1998;39(suppl I):39-52.  CNS sympathetic outflow 1- receptors  Cardiac sympathetic activity  Sympathetic activity to kidneys + peripheral vasculature 2- receptors 1- receptors Activation of RAS Vasoconstriction Sodium retention Myocardial toxicity Increased arrhythmias Disease progression 1- b1-
Slide 17-

Mineralocorticoid Receptor Antagonist (MRA) Effects of RAAS activation is also mediated through aldosterone. Increase in aldosterone level persist in the circulation even in the presence of angiotensin II inhibition. It is associated with increased myocardial fibrosis, inflammation, myocyte hypertrophy, and apoptosis. MRAs inhibit aldosterone
Slide 18-

Ivabradine (Corlanor) Hyperpolarization-activated cyclic nucleotide-gated (HCN) channel blocker. Reduces diastolic depolarization slope in the SA node, thereby decreasing heart rate via direct sinus node inhibition without direct effects on myocardial contractility and intracardiac conduction Indicated to reduce the risk of HF hospitalization in patients with stable, symptomatic chronic HF with LVEF ≤35%, who are in sinus rhythm with resting heart rate ≥70 bpm and either are on maximally tolerated doses of beta-blockers or have a contraindication to beta-blocker use 2016 ACC/AHA Update on New Pharmacological therapy for Heart Failure
Slide 19-

Hydralazine and Isordil The combination of hydralazine and isosorbide dinitrate is recommended to reduce morbidity and mortality for African Americans patients with LVEF <40%, NYHA class III–IV symptoms receiving optimal therapy with ACE inhibitors and beta blockers. Indicated for patients with LVEF <40% who can not tolerate ACEI/ARB secondary to renal insufficiency/impairment.
Slide 20-

Benefits of Medical Therapy Demonstrated in RCTs 2013 ACC/AHA Guideline for Management of Heart Failure
Slide 21-

Digoxin No mortality benefit Decrease hospitalization Increase exercise tolerance May help for rate control in patients with Afib
Slide 22-

Drugs to Avoid in HF Nonsteroidal anti-inflammatory drugs (NSAIDs) Thiazolidinediones Calcium channel blockers – nondihydropyridine Dietary supplements Mann & Felker, 2016
Slide 23-

ACC/AHA HF Management Algorithm Yancy et al. 2013 ACC/AHA Guideline for Management of Heart Failure
Slide 24-

Advanced/End Stage HF Inability to tolerate HF medication or reduction of dose Recurrent hospitalization Severe exercise intolerance Heart failure wasting syndrome Cardiorenal syndrome Right heart failure Inotrope dependence
Slide 25-

Definition of Advanced Heart Failure GDMT: Guideline Directed Medical Therapy CRT: Cardiac Resynchronization Therapy
Slide 26-

Prognostic Models in HF Ambulatory Allen et al. Circulation. (2012). 125(15). 1928-1952
Slide 27-

Seattle Heart Failure Model
Slide 28-

VO2 Max Exercise testing has been used for prognostic purposes and exercise capacity has been demonstrated to be an important component to the risk profile in chronic heart failure. VO2 max refers to the maximum amount of oxygen that an individual can utilize during intense or maximal exercise. It is shown to be a strong predictor of hospitalization and death and a predictor of survival in patients with more advanced HF considered for advanced HF therapy.
Slide 29-

HF Progression
Slide 30-

Transition to Advanced HF Allen et al. Circulation. (2012). 125(15). 1928-1952
Slide 31-

Advanced Heart Failure Limited treatment option - Heart transplantation - Mechanical circulatory support (MCS) - Long-term inotropic therapy - Palliative care
Slide 32-

Inotropes Indicated in the presence of acute or chronic hemodynamic compromise with end organ dysfunction. Bridge to mechanical circulatory support (MCS) Bridge to transplant Palliative
Slide 33-

Inotropes in Advanced HF Milrinone and Dobutamine are currently the only two inotropes approved for use in the US. Both increase cardiac output by increasing the intracellular level of cyclic adenosine monophosphate (cAMP) Dobutamine increases cAMP indirectly through adrenergic agonism. Milrinone, a phosphodiesterase inhibitor, directly blocks cAMP breakdown
Slide 34-

Dobutamine Sympathomimetic amine, which acts on beta-1, beta-2, and alpha-1 adrenergic receptors. Strong inotropic effect and relatively weak chronotropic effect No significant change in BP due to its alpha-1 agonist activity causing vasoconstriction, that balances the beta-2 vasodilatory effect. The use is problematic in patients who take beta blockers due to its adrenergic properties
Slide 35-

Milrinone Milrinone inhibits phosphodiesterase 3 (PDE3), which prevents the degradation of cAMP and ultimately leads to an increase in protein kinase A (PKA). It is an inodilator, both increasing cardiac contractility and reducing afterload with a consequent reduction in left ventricular filling pressures. PKA increases contractility of the left ventricle and cardiac output through cAMP dependent-PKA
Slide 36-

Milrinone Less myocardial oxygen consumption with milrinone when compared to dobutamine. Can be used in patients on beta blockers, because its effects are not dependent on beta adrenoreceptors. Milrinone not only acts as a systemic but also a pulmonary vasodilator. It is the preferred agent in patients with pulmonary hypertension and HF.
Slide 37-

Similarities Most of the hemodynamic effects of dobutamine and milrinone are similar. Increase cardiac output Cause peripheral vasodilation Decrease pulmonary capillary wedge pressure
Slide 38-

Differences
Slide 39-

Mortality on Inotropic Support Rogers JG, Butler J, Lansman SL, et al. 2007;50(8):741-47
Slide 40-

Advanced HF therapies Cardiac Transplantation Mechanical Circulatory support
Slide 41-

Time to Transition: Red Flags Repeated (≥2) hospitalizations or ED visits for HF in the past year Progressive deterioration in renal function Weight loss without other cause (e.g. cardiac cachexia) Intolerance to ACE inhibitors due to hypotension and/or worsening renal function Intolerance to beta blockers due to worsening HF or hypotension Frequent systolic blood pressure < 90 mmHg Persistent dyspnea with dressing or bathing requiring rest Inability to walk 1 block on the level ground due to dyspnea or fatigue Recent need to escalate diuretics to maintain volume status, often reaching daily furosemide equivalent dose > 160 mg/d and/or use of supplemental metolazone therapy Progressive decline in serum sodium, usually to < 133 mEq/L Frequent ICD shocks Yancy et al. 2013 ACC/AHA Guideline for Management of Heart Failure
Slide 42-

Cardiac Transplantation Ideal treatment for advanced HF Provides increased longevity and symptomatic relief Approximately 3,000 people are on waiting list at any given time In 2015, there was only 2804 donors in US United Network for Organ Sharing [UNOS] (2017)
Slide 43-

Listing criteria for Heart transplantation Cardiopulmonary exercise testing: VO2 max <14ml/kg/min if patients intolerant to BB; <12ml/kg/min in the presence f BB; or <50% of predicted VO2 in young patients (50yrs) and women. Acceptable pulmonary artery pressure Age <70 Diabetes well controlled Absence on neoplasm Psychosocial support
Slide 44-

Contraindication Noncompliance with medical regimen Active substance abuse Severe symptomatic cerebrovascular disease Severe organ dysfunction (lung, kidney, liver, coagulopathy) Active infection Active mental illness Inadequate social support Fixed, severe pulmonary hypertension Morbid obesity (BMI > 35 kg/m2) Age > 70 years Recent or uncured malignancy
Slide 45-

Transplant Listing Each US transplant center is part of the nationwide United Network of Organ Sharing (UNOS), which is divided into eleven regions, each with specific local organ procurement organizations (OPO) Patients are listed by OPO, transplant center, and ABO blood type, and prioritized by medical urgency (UNOS Status). Medical urgency status: 1A, 1B, 2, 7
Slide 46-

Post Transplant Care Immunosuppression 1. Calcineurin Inhibitor (CNI) Tacrolimus (Prograf) Cyclosporine (CyA) 2. Antiproliferative Agent/Antimetabolite Sirolimus (Rapamycin) Mycophenolate mofetil (MMF); Cellcept Azathiaprine (AZA)(Imuran) Everolimus 3. Corticosteriods Prednisone Methylprednisolone (Solu-medrol) Prednisolone Prophylactic antimicrobials Agents to treat post-transplant complications and comorbidities
Slide 47-

Survival After Transplant Katz, N. J et al. 2015
Slide 48-

Mechanical Circulatory Support MCS with left ventricular assist device (LVAD) is a treatment option. - Bridge to transplant (BTT) - Destination therapy (DT) - Bridge to decision (BTD) - Bridge to recovery Improves Survival and QOL It is a rapidly evolving field
Slide 49-

Indication NYHA IV functional class Life expectancy <2 years Failure to respond to optimal medical management LVEF ≤25% Refractory cardiogenic shock or cardiac failure VO2 ≤14 mL/kg/min Need for IV inotropes therapy Recurrent symptomatic sustained VT or VF in the presence of an untreatable arrhythmogenic substrate
Slide 50-

Exclusion Criteria Active systemic infection Uncorrectable aortic insufficiency Renal insufficiency that may require dialysis in the near future History of cardiac transplant Any condition, other than heart failure, which is expected to limit survival to less than 2 years
Slide 51-

INTERMACS Profiles of Advanced Heart Failure Profile 1: Critical cardiogenic shock Profile 2: Progressive decline- sliding on inotrope Profile 3: Stable but inotrope dependent Profile 4: Resting symptoms Profile 5: Exertion Intolerant Profile 6: Exertion Limited Profile 7: Advanced NYHA Class 3
Slide 52-

Types of MCS Left ventricular assist device (LVAD) Biventricular support (BiVAD) Total artificial heart (TAH)
Slide 53-

Types of LVADs First generation pumps - Pulsatile pumps Second generation pumps - Continuous axial flow pumps Third generation pumps - Magnetically levitated pump rotor
Slide 54-

Commonly Used Durable LVADs HeartMate II Axial Flow LVAD Ruby Bearing HVAD Centrifugal LVAD Magnetic Drive Hemodynamic Bearing HeartMate 3 Centrifugal LVAD Magnetic Levitation No Bearing
Slide 55-

Comparison of Devices
Slide 56-

Improved Survival with MCS Miller L W et al. Circulation. 2013;127:743-748
Slide 57-

LVAD Survival Survival significantly greater (up to 7 times) than that reported with medical therapy for inotrope dependent heart failure based on multiple trials Landmark trial: REMATCH (Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure) trial. Jorde, S.S., et al. 2013
Slide 58-

LVAD Survival
Slide 59-

HM 3 LVAD Trial Multicenter Study of MagLev Technology in Patients Undergoing Mechanical Circulatory Support Therapy with HeartMate 3 (MOMENTUM 3) ongoing trial. Mehra, M.R. et al. 2017
Slide 60-

Improved Outcomes Improvements in patient selection Improvements in technology Improvements in patient management
Slide 61-

Anti-Coagulation Guidelines Medications Aspirin – prevents platelet aggregation Persantine – prevents platelet aggregation Plavix/Effient- occasionally used for platelet aggregation Coumadin- required, goal INR depends on patients underlying comorbidities HeartMate II: Aspirin + Persantine or Plavix/Effient + Coumadin HeartMate 3: Aspirin + Coumadin
Slide 62-

Complication with LVAD Infections Bleeding Hemolysis Thrombosis Stroke Aortic insufficiency
Slide 63-

Key Success Patient selection Patient management Multidisciplinary approach Psychosocial support
Slide 64-

Total artificial heart (TAH)
Slide 65-

Biventricular support (BiVAD) Paracorporeal VAD (P-VAD)
Slide 66-

Summary Advanced heart failure patients has limited treatment options. Timely referral of end stage HF patients to advanced HF center is essential for success. Heart transplantation is the ideal therapy for refractory end stage HF. However organ shortage limits the therapy. RCTs have demonstrated benefits LVADs in reducing mortality and improving QOL.